Readings

• CHF(Chronic heart failure): heart disease caused by weakness of contractile force of myocardium
• Pulmonary edema is associated with left sided heart failure; peripheral edema is associated with right sided heart failure
• cardiac glycoside: drug obtained from plants of the genus digitalis
• chronic heart failure: condition in which the heart is unable to pump sufficient blood to the tissues of the body
• digitalization: method of dosage with cardiac glycosides that rapidly produces effective drug levels
• ectopic beat: extra heartbeat, a type of cardiac arrhythmia
• Na/K ATPase: enzyme that energizes the Na/K pump and is inhibited by cardiac glycosides
• Vasodilators that primarily dilate veins and decrease venous return decrease preload while vasodilators working on arteries reduce peripheral vascular resistance and decrease afterload
• Diuretics are widely used in the treatment of CHF and its main effect is to eliminate excess Na and water by the kidneys; this reduces the edema and congestion caused by CHF. Excretion of Na also produces a vasodilatory effect.
• 3 types of diuretics used for CHF: thiazides, organic acids and aldosterone antagonists
• Thiazide diuretics block the reabsorption of Na at the DCT of the kidneys; moderate in potency but can cause loss of potassium leading to hypokalemia
• Organic acid diuretics are referred to as loop diuretics cuz they work on the ascending limb of the loop of Henle. These are the most potent diuretics. Also increase excretion of Na and K+.
• Aldosterone antagonists are weak diuretics that act on the collecting ducts of the nephron
• Aldosterone antagonists increase the excretion of Na and retention of K+
• Adverse effects of thiazide and loop diuretics are nausea, hypotension, hypokalemia, hyperuricemia and hyperglycemia. Aldosterone antagonists can cause hyperkalemia
• ARBs stand for angiotensin receptor blockers
• ARBs and ACE inhibitors are the preferred drugs to treat CHF
• Vasodilators are divided into arterial, venous and balanced dilators
• NTG is a venodilator which is why it's contraindicated in preload dependent MIs
• Balanced vasodilators consists of ace inhibitors and ARBs
• ACE inhibitors first inhibit ACE which causes an indirect increase of bradykinin; an endogenous vasodilator
• ARBs block the angiotensin 2 receptor but don't affect bradykinin.
• ACEIs and ARBs cause these adverse effects: dizziness, headaches, hypotension, hyperkalemia and GI disturbances
• Cardiac glycosides increase the force of myocardia contractions in CHF without causing an increase in MVO2
• Cardiac glycosides can also stimulate the vagus nerve to slow down the SA and AV nodes
• Cardiac glycosides inhibits the Na/K ATPase enzyme so Na ions accumulate inside heart muscle cells which inhibits Na/Ca exchanger and slows loss of intracellular Ca+. That all leads to an increase in myocardial contraction
• antiarrhythmic drug: used to restore normal cardiac rhythm
• Cinchonism: quinidine toxicity which is characterized by tinnitus(ringing in ears), dizziness and headache
• Ectopic focus: area of the heart from which abnormal impulses originate
• Premature atrial contraction(PAC): premature contraction of the atria, usually caused by an ectopic focus
• Premature ventricular contraction(PVC) is caused by an ectopic focus
• Proarrhythmia: caused by the admin of an antiarrhythmic drug.
• Supraventricular arrhythmia: originates above the AV node
• Torsade de pointes: type of proarrhythmia that causes v tac and fainting
• Type of arrhythmia depends on location within the heart and severity of electrical disturbance
• Arrhythmias are caused by CAD, electrolyte imbalances, diuretics/drug toxicities and myocardial infarctions and other pathologies
• Paroxysmal atrial tachycardia is a type of supraventricular arrhythmia that is characterized by a rate of 150-200 BPM. It's unpredictable and can start/stop suddenly. S/S are palpitations, anxiety and symptoms of heart failure if it persists
• In Atrial flutter, the HR is 250-350 BPM and instead of a p wave, it look smaller with a serrated pattern.
• In A Fib, the atrial rate is over 350 BPM and ventricular rhythm is also irregular; predisposes atria to development of blood clots
• PVCs cause an impulse to travel up the conduction system instead of down; this results in an inverted QRS wave and disrupts normal ventricular contraction