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Coma Scale – Patients with low scores(3-4) have high mortality and poor prognosis for cognitive recovery compared to patients with higher scores (8 and above)
Eye Opening Spontaneously To speech To pain None Verbal response Oriented Confused Inappropriate Incomprehensible None Motor Response Obeys Command Localizes pain Withdraws (pain) Flexion (pain) Extension (pain) None
4 3 2 1 5 4 3 2 1 6 5 3 1
Glasgow Coma Scale Maximum score: 15
P Q R S T
Pattern Quality Reaction Severity Treatment done
AMPLE Mnemonic For Multiple Trauma A=Allergies, M=Medication, P=Past medical history, L=Last food intake, E=Events preceding the injury
A=Airway B=Breathing C=Circulation D=Disability E=Exposure
A=Is patient ALERT? V=Is patient responding to VERBAL stimulus? P=Is patient responding to PAINFUL stimulus? U=Is patient UNCONCIOUS?
Components C - Circulation
Normal capillary refill and BP>=100 2 Delayed capillary refill or BP>=85<100 1 No capillary refill or BP<85 0
R - Respiration
Normal Abnormal (labored or shallow) 1 Absent 2 0
- Abdomen Abdomen and thorax non-tender 2 Abdomen and thorax tender 1 Abdomen rigid or flail chest* 0 2
M - Motor Normal Responds only to pain 1 (other than decerebrate) no response (decerebrate) 0
- Speech Normal Confused No intelligent words Trauma Trauma Score <= 8: Major Score >= 9: Minor
2 1 0
– loose fitting of the heart composed of membranes and 5-20ml fluid Cardiac layers – epicardium, myocardium, endocardium Chambers – right and left atria; right and left ventricles Valves –Tricuspid, bicuspid, semi-lunar Coronary circulation Left coronary – LAD, LCA Right coronary
Gallop- ventricular overload; heard after S2; “ken-tuck-y” S4 Gallop- increased resistance to ventricular filling; heard late in diastole; “ten-ne-see” Splitting heart sounds –Aortic and pulmonic valve does not close simultaneously Systolic Murmur- turbulent blood flow
angiography Electrocardiogram Serum Studies
– (3-4 days) LDH – Lactate dehydrogenase (7-14 days) Troponin –T (14-21 days) Aspartate Transaminase (3-4 days) C- Reactive Protein Myeloperoxidase
blood pressure(80-90 60-65
mmHg) Central venous pressure ( 1-8 mmHg or 4-12 cm water) Pulmonary artery pressure ( 8-12 mmHg) Cardiac output (4-8 L/min) Venous oxygen Saturation (60-80%)
Consent Explain procedure – cooperation Trendelenberg position – lower extremity source Assist during procedure – local anesthesia Instruct for deep breath and hold; neck flexion for PICC Correct reading Sterile and Aseptic technique – prevent infection.
of central vein or arterial
wall Pneumothorax and hemmorrhage Infection by the indwelling invasive device Catheter occlusion Ischemia distant to the site of catheter Disturbance of cardiac rhythym
BLOOD GASES: ARTERIAL/VENOUS
Normal Values pH
PO2 PCO2 HCO3 (mEqL) Anion gap (mEq/L)
7.35-7.45 80 to 100 35 to 45 22 to 26 10 to 18
7.31 to 7.42 35 to 45 39 to 52 22 to 26 8 to 16
ANALYSIS OF ARTERIAL BLOOD GASES COMPONE NT DESCRIPTION Measures hydrogen ion (H+) concentration Increase in ions, acidosis Decrease in ions, alkalosis •Partial pressure of in CO2 arteries •Respiratory component of acidbase regulation Hypercapnia, respiratory acidosis Hypoventilation, respiratory alkalosis •Measures serum bicarbonate •May reflect primary metabolic disorder or compensatory mechanism to respiratory acidosis Metabolic acidosis Metabolic alkalosis VALUES 7.35-7.45 <7.35 >7.45 35 to 45 mmHg >45 mmHg <35 mmHg Normal: 22 to 26 mEq/L
<22 mEq/L >26 mEq/L
The GOAL is to maintain alveolar ventilation, correct hypoxemia and maximize O2 transport when client cannot sustain spontaneous and effective respirations.
Initiating Mech. Ventilation/ Setting up machine
1.Set up the machine 2. Plug to emergency outlet 3. Select ventilatory settings ( per doctor’s orders)
Tidal volume, FiO2, peak inspiratory flow rate, Mode ( A/C, IMV, SIMV, PSV), Sensitivity, Pressure limit, I:E ratio, respiratory rate.
Types of Ventilators 1. Pressure- Cycled 2. Volume- Cycled 3. Time- Cycled
Nursing Care 1.Note ETT position. Monitor cuff pressure 2. Restrain only if needed 3. Administer sedatives prn.( To keep patient calm) 4. Auscultate breath sounds
5. 6. 7. 8.
Monitor ventilator settings Change tubings prn. Perform CPT as needed Monitor ABG, O2 sat. , V/S
9. Assess position change 10. Provide alternate communication measures 11. Suctioning prn. 12. Respond to alarms
is over 70-80 mmHg PaCO2 = normal Acceptable general respiratory status Correction of underlying problem
Description: a visual representation of the electrical activity of the heart reflected by changes in the electrical potential at the skin surface
P Q S
P Q S
P Q S
P Q S
1,II, III, AVF, V6 – all waveforms are upright aVR – all waveforms are negatively deflected aVL – P and T are negative, QRS are biphasic V1,V2 – P and T positive, QRS negative V3, V4, V5 – P and T positive, QRS biphasic
( 60-100 Bpm) Junctional ( 40-60 Bpm) Ventricular (30-40 Bpm and lower)
Foci- may arise from any part of the heart atria or ventricles causing abnormal heart rates and activity.
The following conditions can interfere with normal heart functioning: A. Disturbances of rate or rhythm B. Disorders of conductivity C. Enlarged heart chambers D. Presence of myocardial infarction E. Fluid and electrolyte imbalances.
Each EKG should include identifying information of patient The standard EKG is the 12-lead EKG. Bedside monitoring through telemetry is more commonly seen in the clinical setting using 3-5 leads A portable continuous monitor (Holter monitor) can be placed on the client to provide a magnetic tape recording; patient to record
The EKG graph paper consists of small and large squares:
A. The small squares represent 0.04
seconds with five of these small squares combining to form one large square. B. Each large square represents 0.20 seconds (0.04 seconds x 5). Five large squares represent 1 second.
Boxes – 300-150-100-75-60
of heart rate using the six-second rule:
1. The easiest means of calculating the heart rate. 2. Can not be used when the heart rate is irregular. 3. 30 large squares equal one-six second interval. 4. Count the number of R-R intervals
P wave: atrial systole A. Represents depolarization of the atrial muscle B. Should be rounded without peaking or notching. QRS complex: ventricular systole A. Represents depolarization of the ventricular muscle. B. Normally follows P wave. C. QRS interval measured from beginning of the QRS to the end
T wave: ventricular diastole 1. Represents repolarization of the ventricular muscle. 2. Follows QRS complex. 3. Usually slightly rounded without peaking or notching. U wave – a small wave following the T-wave indicating potassium depletion
ST segment: A. Represents every ventricular repolarization. B. Measured from the end of the S wave to the beginning of the T wave. PR interval: A. Represents the time required for the impulse to travel through the atria (SA node), through the A-V node, to the Purkinje fibers in the ventricles. B. Measured from the beginning of the P wave to the beginning of the QRS complex.
U wave: A. Not always present. B. Most prominent in the presence of hypokalemia. QT interval: A. Represents the time required to completely depolarize and repolarize the ventricles. B. Measured from the beginning of the QRS complex to the end of the T wave. (0.32-0.44 sec.) R-R interval: A. Reflects the regularity of the heart rhythm.
sinus rhythm (60-100) Sinus bradycardia (below 60) Sinus tachycardia (101-180) Sinus arrhythmia (irregular)
Normal Sinus Rhythm
Look at the p waves:
rate is 60-100/min cycle length do not vary by 10% PR interval is 0.12 sec. or more
Regularly occurring PQRST Rate < 60 / min Rate = 48/min
Rate = 48/min
Regularly occurring PQRST Rate > 100 / min
Rate = 111/min Rate = 111/min Rate = 111/min
Identical but irregularly occurring PQRST longest PP or RR > the shortest by 0.16 sec or more
Rate = 71/min Rate = 94/min Rate = 79/min Rate = 94/min
– P waves are premature Atrial tachycardia – (150-250) difficult to distinguish P from T waves Atrial flutter – atrial (250-450) no p waves but replaced by saw-toothed waves before a QRS Atrial fibrillation- atrial (400-600) bizzare P waves before a QRS
Premature Atrial Contraction
Prematurely occurring PQRTS complex P wave different in configuration from the sinus beat. PR interval often long. QRS narrow.
Multifocal Atrial Tachycardia
Impulses originate irregularly and rapidly at different points in the atrium Varying P wave, PR, PP and RR intervals Ventricular rate > 100/min
Atrial rate = 220-300/min ( P as flutter waves ) Variable degree of AV block ( irregular RR interval )
No discernible P waves Irregular RR interval
– P wave absent with wide Bizzare QRS Ventricular Tachycardia- wide sawtoothed QRS (200-250) without P or PR Ventricular Fibrillation- rate cannot be determined, rapid and chaotic; coarse or fine Asystole- flat line
Premature Ventricular Contraction
Prematurely occurring complex. Wide, bizarre looking QRS complex. Usually no preceding P wave. T wave opposite in deflection to the QRS complex. Complete compensatory pause following every premature beat.
At least 3 consecutive PVC’s Rapid, bizarre, wide QRS complexes (> 0.10 sec) No P wave (ventricular impulse origin) Rate > 140 / min
degree AV – Normal rate and rhythm with prolonged constant PR interval Second degree AV 1 or 2– Atrial regular, ventricular irregular, more P waves than QRS , PR lengthens then drops a QRS periodically or QRS maybe absent Third degree AV - Atrial -ventricular no relationship, more P waves than QRS , No PR ; QRS narrow or wide
FIRST DEGREE AV BLOCK
PR interval > 0.20 sec
Second Degree Atrioventricular Blocks
Do you have a normal P wave? Yes No No
Do you have a normal PR segment? Do you have a normal PR interval?
Will there be intermittent P waves not followed by QRS complex? Yes (dropped beats)
THIRD DEGREE AV BLOCK
Complete atrioventricular block Impulses originate at both SA node and at the subsidiary pacemaker below the block Do you have regularly occurring P waves and QRS complexes? Are the P waves related to the QRST complexes? No Is the atrial rate < = > ventricular rate? greater
Ventricular rate = 83 BPM Ventricular rate = 83 BPM
Atrial rate = 100 BPM
Atrial rate = 100 BPM
Atrial rate = 100 BPM
PVC’s, Salvo, V-tach Lidocaine to regulate rhythm to normal; cardioversion Asystole – epinephrine, atropine to initiate rhythm and contractions, then defibrillation if with pulse Coarse V-Fibrillation with pulse – defibrillation, then medications to regulate rhythm
Coronary Artery Disease ( CAD)loss of oxygen and nutrients to myocardial tissue due to poor coronary blood flow. The most common cause is atherosclerosis ( fatty, fibrous, possibly calcium deposits in the lumen of coronary arteries) Risk factors: Non- modifiable/ non-controllable: Heredity Age ( above 40), Sex/gender( more men , more likely in women who smoke and those on oral contraceptive) Race ( more in blacks)
• Diet • Habit/ Lifestyle ( sedentary; smoking- risk drops
within 1 year of quitting) • Contributing: Obesity, Response to stress, other diseases like DM, • Increased LDL ; decreased HDL; Hypertension; • Coronary artery spasm associated with atherosclerosis or from unknown cause
The mnemonic A B C D E to control risk factors A for aspirin and antianginal therapy, B for beta-blocker therapy and BP control, C for cigarettes and cholesterol, D for diet and diabetes, E for education and exercise.
Angina/ Angina Pectorisa
transient ischemic attack resulting from decreased blood supply through partially occluded coronary arteries. Precipitating factors include: extreme changes in temperature, physical exercise, emotional factors, eating a heavy meal, sexual intercourse, valsalva maneuver, cigarette smoking, stimulants.
Transluminal Coronary Angioplasty (PTCA), Coronary Artery Bypass graft ( CABG), or Stress Test may cause angina. or chest discomfort may be described as burning, suffocating squeezing or crushing tightness in the substernal or precordial areas that radiates to the left arm ( or both), neck, jaw or shoulder blade. may clench his fist or rub his left arm when describing it. Commonly accompanied by nausea, vomiting, fainting, sweating, and cool extremities.
Stable ( chronic) Angina :
usually precipitated by physical exertion, emotional stress, or cold weather. Has stable pattern of onset, duration and severity and relieving factors pain or discomfort may vary from mild to severe and usually lasts for 1 to 5 minutes . Relieved with rest and sublingual NTG, or both.
Preinfarction angina, crescendo angina or intermittent coronary syndrome Triggered by unpredictable degree of exertion or emotion, which may occur at night. It must be treated as a medical emergency with the client receiving immediate medical attention Often described as progressive, prolonged, or frequent angina with increasing severity.
or discomfort is more intense lasting up to 30 minutes, often arouses patient from sleep. Pain is not completely relieved with NTG, may require narcotics (like Morphine Sulfate) Without significant EKG changes like ( T wave inversion =Ischemia ) diagnosis is based on history and clinical condition 10-30% of clients progress to having an MI in 1 year, and 29% die from MI in 5 years
Prinzmetal’s angina :
Variant angina similar to classic angina ; chest pain of longer duration; may occur at rest Attacks tend to happen between midnight and 8am Results from coronary artery associated with elevation of ST segment in the EKG NTG generally yields quick relief. Calcium channel blockers ( Verapamil, Nifedipine, Dialtezem ) are most effective Goal: vasodilation and reduce myocardial oxygen demands
administering Nitroglycerin: Take baseline V/S, give it sublingually x 3 every 5 min. take V/S after each dosage. the BP is less than 100mmHg or less than 25mmhg lower than the previous reading, do not give it, the nurse lowers the head of the bed and notifies the physician segment depression and T-wave inversion occur with chest pain and return to normal when episode subsides; ST segment elevation ( Prinzmetal’s) which goes back to normal when spasm subsides.
Definition 1. Necrosis of myocardial cells is lifethreatening event 2. Loss of functional myocardium affects heart ability to maintain effective cardiac output
or rupture of complicated atherosclerotic lesion Substances released which lead to platelet aggregation, thrombin generation, local vasomotor tone Formation of clot which occludes vessel and blocks blood to myocardium distal to obstruction Prolonged ischemia (>20 – 45 minutes): irreversible hypoxemic damage Cellular metabolism shifts from aerobic to anaerobic metabolism producing hydrogen ions and lactic acid
Depth of Infarction Subendocardial or non-Q-wave infarction 1. Damage is limited to subendocardial tissue 2.Occurs within 20 minutes of injury 3. Common complication is recurrent ischemia 4. S-T segment depression with small infarct Intramural infarction – in myocardium ; associated with angina pectoris Transmural infarction or Q- wave infarction 1.All layers of myocardium to epicardium
Pain: classic manifestation Lasts > 15 – 20 minutes Unrelieved by rest or nitroglycerine Onset sudden and usually not associated with activity Described as crushing and severe; as a pressure, heavy or squeezing sensation; tightness or burning in the chest Location: center of chest (substernal) and may radiate to shoulders, neck, jaw, arms
and older adults have atypical chest pain with complaints of indigestion, heartburn, nausea, vomiting No chest discomfort in 25% of clients with acute MI
Additional symptoms relate to sympathetic nervous system stimulation: Cool, clammy, mottled skin Tachypnea Sense of impending doom and death
Depending on location and amount of infarct Hypertension or hypotension Signs of heart failure Nausea and vomiting, bradycardia Hiccups Sudden death (large blood vessel involvement)
chest pain Reduce extent of myocardial damage Maintain cardiovascular stability Decrease cardiac workload Prevent complications
Rapid assessment and early diagnosis key:
is muscle” Initiation of definitive treatment within 1 hour of entry into health care system Major problem: delay in seeking medical care post onset of symptoms (44% wait > 4 hours to seek treatment)
cardiac markers: Proteins released from necrotic heart muscle; ordered on admission and for 3 succeeding days a. Creatine phosphokinase (CK) Appears 4 – 6 hours postacute MI; peaks 12 –24 hours; declines over next 48 – 72 hours b. CK-MB
Isoenzyme of CK most sensitive indicator of MI CK-MB elevation > 5% positive indicator of
Cardiac-specific troponin T (cTnT) and Cardiac-specific troponin I (cTnI)
released during myocardial infarction; sensitive indicators for myocardial damage Released and levels rise with necrosis of cardiac muscle Sensitive enough to detect very small infarction and remain in blood 10 – 14 days post MI
Other laboratory tests
Erythrocyte Sedimentation Rate: WBC and ESR elevated of because of inflammation Blood Gases: assessment secondary to physical effects of MI T wave
inversion; Elevation of S-T segment; Formation of Q wave
Pain Ineffective Tissue Perfusion: obtain 12-lead ECG to assess significant chest pain Ineffective Coping: overuse of denial may interfere with learning and compliance with treatment Fear
of pain- MONA is the guide of treatment of clients with chest pain. M for Morphine sulfate, O for Oxygen therapy, N for nitrates and A for aspirin. 2. Promote measures to maintain cardiac parameters• Cardiac monitoring ( place client on Lead II), • Report changes in LOC, Heart /Lung sounds, • Peripheral pulses, Capillary refill time (less
than 3 sec), • JVD (jugular vein distention),
• Monitor Pulmonary artery wedge pressure( PAWP) if patient has a Swan- Ganz catheter (PAWP less than 18 mmHg shows volume depletion and PAWP more than 18 mmHg signifies pulmonary congestion or cardiogenic shock • Monitor urinary output, Decreased activity level, Schedule rest periods, Adm. stool softeners.
Promote measures to maintain adequate O2 and carbon dioxide exchange
• O2 Administration, • Pulse oximetry, Monitor ABG
results, Monitor secretions by coughing and suctioning, • Prepare for intubation as necessary.
Thrombolytics- agents which cause lysis of a pathogenic clot and a hypercoagulable state in the entire circulatory system. For coronary artery thrombi treatment should be initiated within 4-6 hours from onset of symptoms.
A. Streptokinase (SK) B. Urokinase C. Anisoylated Plasminogen –Streptokinase Activator Complex ( APSAC) D. Tissue Plasminogen Activator (t-PA) or recombinant tissue-type plasminogen activator ( rt-PA)
Other Medications: used to reduce oxygen demand and increase oxygen supply Analgesics – Morphine Sulfate Angiotensin converting enzyme inhibitor-vasodilation Beta adrenergic blockers- decrease contractility & O2 demand; increase coronary blood flow Anticoagulants( Heparin, Coumadin) Calcium channel blockers (Verapamil) Antidysrhythmic drugs( Lidocaine is the most common)
Other Medical Interventions: 2.Percutaneous Transluminal Angioplasty ( PTCA)- a non surgical procedure performed under fluoroscopy, that uses pressurized balloon catheter to expand stenotic coronary artery. 3.Intracoronary stents- placement of a tubular mesh or coilspring device which is place in the lumen of the coronary artery. 4.Laser surgery- coronary artery is dilated with use of laser.
4. Intra-aortic Balloon Pump ( IABP)inflation of a balloon in the coronary artery during diastole and deflated during sysytole. 5. Coronary Artery Bypass Graft( CABG)-diversion of blood flow around an occluded artery. This conduit is accomplished through anastomosing of the saphenous vein or internal mammary artery.
1. Dysrhythmias – due to myocardial irritability ; Fibrillation is the most common. 2. Heart Failure. 3. Cardiogenic Shock- due to massive left ventricular failure. 4. Ventricular aneurysm- a healing necrotic tissue can cause thinning and weakening of the ventricular wall.
5. Pericarditis-an inflammatory response to myocardial damage. 6. Dressler’s syndrome ( AKA postmyocardial infarction syndrome)- a late Pericarditis, with precordial pain, friction rub, fever, peuritis and/or pleural effusion. 7. Pulmonary embolism. 8. Interventricular septal rupture. 9. Papillary muscle rupture.
Description: the exchange of oxygen for carbon dioxide in the lungs is inadequate for oxygen consumption and carbon dioxide production within the body’s cells. ARDS is characterized by: Hypoxemia: PO2 below 50mmHg. Hypercapnia: PCO2 above 45 mmHg. ARDS is an unexpected, catastrophic pulmonary complication occurring in a person with no previous pulmonary problems. The mortality rate is high
Common causes of respiratory failure include: 3. 4. 5. 6. 7. 8. COPD 1. Pneumonia 2. Tuberculosis 3. Contusion 4. Aspiration 5. Inhaled toxins Emboli Drug overdose Fluid overload DIC Shock
• Dyspnea, tachypnea • Intercoastal retractions • Cyanosis • Hypoxemia: PO2< 50 mmHg with FiO2 > 60% • Diffuse pulmonary infiltrates seen on chest x-ray as “whiteout” appearance • verbalized anxiety; restlessness
• Impaired gas exchange • Ineffective airway clearance • Ineffective breathing pattern • decreased cardiac output • Fluid volume excess
Maintain client on a ventilator with the correct settings. • Provide care for either an oral airway or a tracheostomy. (Suction ONLY when secretions are present) • Monitor breath sounds for pneumothorax especially when positive end expiratory pressure (PEEP) is used to keep small airways open. The amount of pressure can be set with the ventilator and is usually around 5-10 cm of water. • Provide emotional support to
1. Monitor client hemodynamically with essential vital signs and cardiac monitor. 2. Monitor ABGs routinely. 3. Monitor vital organ status: central nervous system, level of consciousness, renal system output and myocardium (apical pulse, blood pressure). 4. Monitor fluid and electrolyte balance.
Surfactant (Survanta/Beractant) ? Nitric Oxide –pulmonary vasodilator ? Dobutamine/Dopamine for fluid instability Steroids Antibiotics Ventilatory support with PEEP
trauma, VA pneumonia, pulmonary fibrosis, Pulmonary embolism Stress ulcers, GIT hemorrhage Arrhythmias ARF Pneumothorax and tracheal stenosis Malnutrition and electrolyte inbalance MOSF – from endothelial damage by circulating immune complexes
Description: Widespread, serious reduction of tissue perfusion (lack of oxygen and nutrients), which, if prolonged, leads to generalized impairment of cellular functioning.
At risk for developing shock include:
2.The very young or the very old client 3.Post-MI clients 4.Clients with severe dysrhythmia 6.Clients with adrenocortical dysfunction 8.Persons with a history of recent hemorrhage or blood loss. 11.Clients with burns
TYPES OF SHOCK
CARDIOGENI C/OBSTRUCTI VE
Related to external or internal blood/fluid loss (most common cause of shock); hemorrhage, burns, Related to dehydration ischemia/impairment in tissue perfusion from myocardial infarction, serious arrhythmia, or congestive heart failure. All of these
Distributiv e SHOCK
Results from inadequate vascular tone. Blood volume remains normal Vascular space increases dramatically because of massive vasodilation Blocking of the sympathetic NS in SCI leads to massive peripheral vasodilation from an unopposed parasympathetic NS.
Related to allergens VASOGENI (anaphylaxis), spinal cord C ANAPHYLACT injury, or peripheral IC neuropathies, all resulting in venous pooling and decreased blood return to the heart, which decreases cardiac output over time.Warm to skin, 3. Related endotoxins SEPTIC bronchoconstriction bacteria, rashes released from may observed with which be causes vascular products of inflammation pooling, diminished venous
STAGES OF HYPOVOLEMIC SHOCK
STAGE SIGNS AND SYMPTOMS CLINICAL DESCRIPTION
STAGE I: INITIAL STAGE Blood loss of less than 10%. Compensa tory mechanis ms triggered.
•Apprehension and restlessness (first signs of shock) •Increased heart rate •Cool, pale skin •Fatigue
•Arteriolar constriction •Increased production of ADH •Arterial pressure is maintained •Cardiac output usually normal (for healthy individuals) •Selective reduction of blood
•Flattened neck veins COMPENSATO and delayed RY STAGE venous filling Bloodvolu time me •Increased reduced pulse and by 15 to respirations 25%. •Pallor, Decompens diaphoresis ation and cool skin begins. •Decreased urinary output STAGE II:
•Marked reduction in cardiac output •Arterial pressure decline (despite compensatory arteriolar vasoconstriction) •Massive adrenergic compensatory response resulting in: tachycardia,
STAGE •Edema •Increased III: PROGRESSI blood viscosity VE STAGE •Excessively low blood pressure •Dysrhythmia, ischemia and MI •Weak, thready, or absent peripheral
•Rapid circulatory deterioration •Decreased cardiac output •Decreased tissue perfusion •Reduced blood volume
STAGE IV: Irreversible STAGE
•Profound hypotension, unresponsive to vasopressor drugs •Severe hypoxemia, unresponsive to oxygen administration •Anuria, renal shutdown •Heart rate slows, BP falls,
•Cell destruction so severe death is inevitable •Multiple organ system failure
Vital Signs: 4.Tachycardia (>100 bpm) 5.Tachypnea (>24 cpm) 6.Blood pressure decreased (systolic <80 mmHg) Mental Status Exam: 9.Early shock: restless, hyper-alert 10.Late shock: decreased alertness, lethargy, coma
Skin Changes: 2.Cool, clammy (warm skin in vasogenic and early shock) 3.Diaphoresis 4.Pale Fluid Status (acute tubular necrosis can happen quickly in shock): • Urine output decreases or an imbalance between intake and output occurs • Abnormal CVP (>4 cm of H2O). • Urine specific gravity >1.020
Fluid volume deficit Decreased cardiac output Altered thought process Anxiety (family and individual)
Monitor arterial pressure by understanding the concepts related to arterial pressure Monitor vital signs and arrhythmias every 15 minutes or more often depending on the stability of the client. Assess urine every hour to maintain at least 30 ml/hr. Notify healthcare provider if urine output drops below 30
Administer fluids as prescribed by provider: blood, colloids, or electrolyte solutions until designated CVP is reached. (In shock, the healthcare provider often orders fluids to elevate CVP 16-19 cm of H2O as compensation for decreased cardiac output). Place client in modified Trendelenburg’s position (feet up 30-45 degrees, head flat). Administer medications IV (not IM or subQ) until perfusion improves in
HINT: If cardiogenic shock exists with the presence of pulmonary edema, i.e. from pump failure, position client to REDUCE venous return (high-Fowler’s with legs down) in order to decrease venous return further to the left ventricle.
Keep client warm (increase heat in room or put warm blankets in client, but not too hot). Keep side rails up during all procedures (clients in shock experience mental confusion and may easily be injured by falls). Obtain blood for laboratory work as prescribed: CBC, electrolytes, BUN, creatinine (renal damage), and blood gases (oxygenation).
Drugs of choice for shock: 2. Digitalis preparations: increase contractility of the heart muscle 3. Vasoconstrictors ( Dopamine): generalized vasoconstriction to provide more available blood to the heart to help maintain cardiac output.
– for blood supply to important organs and in cardiogenic shock Steroids Heparin Naloxone- reverses the effects of hypotension as an opiate antagonist Epinephrine- for anaphylactic shock H2 receptor antagonists – ulcers Opioids – for cardiogenic shock Calcium gluconate- for blood clotting and muscular function
whole ( to replace large volume loss), packed RBC 9 for moderate blood loss bec they replenish RBC and improve oxygen – carrying capacity without adding excessive volume), autotransfusion (trauma). As a rule of thumb, Hct. Rises about 4% and Hgb rises about 1 g % for each unit of packed RBC administered.
replacement- Crystalloids ( for F/E replacement) ,Colloids( plasma protein fraction, fresh-frozen plasma, albumin, dextran, hetasarch ( plasma expander) are used to restore plasma volume and colloidal osmotic pressure bec. they contain large molecules usually proteins or starches)
•Isotonic solutions: •Normal saline (0.9% NS) •Lactated Ringers (LR) •5% dextrose in water (D5W is on the low end of isotonic-some sources classify as hypotonic) Hypotonic solutions: 6.0.3 % NaCl 7.0.45 NS 8.D 2.5 in H20
•Hypertonic saline solutions are available but used only when serum osmolality is dangerously low •5% dextrose in LR (D5LR) •5% dextrose in 0.45% saline (D5 ½ NS) •5% dextrose in 0.9% saline (D5NS)
coagulation disorder with paradoxical thrombus and hemorrhage. DIC is an acute complication of conditions such as hypotension and septicemia, suspected when there is bloody oozing from two or more unexpected sites. The first phase involves abnormal clotting factors, and results in an
The diagnosis is based on laboratory findings:
2. 3. 4. 5. 6.
Prolonged PT Prolonged PTT Decreased fibrinogen Decreased platelet count Increased Fibrin Degradation (split) Products (FDP)
Nursing Assessment Petechiae, purpura, hematomas Oozing from IV sites, drains, gums and wounds GI and GU bleeding Hemoptysis Hypotension, tachycardia Pain Nursing Diagnoses 10. Potential for injury 11. Alteration in tissue perfusion
Nursing Plans and Interventions 2. Monitor client for bleeding. 3. Monitor vital signs. 4. Protect client from injury and bleeding: • Provide gentle oral care with mouth swabs • Minimize needle sticks, use smallest gauge needle possible. • Turn frequently to eliminate pressure points. • Minimize number of blood pressures taken by cuff.
4. Administer Heparin IV during the first phase to inhibit coagulation. 5. If in hemorrhagic phase, administer clotting factors 6. Provide emotional support to decrease anxiety.
Description: dilation of the abdominal
aorta caused by an alteration in the integrity of its wall.
common cause of AAA is atherosclerosis It can also be a late manifestation of syphilis Without treatment, rupture and death will occur It is often asymptomatic Most common symptom is abdominal pain or low back pain with the
Bruit (swooshing sound heard over a constricted artery when auscultated) heard over abdominal aorta, pulsation in upper abdomen. Abdominal or lower back pain. Abdominal x-ray will confirm diagnosis if aneurysm is calcified (aortagram, angiogram, abdominal ultrasound). Symptoms of rupture: hypovolemic or cardiogenic shock with sudden,
2. 3. 4.
Activity intolerance Impaired skin integrity Anxiety
Nursing Plans and Interventions
3. 4. 5.
Assess all peripheral pulses and vital signs regularly Observe for signs of occlusion after graft Observe renal functioning for signs of kidney damage (artery clamped during surgery may result in kidney damage).
MOSF= Multiple Organ System Failure Multiple Organ Dysfunction Syndrome ( MODS)
syndrome that occurs when one or more than one system/organ cannot support its activities. Factors Influencing the development of MODS: Gram negative sepsis ( #1 risk), immunosuppressants, traumatic injury, sleep deprivation, malnutrition, blood transfusions, age over 65. Pathophysiology: the 3 Is of MODS are: persistent Inflammation, Infection (sepsis), Ischemia.
precursor of MODS is systemic inflammatory response syndrome ( SIRS)
of the inflammatory-immune response ( IIR) which 4. Sympathetic nervous system stimulation and release of catecholamines 5. Endothelial damage and embolus formation. Complement activation occurs
is to induce inflammation, the goal of inflammation is to protect the body, limit injury extent , and promote healing at the damaged site)
Mediators involved in the IIR are WBC, platelet, T cells, B cells, and histamine. Altered perfusion r/t to small microvasculature emboli and respiratory insufficiency causes shunting of blood to major organs until compensatory mechanisms fail. The organs affected are usually the lungs, liver kidney, heart and brain.
Modified APACHE II Criteria for Diagnosing Multiple Organ System Failure ( Black and Jacobs, 1997)
I. Cardiovascular Failure ( presence of one or more of the ff) HR less than 54 beats / min Mean arterial pressure equal or less that 49 mm Hg (systolic pressure of equal or less than 60mmHg) Occurrence of Ventricular Tachycardia/ Fibrillation Serum pH of equal or less than 7.24 with a PaCo2 of equal or less than 40 mmHg
II. Respiratory Failure ( presence of one or more of the following)
of less than or equal to 5/min. equal to or greater than 49/min, PaCO2 equal or greater than 50mmHg Alveolar Arterial Oxygen difference equal or greater then 350mmHg calculated as follows: (713 x % Oxygen in inspired gas)PaCO2- PaO2 Dependent on ventilator on the 2nd day
III. Renal Failure ( presence of one or more of the ff) *Urine output equal or less than 479 ml/24 hrs. or equal or less than 159ml/8 hrs. * Serum BUN equal to or greater than 100mg/dl * Serum Creatinine equal to or greater than 3.5 mg/dl
IV. Hematologic Failure ( presence of one or more of the ff)
equal or less than 1000/ul ( Normal is 4,000 to 10,000/ ul) *Platelet equal or less than 20,000 /mm3 * Hematocrit equal or less than 20%
V. Neurologic Failure
coma score equal or < than 6 ( in the absence of sedation )
VI. Hepatic Failure Serum Bilirubin equal or greater than 6 mg/dl Prothrombin Time equal to or greater than 4 sec over control in the absence of systemic anticoagulation
Vasodilation and ↓ PR With normal BP, Cardiac output increases to maintain blood pressure= initial hyperthermia ( skin warm, pink, and dry with shaking chills although the reverse may occur in the elderly) , Increase renal blood flow ( polyuria), Hyperventilation (Causes resp alkalosis), Signs of tissue hypoxia manifest due to oxyhemoglobin dissociation ; Hemoglobin is reluctant to release oxygen to cells.
Hypotension due decreased cardiac output ( PR is ↑ via catecholamine release due to sympathetic nervous system stimulation) ; Pulse becomes weak and thready; ST and T wave changes on ECG ( due to ↓ myocardial perfusion); Cold, moist, pale skin, mottling and cyanosis, hematologic changes( DIC or primary bleeding problem), Hypoxia (↑HR,↑RR, restlessness, diaphoresis, lethargy, confusion, and pallor) and ↓perfusion evident metabolic acidosis develops.
Others: Glucose: initially increased, gluconeogenesis occurs leading to lactic acidiosis; protein catabolism causes negative nitrogen balance and proteinuria Generalized acidotic state and decreased cellular energy cause cell death and organ failure Mortality is up to 90%
Management: Monitor V/S, Neuro status, Measure I/O, Bowel sounds/ Abdominal distention, Abdominal girth, Occult blood Ventilatory support, ABG monitoring, pulse oximetry Maintain + nitrogen balance ( enteral feeding)
MEDICATIONS : antibiotics, antacids, histamine antagonists, analgesics, anti-anxiety agents, sedate as ordered to ↓ metabolic needs, anti-inflammatories, vasoactive agents, inotropes, fluids , steroids ( not proven to be beneficial) FUTURE TRENDS in therapy: Cyclosporine vs. FK-586; monoclonal/polyclonal antibodies.
Sample Questions Which of the following nursing orders would be found on the care plan for a client for the first 24 hours after an MI? A. Utilize bedside commode for bowel movements B. 200 calorie soft diet C. Feed the patient D. Administer promethazine daily
Which of the following would be included in the discharge plan for a client after MI? A. Don’t begin sexual intercourse until after 3 months B. Begin walking frequently C. Take one aspirin every 8 hours as ordered D. Continue previous lifestyle when ready
To prevent the leaking of blood into surrounding tissue following blood extraction for ABG determination, the nurse should implement which nursing measure: A. Apply ice to the puncture site B. Maintain manual compression over the puncture site for at least one minute C. Elevate the limb on several pillows
The client is an asthmatic and in acute respiratory distress. The nurse auscultates the lungs and notes no inspiratory wheezing. What should this finding suggest to the nurse? A. Airway constriction requiring intensive interventions B. An appropriate reaction to the medications used in the management of the client C. The need to assess the client further for signs of pleural effusion D. Overuse of the intercostal
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