Category: Fundamentals Patients should not receive an ACE inhibitor if they have experienced life-threatening adverse effects (angioedema or anuric renal failure) during previous exposure or if they are pregnant.
Category: Fundamentals The hemodynamic effects of ACE inhibitors in heart failure include decreased preload, afterload and mean arterial pressure, as well as increased cardiac output. Ejection fraction is also improved.
Category: Fundamentals Because angiotensin II stimulates aldosterone secretion by the adrenal cortex and provides negative feedback for plasma renin, inhibition of angiotensin II may lead to decreased aldosterone and increased renin activity.
Category: Fundamentals Angiotensin II interacts with at least two known membrane receptors, type 1 and type 2 (AT1 and AT2). By blocking the formation of angiotensin II, ACE inhibitors produce vasodilation and a decrease in systemic vascular resistance (LV afterload).
Category: Fundamentals Activation of the RAAS is an important compensatory mechanism in heart failure. ACE catalyzes the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and stimulant of aldosterone secretion.
Category: Fundamentals The New York Heart Association (NYHA) classifies the functional incapacity of patients with cardiac disease into four levels depending on the degree of effort needed to elicit symptoms.
Category: Fundamentals Depressed ventricular function can be confirmed by echocardiography, ventriculography or cardiac catheterization. Abnormalities in the ECG are common and include arrhythmias, conduction delays, hypertrophy and ST changes.
Category: Fundamentals When the left ventricle malfunctions, congestion initially occurs in the lungs. When the right ventricle functions inadequately, congestion in the supplying systemic venous circulation results in peripheral edema and liver congestion.
Category: Fundamentals When the heart fails as a pump and cardiac output (the volume of blood pumped out of the ventricle per unit of time) decreases, a complex scheme of compensatory mechanisms to raise and maintain cardiac output occurs.
Category: Fundamentals Heart failure is a pathophysiologic state in which abnormal myocardial function inhibits the ventricles from delivering adequate quantities of blood to metabolizing tissues at rest or during activity.
Category: Fundamentals Gradual development of heart failure may be caused by liver or renal disease, primary cardiomyopathy, cardiac valve disease, bacterial endocarditis, myocarditis, thyrotoxicosis, chemotherapy, excessive sodium intake and ethanol abuse.
Category: Fundamentals Coronary artery disease, hypertension and idiopathic cardiomyopathy are the most frequently cited risk factors for heart failure. Acute conditions that may result in heart failure include MI, arrhythmias, pulmonary embolism and sepsis.
Category: Fundamentals In patients with angina, monitoring is important to evaluate for progression or stability of the disease, response to therapy and presence or absence of adverse events. Patient monitoring begins with a stress test.
Category: Fundamentals Clopidogrel is an antiplatelet agent that may be used in patients with angina. It reduces ADP-induced platelet activation by antagonizing the platelet ADP receptors. Clopidogrel is recommended for the prevention of MI.
Category: Fundamentals Adverse events associated with aspirin use include dyspepsia, bruising and bleeding. Enteric-coated aspirin may be prescribed to minimize gastrointestinal symptoms. Aspirin is contraindicated in patients with aspirin hypersensitivity.