Ventricular resistance

Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with Udo-caine for shosk-resistant ventricular fibrillation. NEJM 2002 346(12) 884-90. 

Winkle RA, Mason JW, Harrison DC. Tocainide for drug-resistant ventricular arrhythmias efficacy,... 

III Potassium channel blocking Amiodarone Bretylium Resistant ventricular fibrillation... 

Hoffmann A, Follath F, Burckhardt D. Safe treatment of resistant ventricular arrhythmias with a combination of amio one and quinidine or mexiletine Lancet 9Zy) i, 704-5. 

Duff HJ, Roden D, Primm RK, Oates JA, Woosley RL. Mexiletine in the treatment of resistant ventricular anhythmias enhancement of efficacy and reduction of dose-related side effects by combination with quinidine. Circulation (1983) 67,1124-8. 

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2). 

ACE inhibitors lower the elevated blood pressure in humans with a concomitant decrease in total peripheral resistance. Cardiac output is increased or unchanged heart rate is unchanged urinary sodium excretion is unchanged and potassium excretion is decreased. ACE inhibitors promote reduction of left ventricular hypertrophy. 

Practitioners must have a good understanding of cardiovascular physiology to diagnose, treat, and monitor circulatory problems in critically ill patients. Eugene Braunwald, a renowned cardiologist, described the interrelationships between the major hemodynamic variables (Fig. 10-1).1 These variables include arterial blood pressure, cardiac output (CO), systemic vascular resistance (SVR), heart rate (HR), stroke volume (SV), left ventricular size, afterload, myocardial contractility, and preload. While an oversim-... 

SVRI Systemic vascular resistance index VT Ventricular tachycardia... 

In vivo Hemodynamic and cardiac parameters pressure (arterial, venous, ventricular, e.g., ventricular contractility, cardiac output), HR, peripheral resistance, ECG parameters, body temperature, flow Conscious (restrained or telemetry) and anesthetized Takahara et al. 97 Sato et al. 98 Nekooeian and Tabrizchi99... 

In heart failure, cardiac output rises again because ventricular afterload diminishes due to a fall in peripheral resistance. Venous congestion abates as a result of (1) increased cardiac output and (2) reduction in venous return (decreased aldosterone secretion, decreased tonus of venous capacitance vessels). 

Factors determining oxygen demand. The heart muscle cell consumes the most energy to generate contractile force. O2 demand rises with an increase in (1) heart rate, (2) contraction velocity, (3) systolic wall tension ( afterload ). The latter depends on ventricular volume and the systolic pressure needed to empty the ventricle. As peripheral resistance increases, aortic pressure rises, hence the resistance against which ventricular blood is ejected. O2 demand is lowered by 3-blockers and Ca-antago-nists, as well as by nitrates (p. 308). 

Thus, the nitrates enable myocardial flow resistance to be reduced even in the presence of coronary sclerosis with angina pectoris. In angina due to coronary spasm, arterial dilation overcomes the vasospasm and restores myocardial perfusion to normal. O2 demand falls because of the ensuing decrease in the two variables that determine systolic wall tension (afterload) ventricular filling volume and aortic blood pressure. 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

Pharmacology The principal pharmacological action of nitrates is relaxation of the vascular smooth muscle and consequent dilation of peripheral arteries and especially the veins. Dilation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload). Dilation of the coronary arteries also occurs. The relative importance of preload reduction, afterload reduction, and coronary dilation remains undefined. 

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. 

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