Heart Failure Flashcards
Heart Failure =
Complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation accompanied by effort intolerance, fluid retention and decreased longevity
CV Causes of Heart Failure
Ischemic heart disease
Toxic cardiomyopathy such as alcohol or chemotheraputic agents
Idiopathic cardiomyopathies such as dilated, hypertrophic or restricted
Hypertension
Vavular heart disease
Pericardial disease
Congenital defects
Chronic tachycardia such atrial fibrillation with rapid ventricular response
Noncardiac Causes
Endocrine or metabolic disorders (high output heart failure)
Thyrotoxicosis
Anemia
Pregnancy
Fever, sepsis
Vitamin B1 deficiency
Connective tissue diseases such as lupus, polymyositis or scleroderma
Pulmonary diseases such as pulmonary HTN or cor pulmonale secondary to COPD
Pathophysiology
Decline in the heart’s ability to pump enough blood at a sufficient rate to sustain the body’s physiological functions (systolic heart failure) or elevated filling pressures (diastolic heart failure)
Diastolic Dysfxn
Increased ventricular stiffness and reduced compliance
Produces a rise in in cardiac pressures during diastole filling and the inability of the left ventricle to relax and accommodate a sufficient amount of blood from lungs
Left ventricular distendability is reduced during diastole and filling pressures must increase to maintain a constant ventricular volume
Results in an increase in cardiac filling pressures during rest and activity, failure of normal rise in cardiac output during exertion and reduction in cardiac output at rest
Most common causes are HTN, left ventricular hypertrophy, CAD, aortic stenosis and infiltrative or restrictive cardiac diseases
Systolic Dysfxn
Most common type of heart failure
3 determinants of ventricular dysfunction are altered preload, contractility and afterload
Preload is degree of myocardial fiber stretch at the end of ventricular filling. In systolic heart failure, the myocardial fibers are both excessively overloaded and stretched beyond lengths commensurate with the normal reflex-increased force of contraction. Cardiac output eventually falls
Ventricular dysfunction causes a decrease in myocardial contractility and causes a reduction in ejection fraction, stroke volume and cardiac output
Afterload is the amount of left ventricular wall tension that develops during systole to eject blood. Because afterload determines the ease or speed of ventricular contraction, the ejection fraction is a function of afterload
Compensatory Mechanisms
Sympathetic adrenergic activity
Neuroendocrine activation
Ventricular remodeling
Classification
Class I: No limitations. Ordinary physical activity does not cause undue fatigue, dyspnea or palpitations
Class II: Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results if fatigue, palpitations, dyspnea or angina
Class III: Marked limitation of physical activity. Although patients are comfortable at rest, less than ordinary activity will lead to symptoms
Class IV: Inability to carry on any physical activity without discomfort. Symptoms are present at rest. With any physical activity, increased discomfort is experienced
Clinical Presentation: Right-sided failure
Signs of fluid retention predominate Elevated jugular venous pressure Abdominal bloating and fullness Hepatomegaly Elevated liver enzymes due to passive liver congestion Peripheral edema Nocturia Feeling bloated/anorexia OSA
Clinical Presentation: Left-sided Failure
Have symptoms of low cardiac output and elevated pulmonary venous pressure Dyspnea-predominant symptom Fatigue Orthopnea Paroxysmal nocturnal dyspnea Bronchospasm and wheezing Crackles Hemoptysis and dysphasia Pulmonary edema Pleural effusion Extra heart sounds S3 or S4 Lateral displacement of apical impulse Murmurs
Dx Tests
BNP - elevated when ventricular filling pressures are high
CXR - cardiomegaly
Echocardiography - gold standard for dx HF
Exercise testing
Cardiac Catheterization
Cardiac MRI
Routine labs: CBC, CMP, thyroid studies, autoimmune studies if indicated
DD
Chronic pulmonary conditions PNA Asthma/URI Airway obstructions OSA Pleural effusions Pulmonary embolism Neuromuscular disorders Anxiety Depression
Treatment goals
Prevention of further myocardial injury
Prevention of recurrence of clinical failure
Relief of symptoms and signs
Improvement of prognosis
Pharm Tx
Therapy for heart failure can be subdivided by pathophysiology (systolic vs. diastolic dysfunction) and by the symptomatic presentation defined by the NYHA classification
With an ejection fraction < 40%, treatment is based on volume status. No evidence of fluid excess, start therapy with an ACE inhibitor
Once ACE dose is stabilized, start a beta blocker
If evidence of fluid overload, start ACE inhibitor and loop diuretic. Digoxin may be started to reduce symptoms and increase exercise tolerance. Once fluid overload is stabilized, a beta blocker should then be added
ACE-Is
Cornerstone of chronic management of heart failure
By suppressing the production of angiotension II, a potent vasoconstrictor, ACE inhibitors decrease systemic and pulmonary vascular resistance by preventing the release of aldosterone and norepinephrine while elevating the levels of vasodilator hormone bradykinin
Potential counterindications include history of compelling intolerance or adverse reaction, serum potassium greater than 5.5, serum creatinine >3.0 or worsening renal function and SYMPTOMATIC hypotension
ACE inhibitors have been shown to significantly reduce mortality, improve functional status and reduce hospital readmissions
ARBs
Act directly on the angiotension-renin-aldosterone system. Modify the effects of angiotension II, the substance that promotes vasoconstriction, abnormal cell growth and the release of aldosterone
Use for patients unable to tolerate ACE inhibitors or in addition to ACE inhibitor
Potential counterindications same as ACE inhibitor
Hydralazine and Nitrates
Combination of hydralazine and nitrates used for patients who ACE inhibitors are absolutely counterinicated
Hydralazine is a direct arterial vasodilator and nitrates are venous dilators that result in increased cardiac output secondary to decreased impedance to ventricular ejection and preload
Can improve survival and exercise tolerance in patients with heart failure
Frequent side effects that include headache, palpitations and nasal drainage
Can cause significant hypotension or orthostatic hypotension and doses need slow titration
Beta Blockers
produce a substantial rise in ejection fraction averaging 10% over a 6-month period
Initiate gradually and with care to avoid deterioration in heart failure
Counterinicated in patients with acute exacerbations of failure, reactive airway disease and severe bradycardi
Diuretics
Most effective means of preventing symptomatic relief to patients with moderate to severe heart failure
Mild fluid retention-thiazide diuretic or similar type of agent
More severe heart failure-loop diuretics
Refractory edema-may respond to combination of a loop diuretic and thiazide diuretic
Must monitor electrolytes and kidney function frequently and use potassium replacement as indicated
Spironolactone
Baseline BMP and F/U in 2-4 weeks
Evidence that aldosterone mediates some of the major effects of the renin-aldosterone-angiotension system activation, such as myocardial remodeling and fibrosis as well as sodium and potassium loss at the distal tubule
Should be considered as a neurohormonal antagonist rather than a potassium sparing diuretic
Counterindicated in renal failure, hyperkalemia and hyponatremia
Need frequent monitoring of electrolytes and kidney function
Digoxin
Use of digoxin has declined
Lacks the benefits of the neurohormonal antagonists
Safety concerns secondary to high incidence of toxicity
Efficacy in decreasing the symptoms of heart failure has been established
Must monitor levels for toxicity and dose adjust in patients with renal impairment
Antiarrhythmic Therapy
Use of antiarrhytmic tx has declined d/t permanent pacers
Patients with moderate to severe heart failure have a high incidence of symptomatic and asymptomatic ventricular arrhythmias
70% of patients have asymptomatic nonsustained ventricular tachycardia
<10% of patients have syncope or presyncope related to ventricular tachycardia
Empiric antiarrhythmic therapy does not improve survival and beta blockers should be used for these patients
Nonpharm Tx
Birventricular pacing for EF <0.12 msec Implantable cardioverter defibrillators Case management, diet and exercise training Coronary revascularization Cardiac transplantation Left-ventricular assist devices Palliative care
Treatment Stage A
At risk for heart failure without structural heart disease or symptoms of heart failure Treat hypertension Smoking cessation Treat lipids Exercise Discourage alcohol or drug use Control metabolic syndrome ACE inhibitors in appropriate patients
