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CARDIAC HEMODYNAMICS
Basic function of the heart: to pump blood Measured by CO: HR x SV SV: amount of blood pumped out of the ventricle with each contraction HR: primarily controlled by the ANS Determinants of SV
PRELOAD
Is the amount of blood presented to the ventricle just before systole Increases pressure in the ventricle ---> stretching the ventricular wall (by blood to produce optimal recoil & forceful ejection of blood) ---> too little or too much muscle fiber stretch decreases the volume of blood ejected
PRELOAD
Major Determinants of PRELOAD Venous return of blood to the heart creating the volume of the blood entering the ventricle during diastole Ventricular compliance: the elasticity or amount of give when blood enters the ventricle
Decrease elasticity due to thickening of the muscles (hypertrophic cardiomyopathy) Increased fibrotic tissue within the ventricle (MI)
AFTERLOAD
The amount of resistance to the ejection of blood from the ventricle To eject blood: the ventricle must overcome the resistance caused by tension in the aorta and systemic vessels Inversely related to SV An increase in afterload causes the ventricle to work harder and may decrease the amount of blood ejected DETERMINANTS The diameter and distensibility of the great vessels (aorta / PA) Competence of the semilunar valves Significant vasoconstriction, HTN, or a narrowed valvular opening from stenosis ----> resistance (afterload) increases
CONTRACTILITY
The force of contraction is related to the status of the myocardium Increase contractility and SV Catecholamines released by sympathetic stimulation during exercise Administration of positive inotropic medications MI: necrosis and fibrosis of the myocardial cells
RV PRELOAD:
estimated by measuring the jugular venous distention (JVD) Mean Arterial Blood Pressure
LV AFTERLOAD:
Activity Tolerance
Heart Failure
The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients A syndrome characterized by fluid overload or inadequate tissue perfusion The term HF indicates myocardial disease, in which there is a problem with the contraction of the heart (systolic failure) or filling of the heart (diastolic failure). Some cases are reversible. Most HF is a progressive, lifelong disorder managed with lifestyle changes and medications.
ETIOLOGY
CLINICAL MANIFESTATIONS
GENERAL
Fatigue Decreased activity tolerance Dependent edema Weight gain Third heart sound (S3) Apical impulse enlarged with left lateral displacement Pallor and cyanosis Jugular venous distention (JVD)
CARDIOVASCULAR
CLINICAL MANIFESTATIONS
RESPIRATORY
Dyspnea on exertion Pulmonary crackles that do not clear with cough Orthopnea Paroxysmal nocturnal dyspnea (PND) Cough on exertion or when supine
CLINICAL MANIFESTATIONS
CEREBROVASCULAR
Unexplained confusion or altered mental status Lightheadedness Oliguria and decreased frequency during the day Nocturial Anorexia and nausea Enlarged liver Ascites Hepatojugular reflux
RENAL
GASTROINTESTINAL
Clinical Manifestations
Right-sided failure
RV cannot eject sufficient amounts of blood, and blood backs up in the venous system. This resuts in peripheral edema, hepatomegaly, ascites, anorexia, nausea, weakness, and weight gain.
LV cannot pump blood effectively to the systemic circulation. Pulmonary venous pressures increase, resulting in pulmonary congestion with dyspnea, cough, crackles, and impaired oxygen exchange.
Left-sided failure
CLINICAL MANIFESTATIONS
Dyspnea Cough Pulmonary crackles Low oxygen saturation levels S3 or ventricular gallop Orthopnea PND Nocturia
CLINICAL MANIFESTATIONS
RIGHT-SIDED HEART FAILURE JVD Edema Hepatomegaly Ascites Anorexia and nausea
NYHA classification of HF
ACC/AHA classification of HF
PROGNOSIS
Ordinary physical activity does not cause undue GOOD fatigue, dyspnea, palpitations, or chest pain No pulmonary congestion or peripheral hypotension Patient is considered asymptomatic Usually no limitations of ADLs Slight limitation on ADLs GOOD Patient reports no symptoms at rest but increased physical activity will cause symptoms Basilar crackles and S3 murmur may be detected
II
III
Marked limitation on ADL Patient feels comfortable at rest but less than ordinary activity will cause symptoms Symptoms of cardiac insufficiency at rest
FAIR
IV
POOR
STAGE B
STAGE C
STAGE D
Medical Management of HF
Eliminate or reduce etiologic or contributory factors. Reduce the workload of the heart by reducing afterload and preload. Optimize pharmacologic and other therapeutic regimens. Prevent exacerbations of HF. Medications are routinely prescribed for HF. Promote a lifestyle conducive to cardiac health
PHARMACOLOGIC THERAPY
Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers Hydralazine and Isosorbide Dinitrate Beta-blockers Diuretics Digitalis Calcium Channel Blockers Intravenous Infusions Other medications
ACE INHIBITOR
Slow the progression of HF Improve exercise tolerance Decrease the number of hospitalizations for HF Form: oral, IV
ACE INHIBITOR
Promote vasodilation and diuresis by decreasing afterload and preload -----> decrease the workload of the heart Vasodilation reduces resistance to left ventricular ejection of blood -----> diminish the hearts workload and improving ventricular emptying Promoting diuresis: decrease the secretion of aldosterone (hormone causing kidneys to retain sodium & water) Stimulate the kidneys to excrete Na & H20 (retaining K) -----> reducing left ventricular filling pressure & decreasing pulmonary congestion
ACE INHIBITOR
THERAPEUTIC EFFECTS
Dec BP and afterload Relieve signs and symptoms of HF Prevents progression of HF Hypotension Hypovolemia Hyperkalemia Hyponatremia Alterations in Renal Function
ACE INHIBITOR
Lisinopril (Prinivil, Zestril) Benazepril (Lotensin) Captopril (Capoten) Enalapril/Enalaprilat (Vasotec) Fosinopril (Monopril) Moexipril (Univasc) Perindopril (Aceon) Quinapril (Accupril) Ramipril (Altace) Trandolapril (Mavik)
Dec BP and afterload Dec SVR Improved CO Relieves signs and symptoms of HF Prevents progression of HF Similar with ACEI
ARBs
Valsartan (Diovan) Candesartan (Atacand) Eprosartan (Teveten) Irbesartan (Avapro) Telmisartan (Micardis) Losartan (Cozaar)
Venous dilation -----> reduces the amount of blood return to the heart -----> lowers PRELOAD Lowers SVR and left ventricular AFTERLOAD
Hydralazine:
Dilates blood vessels and dec afterload Dec signs and symptoms of HF Improves exercise capacity KEY NURSING CONSIDERATION
BETA BLOCKERS
DIURETICS
To remove excess extracellular fluid -----> increasing the rate of urine produced Dec fluid volume overload Dec signs and symptoms of HF KEY NURSING CONSIDERATIONS
Electrolyte abnormalities Renal dysfunction Diuretic resistance Dec BP Monitor I&O Daily weight
DIURETICS
LOOP
THIAZIDE
ALDOSTERONE ANTAGONIST
DIGITALIS
Increases the force of myocardial contraction Slows conduction through the AV node Improves contractility, increasing LV output --> enhances diuretics KEY CONCERN: DIGITALIS TOXICITY DIGOXIN (Lanoxin)
Tablets: 0.125, 0.25, 0.5 mg (Lanoxin) Capsules: 0.05, 0.1, 0.2 mg (Lanoxicaps) Elixir: 0.05 mg/mL (Lanoxin Pediatric Elixir) Injection: 0.25 mg/mL, 0.1 mg/mL (Lanoxin)
Changes in HR or rhythm; onset of irregular rhythm ECG changes indicating ventricular dysrhythmias, atrial tachycardia with block, junctional tachycardia, ventricular tachycardia
REVERSAL OF TOXICITY
Assess the patients clinical response to therapy through evaluation of relief of symptoms
MONITOR THE PATIENT FOR FACTORS THAT INCREASE THE RISK OF TOXICITY
Hypokalemia Use of medications that may enhance the effects of digoxin Impaired renal function
STANDARD PRACTICE: ASSESS FOR APICAL HR!!!
Before administration
Dihydropyridines
Amlodipine (Norvasc) Felodipine (Plendil) Verapamil (Calan0 Nifedipine (Procardia) Diltiazem (Cardizem)
INTRAVENOUS INFUSIONS
NESIRITIDE (Natrecor)
32 amino acid recombinant technology BNP Binds to vascular smooth muscle and endothelial cells ---> dilation of arteries and veins Suppression of neurohormones responsible for fluid retention ---> diuresis END RESULT
MILRINONE (Primacor)
A phosphodiesterase inhibitor delaying the release of Calcium from intracellular reservoirs ---> prevents uptake of extracellular Calcium by the cells ---> vasodilation ---> decreased PRELOAD & AFTERLOAD ---> REDUCED CARDIAC WORKLOAD Hypotension GI dysfunction Increased ventricular dysrhythmias
KEY CONSIDERATION
DOBUTAMINE (Dobutrex)
Stimulates the beta-1-adrenergic receptors ---> increase cardiac contractility Increases the heart rate Precipitate ectopic beats Tachydysrhythmias
KEY CONSIDERATION
Anticoagulants Statins
CAD: coronary artery revascularization DYSRHYTHMIAS: ICD No Improvement with Standard Therapy: CRT Severe Fluid Overload: ULTRAFILTRATION End Stage HF: CARDIAC TRANSPLANTATION
GERONTOLOGIC CONSIDERATIONS
GERONTOLOGIC CONSIDERATIONS
Resistant to diuretics More sensitive to changes in volume Requires nursing surveillance for bladder distention
Health history Signs and Symptoms of HF Sleep and activity Knowledge and coping Physical exam Mental status JVD Hepatojugular Reflux Lung sounds: crackles and wheezes Heart sounds: S3 Fluid status/signs of fluid overload Daily weight and I&O Assess responses to medications
Activity intolerance and fatigue Excess fluid volume Anxiety Powerlessness Ineffective therapeutic regimen (Noncompliance)
Hypotension, Poor Perfusion, Cardiogenic shock Dysrhythmias Thromboembolism Pericardial effusion and cardiac tamponade
Bed rest for acute exacerbations Encourage regular physical activity; 30-45 minutes daily Exercise training Pacing of activities Wait 2 hours after eating before doing physical activity. Avoid activities in extremely hot, cold, or humid weather. Modify activities to conserve energy. Positioning; elevation of HOB to facilitate breathing and rest, support of arms
Assessment for symptoms of fluid overload Daily weight I&O Diuretic therapy; timing of meds Fluid intake; fluid restriction Maintenance of sodium restriction See Chart 30-4
Controlling Anxiety
With difficulty maintaining adequate oxygenation Restless and anxious Overwhelmed by breathlessness Interfere with sleep Emotional Stress ---> stimulates SNS Oxygen administration during an acute event Promote physical comfort Provide psychological support Identify factors contributing to anxiety How to use relaxation techniques to control anxious feelings
Minimizing Powerlessness
Taking time to listen actively to patients Provide the patient with decision-making opportunities Provide encouragement
Hypokalemia
Hyperkalemia Hyponatremia Dehydration and hypotension Increased serum creatinine and hyperuricemia
Patient Teaching
Medications Diet: low-sodium diet and fluid restriction Monitoring for signs of excess fluid, hypotension, and symptoms of disease exacerbation, including daily weight Exercise and activity program Stress management Prevention of infection Know how and when to contact health care provider Include family in teaching
CONTINUING CARE
END-OF-LIFE CONSIDERATIONS
EVALUATION
Describes adaptive methods for usual activities Schedules activities to conserve energy and reduce fatigue and dyspnea Maintains HR, BP, RR, and pulse oximetry within the targeted range Exhibits decreased peripheral and sacral edema Demonstrates methods for preventing edema
EVALUATION
Is less anxious
Avoids situations that produce stress Sleeps comfortably at night Reports decreased stress and anxiety Denies symptoms of depression
EVALUATION
Performs and records daily weights Ensures dietary intake includes no more than 2 to 3 g of sodium per day Takes medications as prescribed Reports any unusual symptoms or side effects
Thromboembolism
Decreased mobility and decreased circulation increase the risk for thromboembolism in patients with cardiac disorders, including those with HF. Pulmonary embolism: blood clot from the legs moves to obstruct the pulmonary vessels
The most common thromboembolic problem with HF Prevention Treatment Anticoagulant therapy
Pulmonary Emboli
Umbrella Filter
Pericardial effusion is the accumulation of fluid in the pericardial sac. Cardiac tamponade is the restriction of heart function due to this fluid, resulting in decreased venous return and decreased CO. Clinical manifestations: ill-defined chest pain or fullness, pulsus parodoxus, engorged neck veins, labile or low BP, shortness of breath Cardinal signs of cardiac tamponade: falling systolic BP, narrowing pulse pressure, rising venous pressure, distant heart sounds
Medical Management
Pericardiocentesis Pericardiotomy
END
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