Cardiac Nursing Applied Anatomy And Physiology
hollow muscular behind the sternum and between the lungs has heart wall has 3 layers:
Endocardium – thin lining, covers valves Myocardium – muscular layer Epicardium – thin covering(mesothelium) Pericardium – invaginated sac Visceral – attached to the exterior of myocardium Parietal – attached to the great vessels and diaphragm
separated into 2 pumps: right heart – pumps blood through the lungs left heart – pumps blood through the peripheral organs chambers of the heart atrium – weak pump and blood reservoir ventricle – main force that propels blood to pulmonary and peripheral circulation Blood Supply
Arteries Coronary artery – 1st branch of aorta • Right Coronary o SA nodal Branch – supplies SA node o Right marginal Branch – supplies the right border of the heart o AV nodal branch – supplies the AV node o Posterior interventricular artery – supplies both ventricles • Left Coronary o Circumflex branch – supplies SA node in 40 % of people o Left marginal – supplies the left ventricle o Anterior interventricular branch aka Left anterior descending(LAD)–supplies both ventricles and interventricular septum
o Lateral branch – terminates in ant surface of the heart Veins Coronary sinus – main vein of the heart Ant interventricular vein or Great Cardiac vein – main tributary of the coronary sinus Post interventricular vein or Middle cardiac vein Small Cardiac vein Left Posterior ventricular vein Left Marginal Vein Oblique vein – remnant of SVC, small unsignificant Smallest cardiac veins- valveless Action Potential Resting Membrane Potentials -85 to -95 mV – cardiac muscle -90 to -100 mV – Purkinje fibers Circulation
Blood from head and UE; Trunk and LE Superior Vena Cava: Inferior Vena Cava Right Atrium Tricuspid Valve Right Ventricle Pulmonary Valve Pulmonary Artery Lungs Pulmonary Vein Left Atrium
Mitral Valve Left Ventricle Aortic valve Aorta
Myocardial cell Intercalated disks Cell membranes that separates individual cells from each other Two Groups of Myocardial Cells Cells specialized for impulse generation and conduction • Automatic cells • Found in SA, AV nodes and Purkinje system(transitional cells) Cells specialized for contraction • Non Automatic Cells Specialized Cardiac Cells
Nodal tissues SA Node( Sino-atrial, Keith and Flack) • Primary Pacemaker • Between SVC and RA • Vagal and symphatetic innervation • Sinus Rhythms AV Node( Atrioventricular , Kent and Tawara) • At the right atrium
• 3 zones o AN Zone(atrionodal) o N Zone (nodal) o NH zone (nodal –HIS) Internodal and Interatrial Pathways Connects SA and AV Node Ant. Internodal(bachman) tract Middle Internodal(wenkebach) tract Posterior internodal(Thorel) tract Bundle of His/ Purkinje Fibers Provides for ventricular conduction system Fastest conduction among cardiac tissues Right bundle Left Bundle • Septal branches and 2 fascicles Mechanism of Contraction of Contractile Cardiac Muscle Fibers 1. Na+ influx from extracellular space, causes positive feedback opening of voltage-gated Na+ channels; membrane potential quickly depolarizes (-90 to +30 mV); Na+ channels close within 3 ms of opening. Depolarization causes release of Ca++ from sarcoplasmic reticulum (as in skeletal muscle), allowing sliding actin and myosin to proceed. Depolarization ALSO causes opening of slow Ca++ channels on the membrane (special to cardiac muscle), further increasing Ca++ influx and activation of filaments. This causes more prolonged depolarization than in skeletal muscle, resulting in a plateau action potential, rather than a "spiked" action potential (as in skeletal muscle cells).
Differences Between Skeletal & Cardiac MUSCLE Contraction
All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked electrochemically, so that activation of a small group of cells spreads like a wave throughout the entire heart. This is essential for "synchronistic" contraction of the heart as opposed to skeletal muscle. Automicity (Autorhythmicity) - some cardiac muscle cells are "self-excitable" allowing for rhythmic waves of contraction to adjacent cells throughout the heart. Skeletal muscle cells must be stimulated by independent motor neurons as part of a motor unit. Length of Absolute Refractory Period - The absolute refractory period of cardiac muscle cells is much longer than skeletal muscle cells (250 ms vs. 2-3 ms), preventing wave summation and tetanic contractions which would cause the heart to stop pumping rhythmically. Internal Conduction (Stimulation) System of the Heart A. General Properties of Conduction 1. 2. heart can beat rhythmically without nervous input nodal system (cardiac conduction system) - special autorhythmic cells of heart that initiate impulses for wave-like contraction of entire heart (no nervous stimulation needed for these) gap junctions - electrically couple all cardiac muscle cells so that depolarization sweeps across heart in sequential fashion from atria to ventricles
"Pacemaker" Features of Autorhythmic Cells 1. pacemaker potentials - "autorhythmic cells" of heart muscle create action potentials in rhythmic fashion; this is due to unstable resting potentials which slowly drift back toward threshold voltage after repolarization from a previous cycle.
Theoretical Mechanism of Pacemaker Potential: a. b. c. K+ leak channels allow K+ OUT of the cell more slowly than in skeletal muscle Na+ slowly leaks into cell, causing membrane potential to slowly drift up to the threshold to trigger Ca++ influx from outside (-40 mV) when threshold for voltage-gated Ca++ channels is reached (-40 mV), fast calcium channels open, permitting explosive entry of Ca++ from of the cell, causing sharp rise in level of depolarization when peak depolarization is achieved, voltage-gated K+ channels open, causing repolarization to the "unstable resting potential" cycle begins again at step a. C. Anatomical Sequence of Excitation of the Heart 1. Autorhythmic Cell Location & Order of Impulses (right atrium) sinoatrial node (SA) (right AV valve) atrioventricular node (AV) atrioventricular bundle (bundle of His) right & left bundle of His branches Purkinje fibers of ventricular walls (from SA through complete heart contraction = 220 ms = 0.22 s) a. sinoatrial node (SA node) "the pacemaker" - has the fastest autorhythmic rate (70-80 per minute), and sets the pace for the entire heart; this rhythm is called the sinus rhythm; located in right atrial wall, just inferior to the superior vena cava
atrioventricular node (AV node) - impulses pass from SA via gap junctions in about 40 ms.; impulses are delayed about 100 ms to allow completion of the contraction of both atria; located just above tricuspid valve (between right atrium & ventricle) atrioventricular bundle (bundle of His) - in the interATRIAL septum (connects L and R atria) L and R bundle of His branches - within the interVENTRICULAR septum (between L and R ventricles) Purkinje fibers - within the lateral walls of both the L and R ventricles; since left ventricle much larger, Purkinjes more elaborate here; Purkinje fibers innervate “papillary muscles” before ventricle walls so AV can valves prevent backflow External Innervation Regulating Heart Function 1. 2. heart can beat without external innervation external innervation is from AUTONOMIC SYSTEM
c. d. e.
Parasympathetic (acetylcholine) DECREASES rate of contractions cardioinhibitory center (medulla) vagus nerve (cranial X) heart Sympathetic (norepinephrine) INCREASES rate of contractions cardioacceleratory center (medulla) lateral horn of spinal cord to preganglionics Tl-T5 postganlionics cervical/thoracic ganglia heart The Normal Cardiac Cycle
General Concepts 1. 2. 3. systole - period of chamber contraction diastole - period of chamber relaxation cardiac cycle - all events of systole and diastole during one heart flow cycle Events of Cardiac Cycle 1. mid-to-late ventricular diastole: ventricles filled the AV valves are open pressure: LOW in chambers; HIGH in aorta/pulmonary trunk aortic/pulmonary semilunar valves CLOSED blood flows from vena cavas/pulmonary vein INTO atria blood flows through AV valves INTO ventricles (70%) atrial systole propels more blood > ventricles (30%) atrial diastole returns through end of cycle 2. ventricular systole: blood ejected from heart filled ventricles begin to contract, AV valves CLOSE isovolumetric contraction phase - ventricles CLOSED contraction of closed ventricles increases pressure ventricular ejection phase - blood forced out semilunar valves open, blood -> aorta & pulmonary trunk 3. isovolumetric relaxation: early ventricular diastole
ventricles relax, ventricular pressure becomes LOW semilunar valves close, aorta & pulmonary trunk backflow dicrotic notch - brief increase in aortic pressure TOTAL CARDIAC CYCLE TIME (normal 70 beats/minute) atrial systole (contraction) ventricular systole (contraction) quiescent period (relaxation) Heart Sounds: Stethoscope Listening
= = =
0.8 second 0.1 second 0.3 second = 0.4 second
Overview of Heart Sounds 1. lub-dub, - , lub, dub, 2. lub - closure of AV valves, onset of ventricular systole 3. dub - closure of semilunar valves, onset of diastole 4. Pause - quiescent period of cardiac cycle 5. Tricuspid valve (lub) - RT 5th intercostal, medial 6. Mitral valve (lub) - LT 5th intercostal, lateral 7. Aortic semilunar valve (dub) - RT 2nd intercostal 8. Pulmonary semilunar valve (dub) - LT 2nd intercostals
1. S1- due to closure of the AV valves 2. S2- due to the closure of the semi-lunar valves 3. S3- due to increased ventricular filling 4. S4- due to forceful atrial contraction B. 1. 2. 3. Heart Murmurs murmur - sounds other than the typical "lub-dub"; typically caused by disruptions in flow incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valve does not completely close, some regurgitation of blood stenotic valve - high pitched swishing sound when blood should be flowing through valve; narrowing of outlet in the open state
Cardiac Output - Blood Pumping of the Heart A. General Variables of Cardiac Output
1. Cardiac Output (CO) - blood amount pumped per minute CO (ml/min) = HR (beats/min) X SV (ml/beat) normal CO = 75 beats/minX 70 ml/beat = 5.25 L/min 2. Stroke Volume (SV) - ventricle blood pumped per beat 3. Heart Rate (HR) - cardiac cycles per minute Normal range is 60-100 beats per minute
Tachycardia is greater than 100 bpm Bradycardia is less than 60 bpm Sympathetic system INCREASES HR Parasympathetic system (Vagus) DECREASES HR 4. Blood pressure - Cardiac output X peripheral resistance Control is neural (central and peripheral) and hormonal Baroreceptors in the carotid and aorta Hormones- ADH, aldosterone, epinephrine can increase BP; ANF can decrease BP B. Regulation of Stroke Volume (SV) 1. 2. end diastolic volume (EDV) - total blood collected in ventricle at end of diastole; determined by length of diastole and venous pressure (~ 120 ml) end systolic volume (ESV) - blood left over in ventricle at end of contraction (not pumped out); determined by force of ventricle contraction and arterial blood pressure (~50 ml) 70 ml/beat
SV (ml/beat) =EDV (ml/beat) - ESV (ml/beat) normal SV = 120 ml/beat - 50 ml/beat = 3.
Frank-Starling Law of the Heart - critical factor for stroke volume is "degree of stretch of cardiac muscle cells"; more stretch = more contraction force a. increased EDV = more contraction force i. ii. slow heart rate = more time to fill exercise = more venous blood return
Regulation of Heart Rate (Autonomic, Chemical, Other) 1. Autonomic Regulation of Heart Rate (HR) a. sympathetic - NOREPINEPHRINE (NE) increases heart rate (maintains stroke volume which leads to increased Cardiac Output)
b. c. d.
parasympathetic - ACETYLCHOLINE (ACh) decreases heart rate vagal tone - parasympathetic inhibition of inherent rate of SA node, allowing normal HR baroreceptors, pressoreceptors - monitor changes in blood pressure and allow reflex activity with the autonomic nervous system
2. Hormonal and Chemical Regulation of Heart Rate (HR) a. b.
epinephrine - hormone released by adrenal medulla during stress; increases heart rate thyroxine - hormone released by thyroid; increases heart rate in large quantities; amplifies effect of epinephrine Ca++, K+, and Na+ levels very important; * * * * * 3. a. hyperkalemia - increased K+ level; KCl used to stop heart on lethal injection hypokalemia - lower K+ levels; leads to abnormal heart rate rhythms hypocalcemia - depresses heart function hypercalcemia - increases contraction phase hypernatremia - HIGH Na+ concentration; can block Na+ transport & muscle contraction
Other Factors Effecting Heart Rate (HR) normal heart rate fetus 140 - 160 beats/minute female 72 - 80 beats/minute male 64 - 72 beats/minute
b. c. d. e.
exercise - lowers resting heart rate (40-60) heat - increases heart rate significantly cold - decreases heart rate significantly tachycardia - HIGHER than normal resting heart rate (over 100); may lead to fibrillation f. bradycardia - LOWER than normal resting heart rate (below 60); parasympathetic drug side effects;
physical conditioning; sign of pathology in non-healthy patient
Assessment Diagnostic Tests: Laboratory Test Rationale 1. To assist in diagnosing MI 2. To identify abnormalities 3. To assess inflammation 4. To determine baseline value 5. To monitor serum level of medications 6. To assess the effects of medications LABORATORY PROCEDURES CARDIAC Proteins and enzymes 1. CK- MB ( creatine kinase) Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days Normal value is 0-7 U/L 2. Lactic Dehydrogenase (LDH) Elevates in MI in 24 hours, peaks in 48-72 hours Normally LDH1 is greater than LDH2 Lactic Dehydrogenase (LDH) MI- LDH2 greater than LDH1 (flipped LDH pattern) Normal value is 70-200 IU/L 3. Myoglobin Rises within 1-3 hours Peaks in 4-12 hours
Returns to normal in a day Not used alone Muscular and RENAL disease can have elevated myoglobin 4. Troponin I and T Troponin I is usually utilized for MI Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks! Normal value for Troponin I is less than 0.6 ng/mL REMEMBER to AVOID IM injections before obtaining blood sample! Early and late diagnosis can be made! 5. SERUM LIPIDS Lipid profile measures the serum cholesterol, triglycerides and lipoprotein levels Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL LDH- 130 mg/dL HDL- 30-70- mg/dL NPO post midnight (usually 12 hours) ELECTROCARDIOGRAM (ECG)
A non-invasive procedure that evaluates the electrical activity of the heart
A. Deflection Waves of ECG 1. P wave - initial wave, demonstrates the depolarization from SA Node through both ATRIA; the ATRIA contract about 0.1 s after start of P Wave 2. QRS complex - next series of deflections, demonstrates the depolarization of AV node through both ventricles; the ventricles contract throughout the period of the QRS complex, with a short delay after the end of atrial contraction; repolarization of atria also obscured 3. T Wave - repolarization of the ventricles (0.16 s) 4. PR (PQ) Interval - time period from beginning of atrial contraction to beginning of ventricular contraction (0.16 s) 5. QT Interval the time of ventricular contraction (about 0.36 s); from beginning of ventricular depolarization to end of repolarization Electrodes and wires are attached to the patient
Holter Monitoring A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded
continuously over a period of 24 hours Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop
ECHOCARDIOGRAM Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound No special preparation is needed
Stress Test A non-invasive test that studies the heart during activity and detects and evaluates CAD Exercise test, pharmacologic test and emotional test Treadmill testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath . Instruct client to avoid taking a hot shower for 10-12 hours after the test Pharmacological stress test Use of dipyridamole
Maximally dilates coronary artery Side-effect: flushing of face Pre-test: 4 hours fasting, avoid alcohol, caffeine Post test: report symptoms of chest pain
Cardiac Catheterization Insertion of a catheter into the heart and surrounding vessels Determines the structure and performance of the heart valves and surrounding vessels Used to diagnose CAD, assess coronary atery patency and determine extent of atherosclerosis Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses Pretest: Fast for 8-12 hours, teachings, medications to allay anxiety Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart; inform the patient that a feeling of warmth and metallic taste may occur when dye is administered Post-test: Monitor VS and cardiac rhythm Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site Maintain sandbag to the insertion site if required to maintain pressure Monitor for bleeding and hematoma formation Central Venous Pressure(CVP)
Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O
Elevated CVP indicates increase in blood volume, excessive IVF or heart/renal failure Low CVP may indicated hypovolemia, hemorrhage and severe vasodilatation Measuring CVP 1. Position the client supine with bed elevated at 45 degrees 2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4th ICS
3. Instruct the client to be relaxed and avoid coughing and straining.
CARDIAC IMPLEMENTATION 1. Assess the cardio-pulmonary status VS, BP, Cardiac assessment 2. Enhance cardiac output Establish IV line to administer fluids 3. Promote gas exchange Administer O2 Position client in semi-Fowler’s Encourage coughing and deep breathing exercises 4. Increase client activity tolerance Balance rest and activity periods Assist in daily activities 5. Promote client comfort Assess the client’s description of pain and chest discomfort Administer medication as prescribed 6. Promote adequate sleep 7. Prevent infection Monitor skin integrity of lower extremities Assess skin site for edema, redness and warmth Monitor for fever Change position frequently 8. Minimize patient anxiety Encourage verbalization of feelings, fears and concerns
Answer client questions. Provide information about procedures and medications Imbalance of Cardiac Output & Heart Pathologies 1. congestive heart failure - heart cannot pump sufficiently to meet needs of the body a. coronary atherosclerosis - leads to gradual occlusion of heart vessels, reducing oxygen nutrient supply to cardiac muscle cells; (fat & salt diet, smoking, stress) b. high blood pressure - when aortic pressure gets too large, left ventricle cannot pump properly, increasing ESV, and lowering SV c. myocardial infarct (MI) - "heart cell death" due to numerous factors, including coronary artery occlusion d. pulmonary congestion - failure of LEFT heart; leads to buildup of blood in the lungs e. peripheral congestion - failure of RIGHT heart; pools in body, leading to edema (fluid buildup in areas such as feet, ankles, fingers) Angina Pectoris Chest pain resulting from coronary atherosclerosis or myocardial ischemia Clinical Syndromes: Three Common Types of ANGINA 1. STABLE ANGINA The typical angina that occurs during exertion, relieved by rest and drugs and the severity does not change 2. Unstable angina Occurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and drug 3. Variant angina, Prinzmetal angina results from coronary artery VASOSPASMS, may occur at rest
ASSESSMENT FINDINGS: Chest pain- ANGINA The most characteristic symptom PAIN is described as mild to severe retrosternal pain, squeezing, tightness or burning sensation Radiates to the jaw and left arm Precipitated by Exercise, Eating heavy meals, Emotions like excitement and anxiety and Extremes of temperature Relieved by REST and Nitroglycerin Diaphoresis Nausea and vomiting Cold clammy skin Sense of apprehension and doom Dizziness and syncope LABORATORY FINDINGS ECG may show normal tracing if patient is pain-free. Ischemic changes may show ST depression and T wave inversion Cardiac catheterization Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions NURSING MANAGEMENT
Administer prescribed medications Nitrates- to dilate the coronary arteries Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP and HR Calcium-channel blockers- to dilate coronary artery and reduce vasospasm Teach the patient management of anginal attacks Advise patient to stop all activities Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention Obtain a 12-lead ECG
Promote myocardial perfusion Instruct patient to maintain bed rest Administer O2 @ 3 lpm Advise to avoid valsalva maneuvers Provide laxatives or high fiber diet to lessen constipation Encourage to avoid increased physical activities Assist in possible treatment modalities o PTCA- percutaneous transluminal coronary angioplasty To compress the plaque against the vessel wall, increasing the arterial lumen o CABG- coronary artery bypass graft To improve the blood flow to the myocardial tissue Provide information to family members to minimize anxiety and promote family cooperation Assist client to identify risk factors that can be modified Refer patient to proper agencies Myocardial Infarction terminal stage of coronary art dse resulting from permanent mal-occlussion, necrosis and scarring types of MI: 1. Transmural most dangerous form of MI characterized by occlussion of right and left coronary art. 2. Subendocardial critical period of MI: 24-48 hours - arrythmias, PVC (lidocaine as ordered) S/S: a. Pain: sharp, excruciating visceral pain substernal: radiates to back, arms, shoulder, axilla, jaw and abdominal ms not usually received by rest b. Dyspnea c. Hyperthermia d. Mild restlessness or apprehension e. Initial inc in bld pressure f. Occasional findings:
Rales or crackles upon auscultation Pericardial friction rub Split S1 and S2 Atrial gallop (S4)
Dx procedures 1. Cardiac enzymes CPK-MB Lactic dehydrogenase SGPT (ALT) SGOT (AST) 2. Troponin test: inc 3. ECG tracing reveals: ST segment elevation Widening of QRS complex Arrythmia in MI: PVCs 4. Serum uric acid and cholesterol: inc 5. CBC: inc in WBC count Nursing Management: 1. Administer meds as ordered a. Narcotic analgesic: morphine sulfate - induce vasodilation, reduce levels of anxiety side effect: resp depression: antidote - Naloxone Naloxone toxicity: - tremor 2. Administer O2 inhalation as ordered 3. Enforce complete bedrest a. Bedside commode dec myocardial O2 demand 4. Instruct client to avoid vasalva manuever 5. semi-fowler's pos'n 6. General liquid -> soft diet 7. Avoid foods rich in caffeine, sodium and saturated fats 8. Monitor VS, I and O 9. Administer meds as ordered: a. Vasodilators nitroglycerin isosorbide dinitrate
b. Anti-arrhythmic agents xylocaine c. Beta blockers propanolol d. ACE-inhibitors captopril, enalopril e. Thrombolytic/fibrinolytic agents streptokinase urokinase TPAF (tissue plasminogen activating factor): monitor bleeding time f. Anticoagulants heparin and coumadin simultaneously: late effect of coumadin 3 days heparin: monitor PTT (partial thromboplastin time) heparin antidote: protamine sulfate coumadine antidote: vit K g. Antiplatelet anti thrombotic property 10. Assist in surgical procedure coronary art by pass PTCA 11. Provide client health teaching concerning: a. Avoidance of precipitating factors b. Dietary restrictions c. Prevention of Complications arrhythmia: PVCs shock: cardiogenic - oliguria as late sign congestive heart failure thrombophlebitis CVA Dressler's Syndrome: post MI syndrome - resistance to pharmacologocal agents: administer 450,000 units of streptokinase as ordered d. Instruct client re resumption of ADL sexual intercourse: 3-6 weeks post carrdiac rehab sex before meals assume a non wt-bearing position
importance of follow-up care Congestive Heart Failure inability to pump blood toward systemic circulation I. Left-sided heart failure Pred. Factors 1. 90% mitral valve stenosis (RHD, aging): ASO titer (anti streptolysin O) = > 300 Todd units complication of RHD -> penicillin CHF aspirin steroids 2. IHD 3. Hypertension 4. MI 5. Aortic stenosis Signs and symptoms: 1. Pulmonary edema and congestion 2. Paroxysmal nocturnal dyspnea (PND) 3. Orthopnea: place client in high Fowler's pos'n 4. Productive cough with bld tinge sputum 5. Frothy salivation 6. Cyanosis 7. Rales or crackles 8. Bronchial wheezing 9. Pulsus alternans 10. Anorexia, gen body malaise 11. Point of max impulse displaced laterally PMI 4th-5th ICS mid clavicular line 12. S3 (ventricular gallop) Dx procedures 1. Chestx-ray:cardiomegaly 2. Angiography, echocardiography: site and extent of mal occlusion 3. ABG: pCO2 inc, pO2 dec -> resp acidosis, hypoxemia 4. PAP (pulmonary art pressure), pulmonary capillary wedge pressure (PCWP): inc Swan Ganz catheterization: done at bedside tracheostomy: bedside, done in O.R if pt has laryngeal or
thyroid cancer Right sided HF Predisposing factors 1. Tricuspid v stenosis 2. Pulm edema 3. COPD B. S/S 1. Jugular vein distention 2. Pitting edema 3. Ascites 4. Wt gain 5. Hepatosplenomegaly 4. Pulm valve stenosis 5. left sided heart failure 6. 7. 8. 9. Jaundice Pruritus Anorexia, gen body malaise Esophageal varices
Dx procedure 1. Chest x-ray: cardiomegaly 2. Echocardiogram: enlarged heart chamber 3. Central venous pressure: measures right atrium pressure - N = 4-10 cm of H2O - if CVP is dec -> hypovolemia -> fluid challenge - if CVP is inc -> hypervolemia - trendelenberg pos'n: CVP catheter insertion 4. Liver enzymes: inc A. SGPT (ALT) B. SGOT (AST) Nursing Mgt 1. Administer meds as ordered A. Cardiac glycoside (Digoxin - lanoxin): monitor heart rate before admin > 60 digitalis toxicity: digibind (antidote) B. Bronchodilator aminophylline (theophylline) toxicity: tachycardia, tremors C. Narcotic analgesic morphine sulfate D. Loop diuretics
Lasix (furosemide): 6 hrs max effect, onset 15 mins E. Vasodilators ISDN F. Anti arrhythmic agents lidocaine bretylium 2. Restrict fluids 3. VS, I and O, breath sounds 4. Weigh pt daily, assess for pitting edema 5. Measure abdominal girth -> notify physician 6. O2 inhalation: 3-4 liters/min via nasal cannula - high inflow 7. High Fowler's position 8. Bloodless phlebotomy: rotating tournique - 3 tournique rotated clockwise every 15 mins to dec venous return 9. Health teaching A. Dietary modification: low Na, saturated fats, caffeine B. Prevent complications Arrhythmia MI Thrombophlebitis Cor pulmonale C. Follow-up care