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Course Code: NCM 106 CARE OF CLIENTS ACROSS THE LIFESSPAN WITH PROBLEMS IN INFLAMMATORY AND IMMUNOLOGIC REACTIONS,

CELLULAR ABERRATIONS, ACUTE BIOLOGIC CRISIS, INCLUDING EMERGENCY AND DISASTER NURSING General Objective Demonstrate comprehensive safe and effective nursing care utilizing the concepts of acute biologic crisis Risk Assessment and Screening Procedures Focus: Standard assessment of the critically ill patients

  

focused history-taking discriminating PE - airway, breathing circulation hemodynamics status

Focus: -results and implications of diagnostic/laboratory examinations

  

Acute biologic crisis/multiorgan problem Non-invasive: ECG, cardiac rhythms, Invasive: ABG, hemodynamic monitoring, CVP, pulmonary capillary wedge pressure (PCWP)

Focus: Concurrent Diseases in Pregnancy A. Cardiac Diseases

   

Right Sided Heart Failure Left Sided Heart Failure Myocardial infarction Cardiac Arrhythmias

B. Hemolytic Disorders

 

RH Incompatibility ABO Incompatibility

C. Metabolic Disorder

 

DKA Thyroid Crisis

Hepatic Coma

D. Renal Disorder

Chronic Renal Failure

E. Toxemias of Pregnancy

 

Pre-eclampsia Eclampsia

E. Infectious Diseases

TORCH

F. Emergency Delivery

Standard Assessment of Critically ill Patients

Definition and Scope of the Problem High-risk pregnancy

      

High-risk pregnancy: life or health of mother or fetus is jeopardized For mother, high risk status arbitrarily extends through puerperium (30 days after childbirth) Maternal complications usually resolved within 1 month of birth Perinatal morbidity may continue for months or years High risk diagnosis imposes crisis on family Loss of pregnancy before anticipated date Development of gestational diabetes mellitus with its potential complications

Neonate who does not meet cultural, societal, or familial norms and expectations Definition and Scope of the Problem Maternal health problems

Leading causes of maternal mortality

Pregnancy-induced hypertension Pulmonary embolism Hemorrhage

Factors related to maternal death include: Lack of prenatal care Low educational attainment Unmarried status Nonwhite race

Definition and Scope of the Problem Assessment begins w/ the first prenatal visit & continuous through puerperium FACTORS: Maternal age : < 18 y/o or nullipara >30y/o Maternal height: 60 inches/ 153 cm or less Weight: Obesity (>20% of standard weight) Assessment of risk factors

Biophysical risks Genetic disorders, nutritional and general health status, and medical or obstetric-related illnesses

Sociodemographic risks arise from mother and family Lack of prenatal care, low income, marital status, and ethnicity

Environmental factors include: Hazards in workplace and environment, including noxious chemicals, radiation, infections, and pollutants

Psychosocial risks Maternal behaviors and adverse lifestyles that have negative effect on health of mother or fetus Nursing Role in Antepartal Assessment for Risk

Psychologic considerations Women undergoing antepartal assessments are anxious

Tests due to suspected fetal compromise, deterioration of maternal condition, or both

Psychologic considerations Third trimester women concerned about protecting themselves and fetuses and consider themselves vulnerable Label of high risk increases sense of vulnerability Psychologic Implications of High Risk Pregnancy

 

When woman is diagnosed with high-risk pregnancy, she and her family will likely experience stress related to the diagnosis The woman may exhibit various psychologic responses, including: Anxiety Low self-esteem and guilt Frustration Inability to function

Antepartum Testing Biophysical Assessment

Magnetic resonance imaging Examiner evaluates: Fetal structure Placenta (position, density, and presence of gestational trophoblastic disease) Quantity of amniotic fluid Maternal structures (uterus, cervix, adnexa, and pelvis) Biochemical status of tissues and organs Soft tissue, metabolic, or functional anomalies Biochemical Assessment

Amniocentesis Maternal Hemorrhage Fetomaternal hemorrhage Infection Labor Abruptio placenta Damage to intestines or bladder Amniotic fluid embolism

AMNIOCENTESIS

refers to aspiration of a sample of amniotic fluid for examination of fetal cells

Percutaneous umbilical blood sampling (PUBS) or cordocentesis Direct access to fetal circulation Insertion of needle directly into a fetal umbilical vessel under ultrasound guidance

Maternal assays Alpha-fetoprotein (AFP) Maternal serum levels screened for neural tube defects (NTDs) 80% to 85% of open NTDs and abdominal wall defects can be detected early Recommended for all pregnant women Coombs test Rh incompatibility Detects other antibodies for incompatibility with maternal antigens INDIRECT COOMBS TEST used for search for agglutination of Rh positive RBCs to determine whether antibodies are present in maternal blood

Laboratory Studies & Diagnostic tests

      

COMPLETE BLOOD COUNT provides info on #, type & health of RBC. PREGNANCY TEST (Hcg) SERUM ALPHA-FETOPROTEIN ULTRASOUND (UTZ) refers to the use of high frequency- sound waves passed through the maternal abdomen. BLOOD GLUCOSE & GLYCOSYLATED HEMOGLOBIN SEROLOGIC TESTS to determine presence & type of STD. CULTURES to determine type of infectious agent.

Cardiovascular System 1. The cardiovascular system consists of the heart, and vessels, arteries, capillaries and veins.

1.

A functional cardiovascular system is vital for supplying oxygen and nutrients to wastes from them.

tissues and removing

Structure of the Heart The heart is a hollow, cone-shaped, muscular pump within the thoracic cavity.

Structure of the Heart Size and Location of the Heart 1. The average adult heart is 14 cm long and 9 cm wide. 2. The heart lies in the mediastinum under the sternum; its apex extends to the fifth intercostal space. Coverings of the Heart 1. 2. The pericardium encloses the heart. It is made of two layers: the outer, tough connective tissue fibrous pericardium surrounding a more delicate visceral pericardium (epicardium) that surrounds the heart.

Wall of the Heart

1. 2. 3. 4.

The wall of the heart is composed of three distinct layers. The outermost layer, the epicardium, is made up of connective tissue and epithelium, and houses blood and lymph capillaries along with coronary arteries. It is the same as the visceral pericardium. The middle layer called myocardium consists of cardiac muscle and is the thickest layer of the heart wall. The inner endocardium is smooth and is made up of connective tissue and epithelium, and is continuous with the endothelium of major vessels joining the heart. a. The endocardium contains the Purkinje fibers. Heart Chambers and Valves 1. The heart has four internal chambers: two atria on top and two ventricles below. a. Atria receive blood returning to the heart and have thin walls and ear-like auricles projecting from their exterior. b. The thick-muscled ventricles pump blood to the body. A septum divides the atrium and ventricle on each side. Each also has an atrioventricular (A-V) valve to ensure one way flow of blood. a.The right A-V valve (tricuspid) and left A-V valve (bicuspid or mitral valve) have cusps to which chordae tendinae attach. b.Chordae tendinae are, in turn, attached to papillary muscles in the inner heart wall that contract during ventricular contraction to prevent the backflow of blood through the A-V valves.

2.

1.

The superior and inferior vena cavae bring de-oxygenated blood from the body to the right atrium.

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The right ventricle has a thinner wall than does the left ventricle because it must pump blood only as far as the lungs, compared to the left ventricle pumping to the entire body.

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At the base of the pulmonary trunk leading to the lungs is the pulmonary valve, which prevents a return flow of blood to the ventricle.

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The left atrium receives blood from four pulmonary veins.

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The left ventricle pumps blood into the entire body through the aorta, guarded by the aortic valve that prevents backflow of blood into the ventricle.

Skeleton of the Heart

1. 2.

Rings of dense connective tissue surround the pulmonary trunk and aorta to provide attachments for the heart valves and fibers. These tough rings prevent dilating of tissue in this area.

Path of Blood through the Heart

1. 2. 3.

Blood low in oxygen returns to the right atrium via the venae cavae and coronary sinus. The right atrium contracts, forcing blood through the tricuspid valve into the right ventricle. The right ventricle contracts, closingthe tricuspid valve, and forcing blood through the pulmonary valve into the pulmonary trunk and arteries

1. 2. 3. 4.

The pulmonary arteries carry blood to the lungs where it can rid itself of excess carbon dioxide and pick up a new supply of oxygen. Freshly oxygenated blood is returned to the left atrium of the heart through the pulmonary veins. The left atrium contracts, forcing blood through the left bicuspid valve into the left ventricle. The left ventricle contracts, closing the bicuspid valve and forcing open the aortic valve as blood enters the aorta for distribution to the body.

Simplified Path of Blood Flow Blood Supply to the Heart

1. 2. 3.

The first branches off of the aorta, which carry freshly oxygenated blood, are the right and left coronary arteries that feed the heart muscle itself. Branches of the coronary arteries feed many capillaries of the myocardium. The heart muscle requires a continuous supply of freshly oxygenated blood, so smaller branches of arteries often have anastomoses as alternate pathways for blood, should one pathway become blocked.

1.

Cardiac veins drain blood from the heart muscle and carry it to the atrium.

coronary sinus, which empties into

the right

Heart Actions

The cardiac cycle consists of the atria beating in unison (atrial systole) followed by the contraction of both ventricles, (ventricular systole) then the entire heart relaxes for a brief moment (diastole).

Cardiac Cycle

1. 2. 3.

During the cardiac cycle, pressure within the heart chambers rises and falls with the contraction and relaxation of atria and ventricles When the atria fill, pressure in the atria is greater than that of the ventricles, which forces the A-V valves open. Pressure inside atria rises further as they contract, forcing the remaining blood into the ventricles.

Heart Sounds

1. 2. 3. 4.

Heart sounds are due to vibrations in heart tissues as blood rapidly changes velocity within the heart. Heart sounds can be described as a "lubb-dupp" sound. The first sound (lubb) occurs as ventricles contract and A-V valves are closing. The second sound (dupp) occurs as ventricles relax and aortic and pulmonary valves are closing.

Cardiac Muscle Fibers

A mass of merging fibers that act as a unit is called a functional syncytium; one exists in the atria (atrial syncytium) and one in the ventricles (ventricular syncytium).

Cardiac Conduction System 1. 2. 3. Specialized cardiac muscle tissue conducts impulses throughout the myocardium and comprises the cardiac conduction system. A self-exciting mass of specialized cardiac muscle called the sinoatrial node (S-A node or pacemaker), located on the posterior right atrium, generates the impulses for the heartbeat. Impulses spread next to the atrial syncytium, it contracts, and impulses travel to the junctional fibers leading to the atrioventricular node (A-V node) located in the septum.

1.

Junctional fibers are small, allowing the atria to contract before the impulse spreads rapidly over the ventricles.

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Branches of the A-V bundle give rise to Purkinje fibers leading to papillary muscles; these fibers stimulate contraction of the papillary muscles at the same time the ventricles contract.

Cardiac Diseases Cardiac Disease Affects a small percentage of pregnant women Rheumatic Heart Disease : most common in the past. Congenital disease : most common cardiac problem encountered in pregnancy now Incidence Successful txt of congenital anomalies or mitral stenosis from RHD allows girls to reach childbearing age & bear children. What affects childbearing women is that they already have the disease like hypertension w/c could lead to disorders of the heart & its structures Cardiovascular Disorders Incidence of congenital heart lesions increased in children of mothers with congenital heart disease Preconception counseling crucial Major cardiovascular changes during pregnancy that affect women with cardiac disease are:

   

Increased intravascular volume Decreased systemic vascular resistance Cardiac output changes during labor and birth Intravascular volume changes that occur just after childbirth Normal heart compensates for increased workload

Diseased heart is hemodynamically challenged Degree of disability often more important in treatment and prognosis Miscarriages increase Preterm labor and birth more prevalent Maternal mortality rate of more than 50% during pregnancy associated with pulmonary hypertension Woman with cardiac disease must be assessed and diagnosed as soon as possible

Cardiovascular Disorders Peripartum cardiomyopathy (PPCM) Rheumatic heart disease (RHD) Mitral valve stenosis Mitral valve prolapse (MVP) Infective endocarditis Eisenmenger s syndrome Atrial septal defect (ASD) Tetralogy of Fallot Marfan syndrome CV Physiology of Pregnancy v v v v v Blood volume increases 30 to 50% Plasma volume increase more than RBC mass leading to physiologic anemia An estrogen mediated stimulation of the renin-angiotensin system results in retention of NA and water HR increases 10 to 20 bpm CV Physiology of Pregnancy CO increase up to 45% by 24 wks These increases begin during the 1st trimester Peak by 20-24 wks and are sustained until term In early pregnancy an increase in SV (20-30%) is responsible to the increase in CO Later in pregnancy, the increase in HR is responsible since SV decreased due to IVC compression Concurrently there is a substantial reduction in SVR by 21% with decreases in BP and decreases in PVR by 34%

CV Physiology of Pregnancy Symptoms and PE of normal pregnancy mimic cardiac disease Exertional dyspnea and orthopnea Fatigue and Presyncope Lower extremity edema a and v waves may be pronounced in CVP tracing Maximal apical impulse is displaced 1st Heart sound the pulmonary component of 2nd might are accentuated 3rd HS is heard in 80% of pregnant women Murmurs frequently develop during pregnancy Soft, mid-systolic, and heard along the left sternal border is heard in 90% women Anemia might accentuate it Intensity may increase as CO increases

Cervical venous hums and a continuous murmur due to increased mammary blood flow may also be heard Echocardiography is warranted if: Diastolic, continuous, or loud systolic murmurs (>2/6) A fixed split 2nd sound Associated with symptoms or an abnormal EKG In normal pregnant women, echocardiography demonstrates: Minor increases in the left and right ventricular diastolic dimensions (within the normal range) During labor: CO increases 45% above pre-labor values Uterine contraction boluses the patient It might increase CO up to 65% of pre-labor values The BP increases with uterine contractions/pain Immediately after delivery The cardiac filling pressure increase dramatically due to the decompression of the vena cava and the return of uterine blood into the systemic circulation CO might increase to 80% of pre-labor values The cardiovascular adaptations associated with pregnancy regress by approximately 6 weeks after delivery

Physiology of Pregnancy Pregnancy is also a hypercoagulable state Decreased in Protein activity Stasis Venous hypertension Effect of Pregnancy on the cardiovascular system Pregnancy Blood volume, cardiac output, HR,& stroke volume cardiac workload Normal heart with heart disease

Prenatal Period Assessment Findings Evidence of cardiac decompensation especially when blood volume peaks (weeks 28-32)

Signs of Cardiac Decompensation

Dyspnea Palpitations Pulse irregularity Chest pain Cough crackles @ base of the lungs Sweating,Orthopnea Weakness Progressive generalized edema Pallor

Intrapartal Period Labor increase risk of CHF milking effect of contractions & delivery es bld volume to heart. The New York Heart Association (NYHA) Grading of Functional capacity of the heart Classification Class Class Class Class 1: 2: 3: 4: No limitation of activity Slight limitation of activity Considerable limitation of activity Symptoms present even at rest

Classification Class I ( Uncompromised ) Physical activity is not limited by angina or symptoms of cardiac insufficiency Class II : Slightly Compromised Comfortable at rest but normal activity causes fatigue, palpitations, dyspnea, or angina.

Class III ( Markedly Compromised) Comfortable at rest but normal activity causes excessive fatigue, palpitation, Dyspnea or angina. Class IV ( Severely Compromised) Unable to perform any activity w/out discomfort May experience angina or signs of cardiac insufficiency while at rest Classification of risk The WHO classification What is the mortality associated with the various cardiac lesions ? Mortality associated with specific cardiac lesions What is the prognosis for a woman with a cardiac disease depending on the NYHA classification? What are the clinical features in a normal pregnancy which can mimic a cardiac disease ?

What are the criteria to diagnose cardiac disease during pregnancy ? Heart Failure Heart failure is a medical term that describes an inability of the heart to keep up its work load of pumping blood to the lungs and to the rest of the body.

Signs of low cardiac output Lethargy, dizziness, confusion, agitate Oliguria Weak pulse, tachycardia Narrow pulse pressure Cool, moist skin Sign of etiology or precipitating factor

Signs of high cardiac output Pulse full, bounding Wide pulse pressure Warm skin Prominent PMI Soft Systolic ejection murmur at LSB

Sign of etiology or precipitating factor Rheumatic Fever Strep throat from the streptococcal infection begins a disease process where the heart valves are damaged affects the connective tissues of the body. Cardiomyopathy stretching and enlarging of the heart cavity that occurs making the heart weak so it does not pump correctly Hypertrophic Cardiomyopathy Defects in their contractile proteins, make cells too weak They hypertrophy to do the same amount of work as normal cells Need more oxygen and perform less efficiently, so the person is prone to heart failure and may suffer sudden death during exertion Hypertrophic Cardiomyopathy Ventricular Failure occurs when there are weak spots in the ventricular walls causing a bulge, or an aneurysm. Atherosclerosis

gradual clogging of the arteries by fatty, fibrous deposits tiny lump of fibrous tissue grows as the artery tries to repair the damage. Cholesterol accumulates and more tissue builds up. PCI may be the best option ( > 2nd trimester ) Left Sided Heart Failure Left-Sided Valvular Disorders Mitral valve disorders Mitral valve stenosis Mitral valve regurgitation Mitral valve prolapse Aortic valve disorders Aortic valve stenosis Aortic valve regurgitation Cardiac Disease Left-sided heart failure Orthopnea Paroxysmal nocturnal dyspnea Left-Sided Heart Failure Blood accumulates in left ventricle Left ventricle thickens and enlarges: hypertrophy Blood backs up into lungs Cough and shortness of breath result LEFT-SIDED HEART FAILURE DYSPNEA DRY COUGH CRACKLES WHEEZES ORTHOPNEA HEMOPTYSIS Paroxysmal NOCTURNAL DYSPNEA CHEYNE-STOKES RESPIRATIONS FATIGUE WEAKNESS CYANOSIS NOCTURIA TACHYCARDIA Serious: life threatening Pulmonary Edema Mitral Stenosis

     

Rheumatic MS is the most common valvular abnormality in pregnant women (60%) Associated with pulmonary congestion, edema, and atrial arrhythmias during pregnancy or soon after delivery increased BV load and CO associated with pregnancy lead to an increase in left atrial volume and pressure, elevated pulmonary venous filling pressures, dyspnea, and decreased exercise tolerance Increases in the maternal HR decrease the diastolic filling period, further increasing left atrial pressure and decreasing CO increased atrial pressure may cause arrhythmias Predictors of adverse maternal outcomes Mitral valve area less than 1.5 cm2 Abnormal functional class before pregnancy

Fetal mortality increases with deteriorating maternal functional capacity 30 % when the mother has NYHA class IV

For women with mild or moderate symptoms Medical therapy is directed to the treatment of volume overload Diuretic therapy but avoiding hypotension and tachycardia Na+ restriction Reduction of physical activity

 

Beta-blockers decrease HR and prolong the diastolic filling period which provides symptomatic benefit Development of AF requires prompt treatment, including cardioversion. Beta-blockers and digoxin for rate control Procainamide and quinidine are frequently used if suppressive antiarrhythmic therapy is needed Due to the increased risk of systemic embolism in patients with MS and AF anticoagulant therapy is indicated

 

NYHA class III / IV or a valve area of less than 1.0 cm2 Percutaneous balloon mitral valvuloplasty (PBMV) or valve surgery BEFORE conceiving appear to allow pregnancy with fewer complications than women treated medically Percutaneous aortic balloon valvuloplasty

PBMV, during the 2nd trimester, has been associated with normal deliveries and excellent fetal outcomes Fetal risks associated with exposure to radiation may be reduced by avoiding exposure during the first half of pregnancy

The uterus must be shielded and the patient should be informed about the possible risks

Mitral valvuloplasty has also been performed under TEE guidance

 

Percutaneous mitral balloon valvotomy prior to conception or during pregnancy Open cardiac surgery has been performed during pregnancy for severe MS Maternal outcomes are similar to the non-pregnant Fetal loss in 10 to 30 % of cases MS: Anesthesia management Careful clinical evaluation early on in conjunction with the OB team to have a clear plan ICU consultation Vaginal delivery is the usual approach Hemodynamic goals:

  

Avoidance of tachycardia and fluid overload Preservation sinus rhythm Increase of BV, CO and HR during pregnancy and labor may result in pulmonary congestion, tachycardia and atrial fibrillation Monitoring:

  

A-LINE and probably PAC Labor and delivery is associated with an increase of 8 to 10 mm Hg in the left atrial and pulmonary wedge pressures PAC used before and during delivery facilitates the management of hemodynamics in women with advanced disease

Epidural anesthesia to achieve effective pain control

 

A mixture of LA and opioids is ideal Pain control and minimization of BV/CO increase after delivery

Assisted-delivery devices during the second stage of delivery eliminate hemodynamic effects of valsalva maneuver during pushing Cesarean section should be performed when there are obstetrical indications for it Mitral Regurgitation Women with symptomatic MR may benefit from mitral-valve surgery (preferably repair )before becoming pregnant. However, LV dysfunction associated with MR is unlikely to improve after surgery and will increase maternal risk during pregnancy

Diuretics and vasodilators may be indicated When Will You Hear Murmurs? If a valve is stenotic, you will hear a murmur of blood shooting through the narrow opening when the valve is open If a valve is regurgitant, you will hear a murmur of blood leaking back through when the valve should be closed Aortic Stenosis Congenital valvular abnormalities are usually the cause of AS in young women in the US Severe AS is poorly tolerated during pregnancy Maternal and perinatal mortality of 17% and 32% have been reported The pressure gradient is responsible for the HD changes seen in AS The increased LVSP needed to maintain systemic arterial blood pressure increases stress in the ventricular wall Lt ventricular hypertrophy develops leading to diastolic dysfunction, fibrosis, diminish coronary blood flow reserve and late systolic failure Patients who are symptomatic or who have a peak outflow gradient of more than 50 mm Hg are advised to delay conception until after surgical correction Termination of pregnancy should be strongly considered if the patient is symptomatic before the end of the 1st trimester Aortic-valve replacement and palliative aortic balloon valvuloplasty have been performed during pregnancy with associated maternal and fetal risk Biological valves Aortic Stenosis Hemodynamic goals: Maintain normovolemia NSR Tachycardia decrease diastolic filling time Atrial kick is responsible for up to 40% of ventricular filling in this patients Baseline SVR Aortic Stenosis normal physiological changes of pregnancy can precipitate heart failure in patient with severe AS The further increase of CO and BV during labor in face of the fixed CO of AS patients may precipitate: Tachycardia which decreased diastolic time (and coronary perfusion time) and increases O2 consumption Increases LVEDP Ischemia might result Vaginal delivery is preferred Instrumental delivery to avoid hemodynamic changes of the valsalva manuver Oxytocin may decrease SVR an increase PAP

Monitoring: A-line CVP , PAC Epidural analgesia Pain control and also minimizes BV/CO increase after delivery Avoid epinephrine test dose Careful titration to avoid sudden decrease of SVR Dilute LA with opioids to minimize sympathectomy Cesarean section GA has traditionally being advocated to avoid sudden decreases of SVR Opiod based induction Fetal depression. Pediatric team must be aware Case reports of epidural anesthesia with positive outcomes Careful titration of LA and fluid replacement/vasopressors to counteract sympathectomy Phenylephrine possible a better choice over ephedrine Aortic Regurgitation AI may be due to a dilated Ao annulus (as in Marfan's syndrome), a bicuspid Ao valve, or previous endocarditis The reduced SVR of pregnancy reduces the volume of regurgitated blood Women with an abnormal functional capacity or left ventricular dysfunction are predicted to have a high risk of abnormal maternal outcomes, but few data concerning this population are available Aortic Insufficiency Isolated AI can usually be managed with vasodilators and diuretics ACE inhibitors should be discontinued during pregnancy, and other agents, such as hydralazine or nifedipine, should be substituted Clinical and echo assessment should be performed before conception in women with AI due to Marfan's syndrome Even in the absence of overt cardiac abnormalities, this syndrome predisposes women to unpredictable, but increased, risk during pregnancy. Pulmonary Edema Pathophysiology Pulmonary Edema Capillary fluid moves into alveoli Lung becomes stiffer Harder to inhale Less gas exchange in alveoli Crackles Frothy sputum Hemoglobin not completely oxygenated Pulmonary hypertension

Hemodynamic objectives Maintain the PAP as low as possible and the systemic pressure within the 15% above and below the basal level (the systemic pressure should always be higher than pulmonary pressure) Avoid dysrhythmias and tachycardia, and maintain sinus rhythm

Chest x-ray of rt. lung A. Normal pulmonary vessels B. General increase pulmonary vessels C. Pulmonary congestion D. Pulmonary hypertension Pulmonary hypertension Pregnancy and labor CV changes against goals: Uterine contraction after delivery returns a large bolus of blood to the circulation. This can be poorly tolerated in patients with severe PHTN The sudden hypervolemia can be treated with vasodilators, such as nitroglycerine, and diuretics. A BP cuff inflated between the arterial and venous pressures around the thighs, can suddenly and reversibly decrease RV filling by reducing venous return Air or amniotic fluid embolism could acutely increase pulmonary pressure Monitoring: a-line and CVP or PAC should be used for monitoring or for drug administration Nursing managements

    

Administration of oxygen and intubation and mechanical ventilation if respiratory failure occurs. Positioning the patient to promote circulation Monitor I and O Monitoring pulse rate and blood pressure Examining skin turgor and mucous membranes for signs of DHN.

Assessment symptoms of fluid overload.

PULMONARY EMBOLISM Pulmonary Embolism obstruction of the base or one or more branches of the pulmonary arteries by the thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart.

Gas exchange is impaired in the lung mass supplied by the obstructed vessel. Massive pulmonary embolism is life threatening and can cause death within the first 1 to 2 hours after the embolic event. Common in pregnancy, oral contraceptive use, congestive heart failure, hypercoagulable states, and prolonged immobility. Most thrombi originates in the deep veins of the legs. Clinical Manifestations Symptoms depend on the size of the thrombus and the area of the pulmonary artery occlusion. Dyspnea is the most common symptom. Tachypnea is the most frequent sign Chest pain is common, usually sudden in onset and pleuritic in nature it can be substernal and may mimic angina pectoris Fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, syncope, shock, and sudden death may occur Multiple small emboli in the terminal pulmonary arterioles stimulate symptoms of bronchopneumonia or heart failure Assessment and Diagnostic Methods Ventilation-perfusion scan, pulmonary angiography, chest radiograph Electrocardiogram (ECG), tachycardia, PR interval and T-wave changes, peripheral vascular studies and arterial blood gas (ABG) analysis (for hypoxemia) Prevention Ambulation or leg exercises in patients on bed rest Anticoagulant therapy before abdominothoracic surgery and every 8 to 12 hours until discharge from hospital Application of intermittent pneumatic leg compression devices Right Sided Heart Failure Shunts A shunt is an opening or connection that lets blood move from one side of the circulation to the other Most shunts occur in the heart and move blood either from the left to the right or from the right to the left Because the left side is stronger, blood is usually pushed from the left to the right side Left-to-Right Shunt Right-to-Left Shunt Cardiac Disease Right-side heart failure Distended liver and spleen Ascites Peripheral edema Right-Sided Heart Failure Blood backs up into veins

Causes peripheral edema and organ engorgement Less common than left-sided HF Jugular venous pressure estimation RIGHT-SIDED HEART FAILURE JUGULAR VEIN DISTENSION DEPENDENT PERIPHERAL EDEMA ASCITES WEIGHT GAIN FATIGUE WEAKNESS SPLENOMEGALY HEPATOMEGALY GI DISCOMFORT NOCTURIA TACHYCARDIA

RHD Streptococcal pharyngitis infection Scarring of the heart valves Stenosis of the openings between chambers of the heart Causes Atrial Septal Defects Ventricular Septal Defects Patent Ductus Arteriosus R-L Shunt Occur through Septal Defect or PDA when pulmonary vascular resistance exceeds peripheral resistance & pulmonary hypertension occurs. EISENMENGER SYNDROME ATRIAL SEPTAL DEFECT Produces L-R shunt because pressure of the L side of the heart is higher than the R side. Pregnancy is well tolerated with no complications However pulmonary HPN can occur because the additional blood moves to the R side of the heart is transported into the lungs. VSD Common @ birth Asymptomatic when pregnant Fatigue or pulmonary congestion may occur If heart failure occurs they are managed as nonpregnant patients

Bacterial endocarditis is common with unrepaired defects, antibacterial prophylaxis is usual. PDA The communicating shunt b/w PA & Aorta If untreated physiologic effects are related to size If small, tolerated during pregnancy unless complicated by P HPN Antibiotics is recommended as they are commonly be infected. R-L SHUNT TOF Combination of four defects: Ventricular septal defect Pulmonary valve stenosis Right Ventricular Hypertrophy Displacement of Aorta ( overrides the RV) Symptoms of TOF Cyanosis Clubbing of fingers Inability to tolerate activity If treated ( repaired), & -cyanosis may do well in pregnancy If uncorrected death. EISENMENGER SYNDROME Cyanotic heart condition Pulmonary resistance equals or exceeds systemic resistance to blood flow Several underlying congenital defects: - Large VSD -Large patent ductus arteriosus MITRAL VALVE PROLAPSE One of the most common cardiac conditions Associated with ASD and Marfan Syndrome Leaflets of the valve prolapsed into the left atrium during ventricular contraction Nursing Diagnoses Decrease Cardiac Output Activity Intolerance r/t imbalance between oxygen supply & demands Fluid Volume Excess r/t impaired cardiac pump and water & sodium retention Deficient Knowledge regarding diet and fluid restriction Nursing Interventions Monitor maternal ECG & FHT continuously. Explain to client that vaginal delivery is preferred over C-section. Monitor client s response to stress of labor & watch for signs of decompensation. Administer O2 & pain medication as ordered, epidural preferable. Position client in side-lying/low semi-fowler s position. Provide calm atmosphere.

Encourage open glottal pushing during second stage of labor Monitor VS, any bleeding, strict I&O, lab test values, daily weight, & diet. Promote bed rest in appropriate position. Assist with activities as needed. Prevent infection. Facilitate non stressful mother/baby interaction. Promote frequent rest periods & adequate sleep, decrease stress. Teach client to recognize & report signs of infection, importance of prophylactic antibiotics. Monitor uterine contractions Compare V/S to baseline & normal values expected during pregnancy. Management Antepartum Care The chief aim of management of the patient in pregnancy is to keep patient within her cardiac reserve. It is preferable to have detailed baseline information prior of pregnancy. Limiting activity is helpful in severely affected women with ventricular dysfunction, left heart obstruction, or class III or IV symptoms. Hospital admission by mid-second trimester may be advisable for some. Problems should be identified early and treated aggressively, especially pregnancy induced hypertension, hyperthyroidism, infection, and anemia. Arrhythmias should be treated if warranted Premature atrial or ventricular beats are common in normal pregnancy, and in patients with preexisting arrhythmias, Pregnancy may exacerbate their frequency and hemodynamic severity. These usually are not treated. Sustained tachyarrhythmias, such as atrial flutter or atrial fibrillation, should be treated promptly. If possible, all antiarrhythmic drugs should be avoided during the first trimester, and those known to be teratogenic should be avoided throughout pregnancy. Anticoagulation therapy Oral therapy with warfarin is effective and logistically easy.

However, it can affect embryonic organ development, although some evidence shows that a dosage of 5 mg per day may not be teratogenic. Fetal intracranial bleeding is a risk throughout pregnancy, particularly during vaginal delivery, unless warfarin is stopped before labor. * Heparin in adjusted subcutaneous doses does not cross the placenta and so has no teratogenic effects. However, it may cause maternal thrombocytopenia and osteoporosis and is less effective in preventing thrombosis in patients with prosthetic valves. Mechanical prosthetic heart valves Anticoagulation therapy More recent guidelines recommend either (1) adjusted-dose heparin during the entire pregnancy or (2) adjusted-dose heparin until the 13th week of gestation, warfarin from the 14th week to the middle of the third trimester, and then restart adjusted-dose heparin. Anticoagulation therapy * Low-molecular-weight heparin in adjusted doses is easier to administer and has been suggested as an alternative to adjusted-dose unfractionated heparin.

Bates SM, Greer IA, Hirsh J, Ginsberg JS. Use of antithrombotic agents during pregnancy. Peripartum management Cesarean section is indicated only for the following conditions: Aortic dissection Marfan syndrome with dilated aortic root Taking warfarin within 2 weeks of labor.

Peripartum care Peripartum care Peripartum care Forceps or vacuum extraction should be considered at the end of the second stage of labor to shorten and ease delivery.

Peripartum care Postpartum monitoring Because hemodynamics do not return to baseline for many days after delivery, patients at intermediate or high risk may require monitoring for at least 72 hours postpartum.

Peripartum care Lactation should be encouraged unless patient is in failure. Cardiac output is not compromised during lactation. Lactation is a pathway for fluid excretion and diuretic requirement may actually fall. Cardiopulmonary Resuscitation of the Pregnant Woman For cardiac arrest, standard resuscitative efforts with few modifications implemented If defibrillation needed, paddles must be placed one rib interspace higher than usual MEDICATION DIURETICS: Loop diuretics ex. Lasix (K+loss) VASODILATORS:isosorbide(Isordil),Apresolin INOTROPICS: cardiac glycoside: digoxin please check s/s dig toxicity (grn-yellow halos around objects/lights, n/v/anorexia), Check serum level & hold dose if AP=<60 bpm Digitalis-strengthen the heart s contractions increasing blood flow Beta BLOCKERS: carvedilol or Coreg is often the beta blocker of choice for CHF ACE INHIBITORS: enalapril, lisinopril,catopril Vasodilators-relax blood vessels which lowers the resistance to blood flow. More blood reaches the tissues and the heart works no harder than before. Aldosterone antagonist: (Diuretic) K+ sparing such as spironolactone or Aldactone Diuretics-increase the output of salt and water in urine What is warfarin fetal embryopathy ? Which is the ideal contraceptive for women with heart disease ? Question A client develops left-sided heart failure. An appropriate nursing diagnosis is? 1.Activity intolerance 2.Ineffective airway clearance 3. Deficient fluid volume 4.Pain

Answer? # 1 Activity intolerance: Left sided heart failure impairs cardiac output and affects gas exchange in the lungs. Exchange of O2 and CO2 is compromised. Clients tire easily and may be unable to complete simple activities. Clients with Left-sided heart failure usually experience FVE Question A client develops right sided heart failure. Which of the following s/s would the nurse expect to find? 1. Pulmonary edema 2. Edematous legs and ankles 3. Decreased heart rate 4. Increased urinary output Answer? #2 Clients with right sided heart failure develop edema in the lower extremities and dependent body areas as a result of increase capillary pressure. The workload of the heart is increased leading to tachycardia Pulmonary edema is a complication of left sided heart failure Conclusion Appropriate contraceptive and family planning advice as well as pre-conceptional counselling are also important. The concerted efforts of a team consisting of the obstetrician, cardiologist, anaesthetist, cardiothoracic surgeon, neonatologist, and paediatric cardiologist are mandatory to ensure optimal results. Evaluation The evaluation of a woman with clinically significant valvular heart disease should occur before conception and entail a full cardiac assessment The history should focus on the patient's exercise capacity, current or past evidence of heart failure, and associated arrhythmias Cardiac hemodynamics, including PAP and the severity of valve dysfunction, should be assessed by echo Exercise testing may be useful if the history is inadequate to allow an assessment of functional capacity During pregnancy evaluation each trimester and whenever there is a change in symptoms, in order to assess any deterioration in maternal cardiac status is the rule SURGICAL PROCEDURES HEART VALVE REPAIR OR REPLACEMENT PACEMAKER INSERTION CORONARY ARTERY BYPASS MECHANICAL ASSIST DEVICES HEART TRANSPLANTATION Prosthetic Heart Valves

Women with mechanical valves have a higher rate of thromboembolism and higher 10-year mortality, despite a lower rate of valve loss Pregnancy does not appear to increase the rate of failure of mechanical prostheses associated with an estimated maternal mortality of 1 to 4% with death usually resulting from complications of prosthetic-valve thrombosis. Heart valve repair Examples of remodeling Angioplasty catheterization using a balloon to flatten fatty deposits, used to treat atherosclerosis or other conditions with blocked arteries. artery of an arm or leg is used to guide the catheter through to the blocked artery. An uninflated balloon on the top of a smaller tube is threaded through the larger tube and centered in the plaque narrowed area. The balloon inflates compressing the plaque against the walls and increasing the open area. SURGICAL PROCEDURES Check for Medical Emergency: Acute Pulmonary Edema: frothy sputum, impending doom , panic, orthopnea, cough w/ pink-tinged sputum TX: add morphine to relieve anxiety, slow rr, and decrease peripheral vascular resistance plus cardiac glycoside (Digoxin), and loop diuretic(Lasix), bronchodilators, and oxygen for hypoxia Myocardial Infarction Cholesterol plaques deposited in the walls of coronary artery Hardening of arterial walls and narrowing of the inner channel of the artery Arteries cannot deliver enough blood to maintain normal function of the parts of the body Eventually, the inner chamber of the artery is completely blocked Artery Structure Atherosclerosis in a Nutshell Lipids get into the vascular endothelium White blood cells try to clear them away foam cells

Fatty Streaks and Atherosclerotic Plaques Atherosclerosis in a Nutshell WBCs and vascular endothelium release growth factors that promote plaque formation Plaques block the arteries

Arteriosclerotic Cardiovascular Ischemia Acute: Myocardial Infarction Chronic: Ischemic Cardiomyopathy (Dilated Cardiomyopathy) People Live with Atherosclerosis But Die of Thrombosis! Clinical Manifestations Chest pain Sudden, not relieved by rest or NTG Shortness of breath Anxiety and restlessness Diaphoresis Cold, clammy perspiration Pallor Dizziness or lightheadedness Nausea and vomiting Assessment P - provoking Q - quality R - radiation S - severity T - timing Laboratory tests CK-MB LDH Myoglobulin TROPONIN

An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis Complications of AMI Heart failure Cardiogenic shock Pericarditis Thromboemboli Rupture of the heart Ventricular aneurysms

Morbidity and Mortality Acute MI in 0.0075% (7.5 in 100,000) Overall mortality in pregnancy 28% First trimester 0% Second trimester 21% Third trimester 40% Puerperium up to 75%

Highest mortality rates Delivery within 2 weeks of MI (+) pregnancy complications Fetal mortality 35% Risk factors for MI Older maternal age, multiparity Smoking, obesity, DM Hypertension History of cardiovascular disease Cocaine abuse Management Position during labor Oxygen therapy Epidural anesthesia CVP monitoring

Post myocardial infarction Cardiac Arrhythmias Is an abnormal electrical conduction or automaticity causing changes in the heart rate and rhythm. Predisposing factors: Congenital Myocardial Ischemia, MI Organic heart disease Drug effect and toxicity Conductive tissue degeneration Electrolyte imbalance Acid-base imbalance Cellular hypoxia

Pathophysiology Result in the disturbance in the excitability, automaticity, or conductivity Heart rate and rhythm are altered, reducing cardiac output

Assessment Asymptomatic Palpitation Chest pain

Dizziness Weakness, fatigue Feeling of impending doom Irregular heart rhythm Bradycardia or tachycardia hypotension Syncope LOC Diaphoresis Pallor Cold, clammy skin Life-threatening: pulselessness, (-) respiration, no palpable blood pressure

Diagnosis ECG- change in heart rate, rhythm Blood chemistry : electrolyte imbalance Normal Sinus Rhythm Normal Sinus Rhythm Occurs when the electrical impulse starts at the regular rate and rhythm in the sinus node and travels at through the normal conduction pathway Characteristics: Ventricular and atrial rate: 60 to 100 in adult Ventricular and atrial rhythm: Regular QRS duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape; always in front of QRS PR interval: Consistent interval between 0.12 and 0.20 seconds P: QRS ratio 1:1 Types of Sinus node Dysrhythmias A. Sinus Bradycardia occurs when the sinus node creates an impulse at a slower rate than normal.

Characteristics: Ventricular and atrial rate: Less than 60 in adult Ventricular and atrial rhythm: Regular

 

QRS duration: Usually normal but may be regularly abnormal P wave: Normal and consistent interval between 0.12 and 0.20 seconds

 

P: QRS ratio 1:1 Management The urgency of treatment depends on the effect of the slow rate on maintenance of CO Atropine, 0.5 to 1.0 mg given IV push block vagal stimulation to the SA Node & therefore accelerate heart rate. If bradycardia persists a pacemaker ( electrical device used to re-establish muscular contraction of an arrested heart or to steady heartbeat) may be required. B. Sinus Tachycardia Occur when the sinus node create an impulse at a faster than normal rate. may be caused by acute blood loss, anemia, shock, hypervolemia, hypovolemia CHF, pain, hypermetabolic states, fever, anxiety or sympathomimetic medication.

    

Ventricular and atrial rate: Greater than 100 in the adult Venticular and atrial rhythm: Regular QRS duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape, always in front of the QRS, but may be buried in the preceding T wave. P: QRS ratio 1:1

As the heart rate increases, the diastolic falling time decreases, result in reduced cardiac output and subsequent symptoms of syncope and low blood pressure. If the heart cannot compensate for the decreased ventricular falling the pt may develop acute pulmonary edema

Management It is usually directed at abolishing its causes. Calcium channel blockers and Beta-blockers may be used to reduce the heart rate quickly. C. Sinus Arrhythmias Occur when the sinus node create an impulse at an irregularly rhythm rate usually increase with inspiration and decrease with expiration. Non respiratory cause includes heart disease and valvular disease, but these are rarely seen.

     

Ventricular and atrial rate: 60 to 100 in the adult Ventricular and atrial rhythm: Irregular QRS duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape, always in front of the QRS. PR interval: Consistent interval between 0.12 and 0.20 second P: QRS ratio: 1:1 Atrial Dysrhythmias A. Premature Atrial Complex single ECG complex that occur when an electrical impulse start in the atrium before the next normal impulse of the sinus node. may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety, hypo kalemia (low potassium level), hyper metabolic states or atrial ischemia, injury or infarction.

Characteristics: Ventricular and atrial rate: Depend on the underlying rhythm Ventricular and atrial rhythm: Irregular

     

QRS duration: The QRS that follows the early P wave is usually normal, but it may be abnormal. P wave: An early and different P wave may be seen or may be hidden in the T wave; Other P wave in the strip is consistent. PR interval: The early P wave has a shorter than normal PR interval, but still between 0.12 And 0.20 seconds P: QRS ratio: Usually 1:1 Management If PACs are in frequent, no treatment is necessary. If they are frequent (more tan 6 per minute) this may herald a worsening diseases state or the onset of more serious dysrhythmias, such as atrial fibrillation. Treatment is directed toward the cause. PAC s should be monitored for increasing frequency B. Atrial Flutter Occur in the atrium and creates impulse at an atrial rate between 250 and 400 time per minute. Because the atrial rate is faster than the AV node can conduct, not all atrial impulse are conducted into the ventricle causing a therapeutic block at the AV node.

Characteristics: Ventricular and atrial rate: Atrial range between 250 and 400 ventricular rates usually Range between 75 and 150 Ventricular and atrial rhythm: Usually Regular

   

P wave: Saw toothed shape. These waves referred to as F wave PR interval; Multiple F waves may make it difficult to determine the PR interval. P: QRS ratio: 2:1, 3:1, or 4:1 Sign and Symptoms Chest pain Shortness of breath Low blood pressure.

Management The urgency of treatment depend on the ventricular response rate& resultant symptoms A Calcium channel blocker such as Diltiazem (cardizem) may be used to slow AV Nodal conduction used with caution in the patient with CHF, hypotension Digitalis & Quinidine preparation may be used. A beta adrenergic block drug such as Esmolol may be used. If drug therapy is un successful, trial flutter will often respond to cardiversion.

Small doses of electrical current are often successful C. Atrial Fibrillation May occur for a very short time (paroxysmal) or it may be chronic most common dysrhythmias that cause patients seek medical attention shorter time in diastole reduce the time available for coronary artery perfusion, thereby increasing the risk for myocardial ischemia. erratic atrial contraction promotes the formation of a thrombus within the atria increasing the risk of stroke (brain attack).

Characteristics: Ventricular and atrial rate: Atrial rate is 300 and 600 in untreated atrial fibrillation Ventricular and atrial rhythm: Highly irregular

    

QRS shape and duration: usually normal but may be abnormal P wave: No discernible P waves; irregular undulating waves are seen and are referred to as fibrillatory or waves. PR interval: Cannot be measured P: QRS ratio: many:1 Management Cardioversion (restoration of normal heart rhythm may be indicated for atrial fibrillation that has been present for less than 48 hours, a condition termed acute onset of atrial fibrillation Acute onset, the medication quinidine, Ibutilide,flecanide, dofetilide, profafenon, procanamide, dysopyramide or amiodirone may be given to achieve conversion to sinus rhythm Intravenouse adenosine (adenocard,adenescan) has also been use for conversion, as well as to assist in the diagnosis. Calcium channel blocker and beta blocker are effective in controlling the ventricular rate in atrial fibrillation Use Digoxin is recommended to control the ventricular rate those patient with poor cardiac function Aspirin may be substituted for warfarin. Junctional Dysrhythmias Premature Junction Complex an impulse that starts in the AV nodal before the next normal sinus impulse reaches the AV node Premature junction complex are less common than PAC s The criteria for premature junction complex are the same as for PACs except for the Pwave and the PR interval. The Pwave may be absent QRS, or may occur before the QRS but with a PR interval of less than 0.12 second Treatment for frequency premature junction complexes is the same as for frequent PACs. Junctional Dysrhythmias B. Junctional Rhythm Junctional or idionodal rhythm occur when the AV node, instead of the sinus node, become the pacemaker of the heart.

Characteristics:

Ventricular and atrial rate: 40 to 60 Ventricular rhythm: Regular

   

QRS duration: Usually normal but may be abnormal P wave: May be absent, after the QRS complex, or before the QRS; may be inverted, especially in lead II PR interval: If P wave is in front of the QRS, PR interval is less than 0.12 second P: QRS ratio1:1 or 1:1

C. Atrioventicular Nodal Reentry Tachycardia Occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate. It has an abrupt onset and an abrupt cessation with a QRS of normal duration had been called paroxysmal atrial tachycardia (PAT)

Characteristics: Ventricular and atrial rate: atrial rate 150-250; vent rate: 75-250 Ventricular and atrial rhythm: Regular; sudden onset and termination of the tachycardia

   

QRS duration: Usually normal but may be abnormal P wave: usually very difficult to discern PR interval: If P wave is in front of the QRS, PR interval is less than 0.12 second P: QRS ratio1:1 or 2:1

Ventricular Dysrhythmias A. Premature Ventricular Complex Caused by acute MI other form of heart disease, pulmonary disease, electrolyte disturbance, metabolic instability and drug abuse The wave of impulse originates from an ectopic Focus (Foci) within the ventricles at rate faster than the next normally occurring beat. Because the normal conduction pathway is by passed configuration of the PVC is wider than normal and is distorted in appearance. PVC s may occur in regular sequence with normal rhythm.

Characteristics: Ventricular and atrial rate: Depend on the underlying rhythm. Ventricular and atrial rhythm: Irregular

    

QRS duration: 0.12 second or longer shape is bizarre and abnormal P wave: none PP interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 second P: QRS ratio 0:1, 1:1 Management

standard treatment is Lidocaine hydrochloride (Xylocaine) by IV push Be alert to the development of confusion, slurring of speech and diminished mentation because lidocaine toxicity affects the CNS. If ventricular premature beats occur in conjunction with bradysrhythmias, atropine may be chosen to accelerate the heart rate and eliminate the need for ectopic beat. Atropine should be used with caution in acute MI. the injured myocardium may not be able to tolerate the accelerated rate. B. Ventricular Tachycardia Ventricular tachycardia (VT) is designed as three or more PVCs in a row, occurring at a rate exceeding 100 beats per minute. causes are similar to those for PVC VT is an emergency because the patient is usually unresponsive and pulse less

Characteristics: Ventricular and atrial rate: 100to200 beats per minute Ventricular and atrial rhythm: Usually Regular

    

P wave: atrial rate and rhythm may be indeterminable. PR interval: Very Irregular P: QRS ratio: difficult to determine Ventricular Tachycardia Management Cardioversion may be the treatment of choice, especially if the patient is unstable. VT in a patient who is unconscious and without a pulse treated in the same manner as ventricular fibrillation immediate defibrillation is the action of choice. C. Ventricular Fibrillation rapid but disorganized ventricular rhythm that cause of ventricular fibrillation are the same as for VT may also result from untreated or unsuccessfully treated VT, electrical shock

Characteristics: Ventricular rate: Greater than 300 per minute Ventricular and atrial rhytm: Extremely irregular

 

QRS duration Irregular Management Immediately fibrillation and activation of emergency service importance of defibrillation is evident in one of the recent change in basic life support. Placing a call for emergency assistant and calling for a defibrillator takes precedence over initiating Cardio pulmonary resuscitation in adult victim. Application of an automatic external defibrillator AED is included in basic life support Administering Vaso active and anti arrhythmia medication alternating with defibrillation are treatment used to try convert the rhythm to normal sinus rhythm.

D. Idioventricular Rhythm also called ventricular escape rhythm, occur when the impulse starts in the conduction system below the AV node. Commonly cause the patient to lose consciousness and experience other signs and symptoms of reduced cardiac out put . Intervention may include identify the underlying cause, administering Intravenous atropine andvasopressor medication. Initiating emergency transcutaneous pacing. Bed rest is prescribed so as not to increase the cardiac work load

Characteristics: Ventricular and atrial rate: Between 20and 40 if the rate exceeds 40 Ventricular and atrial rhythm: Regular

  

QRS duration: Bizarre, abnormal, duration is 0.12 second or more. Commonly called flat line, ventricular a systole characterized by QRS complexes, P wave may be apparent for a short duration in two different leads. no heart beat, no palpable pulse and no respiration.

E. Ventricular Asystole Assessment to identify the possible cause which may be hypoxia, acidosis, severe electrolyte imbalance, drug overdose or hypothermia.

Management CPR and emergency service as necessary to keep the patient alive. Transcutaneous pacing may be attempted. A bolus of intravenous epinephrine should be administered and repeated 3 to 5 minutes interval HEART BLOCK Conduction Abnormalities The nurse first to identify is the underlying rhythm.(eg, sinus rhythmia) then the PR interval is assessed for the possibility of an AV block. AV block occurs when the conduction of impulse through the AV nodal are/ is decreased or stopped. These block can caused by medication (eg,digitalis, calcium channel blockers, beta blocker). Clinical sign and symptoms of a heart block vary with the resulting ventricular rate and the severity of any underlying disease processes. treatment is based on the hemodynamic effect of the rhythm Types of Conduction Abnormalities A. First Degree Block Occurs when all the atrial impulse are conducted through the AV node into the ventricle at a rate slower than normal Characteristics:

Ventricular and atrial rate: Depend on the underlying rhythm. Ventricular and atrial rhythm: Depend on the underlying rhythm. QRS duration; usually normal P wave: In front of QRS complex; shows sinus rhythm, regular shape. P: QRS ratio1:1

B.1

Second Degree Atrioventricular Block Type I

Second degree type I heart block occurs when all but one of the atrial impulse are conducted. Through the AV node into the ventricles. Each atrial impulse a take longer time for conduction than the one before, until one impulse is fully blocked.

Characteristics: Ventricular and atrial rate: Depend on the underlying rhythm Ventricular and atrial rhythm: The PP interval is regular if the patient has an underlying normal sinus rhythm; the RR interval characteristically reflect a pattern of change .

QRS duration: Normal may be abnormal

B.2 Second Degree Atrioventricular Block Type II Occurs when only some of the atrial impulses are conducted through the AV node into the ventricles C. Third Degree Atrioventricular Block Occur when no atrial impulse is conducted through the AV node into the ventricle In the third degree heart block two impulses stimulate the heart :one stimulate the ventricle ,represent by the QRS complex, and one stimulate the atria .

Characteristics: Ventricular and atrial rate: Depend on the escape and underlying atrial rhythm. Ventricular and atrial rhythm:The PP interval is regular and the RR interval is regular; however the PP interval is not Equal to the RR interval.

   

QRS duration: Depend on the escape of rhythm P wave: Depend on the underlying rhythm P: QRS ratio: More P wave than QRS complexes Management IF the patient is short of breath, complaints of chest pain or lightheadedness, or has low BP: Intravenous bolus of Atropine is the initial treatment of choice. If the patient does not respond to atropine or has acute MI, trascutaneous pacing should be started. A permanent pacemaker may be necessary if the block persist.

Major assessment include all possible cause of the dysrhythmia and the dysrhythmia s effect on the heart s ability to pump adequate blood volume. When cardiac output is reduced, the amount of O2 reaching the tissue and vital organ is diminished producingthe s/sx associated with dysrhythmia.

Nursing Assessment A health history is obtained to identify any previous occurrence of decreased cardiac output such as syncope (fainting), lightheadedness , dizziness , fatigue, chest discomfort and palpitation Coexisting condition that could be a possible cause of heart block or dysrhythmia (heart disease, chronic obstructive pulmonary disease ) may be also identified. All medications prescribed and over the counter (supplements herbs and nutritional) may be reviewed. nurse conducts physical assessment to the patient with diminished cardiac output especially the level of LOC nurse directs attention to the skin which may be pale and cool. Signs of fluid retention, such as neck vein distention and crackles and wheezes auscultated in the lungs. nurse auscultates for extra heart sounds ( especially S3 and S4 ) and for heart murmur, measure blood pressure indicates reduced cardiac output.

Nursing Diagnosis Decreased cardiac output Anxiety related to fear of the unknown Deficient knowledge about the dysrhythmias and its related treatment.

Collaborative Problems and Potential Complication May developed over time : a heart failure Thromboembolic Cardiopulmonary Resuscitation of the Pregnant Woman Fetus should be monitored during the cardiac arrest THERAPEUTIC MANAGEMENT

CLASS I AND II Limit physical activity Avoid excessive weight gain Prevent infection Undergo physical assessment for the development of CHF pulmonary edema, or cardiac dysrythmias

CLASS III AND IV To prevent cardiac decompensation and development of CHF Protect the fetus from hypoxia and IUGR. Bed rest - increased risk of thrombus formation

DRUG THERAPY ANTICOAGULANTS

   

Clotting factors increase Thrombolytic activities decrease Subcutaneous heparin Enoxaparin (Lovenox) ANTIDHYRHYTHMICS

  

Must balance benefits to the mother against possible harm to the fetus Digoxin, Adenosine , Ca Channel Blockers appears to be safe Beta Blockers causes neonatal respiratory depression, sustained bradycardia and hypoglycemia ANTI-INFECTIVES

   

For endocarditis Gram positive Staph are common to IV drug users Maternal Gonorrhea infection may cause rapidly developing endocarditis Amoxycillin, Penicillin, Ampicillin, Gentamicicn, Ceftraxone, or Vancomycin

Cardiovascular Disorders Heart transplantation Increasing numbers of heart recipients are successfully completing pregnancies Before conception, woman must be assessed for quality of ventricular function and potential rejection of transplant Vaginal birth is desired, but transplant recipients have an increased rate of cesarean births Neonate may exhibit immunosuppressive effects during first week of life Breastfeeding not advised for infants of mothers taking cyclosporine Nursing Process: The Pregnant Woman with Cardiac Disease ASSESSMENT

Health history

(prepregnancy cardiac status)

 

Medical history Family historyReview Level of exercise performance v Breathing pattern v Peripheral tissue perfusion Cardiopulmonary status

NORMAL Fatigue Chest pain Dyspnea Orthopnea Palpitations

ABNORMAL Symptoms at rest Exertional chest pain Severe dyspnea PND Dysrhythmia (>120bpm)

  

Medication intake Emotional status Cultural background Family size Role expectations

Physical Examination Subjective symptoms Objective signs

      

Increasing fatigue, DOB (with usual activities) Frequent cough Palpitations ( heart is racing ) Swelling: face, fingers, feet Weak and irregular PR Progressive, generalized edema Crackles at base of lungs

  

Orthopnea Cyanosis of lips and nailbeds Laboratory and Diagnostic Tests Urinalysis Blood work (CBC, blood chemistry) Baseline ECG or 2D echocardiogram CXR Fetal UTZ, NST (non-stress test)

Nursing Diagnoses Fear Knowledge deficit Risk for Self-care deficit (bathing, grooming, dressing, etc.) peripartum risk Cardiac condition Fatigue or activity intolerance Focus of Treatment To minimize stress to the heart

Management Restriction of activity Nutrition counseling Medication v Prenatal period Promote rest If CO inadequate Peripheral vasoconstriction Uterine/placental constriction REST Program Rest periods (naps and sleeptime) CBR at week 30 of pregnancy Left lateral recumbent position

v Intrapartum period Mode of delivery Vaginal birth under epidural anesthesia

NURSE ALERT! Cesarean section not recommended Dramatic fluid shifts blood loss Sustained hemodynamic changes INTRAPARTUM PERIOD Vital signs monitoring Color and temperature check NURSE ALERT! PR = > 100 bpm RR = > 25 cpm Pale, cool, and clammy skin may indicate cardiac shock ABG to assess oxygenation status ECG and BP monitoring For cardiac decompensation, digitalis diuresis supplemental oxygen v Postpartum period First 24 to 48 hours most hemodynamically difficult

Extravascular fluid remobilized into vascular compartment Cardiac output increases Intra abdominal pressure reduced Pressure on veins removed Splanchnic vessels engorge Blood flow to the heart increased (reflex bradycardia) POST PARTUM PERIOD Care tailored to functional capacity position HOB, patient CBR with or without BRP progressive ambulation NURSE ALERT! Monitor vital signs ECG Rhythm Interpretation ECG Basics

Objectives To recognize the normal rhythm of the heart - Normal Sinus Rhythm. To recognize the 13 most common rhythm disturbances. To recognize an acute myocardial infarction on a 12-lead ECG. Electrocardiogram 1.An electrocardiogram is a recording of the electrical changes that occur during a cardiac cycle. 2.The first wave, the P wave, corresponds to the depolarization of the atria. 3.The QRS complex corresponds to the depolarization of ventricles and hides the repolarization of atria. 4.The T waves end the ECG pattern and corresponds to ventricular repolarization.

Regulation of the Cardiac Cycle 1.The amount of blood pumped at any one time must adjust to the current needs of the body (more is needed during strenuous exercise). 2.The S-A node is innervated by branches of the sympathetic and parasympathetic divisions, so the CNS controls heart rate. 3. Sympathetic impulses speed up and parasympathetic impulses slow down heart rate. 4.Impulses from cerebrum or hypothalamus may also influence heart rate, as do body temperature and the concentrations of certain ions. ELECTROCARDIOGRAM 12-lead electrocardiogram is a representation of the heart's electrical activity recorded from electrodes on the body surface 12 Lead ECG Placement Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers Normal Impulse Conduction Sinoatrial node AV node Bundle of His Bundle Branches

Purkinje fibers The PQRST P wave - Atrial

depolarization

The PR Interval Atrial depolarization + delay in AV junction (AV node/Bundle of His) (delay allows time for the atria to contract before the ventricles contract) Pacemakers of the Heart SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute. AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute. Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm. The ECG Paper

Horizontally One small box - 0.04 s One large box - 0.20 s

Vertically One large box - 0.5 mV Every 3 seconds (15 large boxes) is marked by a vertical line. This helps when calculating the heart rate. NOTE: the following strips are not marked but all are 6 seconds long.

How to Analyze a Rhythm Rhythm Analysis Step 1: Calculate rate. Step 2: Determine regularity. Step 3: Assess the P waves. Step 4: Determine PR interval. Step 5: Determine QRS duration. Step 1: Calculate Rate Option 1 Count the # of R waves in a 6 second rhythm strip, then multiply by 10.

Reminder: all rhythm strips in the Modules are 6 seconds in length. Option 2 Find a R wave that lands on a bold line. Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes 150, 3 boxes - 100, 4 boxes - 75, etc. Memorize the sequence: 300 - 150 - 100 - 75 - 60 - 50 Step 2: Determine regularity Look at the R-R distances (using a caliper or markings on a pen or paper). Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular? Step 3: Assess the P waves Are there P waves? Do the P waves all look alike? Do the P waves occur at a regular rate? Is there one P wave before each QRS? Step 4: Determine PR interval Normal: 0.12 - 0.20 seconds. (3 - 5 boxes) Step 5: QRS duration Normal: 0.04 - 0.12 seconds. (1 - 3 boxes) Rhythm Summary Rate Regularity P waves PR interval QRS duration Normal Sinus Rhythm Normal Sinus Rhythm (NSR) Etiology: the electrical impulse is formed in the SA node and conducted normally. This is the normal rhythm of the heart; other rhythms that do not conduct via the typical pathway are called arrhythmias. NSR Parameters 90-95 bpm regular normal 0.12 s 0.08 s

Rate 60 - 100 bpm Regularity regular P waves normal PR interval 0.12 - 0.20 s QRS duration 0.04 - 0.12 s Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia Arrhythmia Formation

Arrhythmias can arise from problems in the: Sinus node Atrial cells AV junction Ventricular cells

SA Node Problems The SA Node can: fire too slow fire too fast

Sinus Bradycardia

Sinus Tachycardia

Atrial Cell Problems Atrial cells can: fire occasionally from a focus fire continuously due to a looping re-entrant circuit Premature Atrial Contractions (PACs) Atrial Flutter A re-entrant pathway occurs when an impulse loops and results in self-perpetuating impulse formation. Atrial Cell Problems AV Junctional Problems The AV junction can: fire continuously due to a looping re-entrant circuit

Block impulses coming from the SA Node Paroxysmal Supraventricular Tachycardia AV Junctional Blocks Ventricular Cell Problems Ventricular cells can: fire occasionally from 1 or more foci fire continuously from multiple foci fire continuously due to a looping re-entrant circuit Premature Ventricular Contractions (PVCs) Ventricular Fibrillation Ventricular Tachycardia DYSRHYTHMIAS Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart. These disorders can cause disturbances of the heart rate, the heart rhythm, or both Initially evidenced by hemodynamic effect they cause (eg, a change in conduction may change the pumping action of the heart and cause decreased blood pressure) Diagnosed by analyzing the ECG waveform. Electrical impulse stimulates and paces the cardiac muscle & normally originates in the SA node, near superior vena cava in the right atrium. Electrical impulse occurs at a rate ranging between 60 - 100 times a minute in the adult. Sinus rhythm promotes cardiovascular circulation. Electrical impulse causes mechanical contraction of the heart muscle.

Electrical stimulation is called depolarization; mechanical contraction is called systole Electrical relaxation is called repolarization; mechanical relaxation is called diastole

Normal Sinus Rhythm Rate is between 60 and 100 beats/minute The rhythm is regular All intervals are within normal limits There is a P for every QRS and a QRS for every P

The P waves all look the same Sinus Bradycardia Impulse in the sinus node is created at a slower rate. Rate is lower than 60 beats/minute The rhythm is regular All intervals are within normal limits There is a P for every QRS and a QRS for every P Sinus Bradycardia The P waves all look the same Caused by beta-blocker, digitalis, or calcium channel blockers. Normal for athletes Don t treat unless there are symptoms. Can use pacing or atropine Atropine, 0.5 to 1.0 mg given rapidly as an intravenous (IV) bolus, is the medication of choice in treating sinus bradycardia. It blocks vagal stimulation, thus allowing a normal rate to occur. Rarely, catecholamines and emergency transcutaneous pacing also may be implemented. Sinus Tachycardia Impulse in the sinus node is created at a faster rate. Rate above 100 beats/minute The rhythm is regular. All intervals are within normal limits. There is a P for every QRS and a QRS for every P. The P waves all look the same. Sinus Tachycardia Caused by fever, stress, caffeine, nicotine, exercise, or by increased sympathetic tone may be caused by acute blood loss, anemia, shock, hypervolemia, hypovolemia, congestive heart failure, pain, hypermetabolic states Treatment is to take care of the underlying cause Treatment if ischemia occurs administration of beta-adrenergic blocker, calcium channel blocker Sinus Arrhythmia Rate is between 60 and 100 beats/minute The rhythm is irregular. The SA node rate can increase or decrease with respirations All intervals are within normal limits There is a P for every QRS and a QRS for every P. The P waves all look the same Ask the patient to stop breathing and the rate will become regular P-P and R-R are shorter during inspiration and longer during expiration.

More common in children and athletes

Atrial Flutter/ saw-toothed waves Atrial rate is between 250 and 350 beats/minute. Ventricular rate can vary The rhythm is regular or regularly irregular There is no PR interval. QRS may be normal 2:1 to 4:1 f waves to every QRS There are no P waves; they are now called flutter waves or F waves Problem: Loss of atrial kick and ventricular conduction is too fast or too slow to allow good filling of the ventricles Treatment Calcium channel blocker ,Beta adrenergic blocker Amiodarone, ibulitide, procainamide, flecainide. propafenone if arrythmia is present for less than 48 hrs. Anticogulation before cardioversion Synchronized cardioversion

Atrial Fibrillation/ more F waves Atrial rate is between 350 and 600 beats/minute; ventricular rate can vary The rhythm is irregular There is no PR interval; QRS may be normal Atrial Fibrillation/ more F waves There are many more F waves than QRSs Unlike flutter where the f wave will appear the same, in fib the f waves are from different foci so they are different Treatment is the same as atrial flutter Rate is between 100 and 200 bpm Rhythm is regular, but can change to different rhythms No PR interval; QRS is wide and aberrant There may be a P wave, but it is not related to the QRS Hematologic Disorders Iron-deficiency Anemia Anemia reduced ability of the blood to carry oxygen to the cells. In pregnancy Hgb <10mg/dl & Hct 30% Reduces O2-carrying capacity of blood Heart compensates by CO

Cardiac workload Ventricular function is stressed CHF Normal Values Packed RBC volume (HEMATOCRIT) An indirect index of the O2-carrying capacity Effects Blood loss at birth not well tolerated Increased risk for blood transfusions Pregnancy maternal plasma volume & total RBC the viscosity of whole blood

nutrient carrying capacity of the plasma but (disproportionate rise in bld constituents) Hemodilution in Hgb concentration Anemia Fetus requirement for Iron + Poor general nutrition (economic status/nausea & vomiting) Maternal depletion of iron stores

Iron-deficiency anemia Accounts for about 90% of anemia cases in pregnancy Associated with LBW and preterm births Iron Deficiency Anemia Iron absorbed from duodenum into bloodstream Binds to transferrin Transported to liver, spleen and bone marrow Incorporated into hemoglobin (stored as ferritin)

Microcytic (small-sized RBC) Hypochromic ( Hgb than the average RBC) Deficient iron stores results from: Poor nutritional status Heavy menstrual flow

 

Management Oral iron supplements Prophylactic therapy 30-60 mg/day Therapeutic regimen 120-180 mg/day

Dietary instruction: food sources Liver Meats Whole or enriched bread/cereals Deep green leafy vegetables Legumes Dried fruits

Nursing Care Diet history during prenatal visits Dietary teaching PRN Assess other needs (emotional support, financial aid, etc.) Provide for appropriate resources or referral

Nursing considerations Take with orange juice or vitamin C Iron is best absorbed in an acid medium IF NOT TOLERATED, IM or IV Dextran Folic acid deficiency anemia Folic acid deficiency anemia Accounts for about 1 5 % of anemia cases in pregnancy Common in multiple gestations Megaloblastic (enlarged RBC) Effects Early abortion

Abruptio placenta (premature placental separation) Folic acid Folacin (Vitamin B) normal RBC formation prevents neural tube defects v cleft lip v cleft palate Nutritional instruction RDI (recommended dietary intake) 400micrograms/day Therapeutic regimen: 1 mg/day Food sources Fortified ready-to-eat cereals Green leafy vegetables Oranges Broccoli Asparagus Liver Blood Incompatibilities OVERVIEW : ANATOMY AND PHYSIOLOGY STRUCTURES OF THE HEMATOLOGIC SYSTEM BLOOD BLOOD VESSELS BLOOD FORMING ORGANS

    

BONE MARROW SPLEEN LIVER LYMPH NODES THYMUS GLAND

COMPOSITION OF THE BLOOD PLASMA ( 55%) CELLULAR COMPONENTS (45%) 99% - erythrocytes 1% - leucocytes and thrombocytes BLOOD FORMING ORGANS BONE MARROW

  

Site of hematopoeisis or blood cell formation One of the largest organs of the body, making up 4% to 5% of total body weight Consists of cellular components (red marrow) separated by fat (yellow marrow)

BLOOD COMPONENTS ERYTHROCYTES

Biconcave disc; no nucleus, chiefly sacs of hemoglobin PRIMARY FUNCTION: To transport oxygen from the lungs to the various tissues of the body and to assist in the transport of carbon dioxide from tissues to the lungs Two portions of erythrocytes: IRON carried on the heme portion PROTEIN on the second portion Iron- small intestine as ferritin when required released into the plasma binds to transferrintransported into the membranes of the RBC in the marrow incorporated into hemoglobin v LEUKOCYTES

Are spherical cells that are whitish in color because they lack hemoglobin PRIMARY FUNCTION: Involved in the protection from bacteria and other foreign substances TWO CELL TYPES: v Granulocytes

  

Eosinophils involved in phagocytosis and allergic reactions Basophils prevention of clotting and allergic reaction Neutrophils involved in phagocytosis

v Agranulocytes

 

Monocytes

phagocytosis produce substances against foreign cells

Lymphocytes

THROMBOCYTES (PLATELETS) Minute cell fragments surrounded by a plasma membrane and containing granules PRIMARY FUNCTION: Forms platelet plugs, releases chemicals necessary for blood clotting PLASMA Liquid part of the body, yellow in color because of pigments

3 MAJOR TYPES OF PLASMA PROTEINS: Albumin prevents the plasma from leaking into tissues Globulins transports other substances and protects the body against infection fibrinogen a protein molecule that can be activated to form fibrin important in clotting process SPLEEN Located under the diaphragm to the left of the stomach Destroys old imperfect RBCs, breaks down hemoglobin released from these destroyed cells, stores platelets and filters antigens 3 types of tissues:

  

White pulp filled with WBC, esp. lymphocytes and macrophages Red pulp contains vascular enlargements that stores RBCs and platelets Marginal pulp contains end of arteries and other blood vessels

LIVER Largest glandular organ of the body Main production site for prothrombin and most blood clotting factors Converts bilirubin to bile and stores extra iron within the protein ferritin LYMPH NODES Fleshy pea sized structures found in groups or chains throughout the body Traps infection and foreign materials by acting like a sieve Blood Incompatibility Between the Pregnant and Fetus

Rh Incompatibility The Rh-negative Blood type Is An autosomal recessive trait A person must receive a gene for this characteristics from both parents Alternative Names Rh-induced hemolytic disease of the newborn Hydrops fetalis Rh incompatibility - excessive destruction of RBC which develops when a pregnant woman has an Rh(-) blood type + the fetus she carries has Rh(+) blood type

antigen is named Rh because it was

1st identified in the blood of rhesus monkeys Causes During pregnancy, red blood cells from the fetus can get into the mother's bloodstream as she nourishes her child through the placenta If mother is Rh-negative, her system cannot tolerate the presence of Rh (+) RBC mother's immune system treats the Rh (+) fetal cells as if they were: 1. a foreign substance 2. makes antibodies against the fetal blood cells If some of fetus' blood passes into the mother's blood stream, her body will produce antibodies in response mother is said to be sensitized (the process by which a person produces antibodies against the antigens of a different species, eg. Measles virus is called These anti-Rh antibodies may cross the placenta into the fetus, where they destroy the fetus's circulating red blood cells Due to the excessive destruction of fetal blood becomes deficient in RBC cannot deliver Sufficient oxygen to fetal cells

Erythroblastosis Fetalis disease in fetus or newborn caused by transplacental transmission of maternal antibody, resulting from maternal and fetal blood group incompatibility Incidence First-born infants : not affected -- unless the mother has had previous miscarriages or abortions, which could have sensitized her system R: takes time for the mother to develop antibodies against the fetal blood. Second child who is also Rh-positive

may be harmed. Symptoms Polyhydramnios (before birth) Hypotonia Motormental Retardation Slowly or rapidly increasing jaundice Prolonged jaundice Hyperbilirubinemia: bilirubin level in the blood is increased yellowish discoloration of the skin, mucous membrane, sclera and other organs Manifestation Yellowish discoloration = JAUNDICE or ICTERUS Icterus Index :representing the bilirubin concentration in the blood plasma 4-6 units The observations of HDN will include: Hepatosplenomegaly Icterus Gravis anemia & deep Hydrops Fetalis generalized edema

jaundice

The observations of HDN will include: Kernicterus - excessive staining of brain cells with bilirubin - Brain damage - Mental retardation - Nerve deafness - Muscle spasticity - Athethoid movement - Death

results:

Assessment / Diagnosis 1. All pregnant woman should be tested for: blood group Rh factor Routine antibody screening Blood transfusions 2. If the mother is Rh (-), the father of the infant is tested to determine his Rh status. *an Rh (-) father and mother will only produce Rh (-) offspring who will not be affected by Rh incompatibility* 3. Rh (-) pregnant woman who has Rh (+) husband will have to undergo: an anti-D antibody titer (INDIRECT COOMBS TEST) Done on the 16th 20th wk of pregnancy IF the titer is normal (less than 1.8), no intervention is immediately necessary BUT, a repeat indirect Coombs test will be made on the 7th -8th month of pregnancy = IF results are normal, mother will be allowed to progress on with pregnancy and deliver full term.

= once baby is delivered, his blood will be examined for the Rh factor = IF baby is Rh (-), there s no problem. = IF baby is Rh (+),he will undergo cord blood examination to determine presence of maternal antibodies in baby s blood stream, (DIRECT COOMBS TEST) DIRECT COOMBS TEST IF baby is Rh (+) and (-)for Coombs test mother will be given RhoGam BUT If baby is Rh (+) and (+) for Coombs test useless to give RhoGam to the mother IF the INDIRECT COOMBS TEST of a Rh (-) pregnant woman with a Rh (+) husband is positive at the start pregnancy will be allowed to progress But Amniocentesis will have to be repeated at regular intervals If studies revealed that fetus is severely affected, signs & symptoms of Erythroblastosis Fetalis will be observed.

*due to excessive RBC destruction and efforts of the fetus to make more RBC ensue* Laboratory & Diagnostic Findings SPECTROPHOTOMETER used to read amniotic fluid collected Readings are obtained to determine fluid density Plotted on graph & correlated w/ gestational age amt of bilirubin resulting from the hemolysis of RBCs can be estimated. c. Antibody Titer drawn at first prenatal visit on all Rh negative women drawn at 28 & 36 weeks & again at delivery or abortion. Normal value is 0. Ratio: Normal is1:8 If titer is absent or minimal (1:8) no therapy is needed. A rising titer indicates the need for RhoGAM & vigilant monitoring of fetal wellbeing. What is Rhogam ?

Management of Erythroblastosis Fetalis: Fetal intrauterine transfusion Exchange transfusion Phototherapy Fetal Intrauterine Transfusion Purpose: - to replace destroyed RBC s Procedure: Amniotic cavity is penetrated and fetal peritoneal cavity is entered by means of a special needle with radiopaque dye and a catheter is threaded into it 75-100 ml of type O, Rh (-) PRBC will be given to the fetus *the blood to be transfused to the fetus should be exactly the same as that of the mother so as not to be destroyed by the antibodies* FHR and mother s v/s monitoring reaction to the dye should also be observed If satisfactory, mother is discharged and readmitted after 7-10 days for another fetal intrauterine transfusion until fetus is mature. Exchange Transfusion Purpose : relieves baby s anemia : lowers blood s concentration of the bilirubin Procedure: umbilical stump is left longer than usual Wrapped in saline saturated gauze to prevent drying of the stump NPO for 3 hrs prior to transfusion Plastic catheter is inserted into umbilical vein and small amounts (10-20ml)of infants blood are withdrawn. Equal amounts of type O, Rh (-) blood is transfused venous catheter for fluids, meds; arterial catheter for extraction of blood Procedure is continued until most of the infants blood (around 500 ml) has been replaced with Rh (-) blood 1ml of Calcium Gluconate is injected after each 100-200 ml of donor blood -in order to replace ions depleted by citration (acid citrate- dextrose mixture) of donor blood*

Exchange Transfusion NURSING RESPONSIBILITIES: Make sure that thedonor blood is around 37 degrees Celsius to prevent cardiac arrest monitor CVP Give antibiotics as ordered

Monitor for v/s Monitor for serum glucose Observe for muscle twitching and other signs of hypocalcemia Phototherapy Photo oxidation by the use of artificial blue light (bililight) in order to convert bilirubin to an excretable one NURSING RESPONSIBILITIES: Cover infants eyes* Cover infants genetalia* Increase fluid intake* Expose all areas of the body* Assess for loose green stools* Assess temperature every 2hrs* Monitor bilirubin level*

Prevention Completely preventable. Rh-negative mothers to be closely monitored by obstetricians during pregnancy. If father is Rh-positive, mother is given a mid-term injection of RhoGAM ;second injection within afew days of delivery. injections prevent the development of antibodies against Rh-positive blood. An Rh positive person can receive Rh negative blood with no untoward effects ( if all other factors are compatible) Rh negative blood cannot receive Rh positive blood because they are not born with antibodiesagainst the Rh factor. Pregnancy Nursing Management Administer RhoGAM to the unsensitized Rh-negative client as appropriate RhoGAM must be administered to the mother w/in 72h of delivery Type & cross match of the mother s blood & newborn s cord blood must be done before administration to determine the need for the drug. Administer RhoGAM to the unsensitized Rh-negative client as appropriate Do not give RhoGAM to the newborn.

The dose may be given w/in 3-72h after a miscarriage or abortion. Do not administer IV. Administer into the deltoid muscle Monitor for side effects (anemia, pain at injection site, fever. May decrease antibody response to some live virus vaccines, such as measles, mumps and rubella. 2.Focus mgt. of sensitized Rh-negative mother on close monitoring of fetal well being 3. Provide management for ABO incompatibility Phototherapy Initiation of early feeding & exchange blood transfusion 4. Provide client family teaching & counseling. Rh Factor The dose must be repeated after each subsequent delivery. RhoGAM 300 mcg is the standard dose. RhoGAM Rho (d) immune globulin, human ABO Incompatibilty type O ( universal donor but cannot receive from other blood type) ABO Incompatibility Reaction in an infant with type B blood is more serious Hemolysis happens with first pregnancy (antibodies to A and B cell types are present from birth) Large IgM ( do not cross the placenta) Infant is not born anemic Hemolysis begins with birth Destruction may extend for up to 2 weeks Pre term infants do not seem to be affected ( receptor sites for ant A and B antibodies do not appear on RBC till late in fetal life) Even in mature NBs, direct Coomb s test: weakly positive ( few ant A & B sites) Reticulocyte count ( immature or newly formed RBC ) usually elevated as infant attempts to replace destroyed cells Jaundice occurs due to RBC destruction

THROMBOPHLEBITIS and THROMBOSIS

Etiology ASSESSMENT MEDICAL MANAGEMENT ANTICOAGULANTS Metabolic Disorders Normal glucose metabolism Glucose enters bloodstream from food source Insulin aids in storage of glucose as fuel for cells Insulin resistance is defined as insensitivity of cells to insulin, therefore resulting in increased levels of insulin and glucose in the bloodstream Metabolic changes in pregnancy Caloric requirement for a pregnant woman is 300 kcal higher than the non-pregnant woman s basal needs Placental hormones affect glucose and lipid metabolism to ensure that fetus has ample supply of nutrients Lipid metabolism: Increased lipolysis (preferential use of fat for fuel, in order to preserve glucose and protein) Glucose metabolism: Decreased insulin sensitivity Increased insulin resistance Increased insulin resistance Due to hormones secreted by the placenta that are diabetogenic : Growth hormone Human placental lactogen Progesterone Corticotropin releasing hormone Transient maternal hyperglycemia occurs after meals because of increased insulin resistance Relative baseline hypoglycemia Proliferation of pancreatic beta cells (insulin-secreting cells) leads to increased insulin secretion Insulin levels are higher than in pregnant than nonpregnant women in fasting and postprandial states Hypoglycemia between meals and at night because of continuous fetal draw Blood glucose levels are 10-20% lower Lipid metabolism Increased serum triglyceride (300%) and cholesterol (50%) levels Spares glucose for fetus, since lipids do not cross the placenta Provides building blocks for increased steroid hormone synthesis Insulin Synthesis Produced within the pancreas by cells, islets of langerhans Islets of Langerhans 1 million islets

identified by Paul Langerhans in 1869

cells cells

secrete glucagons produce insulin, most abundant

Somatostatin suppress secretion of insulin and glucagon History of Insulin 1920 Insulin is first discovered by Fredrick Banting and Charles Best November 1922 - Eli Lilly and Company is first to produce large amounts of insulin 1923 - MacLeod and Banting receive Nobel Prize in Physiology and Medicine for insulin discovery 1964 - Dorothy Crowfoot Hodgkin receives Nobel Prize in Chemistry for determination of spatial conformation of molecule 1980 - Frederick Sanger, British molecular biologist, receives Nobel Prize in Chemistry for amino acid structure determination DIABETES MELLITUS and PREGNANCY WHAT IS DIABETES? Refers to group of metabolic diseases that lead to high blood glucose levels due to defects in either: insulin secretion insulin action or both WHAT IS DIABETES? DIABETES MELLITUS Is an endocrine disorder of carbohydrate metabolism PATHOPHYSIOLOGY Deficiency or ineffective Insulin Glucose accumulates in the bloodstream (Hyperglycemia) Preexisting Conditions For some women, pregnancy represents significant risk because it is superimposed on preexisting illness Unique maternal and fetal needs due to these conditions must be met in addition to usual pregnancy-related feelings, needs, and concerns Metabolic Disorders Endocrine and metabolic disorders require careful management to promote maternal and fetal well-being and positive pregnancy outcome Diabetes mellitus is the most common endocrine disorder associated with pregnancy What are the Signs and Symptoms? Polyuria (frequent urination) Glucose concentration in blood is high Reabsorbtion of glucose in the proximal renal tubuli is incomplete, glucose remains in urine

Osmotic pressure of urine increases Inhibits reabsorbtion of water by kidney, resulting in increase urine production Dehydration Lost water volume in kidney replaced from water held in body, increased thirst and increased fluid intake polydipsia Polyphagia Increased appetite, no glucose delivered to muscles, tissues, body sends signal to brain to eat something to renourish Weight loss and weakness glucose cannot participate in crib cycle to be used as energy, use of fat as alternative energy source Vision changes changes shapes of lens in eye Importance of Control Complications of Diabetes

Diabetic Ketoacidosis Fat break down accelerates and increase the production of fatty acids Fatty acids converted into ketone bodies Ketones are toxic at high levels Symptoms - rapid, deep breathing, polyuria, nausea, vomiting, abdominal pain, altered states of mind such as hostility, mania, confusion, lethargy, and hypotension, coma, death Hypoglycemia Low blood sugar, too much insulin or not enough glucose to cover insulin treatment Symptoms - sympathetic activation of the autonomic nervous system: immobilized panic, dread, agitated, sweaty, seizures Amputations Heal slowly Fail to heal Infection Vascular diseases Damage to blood vessels Diabetic retinopathy growth of poor quality new blood vessels in retina, retinal damage, blindness Diabetic nephropathy damage to kidney, chronic renal failure dialysis Damage to arteries Coronary artery disease, stroke, peripheral vascular, diabetic myonecrosis ( muscle wasting ) Diabetic foot neuropathy and arterial disease Gestational Diabetes

Hyperglycemia in mother means more than normal glucose crossing the placenta and going to the fetus resulting to hyperinsulinism Diabetes Mellitus Before discovery of insulin in 1922, it was uncommon for a woman with diabetes to give birth to a healthy baby Pregnancy complicated by diabetes considered high risk Care requires nurse fully to understand normal physiologic responses to pregnancy and altered metabolism of diabetes Effects of Pregnancy on Diabetes Classification System: DM WHAT S THE DIFFERENCE?! Type 1 Juvenile diabetes mellitus Don t be fooled by its name!!! -cells that produce insulin are destroyed. Results in insulin dependence: Injection (most common), jet injection, indwelling catheters, & inhaled insulin. Type 2 Adult onset diabetes mellitus 90% of cases are Type 2 Ineffective insulin activity Insulin resistance Eventually leads to insulin dependence: Similar administrative techniques as Type 1. Pregestational Diabetes: Types 1 and 2 MAJOR TARGETED SITES OF DRUG CLASSES GESTATIONAL DIABETES Risk factors for the development of Gestational Diabetes Previous large infants 9lbs or more Family History of DM Glucosuria on two successive occasions Obesity weight >200lbs Unexplained pregnancy wastage (spontaneous abortions, stillbirths) Multiparity Presence of hydramnios Previous infant w/ a congenital anomaly

Gestational Diabetes (GDM) Diabetes Mellitus Metabolic changes associated with pregnancy Pregestational diabetes mellitus Preconception counseling Maternal risks and complications Hydramnios Ketoacidosis Hypoglycemia Fetal and neonatal risks Sudden and unexplained stillbirth Congenital anomalies

   

Cardiac defects Central nervous system Skeletal defects Other problems that cause significant neonatal morbidity

Effect of Diabetes on Pregnancy The fetus is often large ( macrosomia) 4x greater incidence of preeclampsia or Eclampsia Increase incidence of hydramnios & if coupled w/ macrosomia, it can cause cardiopulmonary symptoms rate of CS deliveries (45%) Incidence of congenital anomalies Gestational Diabetes Maternal diabetic acidosis is the most common cause of fetal death in pregnancy of a diabetic mother In ketoacidosis there is no oxygen and placental exchange at placental site results to: fetal asphyxia fetal death If maternal ketoacidosis is not treated, risk of fetal death increases to between 50 -90 % Macrosomia can be reduced by tight maternal blood glucose control before 32 weeks gestation Polyhydramnios ( increased amniotic fluid greater than 2000 ml) occur in 10% of pregnant diabetics. Even if the newborn is large, he is basically immature or premature thus more likely to suffer from respiratory distress syndrome (RDS) PREGNANCY RELATED COMPLICATIONS OF DIABETES

Nursing Assessment Obtain & review client s family & prenatal Hx Observe for the previously identified S/Sx & risk factors Assess client s knowledge on diabetes & her normal physiological Explain importance of screening tests Diabetic screening Important especially for the following: History of delivery of large babies >9 lbs. Unexplained fetal loss Congenital anomalies in previous pregnancies Obesity Family history of diabetes

psychological adaptations in pregnancy

Nursing Assessment Obtain baseline V/S & FHR & record. Obtain results of OGTT & other screening & diagnostic test results Knowledge on the basic testing procedures Assess psycho socioeconomic factors w/ special consideration to the potential stress evoked by the high risk pregnancy & high cost antepartum testing TESTING TESTING Diagnosed according to the following standards: Casual (not fasting) PG concentration: 200mg/dL 2 hour (fasting) PG concentration: 200mg/dL 8-hour (fasting) PG concentration: 126mg/dL Normal resting PG concentration ranges between: 80mg/dL 100mg/dL Fasting PG Test: Detects PG concentrations between 100mg/dL 125mg/dL Inexpensive and fast Oral Glucose Tolerance Test: Detects PG levels between 140mg/dL - 200mg/dL Takes longer since PG level is monitored for approximately two hours.

Medical Diagnosis The diagnosis should be established or ruled out by the evaluation of blood glucose levels. LABORATORY & DIAGNOSTIC FINDINGS Fasting Blood Sugar test (FBS) GLUCOSE SCREENING TEST FBS (fasting blood sugar of at least 8 hours) ORAL GLUCOSE TOLERANCE TEST (OGTT) Oral glucose of 50 mg is given and blood sugar is taken one hour after oral glucose administration Repeated for a 3-hour glucose tolerance test after a positive result of 1-hour screening

GDM: Screening Screening test 50 gm 1-hour glucose challenge test (GCT) Screening thresholds 135mg/dL: 90% sensitivity (23% screen positive) 140mg/dL: 80% sensitivity (14% screen positive) If patient screens positive, she goes on to take a 3-hour glucose tolerance test (GTT)

Glycosylated hemoglobin test(HbAIc) In the normal 120-day life span of the red blood cell, glucose molecules join hemoglobin, forming glycated hemoglobin. A buildup of glycated hemoglobin within the red cell reflects the average level of glucose to which the cell has been exposed during its life cycle. Measures glycemic control 4-8 weeks before test was done. Performed on women with pre-existing Diabetes. Hgb A1C concentration near 10% is associated with fetal anomaly rate of 20-25% Levels between 5 and 6% are associated with fetal malformation rates comparable to those observed in normal pregnancies (2-3%) Goal of normal or near-normal glycosylated hemoglobin (Hgb A1C) level for at least 3 months prior to conception

UTZ often done @ 18 weeks gestation to confirm gestational age & to survey for congenital anomalies fetal structural anomalies, macrosomia, hydramios Urinalysis Opthalmic exam Weekly Non-Stress Test (NST) are administered beginning @ approximately 32 weeks gestation Maternal serum alpha-fetoprotein level assess risk for neural tube defects Medical Diagnosis risk of intrauterine fetal demise in the antepartum period. Lung Maturity Studies (Amniocentesis) determine L/S ratio and Phosphatidylglycerol (PG) predictor of newborn s ability to avoid RDS Nursing Diagnoses Alteration in Carbohydrate Metabolism r/t diabetes Knowledge Deficit r/t diabetic self care during pregnancy

Disturbance in self Concept r/t complications of pregnancy Alteration in Tissue Perfusion; Uteroplacental High risk for Infection High Risk for Impaired Skin Integrity Major objectives of Nursing Care Identification of women at risk for diabetes & provisions of appropriate perinatal care. Maintenance of blood sugar levels. Provisions of adequate client education & counseling for safe self-management of mother & fetus/newborn. Prevention or detection of potential complications Promotion of a positive psychosocial adjustments to childbearing through understanding & acceptance of pregnancy & diabetes. Nursing Interventions Teach client the effects & interactions of diabetes & pregnancy & signs of hyper & hypoglycemia. Prepare & assist client for screening & other diagnostic tests. Teach client how to control diabetes in pregnancy. Advise on changes that need to be made in nutrition & activity patterns to prevent complications. Advise client on how to prevent infection Discuss & demonstrate insulin self-injection Demonstrate how to self-monitor blood glucose level. Provide emotional & psychosocial needs. Nursing Evaluation Understands the effects of her condition Recognizes symptoms of disease progression & reports them promptly. Implements the treatment plan of self care activities & prevents potential complications. Maintains adequate tissue perfusion & oxygenation to maternal-fetal unit. Delivers a healthy infant at or near term SIGNS AND SYMPTOMS of HYPOGLYCEMIA (Insulin reaction) Shakiness, dizziness Pallor, cold, clammy skin Sweating Headache Blurred vision Disorientation, irritability Hunger Nervousness TREATMENT: Hypoglycemia Give 12 fluid oz of orange juice (20 g CHO), 8 oz regular soft drink(not diet), 6-8 Lifesavers, 1 tbs honey, 1-2 tbs jam. Administer glucagon if unable to swallow. NOTE: Wait 20 minutes before repeating the procedure.

INTERVENTIONS

DIET and NUTRITION 1,800 2,200 calories/day divided into 3 meals and 3 snacks (20% CHON, 50% CHO, 30% fat) IVF supplementation if with nausea or vomiting (early pregnancy) or heartburn (late pregnancy) Low fat, high fiber diet

EXERCISE Aerobic or anaerobic exercises; exercise program consulted with physician

THERAPEUTICS INSULIN Combination of short-acting (regular) and Intermediate (NPH) Ratio of 2:1 (NPH to regular) 30 minutes pre-breakfast and a 1:1 ratio 30 minutes pre-supper

Methods for Control Daily Injections Bolus insulin Basal insulin Two to five shots a day

Insulin Pump Therapy Constant insulin delivery One insulin type become the bolus insulin and the basal insulin Catheter changed every three days

Regular Insulin No alteration in structure of human insulin Does not peak until 1 to 2 hours later because hexameric form must be converted to monomeric form Lasts about 4 to 6 hours in body NPH Neutral Protamine Hagedorn Protamine and Zinc added to the insulin structure These additions resulted in more of the hexameric form present in the mixture than the monomeric form Thus, more hexamers had to be transformed to monomers for insulin absorption The duration, onset, and peak of the insulin prolonged

Glucagon Brain can only use glucose, not alternative energy sources like fatty acids Insulin stimulates liver to store glucose in the form of glycogen In liver: 1.Stimulates break down of glycogen stored in liver 2.Activates hepatic gluconeogenisis: (amino acids) are converted to glucose Injection of this hormone is given to patients when seizures from low blood sugars occur Seizures most likely to occur during the middle of the night, most specifically when using Regular insulin and NPH insulin THERAPEUTICS BLOOD GLUCOSE MONITORING CBG (capillary blood glucose) monitoring TID AC or every 6 hours Recent Developments Constant glucose monitoring sensor records blood glucose every 10 seconds and sends an average of the glucose measurements every 5 minutes to the pump for 3 days Calibration by glucometer still required Symlin analog of human amylin, a hormone that contributes to glucose control during postprandial periods Slows gastric emptying Supresses glucagon secretion Implanted Insulin Pump (not yet fully developed) Transplants Pancreas and kidney dual transplants have been successful, must take immunosuppressant for rest of life Islet cell injections several injections must take place, not viable for the whole population because costly and not enough supply, most take immunosuppressant for rest of life Diabetic Ketoacidosis (DKA) Diabetic ketoacidosis <DKA> is near complete deficiency of insulin and elevated levels of stress hormones

   

Glucagon Cathecolamine Cortisol Growth hormone

DKA : acute metabolic complication of diabetes characterized by Hyperglycemia, Hyperketonemia,Metabolic acidosis DKA is a life-threatening complication in Pt. with untreated DM (chronic high blood sugar or hyperglycemia).

DKA occurs mostly in type 1 DM, less common in type 2 DM, may occur in situations of physiologic stress. new undiagnosed Type 1 DM frequently present with DKA Etiology Precipitates DKA -- > 5I s Insulin deficiency c relative or absolute increase in glucagon<Inadequate insulin administration> Infection or Inflammation < pneumonia, UTI, gastroenteritis, sepsis> Ischemia or Infarction < cerebral, coronary, mesenteric, peripheral> Intra-abdominal process <pancreatitis, cholecystitis> Iatrogenesis Drug < glucocorticoids,cocaine> Pathophysiology 1. Hyperglycemia : gluconeogenesis, glycogenolysis , glucose uptake into cell <underutilization> 2. Ketosis : lipolysis, ketogenesis , Peripheral tissue uptake ketone -- >ketonemia

3. Hypertriglyceridemia : free fatty acid 4. Osmotic diuresis : hyperglycemia -- > renal loss glucose, Na & K -- >electrolyte imbalance 5. Volume depletion : hyperglycemia, glucosuria & osmotic diuresis -- >dehydration Signs and Symptoms Initial symptoms of DKA Anorexia, nausea, vomiting, abdominal pain Polyuria, polydipsia Dehydration -- > dry mucous membranes, tachycardia, hypotension Alterated mental function-- > somnolence, stupor,coma Fever is not a sign of DKA -- >signifies underlying infectio Classic signs of DKA Kussmaul s respirations <deep> to compensate for metabolic acidosis with acetone odor on breath Laboratory and Diagnostic Test 1. 2. 3. 4. 5. 1. 2. 3. 4. 5. Glucose & ketone in serum & urine Serum electrolyte, BUN, Cr, Ca, PO4 Blood gas : capillary or arterial blood gas EKG : hypo/ hyperkalemia CBC UA Hemoculture Urine culture Throat swab culture CSF culture Chest x-ray

6. Omission of insulin 7. Physical or emotional stress

LABORATORY EVALUATION Elevated blood glucose level, decreased bicarbonate, decreased arterial pH Urine is strongly positive for sugar and ketone and moderate protein Sodium potassium level decreased, increased creatinine, BUN level Diagnosis Serum glucose > 300 mg/dl euglycemic DKA-- > pregnancy, alcolhol drinking, stravation >

<

Acidosis : serum HCO3 < 15 mEq/ml or pH < 7.25 < wide anion gap: >15 mEq/L> severity of DKA Mild : HCO3 > 15-18 mq/L & pH > 7.3 Moderate : HCO3 10-15 mq/L & pH 7.1-7.3 Severe : HCO3 < 10 mq/L & pH < 7.1 Ketone : positive ketone in urine and / or serum MANAGEMENT: Obtain blood and urine specimen perform PE stat start IVF of isotonic saline solution at a rate of 500 ml/hr- give insulin as directed monitor blood chemistry 1 or more ECG tracings clear liquids Treatment Confirm Dx : BS, positive serum ketone, metabolic acidosis

Assess Serum electrolyte : K, Na, Mg, Cl, HCO3, PO4 Acid-base status : pH, H CO3, Pco2 Renal function : creatinine, urine output Replace fluid Administer regular insulin/ RI Assess patient What precipitated the episode Initial appropriate work up

Measure capillary glucose every 1-2 hr/ E lyte, anion gap every 4 hr for first 24 hr

    

Monitor BP, PR, respiration, mental status, fluid intake/output every 1-4 hr Replace K Continue above until Pt. stable Administer intermediate or long acting insulin as soon as Pt. eating / overlap in insulin infusion & subcutaneous injection. Replace fluid DKA : volume & Na depletion 0.9%NaCl or NSS -- > 1 L/hr in 1-3 hr <5-10 0.45% NaCl or Nss/2-- > 150-300 mL/hr Pt. Na NSS/2 Pt. euglycemic DKA -- > 5% D/NSS/2 Severe DKA volume depletion~ 5-6 L ,Na ~ 500 & Cl ~ 350 mEq When BS < 300 -250 mg/dl change to 5%DN/2 80-100 ml/hr <Severe dehydration add NSS/2 >

mL/kg/hr> then >150 mEq/L-- >

Replace fluid Adequate Fluid replace : plasma volume urine output absorb/action insulin release counter-regulatory hormone Fluid replace : 50 % of volum in 6 hr & 50% in 24 hr Measure BP, PR, urine out put, E lyte, crepitation -- > pulmonary edema Administer regular insulin RI -- > blood sugar , inhibit ketone production low dose intramuscular insulin injection low dose continuous intravenous insulin infusion Potassium Supplement Moderate to severe DKA loss K~ 300-1,000 mEq or

3-5 mEq/kg

Rx :RI ,iv fluid -- > K shift in cell, loss K in urine-- > hypokalemia < cardiac arrhythmia ,muscle weakness > K supplement -- >urine > 40 ml/hr , k< 5.5 mEq/L, EKG normal

Monitor In first 6 hr BP, PR, RR, Mental status-- > q 15 min 1 hr skin turgor, plasma ketone Urine output, urine glucose, urine ketone -- > q 1 hr E lyte, BUN,Cr-- > q 4 hr

Long term F/U K supplement 7-10 day DM type 1 continue insulin usage Advice control BS < 300 mg/dl

Thyroid Crisis Where to look for Thyroid ? Clinical Anatomy of Thyroid Clinical Exam of Thyroid Thyromegaly

Thyroid Diseases Management of thyroid diseases during pregnancy requires special considerations Pregnancy induces major changes in thyroid function, and maternal thyroid disease can have adverse effects on the pregnancy and the fetus THYROID FUNCTION AND PREGNANCY

     

Altered thyroid function is associated with hormone changes in pregnancy as a result of increased levels of HCG and estrogen. Elevated levels of HCG may cause transient hyperthyroidism. Pregnant and lactating women require additional iodine intake Recommended average iodine intake is approximately 250 g/d Thyroid Hormone is Essential for Normal Brain Development Severe iodine deficiency, if inadequately treated, is a major cause of neurological damage

Physiologic Changes in Pregnancy free T4 and T3 increase slightly during the first trimester in response to elevated hCG. decline to nadir in third trimester TSH decreases slightly in first trimester.

The thyroid gland increases slightly in size during pregnancy. Effect to pregnant women:

If hyperthyroidism is inadequately treated, it may result in early

labor and pre-eclampsia.

Women with Grave s disease/ hyperthyroidism (worsens during post partum period) are at high risk of developing thyroid storm.

Considerations

    

Care requires coordination among several healthcare professionals. Avoiding maternal (and fetal) hypothyroidism is of major importance because of potential damage to fetal neural development, an increased incidence of miscarriage, and preterm delivery. Maternal hyperthyroidism and its treatment may be accompanied by coincident problems in fetal thyroid function. Autoimmune thyroid disease is associated with both increased rates of miscarriage, for which the appropriate medical response is uncertain at this time, and postpartum thyroiditis. Universal screening of pregnant women for thyroid disease is not yet supported by adequate studies, but case finding targeted to specific groups of patients who are at increased risk is strongly supported.

THYROID STORM ( Thyrotoxic crisis, Thyroid crisis) DEFINITION A severe, life threatening condition caused by an excess of thyroid hormones Form of severe hyperthyroidism (Grave s disease), usually of abrupt onset THYROID STORM ( Thyrotoxic crisis, Thyroid crisis) DEFINITION If untreated, May be fatal that may lead to stroke or heart attack. Mortality rate is 10-20% if with proper treatment and monitored closely.

Effect to fetus: Uncontrolled maternal hyperthyroidism may lead to:

    

Fetal tachycardia Small Gestational Age Still births Congenital malformations Fetal hyperthyroidism (occurs if mother s TSI (Thyroid Stimulating Immunoglobulins, antibody that stimulates thyroid gland function) levels are very high.

TSI is measured at 3rd trimester

Hypothyroidism Untreated patients with hypothyroidism rarely conceive and carry a pregnancy. Treated hypothyroidism usually has no associated pregnancy complications. Some patients will require increased levothyroxine doses during their pregnancies. Monitor thyroid function tests each trimester and at other clinically indicated times. Prenatal vitamins can decrease the absorption of levothyroxine.

Hyperthyroidism 90- 95% of hyperthyroidism in pregnancy is secondary to Graves Disease. A good pregnancy outcome can be expected in patients with good control. Untreated hyperthyroidism is associated with decreased fertility, an increased rate of miscarriage, intrauterine growth retardation (IUGR), premature labor, and perinatal mortality. Poorly controlled thyrotoxicosis is associated with thyroid storm especially at labor and delivery. Beta Blockers and PTU can be safely used in pregnancy and in nursing mothers. PTU crosses the placenta but does not usually cause fetal hypothyroidism and goiter unless used in high doses. Treatment goals favor mild hyperthyroidism over hypothyroidism. Hyperthyroidism -Grave s Disease Like other immune mediated diseases in pregnancy, Grave s disease tends to improve in the third trimester. Exacerbations may occur in the first trimester and postpartum. Neonatal and fetal thyrotoxicosis may occur because of transplacental passage of thyroid stimulating antibodies. Thyroid Failure - Organ Systems Cardiovascular Decreased ventricular contractility Increased diastolic blood pressure Decreased heart rate Central Nervous Decreased concentration General lack of interest Depression Gastro-instestinal Decreased GI motility Constipation Reproductive Arrest of pubertal development Reduced growth velocity Menorrhagia, Amenorrhea Anovulation, Infertility Hepatic Increased LDL / TC

Elevated LDL + triglycerides CAUSES Infections esp. of the lungs and throat Thyroid surgery Stopping/discontinuing hyperthyroidism medications Too high thyroid dose Treatment using radioactive iodine Pregnancy (Toxemia) Heart emergencies (heart attack/heart failure) Blood sugar changes DKA, insulin-induced hypoglycemia excessive palpation of thyroid Severe emotional stress CLINICAL MANIFESTATION Hyperpyrexia (38.5 C/105-106F and above) major sign/hallmark that differs thyroid storm from hyperthyroidism) Extreme tachycardia (130 bpm and above) Exaggerated symptoms of hyperthyroidism with disturbances of a major system ( GI- wt loss,diarrhea, abd l pain, N & V; Cardio- bp, edema, palpitations, arrythmias; Respi- SOB, DOB, chest pain.) Altered neurologic/mental state (CNS- disoriented, anxiety & irritability, confusion restlessness, delirium, psychosis, exaggerated reflexes, coma) increased sweating weakness MANAGEMENT : Decrease circulating thyroid hormone levels and their formation Treat precipitating cause (infection) Temperature be lowered with hypothermia blanket or cooling mattress, ice packs, cool environment. Acetaminophen is preferred with aspirin. Sedatives (e.g. Phenobarbital) are given to reduce anxiety, irritability and hyperactivity. Phenothiazines in large doses may be prescribed to reduce emesis and anxiety Humidified oxygen is administered to improve tissue oxygenation and meet high metabolic demands ABG level monitoring and pulse oximetry monitoring to monitor respiratory status Administer IVF, electrolytes and vasopressor agents ( treat dehydration and hypertension) Hydrocortisone is prescribed to improve adrenal insufficiency PTU (propylthiouracil)/methimazole (tapazole) administration antithyroid drugs, decreases thyroid hormone synthesis by blocking T4 to T3 conversion Give iodine, Na iodide, K iodide or Lugol s solution to inhibit thyroid hormone release from the thyroid gland Antithyroid drug therapy to the mother can induce fetal hypothyroidism, and transplacental passage of TSH receptor antibodies can cause fetal hyperthyroidism Administer digitalis if heart failure or atrial fibrillation occurs Give propanolol for sinus tachycardia. (controls heart rate, reduces adrenergic hyperactivity symptoms Sustain nutritional requirements Close monitoring of thyroid hormones and TSH.

Anti-thyroid drugs are administered usually at low levels. (Methimazole or PTU) Why low dose? drugs cross placenta and may potentially impair baby s thyroid function and cause fetal goiter R: To minimize development of hypothyroidism in baby. PTU is the drug of choice for maternal hyperthyroidism due to less transplacental passage Beta Blockers can be used sparingly to treat palpitation and tremors. R: used sparingly to avoid impaired fetal growth If allergic to Anti-thyroid drugs, Surgery is done but very rarely due to risks to mother and baby. Surgery is contraindicated during a thyroid storm episode because of patient s adrenergic hyperactivity. Radioiodine is also contraindicated to treat hyperthyroidism R: it crosses placenta and may result in permanent fetal hypothyroidism. Baby s thyroid gland is destroyed. Mother can still breast milk even if treated with anti-thyroid drugs only lower amounts of PTU is present. Hypothyroidism should be corrected before initiation of pregnancy, replacement dosage should be augmented early in pregnancy euthyroidism should be maintained throughout. Overt maternal hypothyroidism has been associated with damage to fetal intellectual developmentpresumably because of inadequate transplacental supply of hormone during early pregnancy Mother can still breast milk even if treated with anti-thyroid drugs only lower amounts of PTU is present. Postpartum Thyroiditis Postpartum thyroiditis is a destructive autoimmune thyroiditis that begins with a period of hyperthyroidism followed by a period of hypothyroidism. The gland is often enlarged. Postpartum Thyroiditis There is usually complete recovery but a chance of recurrence in subsequent pregnancies exists. 80-85% of patients will have positive antithyroid antibodies. A radioactive iodine uptake scan can differentiate postpartum thyroiditis from an exacerbation of Graves Disease. Postpartum thyroiditis in an important consideration in women with postpartum depression.

Perchlorate blocks Radioactive Iodide Uptake (RUI) Thyroid Investigations Nursing mothers who have radioactive iodine uptake scans should pump and discard their milk for 48-72 hours after the test. Hyperemesis Gravidarum associated with abnormal thyroid function tests in a significant number of cases. Hyperthyroidism may be the cause of hyperemesis or hyperemesis may be the cause of the hyperthyroidism. Thyroid Nodules New thyroid nodules should be aggressively investigated during pregnancy because of a high incidence of malignancy. Fine-needle aspiration cytology should be performed for dominant thyroid nodules discovered in pregnancy. Thyroid nodules recognized during pregnancy, or growing,are typically biopsied under ultrasound guidance If appropriate, surgery is performed in the midtrimester Delay in treatment of low-grade tumors until after delivery is not considered a danger Hepatic Coma HEPATIC COMA PORTAL-SYSTEMIC ENCEPHALOPATHY (PSE), HEPATIC ENCEPHALOPATHY A clinical disorder seen in hepatic failure and cirrhosis. Brain and nervous system damage that occurs as a complication of liver disorders. PATHOGENESIS WITH SEVERE LIVER IMPAIRMENT AND IF THERE IS ALSO PORTAL HYPERTENSION, AND SUBSEQUENT BYPASSING OF THE LIVER FILTRATION SYSTEM OF BLOOD FLOWING IN FROM THE INTESTINES, TOXIC SUBSTANCES NORMALLY REMOVED BY THE LIVER ACCUMULATE IN THE BLOOD LEAD TO METABOLIC ABNORMALITIES, MOST SIGNIFICANTLY ELEVATED SERUM AMMONIA,WHICH IS PRODUCED BY THE BODY WHEN PROTEINS ARE DIGESTED TRAVEL DIRECTLY TO THE BRAIN IMPAIRING THE FUNCTION OF BRAIN CELLS.

IMPAIRED COGNITION, (THINKING PROCESS) NEUROMUSCULAR DISTURBANCES (A FLAPPING TREMOR KNOWN AS ASTERIXIS), DECREASED LOC INCLUDING COMA AND DEATH. HEPATIC ENCEPHALOPATHY TRIGGERS : EPISODES OF GASTROINTESTINAL BLEEDING presence of blood in the upper GIT results in increased from the gut. EXCESSIVE INTAKE OF DIETARY PROTEIN ELECTROLYTE ABNORMALITIES (ESP. DECREASE IN K, RESULTING FROM VOMITING OR TREATMENTS SUCH AS DIURETICS OR PARACENTESIS) Decreased serum potassium levels and alkalosis may facilitate the conversion of NH4+ to NH3. INFECTIONS - Infection may predispose to impaired renal function and to increased tissue catabolism, both of which increase blood ammonia levels. RENAL DISEASE - Renal failure leads to decreased clearance of urea, ammonia, and other nitrogenous compounds. ANY CONDITION THAT RESULTS IN ALKALOSIS (ALKALINE BLOOD PH)

ammonia and nitrogen absorption

USE OF MEDICATIONS THAT SUPPRESS THE CENTRAL NERVOUS SYSTEM (E.G. BARBITURATES OR BENZODIAZEPINE TRANQUILIZERS) HEPATIC ENCEPHALOPATHY TRIGGERS : SURGICAL PROCEDURES TO TREAT PORTAL HPN e.g. operations to relieve pressure in the portal vein by connecting it to the splenic vein or other systemic venous vessels, have the effect of diverting incoming intestinal venous blood away from the liver. Ammonia-carrying blood will not be "purified" by the liver. "TIPS" procedure (transjugular intrahepatic portosystemic shunt) CLINICAL SYMPTOMS AN ELEVATED BLOOD AMMONIA LEVEL IS THE CLASSIC LABORATORY ABNORMALITY REPORTED IN PATIENTS WITH HEPATIC ENCEPHALOPATHY. EARLY MANIFESTATIONS OF HEPATIC COMA 1. "DAY-NIGHT REVERSAL" - tend to sleep during the day and stay awake at night 2. IMPAIRMENT IN SPATIAL PERCEPTION - poor ability to copy or draw various simple images, e.g cube, star, clock. This deficit can also be demonstrated by administering a "trail test" or "numbers connecting test . 3. ASTERIXIS Hallmark of hepatic coma on physical examination. Detected by having patient hold out his outstretched arms and hands and cock his wrists back. In the presence of asterixis, there is a non-synchronized, intermittent flapping motion at the wrists STAGES OF PORTAL-SYSTEMIC ENCEPHALOPATHY

STAGE I PRODROMAL SUBTLE MANIFESTATIONS THAT MAY NOT BE RECOGNIZED IMMEDIATELY; PERSONALITY CHANGES, BEHAVIOR CHANGES (AGITATION,BELLIGERENCE) EMOTIONAL LABILITY (EUPHORIA, DEPRESSION) IMPAIRED THINKING,INABILITY TO CONCENTRATE, FATIGUE, DROWSINESS,SLURRED SPEECH SLEEP PATTERN DISTURBANCES STAGE II IMPENDING CONTINUING MEDICAL CHANGES, MENTAL CONFUSION DISORIENTATION TO TIME, PLACE, PERSON, ASTERIXIS STAGE III STUPOROUS PROGRESSIVE DETERIORATION, MARKED MENTAL CONFUSION STUPOROUS,DROWSY BUT AROUSABLE ABNORMAL EEG TRACING MUSCLE TWITCHING HYPERREFLEXIA ASTERIXIS STAGE IV COMATOSE UNRESPONSIVENESS,LEADING TO DEATH, UNAROUSABLE,OBTUNDED, RESPONSE TO PAINFUL STIMULUS, NO ASTERIXIS, POSITIVE BABINSKI SIGN, MUSCLE RIGIDITY, FETOR HEPATICUS-LIVER BREATHMUSTY,SWEET ODOR, SEIZURES PROGNOSIS DEPENDS ON SEVERITY OF THE UNDERLYING CAUSE, PRECIPITATING FACTORS AND DEGREE OF LIVER DYSFUNCTION MANAGEMENT THE GOALS OF TREATMENT INCLUDE LIFE SUPPORT, ELIMINATION OR TREATMENT OF THE CAUSES, AND REMOVAL OR NEUTRALIZATION OF AMMONIA AND OTHER TOXINS. Checking an arterial ammonia level in the initial assessment Precipitants of hepatic encephalopathy, such as metabolic disturbances, GI bleeding, infection, and constipation, should be corrected. Avoid medications that depress CNS function, especially benzodiazepines. Patients with severe agitation and hepatic encephalopathy may receive haloperidol as a sedative. Patients with severe encephalopathy (ie, stage 3 or 4) who are at risk for aspiration should undergo prophylactic endotracheal intubation.

Low-protein diets are recommended for patients with cirrhosis, to decrease intestinal ammonia production and prevent hepatic encephalopathy Cathartics - Lactulose causes osmotic diarrhea, lessens the time available for intestinal bacteria to metabolise protein into ammonia within the bowel. Antibiotics - Neomycin and other antibiotics, such as metronidazole, oral vancomycin, paromomycin, and oral quinolones,rifaximin are administered to decrease the colonic concentration of ammoniagenic bacteria Medications containing ammonium (including certain antacids) should also be avoided Treatments to increase ammonia clearance L-ornithine L-aspartate (LOLA) -LOLA is a stable salt of the 2 constituent amino acids. L-ornithine stimulates the urea cycle, with resulting loss of ammonia Treatments to increase ammonia clearance Zinc -Zinc deficiency is common in cirrhosis. zinc increases the activity of ornithine transcarbamylase, an enzyme in the urea cycle. The subsequent increase in ureagenesis results in the loss of ammonia ions.

Sodium benzoate, sodium phenylbutyrate, sodium phenylacetate -Sodium benzoateinteracts with glycine to form hippurate. The subsequent renal excretion of hippurate results in the loss of ammonia ions. 5g of sodium benzoate p.o. BID can effectively control hepatic encephalopathy. Treatments to increase ammonia clearance Sodium phenylbutyrate is converted to phenylacetate. Phenylacetate reacts with glutamine to form phenylacetylglutamine. This is subsequently excreted in the urine, with loss of ammonia ions. L-carnitine - improves hepatic encephalopathy symptoms in several small studies of patients with cirrhosis. EXAMS AND TESTS Coarse, "flapping" muscle tremor (ASTERIXIS) may be observed during voluntary movement. Mental status examination will be abnormal, particularly cognitive (thinking) tasks such as connecting numbers with lines. Liver disease may be known or may be suspected, and signs of liver disease such as jaundice and ascites may be noted. Musty odor to the breath and the urine (occasional) Blood tests may be nonspecific, or may show liver failure. Blood chemistry may show low albumin, high bilirubin, or other abnormalities. Serum ammonia levels are usually high.

PT may be prolonged and not correctable with Vitamin K. Cranial CT scan may be normal, or may show general atrophy (loss of tissue). EEG shows abnormalities. POSSIBLE COMPLICATIONS Brain swelling Brain Herniation Progressive, irreversible coma Permanent nervous system damage Increased risk of:

   

Sepsis Respiratory failure Cardiovascular collapse Kidney failure

Side effects of medications PREVENTION TREAT LIVER DISORDERS TO PREVENT SOME CASES OF HEPATIC ENCEPHALOPATHY. AVOID HEAVY DRINKING AND INTRAVENOUS DRUG USE TO PREVENT MANY LIVER DISORDERS. Maternal Phenylketonuria Recognized cause of mental retardation caused by deficiency in enzyme phenylalanine hydrolase Absence impairs body s ability to metabolize phenylalanine, found in all protein foods Toxic accumulation of phenylalanine in blood interferes with brain development Key to prevention is identification of women with disorder Renal Disorders Renal Changes in Pregnancy Renal Changes Bladder capacity Increased Glomerular filtration rate (GFR) by 50% Renal plasma flow by up to 80% Blood urea nitrogen (BUN) Creatinine Glucose (in urine) ACUTE RENAL FAILURE ACUTE RENAL FAILURE Sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days Oliguria most common clinical situation TYPES Decreased Decreased Present

Prerenal occurs as a result of impaired blood flow hypoperfusion of the kidney

Intrarenal actual parenchymal damage to the glomeruli or kidney tubules

Postrenal obstruction in the kidney CHRONIC RENAL FAILURE CHRONIC RENAL FAILURE End stage renal disease (ESRD) Irreversible renal failure Fewer nephrons are functioning Remaining nephrons must filter more Hyperperfusion Hypertrophy Progressive, irreversible deterioration in renal function body s ability to maintain metabolic and fluids and electrolyte balance fails Results in uremia and azotemia CAUSES

 

CRF can develop insidiously over many years or it may result from episodes of ARF from which the client has not recovered DM (leading cause)

Pathophysiology renal blood flow GFR Hypertrophy of remaining nephrons Inability to concentrate urine Decreased blood viscosity + Increased blood pressure

+ Decreased oxygen supply Cardiovascular Consequences of CRF Clinical manifestations

     

Severe anemia Elevated serum creatinine level Proteinuria in urine Elevated BP Flank pain with pyelonephritis Edema

Goal of care

 

To preserve renal function To provide an optimal quality of life for self and significant others

Medical management

Drug therapy Corticosteroids Prednisone ALERT: suppresses insulin activity infant hyperglycemic Progesterone Azathioprine (with kidney transplantation) Nursing responsibilities Monitor vital signs, esp BP Emotional support, esp fetal status Stress reduction Restriction of activity Dialysis education Surgical management Dialysis Peritoneal dialysis Hemodialysis Further loss of nephron function Loss of non-excretory renal function Loss of excretory renal function

End- Stage Renal Disease CAUSES Diabetes mellitus Hypertension Chronic glomerulonephritis Pyelonephritis Obstruction of the urinary tract Hereditary lesions (eg. Polycystic kidney disease) Vascular disorder Infections Medications / toxic agents Environmental and occupational agents (eg. Lead, cadmium, mercury, chromium) Pathophysiology Stages of Kidney Failure Stage I - (Reduced renal reserve) Loss of nephron function (40% - 70%) Px usually does not have sx because the remaining function of the kidney

nephrons are able to carry out the normal

Stage II - (Renal insufficiency) Nephron function is lost (75% - 90%) Serum creatinine and blood urea nitrogen rise Kidney loses it s ability to concentrate urine and anemia developsPx may report polyuria and nocturia Stage III - (ESRD) Final stage of chronic renal failure Loss of nephron function (10%) All of the normal regulatory, excretory and hormonal function of the kidney are severely impaired Elevated creatinine and BUN levels as well as electrolyte imbalances Dialysis is indicated Clinical Manifestation Cardivascular: hypertension, pitting and periorbital edema, pericardial friction rub, pericardial tamponade, hyperkalimia Integumentary: ecchymosis, purpura, thin brittle nails, coarse thinning hair, gray-bronze skin color, dry flaky skin Pulmonary: crackles, thick tenacious sputum, depressed cough reflex, shortness of breath, tachypnea, kussmaul type of respiration, uremic pneumonitis Gastrointestinal: ammonia odor of breath, metallic taste, mouth ulceration and bleeding,N/V, constipation or diarrhea, bleeding in GIT Nuerologic: weakness, fatigue, confusion, disorientation, tremors, seizure, burning of sole of feet, behavioral change

Musculoskeletal: muscle craps, loss of muscle strength, renal osteodystrophy, bone pain, fracture, foot drop Reproductive: amenorrhea, testicular atrophy, infertility, decrease libido Hematologic: anemia,thrombocytopenia Assessment and Diagnostic Findings 1. Glomerular filtration rate 24 urinalysis for creatinine clearance = decrease GFR Increase BUN level Serum creatinine (most sensitive indicator of renal function 2. Na and H2O retention Kidney cannot concentrate or dilute urine normally Retain Na and H2O = increase risk for edem, heart failure and HPN Other px tends to lose salt and develop hypotension and hypovolemia Vomiting and diarrhea may produce Na and H2O depletion which worsen the uremic state 3. Anemia Inadequate erythropoietin production Producing fatigue, angina and shortness of breath 4. Ca and Phosporous imbalance Body does not normally respond to the increased secretion of parathormone Active metabolite of vitaminD normally manufactured by the kidney decreases Uremic bone disease develops from the complex changes in Ca, PO4 and parathormone balance Medical Management 1. Medications Antihypertensive - to manage HPN Antiseisure agents - (Diazepam, Phenytoin) Erythropoietin (Epogen) - to manage anemia Administer via IV or SubQ tid A/E: HPN, increased clotting of vascular access sites, seizure and depletion of iron stores Iron supplement PO4 binding agents - suitable for or select not to participate in dialysis or transplantation Antacids Hyperphosphatemia and hypocalemia are treated with aluminium based antacid Magnesium based antacid should be avoided to prevent magnesium toxicit Medical Management Diet therapy Vitamin supplementation CHON restriction Potassium restriction Adequate caloric intake

Fluid intake to balance fluid loses Na intake to balance Na loses Dialysis Used to remove fluid and uremic waste products from the body when the kidney cannot do so. Used to treat px with edema that does not respond to tx, hepatic coma, hyperkalemiam hypercalcemiam HPN and uremia Types of Dialysis Medical Management Methods of Therapy 1. Hemodialysis Commonly used method of dialysis Used for acutely ill and require short term dialysis (days to weeks) Used for ESRD who require long term or permanent therapy to prevent death Uses dialyzer (synthetic semipermeable membrane replacing the renal glomeruli and tubules as the filter for the impaired kidneys) Dialysis disequilibrium Complication includes: Hypertriglyceridemia Heart failure Coronary heart disease Angina pain Stoke Peripheral vascular insufficiency Hypotension Painful muscle cramping Exsanguinations Dysrhythmias Air embolism Dialysis disequilibrium Nursing Diagnosis

     

Excess fluid volume r/t decreased urine output, dietary excesses and retention of Na and H2O Imbalance nutrition: less than body requirements r/t anorexia, N/V, dietary restriction and altered oral mucous membranes Deficient knowledge regarding condition and tx regime Activity intolerance r/t fatigue, anemia, retention of waste product and dialysis procedure Low self-esteem r/t dependency, role changes, change in body image and sexual dysfunction

Nursing Management

 

Assessing fluid status and identifying potential source of imbalance Implementing dietary program to ensure proper nutritional intake

  

Promoting positive feelings by encouraging increase self-care and greater independence Report the health care provider the s/sx of decreased renal fxn Worsening s/sx of renal failure (N/v, change in usual output, ammonia odor or breaths/sx of hyperkalemia s/sx of access problem (clotted fistula or graft andinfection)

Multiple dietary restrictions is required, including fluid intake, NA, K and CHON restriction

Pregnancy Induced Hypertension a condition in which vasospasm occurs during pregnancy in both small and large arteries . TOXEMIAS OF PREGNANCY VASOSPASM ( constriction of Blood vessels) BP level

Physiology Vasospasm Vascular effects Vasoconstriction Poor organ perfusion Increased blood pressure Vasospasm Kidney effects Decreased GFR and increased permeability of glomeruli membranes Increased levels of BUN, UA and creatinine Decreased urine output and proteinuria Vasospasm Interstitial effects Diffusion of fluid from blood stream into interstitial tissue Edema

Predisposing Factors

    

Multiple pregnancy Primiparas Low socio economic status Multiparas Hydramnios

Existing disease cardiac, DM with vessel or renal involvement or essential HPN. Symptoms of developing PIH

Rapid weight gain over 2 lb / wk. in the 2nd trimester 1 lb / wk. in the 3rd trimester

     

Swelling of the face or hands & fingers.Face Hands Flashes of light or dots before the eyes. Dimness or blurring of vision Severe, continuous headache Decreased urine output.

CLASSIC SIGNS Hypertension Edema proteinuria PATHOPHYSIOLOGY Significance and Incidence Hypertensive disorders of pregnancy are most common medical complication reported during pregnancy Significant contributor to maternal and perinatal morbidity and mortality Preeclampsia complicates approximately 12% to 20% of pregnancies Morbidity and Mortality Overall rate of maternal death from preeclampsia/eclampsia is 1.8 per 100,000 Leading cause specific cause of death Large disparity between rates of maternal death by race, in that: African-American women more likely to die of preeclampsia than women of all other races Classification Hypertension, gestational or chronic, defined Systolic BP greater than 140 mm Hg Diastolic BP greater than 90 mm Hg

Mean arterial pressure (MAP) greater than 105 mm Hg Hypertension, gestational or chronic, defined Diagnosis of onset during pregnancy based on two measurements that meet criteria for gestational BP elevation HYPERTENSIVE DISORDERS IN PREGNANCY Gestational Hypertension(GH) Pre-Eclampsia Eclampsia Chronic Hypertension Chronic hypertension with superimposed preeclampsia Classification Gestational hypertension Onset of hypertension without proteinuria after week 20 of pregnancy GESTATIONAL HYPERTENSION BP>140/90 or + 30mmhgSBP/+15mmhgDBP Starts after 20th week of pregnancy No proteinuria BP returns to normal by 6 wks postpartum Classification Preeclampsia Pregnancy-specific syndrome Hypertension develops after 20 weeks of gestation in previously normotensive woman Disease of reduced organ perfusion with presence of hypertension andproteinuria MILD PREECLAMPSIA BP rising to 140/90 mmHg, taken on two occasions at least 6 hours apart proteinuria of 1+ or 2+, on reagent test strip on Diastolic Pressure Value degree of peripheral arterial spasm. Appearance of symptoms b/w 20th & 24th week of Orthostatic Proteinuria long periods standing, excrete protein. 1+ proteinuria ( about 1 gram per day) random sample

pregnancy

Edema weight gain 1st symptom a woman notices. Sudden weight gain (+3lb/mos in second trimester; +1lb/week in 3rd trimester; or Interventions Bed rest Diet Provision of emotional support

+ 4.5lb/week at any time)

Patient education Severe Preeclampsia Assessment Findings Headaches, epigastric pain, nausea & vomiting, visual disturbances, irritability BP of 150-160/100-110mmhg Severe hypertension, 30-40 mmHg on Bedrest. edema & weight gain

Massive anasarca Proteinuria (5g/24hours) (4+) oliguria Hyperreflexia of 4+, possibly w/ clonus Less than 400 mL output in 24 hours. Dizziness, headache, blurring vision, nausea and vomiting, epigastric pain, and irritability. Changes from preeclampsia with tonic-clonic seizure attacks to comatose state. Severe Preeclampsia Assessment Extensive edema Cerebral and visual disturbances Epigastric pain, nausea and vomiting Interventions Bed rest Maternal and fetal vital signs monitoring Nutrition Patient education - I and O - Daily weight Seizure precautions Medications -Anti-hypertensives -Anti-convulsant Administration of Magnesium Sulfate -acts on myoneural junction -diminishes neuromuscula transmission Nursing responsibilities Monitor vital signs, reflexes and urine output Antidote: Calcium gluconate Promote bed rest as long as signs of edema or proteinuria are minimal, preferably side lying Provide well-balanced diet with adequate protein & roughage, low to moderate Na. Explain need for close follow-up, weekly or twice-weekly visits to physician

Monitor I & O Review results of laboratory tests. Take daily weight. Do daily fundoscopic examination Institute seizure precautions. Restrict visitors Minimize all stimuli Monitor for hyperreflexia Adm. sedatives as ordered. Continue to monitor 24-48 hours post delivery. Administer medications as ordered; vasodilator of choice usually hydralazine ( Apresoline) Eclampsia Assessment Findings Increased hypertension precedes convulsions followed by hypotension & collapse. Coma may ensue. Labor may begin, putting fetus in great jeopardy. Convulsions may recur.

ECLAMPSIA 20% of maternal mortality rate due to: (Moldenhauer & Sibai, 2003) Cerebral hemorrhage Circulatory collapse Renal failure Fetal prognosis poor hypoxia and fetal acidosis Abruptio placenta occurs due to vasospasm Fetal mortality rate 10% in preeclampsia Fetal mortality rate 25% in eclampsia PREECLAMPSIA HPN + Proteinuria + Edema Eclampsia Description Most severe classification of PIH High maternal mortality

Assessment Convulsions leading to coma

Interventions Tonic-clonic seizures Oxygen administration; pulse oximetry Cardiac monitoring Positioning Medications Termination of pregnancy COMPLICATION HELLP H emolysis EL elevated liver enzymes LP low platelet Description *Variation of PIH *Occurs in 1 in every 150 births *Maternal mortality 24% *Fetal mortality 35% Assessment Nausea Epigastric pain Body malaise RUQ tenderness Diagnostics & Laboratory studies PBS hemolysis of RBC Platelet thrombocytopenia ALT (alanine aminotransferase) and AST (aspartate aminotransferase) Management TransfusionFFP or platelet IVF hydration and nutrition Termination of pregnancy Eclampsia Nursing Interventions Minimize all stimuli Darken room Limit visitors Use padded bedsides & bed rails Check vital signs & lab values frequently. Seizure precautions: airway, 02, & suction equipment should be available at bedside. Adm. Meds as ordered. Prepare for CS when seizure stabilized Continue monitoring 24-48h postpartum.

elevated liver enzymes

Lateral recumbent position - avoids uterine pressure on the vena cava - prevents supine hypotension syndrome Bed rest evacuation of sodium encouraging diuresis. ABSENCE OF MEDICATION 90% of childbearing age women are working difficult to leave work little swelling - little headache. BEGINNING SIGNS OF HPN seen weekly or more frequently. NO CURE bed rest reduce symptoms Chronic hypertension Present before the pregnancy or diagnosed before week 20 of gestation High BP that occurs before pregnancy or before the 20th week of pregnancy Chronic Hypertension Chronic hypertension associated with increased incidence Abruptio placentae Superimposed preeclampsia Adverse pregnancy outcomes Postpartum complications include: Pulmonary edema Renal failure Hypertensive encephalopathy Chronic Hypertension Increased risk of perinatal deaths, rates of preterm birth, and small-for-gestational-age (SGA) infants Lifestyle changes may be necessary In postpartum, high risk women monitored for complications: renal failure, pulmonary edema, heart failure, and encephalopathy Chronic Hypertension Antihypertensive drugs found in breast milk Methyldopa is choice for woman needing medication for hypertension and wishing to breastfeed CHRONIC HYPERTENSION WITH SUPERIMPOSED PREECLAMPSIA Chronic HPN that has new occurrence of proteinuria or thrombocytopenia &

liver enzymes

HELLP Syndrome H Hemolysis, resulting in anemia & jaundice EL Elevated liver enzymes, resulting in epigastric pain & vomiting LP Low platelets, resulting in thrombocytopenia, abnormal bleeding & clotting time, bleeding gums, petechia, & possibly DIC HELLP SYNDROME Characterized by:

  

RBC hemolysis elevated liver enzymes low platelet count related to severe vasospasm leading to disseminated intravascular coagulation ( DIC ).

Platelet and RBC transfusion often are administered; coagulation factors are monitored Labor is induced if AOG is more than 32 weeks; cesarean if less than 32 weeks. Chronic hypertension with superimposed preeclampsia Women with chronic hypertension may acquire preeclampsia or eclampsia Extreme Edema puffiness on woman s face and hands palpated over bony surfaces Tibia on the anterior leg Ulnar surface of the forearm Cheekbones Assessing type of Edema Nonpitting edema 1+ 2+ swelling cannot be indented with finger pressure. tissue can be indented slightly. Minimal edema of lower extremities. moderate indentation. Marked edema of the lower extremities Assessing type of Edema

3+ 4+ pitting edema

deep indentation. Edema of lower extremities, face, hands, and sacral area. indentation so deep and remains after removal of the finger. Generalized massive edema that includes ascites. Reports about edema UE edema my rings are so tight, I cant get them off . Facial edema when I wake in the morning, my eyes are swollen shut or I cant talk until I walk around awhile . Edema reduce their urine output to approximately 400 600 mL / 24 hours Criteria for admission to healthcare facility BP 160/110 mm Hg With extensive edema With marked proteinuria 3+ to 4+ With cerebral or visual disturbances With marked hyperreflexia Oliguria 500 ml or less Criteria for admission to healthcare facility 36 weeks of pregnancy with confirmed fetal lung maturity Less than 36 weeks and with immature lung function Management

   

Women are hospitalized Visitor restriction Darken the room Do not stress patients receives clear explanation Allow to express feelings

Take BP every 4 hours

Obtain blood studies

assess renal & liver function & development of DIC Blood typing and cross matching Daily Hematocrit Plasma estriol level Electrolytes Optic fundus

 

Obtain daily weight Indwelling catheter: UO 600 mL/ 24 hours more than 30 mL/ hour

24 hour urine sample for protein and creatinine clearance evaluate kidney function

  

Doppler auscultation at 4 hour s intervals External fetal heart monitor Record of fetal movements KICK COUNT

    

Non stress test or biophysical profile O2 administration Moderate to high in protein Moderate in sodium IV line emergency route

DRUGS USED IN PREGNANCY INDUCED HYPERTENSION

HYDRALAZINE (Apresoline) INDICATION Antihypertensive (peripheral vasodilator), used to decrease HPN DOSAGE :5 10 mg / IV Administer slowly to avoid sudden fall in BP. Maintain diastolic pressure over 90 mmHg inadequate placental perfusion can occur HYDRALAZINE (Apresoline) MAJOR ADVANTAGE: increases CO and blood flow to the placenta thus do not interfere with placental circulation.

LABETALOL OR NIFEDIPINE ANTIHYPERTENSIVE HYDRALAZINE (Apresoline) Acts to lower BP by peripheral dilatation Diastolic pressure not be lowered below 80 to 90 mmHg ANTIHYPERTENSIVES: HYDRALAZINE HCl (APRESOLINE) AND DIAZOXIDE (HYPERSTAT) ANTIHYPERTENSIVES: HYDRALAZINE HCl (APRESOLINE) AND DIAZOXIDE (HYPERSTAT) Nursing Care P promote bed rest P prevent convulsion P Prepare the following E Ensure high CHON diet, Na in moderation A Antihypertensive drug (Apresoline) C Convulsion, prevent E Evaluate for MgS04 Toxicity Magnesium Sulfate MECHANISM OF ACTION Prevents seizures and blocks neuromuscular transmission SIDE EFFFECTS: Flushing, thirst, absence of deep tendon reflexes, respiratory depression, cardiac arrhythmias, cardiac arrest, decreased urinary output Medical Management Magnesium Sulfate (Mgso4)

 

Acts upon the myoneural junction, diminishing neuromascular transmission Promotes maternal vasodilation, better tissue perfusion

Prevents CONVULSIONS MAGNESIUM SULFATE INDICATION: Muscle relaxant, prevents seizures & uterine contractions in preterm labor. Loading dose 4 6 g. Maintenance dose 1 g/ hour IV. Infuse loading dose slowly over 15 30 mins. Always administer a piggyback infusion. MAGNESIUM SULFATE Assess RR, UO, DTR s, & clonus every hour. UO should be over 30 mL/hr and RR over 12/min. Serum Mg level should remain below 7.5 mEq/L (4 8 mg / dL Mckinney) Observe for CNS depression & Hypotonia in infant at birth.

Signs of overdose of Mg SO4

    

Decreased UO Depressed respirations (less than 12 cpm) Assess deep respirations. Reduced consciousness / altered sensorium Maternal pulse oximeter reading lower than 95% Sweating , flushing, Hypotension A serum Mg above the therapeutic range Signs of paralysis

Decreased or absence of DTR sAssess for depressed patellar reflex.(absent or <1+)

Nursing Responsibilities when giving magnesium sulfate

 

Monitor client s respirations, BP, & reflexes as well as urinary output frequently Administer medication either IV or deep IM.

ANTIDOTE: calcium gluconate or calcium chloride GLUCONATE CALCIUM Antidote for Mg SO4 intoxication 1 g/IV (10 mL of a 10% solution Prepared at bedside when administering Mg SO4. Administer at 5 mL/ min. DIAZEPAM (Valium) Halt seizures 5 10 mg / IV Administer slowly. Dose maybe repeated q 5 10 (up to 30 mg/hr) DIAZEPAM (Valium ) SALT POOR ALBUMIN high colloid solution used to treat severe Oliguria Mg SO4 given IV 2 hrs before baby s birth baby will be born with respiratory depression drug crosses the placenta. Fetal effects

  

Loss of variability of heartbeat Reduced fetal breathing movements Late deceleration

Drug Management

Pulmonary edema Furosemide (Lasix) is given.

Digitalis - to strengthen contraction of the heart TONIC CLONIC SEIZURES Preliminary signal or aura TONIC PHASE Muscles of the body contract Back arches Extremities becomes stiff / rigid Jaw closes abruptly Respirations stop Woman may grow slightly cyanotic CLONIC PHASE Muscles contract and relax repeatedly Extremities waves widely Inhales and exhales irregularly bladder & bowel muscles contract & relax Urine & fecal incontinence Breathing is not entirely effective Remains cyanotic

May aspirate saliva

May aspirate saliva Priority care: MAINTAIN PATENT AIRWAY Don t put a tongue blade between the woman s teeth Suction patient s mouth and nose Administer O2 via face mask (8 10 L/min) Asses O2 saturation via pulse oximeter.

Apply external fetal monitor Turn the patient on her side POSTICTAL STATE

Patient is in semicomatose stage Cannot be roused except by painful stimuli Priority care: MAINTAIN PATENT AIRWAY Extreme close observation Painful stimulus of contractions NOTE: Hearing is the last sense lost and the 1st one regained Continuously assess fetal heart sounds and uterine contractions Check for vaginal bleeding every 15 minutes

POSTPARTUM HYPERTENSION 10 14 days after birth usually occurs 48 hours after birth Monitoring BP Postpartum check up GRADING PATELLAR REFLEX 0 no response, hypoactive, abnormal. 1+ - somewhat diminished response but not 2+ - average response 3+ - brisker than average but not abnormal. 4+ - hyperactive, very brisk, abnormal. GRADING ANKLE CLONUS Mild Moderate Severe 2 movements 3 to 5 movements over 6 movements

abnormal.

Closely monitoring of maternal vital signs ( esp. BP ) and weight and FHT

      

Bedrest most of the day; side lying position; for 8-12 hours. High protein ( 60-70g/day), Low sodium diet. Calcium ( 1200mg), magnesium, 2-6g of zinc; vitamin C&E. Health teachings for symptoms of mild and severe preeclampsia. Administration of Magnesium Sulfate, Cortecosteroids and anti hypertensives as ordered. HPN drugs are excreted in breast milk. Blood replacements. Monitor for seizure activity and protection from injury.

  

Administer O2 as needed. Prepare mother and her family for early induction of labor. Vaginal delivery is preferred over cesarean. Health teachings on contraception.

Infectious Diseases A group of infections caused by viruses and protozoa that cause serious fetal problems when contracted by the mother during pregnancy. TORCH INFECTIONS

infections transmitted to the fetus in utero OR during passage through the birth canal TORCH INFECTIONS stands for

     

Toxoplasmosis Others: Include gonorrhea, syphilis, varicella, hepatitis A and B virus (HAV, HGBV), HIV, and group B beta-hemolytic streptocci (GBS) Rubella Cytomegalovirus (CMV), causing Cytomegalic inclusion disease (CID) Herpes simplex virus (HSV) TOXOPLASMOSIS a protozoan infection Cause: eating undercooked meat, although organism is spread most commonly by contact with cat stool, or soil with cat litter Manifestations: almost none, except for a few days of malaise and posterior cervical lymphadenopathy (influenzalike symptoms) Toxoplasmosis Cause: Toxoplasmosis protozoan - Toxoplasma Gondii, capable of causing intrauterine infection Incidence: 1:1000 live births TOXOPLASMOSIS Effect on fetus: Infant may be born with any of the following:

    

Central nervous system damage Hydrocephalus Microcephaly Intracerebral calcifications Retinal deformities

TOXOPLASMOSIS Diagnostics - serum analysis for antibody titers Management Sulfadiazine (potentially harmful to the fetus) Pyrimethamine (anti-protozoal) Pathophysiology: parasite primary natural host is the cat family The organisms exist in 3 forms: oocyst, tachyzoite, tissue cyst. The oocyst are excreted in cat feces Ingestion of oocyst is followed by penetration of gastrointestinal mucosa Most maternal organs, including the placenta are seeded by the protozoan In the chronic form of the disease, organisms invade certain body tissues tissue cysts Signs & symptoms: Rarely produces symptoms - IF present, they are generally nonspecific Mononucleosis-like illness with fever Lymphadenopathy Fatigue, Malaise, Myalgia Fever , Skin rash, splenomegaly BUT when the infection is transmitted from the woman through the placenta, condition is called Congenital Toxoplasmosis (Premature infants have a higher incidence) Chorioretinitis Intracranial calcification Obstructive Hydrocephalus triad of symptoms includes: brain, eyes and striated muscle forming

Transmission: contact with soil or litter boxes contaminated with cat feces Development of the infection in the mother is associated with: consumption of ingested raw or undercooked meat unpasteurized milk Transmission: Development of the infection in the mother is associated with:

 

via blood product transfusion (WBC) poor hand washing after handling cat litter

Diagnosis and Laboratory studies Direct Isolation of the organism from body fluids or tissues Cerebrospinal fluid examination Serologic tests Indirect Fluorescent antibody test it measures antibodies to surface antigen (in mother) IgG titers greater than 1:256 acquired a recent infection IgM titers greater than 1:256 acquired an acute infection Radiologic studies a. a skull film or CT scan of the head b. long bone film Other studies a. ophthalmologic examination Effects Maternal effects: Flu-like symptoms in acute phase Fetal effects: Miscarriages in early pregnancy (harmful to the fetus if it is contracted between 10 and 24 weeks of pregnancy) Neonatal effects: CNS lesions can result in: hydrocephaly, microcephaly, chronic retinitis, seizures Management: The efficacy of treatment of pregnant women and infants with congenital infection is unclear Treatment of acute maternal toxoplasmosis appears to reduce the risk of fetal wastage, and decrease the congenital infection Drug of choice: Pyrimethamine (1mg/kg/day orally) + sulfadiazine (25-100mg/kg/day) should be use after the 1st trimester Pyrimethamine is a folic acid antagonist Folic Acid (2mg/6mg, 3x a wk) Prevention: Advise the pregnant women to have someone else clean the cat litter box If there s no one else to perform the cleaning - should wear the gloves avoid eating raw meat all fruits and vegetables washed carefully do hand washing Other infections (like Hepatitis B, Syphilis, Varicella and Herpes Zoster) Hepatitis B Cause: infection with Hepatitis A (HAV) orHepatitis B (HBV) - common Manifestations: Fever, malaise, nausea, vomiting, liver

Tenderness, Jaundice (late symptom) Incidence: acutely affected- approx 1% die of liver disease 85%-90% - completely recover and develop immunity to hepatitis b 10%-15% - chronic carriers and are at higher risk for developing cirrhosis and liver Ca Pathophyiology: Transmitted sexually or through contact with blood or body fluids Be transmitted to fetus by contact with vaginal secretions and blood during delivery Transmission: HAV is spread by droplets or hands Transmission to the fetus is rare BUT it can occur HBV can be transmitted to the fetus via placenta, BUT transmission usually occurs when the infant is exposed to blood and genital secretions during labor and delivery

Diagnosis: For Hepatitis A: Radioimmunoassay and enzyme-linked immunosorbent Assay methods *elevated IgM in the absence of IgG - probable acute hepatitis *elevated IgG in the absence of IgM - chronic stage of HAV

to detect HAV antibodies

For Hepatitis B: Hepatitis B surface antigen (HbsAg) Serology to detect IgM antibody, bilirubin levels VIRAL HEPATITIS Management: Pregnant patients screen for (HbsAg) If the mother if (+) for (HbsAg) the neonate should receive within 12 hours: Hepatitis immunoglobulin (HBIg) provides immediate protection Hepatitis B vaccine provides long protection from infection Hepatitis A Treatment is supportive Condition limiting and does not result in chronic infection Hepatitis B Bed rest

High-protein, low-fat diet Increased fluids HIV (Human Immunodeficiency Virus) leads to acquired immunodeficiency syndrome (AIDS) is the most serious of the STDs The Infected Cell Produces New HIV Pathophysiology Retrovirus Infects T-lymphocytes Body s ability to fight infection is disabled Transmission (by blood or body fluids) Sexual intercourse Exposure to infected blood Vertical transmission across the placenta to the fetus at birth Breast milk to the newborn

Manifestations Weight loss Anemia Diarrhea and fatigue (AIDS-related complex); developing later on to opportunistic infections (toxoplasmosis, candidiasis, GI illness, herpes simplex) Diagnostics Serologic screening Antibody testing Management Symptomatic, based on disease progression Focus on prevention of HIV transmission GROUP B BETA-HEMOLYTIC STREPTOCOCCI (GBS) occurs at a higher incidence during pregnancy (10% to 30%) Manifestations: Usually asymptomatic; symptoms of UTI Transmission: Placental transfer; direct contact at birth Effect on fetus: Pneumonia, meningitis Diagnostics: Cultures from anorectal and vaginal areas obtained at 36-37 weeks gestation

Management: Penicillin or ampicillin during labor; if given earlier, recolonization may occur, with subsequent infection of infant v Syphilis Cause: It is caused by a spirochete (spiral- or coil-shaped bacterium), Treponema pallidum. crosses the placenta only after the 18th week of pregnancy Transmission: It is transmitted sexual contact or through broken skin Symptom: Painless red pustule, appears within 2-6 weeks after exposure Pathophysiology: The pustule quickly erodes and develops a painless, bloodless ulcer called chancre Because it is painless, the newly infected person may not notice the chancre The chancre, which sheds infectious fluids IF the pregnant woman becomes infected with Syphilis, the bacteria can cross the placenta causing infection to the growing fetus Manifestations dependent on stage Primary: a painless chancre (lesion or deep ulcer) seen generally on the genitalia, but may also be present on the mouth or rectal area Secondary (4 to 6 weeks after the chancre): generalized maculopapular rash on palms and soles Tertiary or latent: neurologic symptoms such as mental confusion, slurred speech and lack of coordination Maternal effects: Preterm birth, miscarriage, or stillbirth If the woman carries the pregnancy to the age of viability, there is a 40% to 70% chance infected Fetal / Neonatal effects: Birth defects such as: blindness, deafness or other deformities Hutchinson s triad- includes inflammation of the cornea, deafness notched teeth Fetal / Neonatal effects: Swollen lymph glands , spleen, and liver enlargement, jaundice , anemia, bone deformities, and vesicular rash contagious Diagnosis: VDRL slide test Venereal Disease Research Laboratory a routine blood test, performed for every pregnant woman in early pregnancy Diagnosis: FTA-ABS (fluorescent treponemal antibody absorption) infant will be born

Management: Drug of choice: Benzathine Penicillin G

v Varicella and Herpes Zoster Cause: Herpes varicella virus Incidence: 1-5 of 10,000 pregnancies Transmission of Varicella Zoster: respiratory droplet, highly contagious the virus incubates for approximately 2 wks and is contagious 2 days before onset of the skin lesions until the lesions crust over generally 5 days after the initial onset v Herpes Zoster: localized painful rash within a Dermatome - an area on the body surface supplied by a particular sensorynerve. *Anyone who has had chickenpox is at risk for developing Shingles* Fetal / Neonatal effects: Low birth weight, skin lesions Contractures, damage to the ears, eyes CNS leading to mental retardation, paralysis and seizures Management: Serologic test to detect varicella antibodies Varicella zoster immune globulin (VZIG) - given within 96 hours of exposure to help prevent the development of chickenpox. (VZIG) may also be given to the neonate IF the woman develops chickenpox 5 days before or within 48 hours after delivery Best is Prevention vaccination v GONORRHEA Cause: gram-negative coccus Neisseria gonorrheae Manifestations Yellow-green vaginal discharge Male partner: severe pain on urination, purulent yellow penile discharge Effect on fetus (esp. with vaginal delivery) destructive conjunctivitis (opthalmia neonatorum)

Diagnostics: vaginal, rectal or urethral cultures Management: Antibiotics, like Ceftriaxone and Cefixime v Rubella AKA German Measles / 3 Day Measles Cause: infection with the rubella virus Transmission: by droplet RUBELLA German measles virus causing extensive fetal damage (teratogenic effects) Greatest risk to embryo: early pregnancy (organogenesis period) Frequency of defects: 50% if infection occurs in first 8 weeks, 20% in the 9th 16th week Manifestations: Rash, low grade fever, headache, lymphadenopathy Effect on fetus: Deafness, mental and motor retardation, cataracts, cardiac defects (PDA and pulmonary stenosis), dental and facial clefts (cleft lip and palate) Diagnostics: Serum for antibody titers Management: No treatment available; vaccination of pregnant women not recommended because of the risk of developing a rubella infection Prevention Immunization; women of childbearing age who received vaccination advised to avoid getting pregnant for 3 months time Diagnosis: IgG antibodies to rubella are measured to determine the client s rubella immunity status: A titer of 1:10 or greater indicates that the woman is immune to rubella. A titer of 1:8 or less indicates minimal or no immunity Effects Maternal effects: Fever, rash and mild lymphedema Fetal/neonatal effects: spontaneous abortion, stillbirth, congenital anomalies, and death Risks: occurs if the woman develops rubella in the 1st trimester (first 11 weeks) = multiple anomalies Management: There is no cure for congenital rubella infection Treatment are of symptoms and complications Best tx.= prevention rubella vaccine Management: Avoid anyone with flu-like symptoms or rash during the pregnancy combination of MMR Vaccine (measles , mumps, rubella) == to children at 12-15 months, 2nd dose = 4-6 yrs before starting to school v Cytomegalovirus Cause: exposure to the cytomegalovirus Transmission: Can be transmitted through respiratory droplet (most common), semen, cervical and vaginal secretions, breast milk, placental tissue, urine, feces and banked blood At risk: workers in day care centers, institutions for the mentally retarded, health settings. Manifestations: Possibly asymptomatic Effect on fetus: Severe brain damage (hydrocephalus, microcephaly, spasticity); eye damage or chronic liver disease. Child s skin may be covered with large petechiae ( blueberry muffin lesions)

Diagnostics Serology: positive viral titers Management: No treatment available in pregnancy or for the infected newborn Diagnosis: a viral culture is the most definitive tool CMV antibodies indicate a recent infection a fourfold increase in CMV titer in paired sera drawn 10-14 days apart is usually indicative of an acute infection Maternal effects: asymptomatic illness, cervical discharge, mononucleosis- like symptoms Fetal/ neonatal effects: Fetal death or severe generalized disease with hemolytic anemia and jaundice, hydrocephaly or microcephaly, Pneumonitis, hepatosplenomegaly, deafness Management: Antiviral agents Ganciclovir Prevention: Pregnant woman who have contact with small children should practice meticulous hand washing, particularly after contact with saliva and urine Proper disposal of the diapers, tissues, and other potentially infected items Drinking glass and utensils should not be shared Pregnant woman should practice universal precaution Although CMV is passed through breast milk, breast feeding is not contraindicated bec. CMV infection contracted during birth or from breast-feeding rarely cause serious problems v Herpes Simplex virus (HSV) Cause: exposure to the herpes simplex virus Transmission: HSV type II is a sexually transmitted disease transmitted by exposure to vesicular lesions on the penis, scrotum, vulva, perineum, perianal region, vagina, or cervix Infant= infected during exposure to a lesion in the birth canal, most at risk Virus causing genital herpes infection Transmission: Placental transmission, or during vaginal delivery Effects: First trimester severe congenital anomalies, spontaneous miscarriage; second trimester premature birth, IUGR Method of delivery: CS Management: Acyclovir (Zovirax) Diagnosis: Viral culture is used for definitive diagnosis; serologic test have a lower accuracy Effects Maternal effects: blisters, rash, fever, malaise, nausea and headache Fetal/ neonatal effects: miscarriage, preterm labor, stillbirth, intrauterine growth retardation, mental retardation Management: Ante partum cultures should be done when there is active lesions during pregnancy to confirm diagnosis Management: Neonatal treatment: * Isolation

* Pharmacologic therapy drug-Acyclovir - the 2nd line- Vidarabine * Feedings STIs and Pregnancy v Syphilis Associated with miscarriages, preterm labor, stillbirth and congenital anomalies v Herpes Simplex Virus Type 2 Associated with infection in the newborn v STIs and Pregnancy v Gonorrhea Associated with severe eye infection and blindness v Human Papillomavirus May obstruct birth canal

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Nursing Process: A Woman Who Develops A Complication Pregnancy Related Complications Hemorrhagic Complications of Early Pregnancy Abortion Incompetent Cervical Os Ectopic Pregnancy Hydatidiform Mole Choriocarcinoma Hyperemesis Gravidarum Hemorrhagic Disorders Hemorrhagic disorders in pregnancy are medical emergencies Maternal blood loss decreases oxygen-carrying capacity Increased risk for hypovolemia, anemia, infection, preterm labor, and preterm birth Hemorrhagic Disorders Maternal blood loss decreases oxygen-carrying capacity Adversely affects oxygen delivery to fetus Fetal risks include blood loss or anemia, hypoxemia, hypoxia, anoxia, and preterm birth Bleeding Development of shock Blood pressure Pulse Fetal heart Rate Treatment

1st Trimester Bleeding Spontaneous miscarriage Threatened Imminent Complete Missed Recurrent pregnancy loss Complications of Miscarriage Hemorrhage Infection Septic abortion Isoimmunization Powerlessness or anxiety 1st Trimester Bleeding Ectopic pregnancy Implantation occurs outside of the uterine cavity Abdominal pregnancy Clinical manifestation Scant to dark brown vaginal bleeding Abdominal pain usually develop 3-5 weeks after a missed menstrual period PAIN is the predominant symptom of tubal rupture- localized on one side or felt over the entire abdomen CHARACTERISTIC of PAIN: Cramping or sharp, sudden, knifelike pain, often of extreme severity Shoulder tip pain- presence of intraperitoneal bleeding extending to the diaphragm (Phrenic nerve) Ectopic pregnancy Fertilized ovum implanted outside uterine cavity 95% occur in uterine (fallopian) tube Most located on ampullar Ectopic pregnancy Other sites include: Ovary (0.5%) Abdominal cavity (1.5%) Cervix (0.3%) ECTOPIC PREGNANCY Sites of Ectopic pregnancy Ampullar Isthmus Interstitial Cornual

Cervical Abdominal Ovarian 2nd Trimester Bleeding Gestational trophoblastic disease (hydatidform mole) Abnormal proliferation and degeneration of the trophoblastic villi HYDATIDIFORM MOLE a gestational trophoblastic neoplasm Occurs when the chorionic villi abnormally increases & develop vesicles that resembles tiny grapes 2 Types of Molar Growth PARTIAL MOLE normal villi intermingled with hydropic villi some fetal material or an amnionic sac. Usually associated with one haploid maternal & two haploid paternal sets of chromosomes Triploid karyotype COMPLETE MOLE large amount of edematous enlarge villi without a fetus or fetal membranes. Almost uniformly diploid w/ paternal chromosomal markers Clinical Manifestation Pregnancy appears to be normal at first. 1/3 to of women with complete moles has a uterus larger than expected for gestational dates. Initial hCG levels are lower in patients with apartial mole than those with a complete mole. Bleeding may vary from brownish-red spotting to heavy bright red. Vomiting FHT is absent Pre eclampsia may appear before the 20th week of gestation Those with partial moles typically have a clinical diagnosis of spontaneous or missed abortion. Vesicles may be evident in the vaginal discharge or the abortus. Causes Exact cause is unknown Partial moles believed to originate from dispermic fertilization of a haploid ovum or fertilization of a haploid ovum with a diploid sperm. Complete moles often result from fertilization of an empty egg by haploid sperm that reduplicates

Associated factors: age, multiparity, diet Medical Diagnosis & Prognosis UTZ

With appropriate therapy, H-mole generally not associated with maternal mortality Complete H-mole- has a higher incidence of malignant sequelae(10-30%);partial moles Medical management FIRST PHASE Emptying the uterus through D & C. Evaluation of the tissue by a pathologist SECOND PHASE hCG level surveillance by radioimmunoassay to detect any c Protocol for hCG monitoring/measurements 1 YEAR Weekly until they are normal for 3 weeks Then monthly until they are normal for 6 mos. 1 YEAR Then q 2 mos for the next 6 months. Negative hCG should be evident after 6 weeks of evacuation Assessment Assessment of fundal height Careful auscultation for fetal heart sounds reveals no findings Positive pregnancy test Intense nausea & vomiting Check V/S; BP evaluation may reveal HPN before 20th week of pregnancy Blood should be assessed for clear, fluid vesicles. Lab tests: Hgb,Hct and proteinuria. Nursing Intervention Prepare the client for the evacuation of the uterus. Provide client education Family counseling to assist the woman in selecting desirable contraceptive Pregnancy should be avoided for at least 1 year, after which time conception is permitted. Provide psychosocial support Encourage verbalization or expression of feelings. 2nd Trimester Bleeding Premature cervical dilatation Cannot hold the fetus until term Cervical cerclage 10%

hanges suggestive of trophoblastic malignancy.

Incompetent Cervix Incidence and etiology Medical management Conservative management of bed rest, progesterone, antiinflammatory drugs, and antibiotics Shirodkar or McDonald procedure Prophylactic cerclage is placed at 11 to 15 weeks of gestation Nursing care and home care also called cervical insufficiency. premature opening (dilation) of the cervix usually in mid-pregnancy (18 to 22 weeks or 4 to 6 months of pregnancy). INCOMPETENT CERVICAL OS Mechanical defect in the cervix that cause it to dilate prematurely occurs during midtrimester of pregnancy Late habitual abortion or preterm labor Incompetent Cervix ccurs in about 1 out of every 100 pregnancies and may be responsible for 20 to 25 percent of second trimester miscarriages. Causes: Congenital anomalies of the uterus or the cervix Prior trauma S/Sx: Painless dilatation Bloody show Premature rupture of the membranes Treatment CERVICAL CERCLAGE may be done at approx. 12 to 14 weeks gestation. Removed @ 37 wee gestation

2 Types of Cervical Cerclage SHIRODKAR TECHNIQUE vaginal mucous membrane is elevated band of homologous fascia or a narrow strip of material is carried around the internal os & tiedvaginal mucosa is restored to its original position & sutured.

McDONALD TECHNIQUE placement of a non absorbable suture around the cervix high on the cervical mucosa. Nursing Management Monitor FHR. Observe for signs of rupture of the membranes or uterine contractions. If contractions ensue, place client on bed rest. Administer prescribed medicine to control contractions such as ritodrine hydrochloride. PREGNANCT RELATED COMPLICATION Hemorrhagic complications of late pregnancy Placenta Previa Abruptio Placentae 3nd Trimester Bleeding v Placenta previa Low implantation of placenta Risk factors Assessment Management PLACENTA PREVIA

Is the development of the placenta in the lower uterine segment so that either partially or wholly covers the region of the cervix. Types of Placenta Previa

  

Total Placenta Previa placenta completely covers the internal os. Partial Placenta Previa placenta partially covers the internal os. Low implantation of the Placenta- placenta encroaches on the region of the internal os; can be palpated by the AP; does not extend beyond the margin of internal os.

Clinical Manifestation Sudden onset of painless, bright-red vaginal bleeding The uterus usually remains soft FHR is stable & within normal limits Causes No known cause PREDISPOSING FACTORS: Multiparity Advancing maternal age Multiple gestation previous Cesarean birth

Uterine incisions Medical Diagnosis & Prognosis Transabdominal UTZ Internal examination (IE) in the operating room under UP Medical Management Planned based on the location of the placenta, the amount of bleeding, and the gestational age of the fetus. Conservative management is appropriate when the fetus is premature & bleeding is not excessive Bedrest Medical Management Administration of magnesium sulfate, terbutaline, or ritodrine. To confirm fetal maturity, amniocentesis is often performed Delivery must be performed irrespective of gestational age under emergency situation. Cesarean birth is the approach of choice for delivery Vaginal delivery may be accomplished with low implantation of the placenta, especially if the baby is small & the cervix is partially dilated. Nursing Assessment Assessment include: Baseline V/S Amt, chartx of bleeding Uterine activity & condition( size, contour, irritability, relaxation) Pain or tenderness, especially in the abdomen; FHT & actvy LOC Nursing Diagnosis Fluid Volume deficit; Hypovolemia r/t bleeding secondary to abnormal placental implantation Alteration in Tissue Perfusion r/t High RisK for Infection r/t Nursing Intervention Depends on whether conservative or active medical management Home Care: Provide client & family education Importance of bedrest & restriction of activitiesInstruct the client to save all perineal pads Advise client to report if she feels any fluid escaping from her vulva. HOSPITAL CARE Periodically palpate the uterus gently to detect contractions suggesting onset of labor. Monitor for signs of shock.

Monitor lab tests such as hgb, hct.Address emotional & psychosocial needs Prepare for possible transfusion of blood 3nd Trimester Bleeding Abruptio Placentae Premature separation of placenta Occurs suddenly Most frequent cause of perinatal death Risk factors Assessment Management ABRUPTIO PLACENTA Premature separation of a normally implanted placenta after the 20th week of pregnancy Clinical Manifestation Clinical picture varies depending on the type of premature separation present; Type of Abruptio Placentae COVERT or SEVERE ABRUPTIO PLACENTAE characterized by central separation that entraps lost blood between the uterine wall & the placenta concealed hemorrhage masks the seriousness of the problem. OVERT or PARTIAL PLACENTAE separation occurs at the margin, blood passes b/w the uterine wall & fetal membranes creating an external hemorrhage. PLACENTAL PROLAPSE involving complete or almost total separation.

Associated with massive vaginal bleeding. Anomalies of Placenta and Cord Two-vessel cord Unusual cord length Signs & Symptoms Vaginal bleeding that is dark abdominal pain( sudden, severe, knifelike) firm, tender uterus Signs of shock Fetal distress may be present Contraction is frequent, low-amplitude with an increase in resting tone. Causes Exact cause is unknown PREDISPOSING FACTORS: Maternal hypertension Grand multiparity ( 5 or more pregnancies)

Short umbilical cord Automobile accidents & trauma Multiple gestation hydramnios

Medical Diagnosis & Prognosis UTZ CAT scans Perinatal mortality rates vary greatly with the type of abruptio, ranging from 15% to approaching 100% for infants experiencing nearly total or complete abruptions. Medical Management Treatment is dependent on the condition of the fetus & the mother at the time the diagnosis is made. Prompt delivery either vaginal or cesarean depending on the condition of the fetus. Disseminated Intravascular Coagulation (DIC) Disorder of blood clotting

Fibrinogen levels fall below effective limits Symptoms Bruising or bleeding Preterm Labor Labor that occurs before the end of week 37 of gestation 9-11% of all pregnancies 2/3 of all infant deaths Management Preterm Labor Drug administration Antibiotics Steroids Magnesium sulfate Beta sympathomimetics Fetal Assessment

Fetal movement Labor that cannot be stopped Assessment Management Preterm Rupture of Membranes Rupture of fetal membranes with a loss of amniotic fluid Before 37 weeks gestation

Associated with chorioamnioitis Complications Assessment Management

Nursing Process: Pregnant Woman With Special Needs Pregnant Adolescent Developmental tasks Prenatal assessment

  

Health history Family profile Day history Physical examination Prenatal health teaching Nutrition Activity and rest Pregnancy information Childbirth

Complications Pregnancy-induced hypertension Iron-deficiency anemia Preterm labor

Pregnant Adolescent Complications and concerns of labor, birth and postpartum Cephalopelvic disproportion Postpartal hemorrhage Inability to adapt Lack of knowledge Over Age 40 Developmental tasks Prenatal assessment

  

Health history Family profile Day history Physical examination Chromosomal assessment Nutrition Prenatal classes Complications

Pregnancy-induced hypertension Complications and concerns of labor, birth and postpartum Failure to progress Difficulty accepting event Postpartal hemorrhage Physically or Cognitively Challenged Rights Modifications for pregnancy Safety

    

Emergency contacts Transportation Mobility Elimination Autonomic responses

Prenatal care modifications Pregnancy education Labor and birth modifications Postpartum modifications Planning child care

Substance Dependent Withdrawal symptoms following discontinuation of the substance Abandonment of important activities Spending increased time in activities related to substance use Using substance for a longer time than planned Drugs commonly used during pregnancy Cocaine Amphetamines Marijuana and hashish Phencyclidine Narcotic agonists Inhalants Alcohol Nursing Process: Labor or Birth Complications Complications: Force of Labor Ineffective uterine force Hypotonic contractions

Hypertonic contractions Uncoordinated contractions Dysfunctional Labor First stage Prolonged latent Protracted active Prolonged deceleration Secondary arrest of dilatation Second stage Prolonged descent Arrest of descent Complications: Force of Labor Contraction rings Precipitate labor Uterine rupture Inversion of the uterus Amniotic fluid embolism ABORTION Termination of pregnancy at any time before the fetus has attained a stage of viability Before it is capable of extrauterine existence Occur in about 10%-20% of all pregnancies. Causes 1. Fetal Factors Defective embryologic development Faulty ovum implantation Rejection of the ovum by endometrium Chromosomal abnormalities 2. Placental Factors Premature separation of the normally implanted placenta Abnormal placental implantation Abnormal placental function 3. Maternal Factors Infection Severe malnutrition Reproductive system abnormalities (eg, incompetent cervix) Endocrine problems (eg, thyroid dysfunction) Trauma, Drug ingestion Pathophysiology Fetal, placental defect & maternal condition results in the disruption of blood flow, containing oxygen and nutrients, to the developing fetus. The fetus is compromised

subsequently expelled from the uterus. ABORTION VS. PRETERM DELIVERY ABORTION Has not reached stage of viability (about 20 wks or less) 500g or less PRETERM INFANT born after the stage of viability has been reached but before it has the same chance for survival as a full term infant 2500g or less Division of Abortion

1.

SPONTANEOUS ABORTION

1.

INDUCED ABORTION

SPONTANEOUS ABORTION ONE IN WHICH THE PROCESS STARTS ON ITS OWN ACCORD THROUGH NATURAL CAUSES Types of Spontaneous Abortion INDUCED ABORTION ONE THAT IS ARTIFICIALLY INDUCED, WHETHER FOR THERAPEUTIC OR OTHER REASON Clinical manifestations About 80% occur during first 12 weeks of pregnancy. 15-20% terminate in spontaneous abortion Generally occur 1 to 3 weeks after the death of the embryo or fetus SIGN & SYMPTOMS Bleeding Uterine cramps Softening and dilatation of the cervix Complete or incomplete expulsion of the products of conception Medical diagnosis & Prognosis Internal Examination (IE) UTZ Medical management Bed rest and sexual abstinence prescribed Sedatives Hospital confinement necessary If bleeding becomes copious & accompanied by cramps or uterine contractions IVF/BT

Oxytocin administration Surgical removal of the retained products Dilatation and curettage Vacuum extraction Forcep removal Administration of RhoD immune globulin (RhoGAM) within 72h after the abortion is indicated for Rh-negative women Antibiotic therapy Nursing Assessment Obtain a detailed, accurate hx. Ask client to describe the quantity of bleeding Assess characteristic of blood loss Assess for presence, nature, and location of accompanying discomforts such as cramping, dull or sharp pain, and dizziness. Nursing Diagnosis Knowledge deficit related to physiological alterations in the reproductive system Fluid volume deficit High risk for infection Grieving r/t actual or threatened loss of pregnancy Nursing Interventions Advise bed rest and eat a well balanced diet. Provide information regarding the client s condition. Counsel to save all perineal pads as well as all tissue and clots passed. Counsel to avoid coitus for 2 weeks following the last evidence of bleeding. Give psychosocial support. Encourage verbalization of feelings. EVALUATION Understands the physiological alteration occuring w/ her codition & r/t tx. Fluid volume corrected No signs of infection noted Appropriately progresses through the grieving process Medical Management Early diagnosis of ectopic pregnancy based on health history, physical exam, diagnostic test. DIAGNOSTIC TESTS: HCG level UTZ Lab tests: CBC (hgb, Hct , leukocytosis) Culdocentesis checks for abnormal fluid in the space that is just behind the vagina, the posterior cul-de-sac. v Colpotomy Surgical Management

Laparoscopy Curettage SALPINGECTOMY with or without ipsilateral oophorectomy. Nursing Assessment Assess for the 3 main classic symptoms of ectopic pregnancy. Missed menstruation Abdominal pain Vaginal spotting CHARACTERISTICS OF PAIN: crampy , dull or restricting to the shoulder & back. Ask client about the use of IUD or history of previous tubal damage caused by dse or developmental problems. Assess V/S Assess for signs of hypovolemic shock

  

Thready pulse Tachypnea Hypotension Check for cullen s sign- blue tinge color in the umbilicus indicative of peritoneal bleeding.

Nursing Interventions Explain various dxtc tests & provides support for the patient with a suspected ectopic pregnancy. Acurately record the perineal pad count. Prepare for surgery Adm. IVF Monitor V/S Monitor I & O After surgery, early ambulation is encouraged. Administer antibiotic Provide emotional support and encourage verbalization of feelings Assist them in resolving feelings of guilt and self-blame.

Evaluation Understands the pathophysiology of her condition & treatment alternatives. No signs of infection or complications noted. Appropriately progresses through grieving process & accepts the loss of her child. HYPEREMESIS GRAVIDARUM also known as Pernicious vomiting

Severe & excessive nausea & vomiting during pregnancy, which leads to electrolyte, metabolic, and nutritional imbalances in the absence of other medical problems. Clinical manifestation Nausea on arising in the morning or may occur at other times of the day Persists for weeks & suddenly ceases may last 4 to 8 weeks or longer. Signs of dehydration & starvation urine output Dryness of the skin Hypovolemia w/ associated hypotension if dehydration is not corrected. Causes exact cause is unknown. Endocrine imbalance caused by high level of hCG & estrogens Metabolic changes of normal gestation Fragments of chorionic villi entering the maternal circulation Diminished motility of the stomach psychological Medical Diagnosis & Prognosis Diagnostic testing to detect underlying causes of nausea & vomiting Perinatal outcome may be improved through early tx to prevent significant lo weight loss Recovery is usually rapid once fluid & electrolyte balance are restored Directed toward preventing significant weight loss, correcting fluid & electrolyte imbalance, and treating acidosis & alkalosis hospitalization if unable to remedy symptoms & hyperemesis Goals of Intervention 1. Treat the dehydration by liberal administration of parenteral fluids ( approx. 3000ml/24h) 2. Treat emotional component with an understand in attitude.

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Reverse starvation by administration of glucose IV, thiamine chloride SQ, if necessary, feeding a high caloric, high vitamin fluid diet through NGT or hyperalimentation method.

Nursing Diagnoses Altered Nutrition; less than body requirement r/t pernicious vomiting Risk for Impaired Skin Integrity r/t excessive vomiting & dehydration Ineffective individual coping with the psychological tasks of pregnancy & motherhood

Nursing Assessment Assess the particular pattern of nausea & vomiting experience by the client Review laboratory tests Elevated hgb, Hct k, Na & Cl Nursing Assessment Vit B deficiency Measure current weight, compare w/ her nonpregnant weight. Ask about ADL, lifestyle & attitude about herelf & pregnancy. Nutritional habits are assessed in detail & then compared w/ findings on P.E Nursing Intervention Monitor I & O Restrict oral fluid intake until vomiting ceases. Start oral feeding once vomiting ceases. Ex. small quantities of dry food may be given hourly alternating with small quantities of water then progress slowly as tolerated. Provide a hygienic environment Provide psychological support

Surgery during Pregnancy Appendicitis Intestinal obstruction Gynecologic problems Trauma during Pregnancy Significance Special considerations for mother and fetus Physiologic alterations of pregnancy Presence of fetus Special considerations for mother and fetus Presence of fetus Fetal survival depends on maternal survival Pregnant woman must receive immediate stabilization and care for optimal fetal outcome Effect of trauma on pregnancy influenced by: Length of gestation Type and severity of the trauma Degree of disruption of uterine and fetal physiologic features Maternal physiologic characteristics Requires strategies adapted for appropriate resuscitation, fluid therapy, positioning, assessments, and other interventions Uterus and bladder positioning Elevated levels of progesterone Decreases tolerance for hypoxia and apnea

Cardiac output Circulating blood volume Fetal physiologic characteristics Careful monitoring of fetal status assists greatly in maternal assessment Fetal monitor tracing works as oximeter of internal maternal well-being Mechanisms of trauma Blunt abdominal trauma Penetrating abdominal trauma Thoracic trauma Care management of trauma Immediate stabilization Primary survey Secondary survey Electronic fetal monitoring Postmortem cesarean delivery Discharge planning Emergency Delivery Precipitate Labor Labor that lasts less than 3 hours with titanic-like contractions and rapid delivery. Complications are uterine rupture, severe laceration of birth canal, hypotonic uterus after delivery with profuse bleeding, and fetal hypoxia. Nursing Diagnosis are pain and risk for injury. Nursing Implementation: Safe delivery of infant between contractions using Ritgen s maneuver; Newborn care. Preterm Labor Labor occurring after 20th Week but before 37th. May cause fetal death if delivered with low birth weight. From 35th week onwards, there s good chance o survival. Maternal complications requiring delivery of preterm infants placental separation with untrolled hemorrhage; Severe eclampsia or preeclampsia; uncontrolled renal or CVD; Premature rupture of membrane; and Chorioamnionitis . Preterm Labor Main Nursing Diagnosis: Fear. Nursing Implications: Bedrest in less stimulating environ at lateral recumbent position; Adequate hydration; Use of steroids to prevent respiratory distress syndrome for infants; Prepare for delivery; Administer tokolytic agents ( Vasodilan, Ritodrine, Terbutaline, Magnesium Sulfate) as ordered, but prepare calcium gluconate as an antidote. Dystocia Difficult labor and delivery due to problems with one of the five P s leading to maternal exhaustion, infection, trauma, and fetal injury and death. Diagnostic exams include vaginal exam, pelvimetry, ultrasound, Leopold s maneuver. Dystocia Defined as long, difficult, or abnormal labor

Dysfunctional labor from abnormal uterine contractions preventing normal progress of: Cervical dilation Effacement (primary powers) Descent (secondary powers) Increased risk for uterine dystocia includes: Body build Uterine abnormalities Malpresentation and position of fetus Overstimulation with oxytocin Cephalopelvic disproportion (CPD) Increased risk for dystocia includes: (cont d) Maternal fatigue, dehydration and electrolyte imbalance, and fear Inappropriate timing of analgesic or anesthetic administration Dysfunction of uterine contractions Hypertonic or primary dysfunctional labor Hypotonic or secondary uterine inertia Secondary powers Bearing-down efforts are compromised when large amounts of analgesia are given Analgesics may also block the bearing-down reflex Dystocia Alterations in pelvic structure Pelvic dystocia Contractures of pelvic diameters that reduce the capacity of the bony pelvis, inlet, midpelvis, or outlet Soft-tissue dystocia Results from obstruction of the birth passage by an anatomic abnormality other than the bony pelvis Dystocia Fetal causes of dystocia Anomalies Cephalopelvic disproportion (CPD) Malposition Malpresentation Multifetal pregnancy Dystocia Main Nursing Diagnosis are Pain and Anxiety Management sedation for hypertonicity; Stimulation of labor for hypotonicity; C/S; Prophylaxis antibiotic; Constant monitoring of fetal and maternal vital signs; Provide rest ; monitor presence of cord prolapse or rupture of membrane; Regularly assess fatigue and pain. Care Management Assessment and nursing diagnoses Diagnoses that might be identified in women experiencing dystocia Expected outcomes of care Plan of care and implementation Nurses assume many caregiving roles when labor is complicated Nurses also work collaboratively with other health care providers in providing care Care Management

Plan of care and implementation Version External cephalic version (ECV) Internal version Trial of labor Induction or augmentation with oxytocin Cervical ripening methods Chemical agents Prostaglandin gel Care Management Plan of care and implementation Cervical ripening methods Mechanical methods Amniotomy Care Management Oxytocin Hormone normally produced by posterior pituitary gland Stimulates uterine contractions Used to induce labor or to augment a labor progressing slowly because of inadequate uterine contractions Management of stimulation of labor is same regardless of indication FDA has issued certain restrictions to its use Indications Contraindications Special cautions Augmentation of labor Stimulation of uterine contractions after labor has started but progress is unsatisfactory Implemented for management of hypotonic uterine dysfunction Common augmentation methods Oxytocin infusion Amniotomy Nipple stimulation Obstetric Emergencies Prolapsed umbilical cord When cord lies below presenting part of fetus Contributing factors include: Long cord (longer than 100 cm) Malpresentation (breech) Transverse lie Unengaged presenting part Cord Prolapse Risk factors are breech presentation, multiple pregnancy, prematurity. Assessment includes fetal hypoxia, irregular FHR, and Umbilical cord can be seen or felt. Nursing Implication: Monitor FHR continuously; Elevate fetal presenting part to relieve pressure; Do not push cord back to uterus; Prepare for immediate C/S.

ASSESSMENT NURSING MANAGEMENT Obstetric Emergencies Rupture of the uterus Very serious obstetric injury Most frequent causes Separation of scar of previous classic cesarean birth Uterine trauma: accidents, surgery Congenital uterine anomaly Obstetric Emergencies Rupture of the uterus During labor and birth may be caused by: Intense spontaneous uterine contractions Labor stimulation: oxytocin, prostaglandin Overdistended uterus: multifetal gestation Malpresentation: external or internal version Difficult forceps-assisted birth More often in multigravidas than primigravidas Rupture of Uterus Rupture of uterus from stress of labor from uncontrolled titanic and hypertonic contractions, prolonged labor, prior uterine surgey, fetal abnormalities and faulty use of forceps. Clinical manifestation: sudden onset of sharp, stabbing abdominal pain during labor, shock syndrome, cessation of uterine contraction with rigidity of abdomen. Main Nursing diagnosis: Altered tissue perfusion and Pain. Nursing care involves Close monitoring of labor and fetal and maternal vital signs ; preparation to emergency surgery Obstetric Emergencies Amniotic fluid embolism (AFE) Amniotic fluid containing particles of debris Vernix, hair, skin cells, or meconium enters maternal circulation Obstructs pulmonary vessels Causes respiratory distress and circulatory collapse Subinvolution Retarded involution of puerperal uterus; With enlarged, boggy uterus, profuse and prolonged lochia rubra, backache, pelvic discomfort, and dragging sensation. May be caused by poor uterine tone, retained placenta, endometritis, fibroids and tumors, and displacement of uterus. Main nursing diagnosis: Fluid volume deficit and high risk for infection. Nursing care include: administration of antibiotics and oxytocin; ambulation; and health teachings. Cystitis

Infection of bladder from trauma during delivery, catheterization, and temporary loss of bladder tone. Manifested as urinary frequency, urgency and retention; Dysuria, nocturia, hematuria and tenderness, fever. Main nursing diagnosis: Pain and Knowledge deficit. Nursing Care includes observing closely for bladder function; forcing fluids to 3000 mL per day; antibiotics; Perineal care, Infection precautions. Postpartum Hemorrhage Bleeding of 500 mL or more following delivery; commonly caused by uterine atony. Woman may experience copious amount of vaginal bleeding with or without bright or dark red clots; boggy uterus; maternal shock. Main Nursing Diagnosis: Fluid volume deficit Nursing responsibility includes Monitoring bleeding, hemoglobin and hematocrit, V/S, I&O, fluid replacement and Oxytocin administration; Maintaining asepsis; Iron supplements; follow up care. Predisposing factors of Postpartum Hemorrhage

  

Uterine Atony loss of muscle tone in the uterus. Over distention Over massage

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Laceration 1st degree 2nd degree 3rd degree 4th degree

of the birth canal fourchette, perineal skin - perineal muscles, vaginal muscles involves the anal sphincter, anus includes the rectum and rectal muscles.

Pulmonary Disorders Asthma Therapy objectives Relief of acute attack Prevention or limitation of later attacks Adequate maternal and fetal oxygenation Cystic fibrosis Infants of mothers with cystic fibrosis will be carriers of gene With severe disease, pregnancy is often complicated by chronic hypoxia and frequent pulmonary infections Gastrointestinal Disorders Cholelithiasis (gallstones) Cholecystitis (inflammation of the gallbladder) Inflammatory bowel disease

Integumentary Disorders Dermatologic disorders induced by pregnancy include: Melasma (chloasma) Vascular spiders Palmar erythema Striae gravidarum Skin problems aggravated by pregnancy Acne vulgaris (in the first trimester) Erythema multiforme Herpetiform dermatitis (fever blisters and genital herpes) Granuloma inguinale (Donovan bodies) Condylomata acuminata (genital warts) Neurofibromatosis (von Recklinghausen disease) Pemphigus Neurologic Disorders Epilepsy Failure to take medications is common factor Message that drugs are harmful to the fetus Risks to the infant have been exaggerated Multiple sclerosis (MS) Bed rest and steroids used to treat acute exacerbations Bell s palsy Autoimmune Disorders Systemic lupus erythematosus (SLE) Autoimmune antibody production affects skin, joints, kidneys, lungs, CNS, liver, and other body organs Immunosuppressive medications not recommended during pregnancy Systemic lupus erythematosus (SLE) Myasthenia gravis (MG) Women with MG usually tolerate labor well Vacuum or forceps assistance for birth may be required due to muscle weakness Oxytocin may be given Magnesium sulfate is contraindicated Narcotic analgesia should be avoided Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome Preconception counseling Pregnancy risks Women now fastest-growing population of individuals with HIV infection and AIDS Perinatal transmission 90% of all pediatric AIDS cases are due to transmission of virus from mother to child Obstetric complications Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome Care management

HIV-infected women should be treated with zidovudine during pregnancy Opportunistic infections should be treated with medications specific for infection Every effort should be made to decrease neonate s exposure to blood and secretions Immediately after birth, infants should be wiped free of all body fluids and then bathed All staff working with mother or infant must adhere strictly to infection control techniques Observe Standard Precautions for blood and other body fluids Substance Abuse Alcohol and other drugs easily pass from mother to baby through the placenta Smoking during pregnancy has serious health risks including: Bleeding complications Miscarriage Stillbirth Prematurity Placenta previa Placental abruption Low birth weight (LBW) Sudden infant death syndrome Substance Abuse Barriers to treatment Women fear losing custody of child and criminal prosecution Substance-abuse treatment programs do not address issues affecting pregnant women Long waiting lists and lack of health insurance present further barriers to treatment Legal considerations Women who abuse substances may face criminal charges Nurses who encourage prenatal care, counseling, and treatment are of greater benefit to mother and child than prosecution Care management Women often deny or greatly underreport usage of drugs or alcohol consumption Crucial for nurse to display nonjudgmental and matter-of-fact attitude to gain woman s trust and elicit reasonably accurate estimate Michigan alcohol screening test (MAST) CAGE T-ACE and TWEAK specifically for alcohol use during pregnancy Care management (cont d) Realistic goal may be to decrease substance use Consequences of drug use should be clearly communicated and abstinence recommended Women more receptive to making lifestyle changes during pregnancy than at any other time Women for Sobriety Methadone treatment for pregnant women Cocaine use during pregnancy has increased dramatically Care management (cont d) Breastfeeding definitely contraindicated in women who continue to use amphetamines, alcohol, cocaine, heroin, or marijuana Substance abusers difficult to care for particularly during intrapartum and postpartum periods Substance abuse is an illness; women deserve to be treated with patience, kindness, consistency, and firmness

Care management (cont d) Before discharge Home situation must be assessed for safe environment Someone available to meet infant s needs if mother is unable Family members or friends should become actively involved with mother before discharge If infant s well-being is questionable, case will be referred to child protective services agency Management of Problems Forceps Delivery Forceps-assisted birth Maternal indications Shorten second stage in event of dystocia Compensate for deficient expulsive efforts Reverse a dangerous condition Fetal indications Distress or certain abnormal presentations Arrest of rotation Delivery of head in a breech presentation Forceps delivery Two double-crossed, spoon like articulated blades are used to assist in delivery of fetal head Prerequisites: fully dilated cervix, engaged head, vertex or face presentation, absence of CPD, empty bladder and bowel. Types are: High forceps biparietal dimension of vertex above ischial spine. Midforceps vertex at ischial tuberosities. Low forceps vertex distending introitus, use to control and guide head, easiest to deliver. Low forceps vertex distending introitus, use to control and guide head, easiest to deliver. Complications are perineal lacerations, damage to facial nerve of fetus, fetal death, postpartal hemorrhage, cystocele, rectocele, or uterine prolapse.

Low forceps vertex distending introitus, use to control and guide head, easiest to deliver. Main Nursing diagnosis: Fear and risks of injury to both fetus and mother. Nursing Implications: Closely monitor both fetus and mother during delivery with continual assessment.

Vacuum Delivery Vacuum-assisted birth Attachment of vacuum cup to fetal head, using negative pressure to assist birth of head Prerequisites Vertex presentation Ruptured membranes Absence of CPD ASSESSMENT NURSING MANAGEMENT Cesarean Delivery The birth through an abdominal incision into the uterus. Indications are: CPD, severe PIH, genital herpes or papilloma, previous C/S History, placenta previa, abruption placenta, tranvers fetal lie, breech presentation, extreme low birth weight, fetal distress, large fetus Types of C/S: Low transverse, Classic, Low vertical. Preoperative care measures are Informed consent, overall hygiene, skin prep, GIT prep, MIO, hydration, pre-op meds, role of support system. TYPES OF CESAREAN DELIVERY Postpartum Complications Postpartum Hemorrhage Definition and incidence PPH traditionally defined as loss of more than: 500 ml of blood after vaginal birth 1000 ml after cesarean birth Cause of maternal morbidity and mortality Life-threatening with little warning Often unrecognized until profound symptoms Postpartum Hemorrhage Etiology and risk factors Uterine atony Marked hypotonia of uterus Leading cause of PPH, complicating approximately 1 in 20 births Lacerations of genital tract Retained placenta Nondherent retained placenta Adherent retained placenta Postpartum Hemorrhage Inversion of uterus Subinvolution of uterus Care Management Assessment

Bleeding assessed for color and amount Perineum inspected for signs of lacerations or hematomas to determine source of bleeding Vital signs may not be reliable indicators because of postpartum adaptations Measurements during first 2 hours may identify trends related to blood loss Laboratory studies of hemoglobin and hematocrit levels Care Management Plan of care and implementation Medical management Hypotonic uterus Bleeding with a contracted uterus Uterine inversion Subinvolution Herbal remedies Nursing interventions Providing explanations about interventions and need to act quickly Instructions in increasing dietary iron, protein intake, and iron supplementation May need assistance with infant care and household activities until strength regained Hemorrhagic (Hypovolemic) Shock Medical management Nursing interventions Fluid or blood replacement therapy Coagulopathies Idiopathic thrombocytopenic purpura (ITP) von Willebrand disease type of hemophilia Disseminated intravascular coagulation (DIC) Pathologic clotting Correction of underlying cause Removal of fetus Treatment for infection Preeclampsia or eclampsia Removal of placental abruption Thromboembolic Disease Results from blood clot caused by inflammation or partial obstruction of vessel Incidence and etiology Venous stasis Hypercoagulation Clinical manifestations Medical management Nursing interventions

Postpartum Infections Puerperal sepsis: any infection of genital canal within 28 days after abortion or birth Most common infecting agents are numerous streptococcal and anaerobic organisms Endometritis, Wound infections Urinary tract infections Mastitis Sequelae of Childbirth Trauma Disorders of uterus and vagina related to pelvic relaxation and urinary incontinence, are often result of childbearing Uterine displacement and prolapse Posterior displacement, or retroversion Retroflexion and anteflexion Prolapse a more serious displacementa Cervix and body of uterus protrude through vagina and vagina is inverted Sequelae of Childbirth Trauma Cystocele and rectocele Cystocele: protrusion of bladder downward into vagina when support structures in vesicovaginal septum are injured Rectocele is herniation of anterior rectal wall through relaxed or ruptured vaginal fascia and rectovaginal septum Urinary incontinence Sequelae of Childbirth Trauma Genital fistulas May result from congenital anomaly, gynecologic surgery, obstetric trauma, cancer, radiation therapy, gynecologic trauma, or infection Vesicovaginal: between bladder and genital tract Urethrovaginal: between urethra and vagina Rectovaginal: between rectum or sigmoid colon and vagina Postpartum Psychologic Complications Mental health disorders in postpartum period have implications for mother, newborn, and entire family Interfere with attachment to newborn and family integration May threaten safety and well-being of mother, newborn, and other children Postpartum Psychologic Complications Postpartum depression without psychotic features PPD: an intense and pervasive sadness with severe and labile mood swings Treatment options Antidepressants, anxiolytic agents, and electroconvulsive therapy Psychotherapy focuses fears and concerns of new responsibilities and roles, and monitoring for suicidal or homicidal thoughts Postpartum Psychologic Complications Postpartum depression with psychotic features Postpartum psychosis: syndrome characterized by depression, delusions, and thoughts of harming either infant or herself Psychiatric emergency, and may require psychiatric hospitalization Antipsychotics and mood stabilizers such as lithium are treatments of choice

Loss and Grief Losses of what was hoped for, dreamed about, and/or planned Any perception of loss of control during the birthing experience Birth of a child with handicap Maternal death Fetal or neonatal death Loss and Grief Conceptual model of parental grief Acute distress Intense grief Reorganization Anticipatory grief Loss and Grief Plan of care and implementation Communicating and care techniques Actualize the loss Provide time to grieve Interpret normal feelings Allow for individual differences Cultural and spiritual needs of parents Physical comfort Loss and Grief Plan of care and implementation Options for parents Seeing and holding Bathing and dressing Privacy Visitations: other family members or friends Religious rituals/funeral arrangements Special memories Pictures Maternal Death Rare for woman to die in childbirth Families are at risk for developing complicated bereavement and altered parenting of surviving baby and other children in family Referral to social services can help combat potential problems before they develop Equipments and Materials Cardiac monitor, EKG machine, oxymeter ventilatory support equipment, endotracheal tubes, tracheostomy tube airway, BP apparatus, stethoscope, oxygen tank, O2 regulator, humidifier, monkey wrench, O2 tubings, O2 cannula/catheter, O12 Equipments and Materials masks, croupette, O2 tent, suction catheters, suction machine, cardiac arrest board, gloves, peak flow meter, tongue depressor, microscope

glass slide, one-way/two-way/three-way water seal drainage, CVP Equipments and Materials manometer and tubing, peritoneal dialysis set, dialyzing solution hemodialysis machine (optional), incubator, Billi light, Isolette Model for basic and advance life support