Heart failure

Davidson

 Describes the clinical syndrome that develops when the heart cannon maintain
adequate output or can do so only at the expense of elevated ventricular filling present.
 Almost all forms of heart disease can lead to heart failure.
 Causes unplanned hospital visit.
 The most common etiology is coronary artery disease and myocardial infarction
 Approximately 50% of patients with severe heart failure due to left ventricular
dysfunction will die within 2 years, because of either pump failure or malignant
ventricular arrhythmias.
 HF may develop suddenly as in MI, or gradually, as in progressive valvular heart disease.
 Pathophysiology:
 Impaired systolic contraction, Impaired diastolic relaxation of both.
 Stimulation of the renin-angiotensin-aldosterone system leads to V.C., sodium and
water retention, and sympathetic activation. This is mediated by angiotensin II, a
potent constrictor of arterioles  prolonged sympathetic stimulation causes
negative effects, including cardiac myotic apoptosis, hypertrophy and focal
myocardial necrosis. Also causes peripheral vasoconstriction and arrythemias.
Sodium and water retention is promoted by the release of aldosterone, endothelin-1
( a potent vasoconstrictor peptide with marked effects on the renal vasculature) and
in severe HF, ADH. Natriuretic peptides arenreleaased from the atria in response to
atrial stretch, and act as physiological antagonists to the fluid-conserving effect of
aldosterone.
 After MI, cardiac contractility is impaired and neurohormonal activation causes
hypertrophy of non-infarcted segment, with thinning, dilatation and expantion of the
infarcted segment.
 Pulmonary and peripheral edema occurs because of high left and right atrial
pressures. This is compounded by sodium and water retention, caused by
impairment of renal perfusion and by 2ry hyperaldosteronism.
 Types of heart failure:
 Left-sided HF
 A reduction in LV output + increase in LA venous pressure + increase in
pulmonary venous pressure.
 an acute increase  pulmonary congestion or pulmonary edema
 a more gradual increase in left atrial pressure as that occurs in mitral stenosis 
reflux pulmonary vasoconstriction  protects the patient from pulmonary
edema  pulmonary hypertension  impair right ventricular function
 right-sided HF
 reduction in RV output and an increase in right atrial and systemic venous
pressure.
 Causes of isolated right HF include chronic lung disease (cor pulmonale),
pulmonary embolism and pulmonary valvular stenosis.
 Clinical assessment:
 Acute left HF:
  Presents with a sudden onset of dyspnea at rest that rapidly progresses to acute
respiratory distress, orthopnea and prostration ( ‫) زي السجود‬.
 The patient is agitated, pale and clammy ( quality of being cold + dry ). The
peripheries are cool to the touch and pulse is rapid.
 The BP is usually high because of sympathetic activation.
 The jugular venous pressure (JVP) us usually elevated.
 Auscultatory findings in pulmonary edema are crepitation at the lung bases, or
throughout the lungs if pulmonary edema is severe.
 Chronic HF:
 With periods of stability and episodes of decompensation, leading to worsening
symptoms that may necessitate hospitalization.
 Low cardiac output causes fatigue, listlessness and poor effort tolerance; the
peripheries are cold, and the BP is low. To maintain perfusion of vital organs,
blood flow is diverted away from skeletal muscle and this may contribute to
fatigue and weakness. Poor renal perfusion leads to oliguria and uremia.
 Pulmonary edema due to left HF presents with inspiratory crepitations over the
lung bases. In contrast, right HF produces a high JVP with hepatic congestion and
dependent peripheral edema. In ambulant patients, the edema affects the
ankles, whereas in bed-bound patients it collects around thighs and sacrum.
Ascites or pleural effusion may occur,
 It is associated with marked weight loss (cardiac cachexia), caused by
combination of anorexia and impaired absorption due to low cardiac output and
skeletal muscle atrophy due to immobility.
 Complications:
 Renal failure:
 By poor renal perfusion due to low cardiac output
 Exacerbated by diuretic therapy, angiotensin-converting enzyme inhibitors and
angiotensin receptor blockers.
 Hypokalemia:
 Result of treatment with potassium sparing diuretics or hyperaldosteronism
 Hyperkalemia
 Hyponatremia
 Impaired liver function
 By hepatic venous congestion and poor arterial perfusion which causes mild
jaundice and abnormal liver function tests; reduced synthesis of clotting factors.
 Thromboembolism
 Atrial and ventricular arrhythmias
 Investigation:
 Serum urea, creatinine and electrolytes, Hb, thyroid function, ECG and chest X-ray.
 Atrial fibrillation:
 Atrial fibrillation (AFib) is the most common heart rhythm abnormality, affecting more than
33 million people worldwide. Patients with AFib are at a higher risk of stroke if not
properly treated.
 Diagnosed by ECG
 Symptoms:
 Heart racing
 Fatigue
 5 times risk for stroke
 Adverse consequences are related to reduced blood flow from the heart and from clots
that may form in the heart