Systemic vascular resistance

Phenylephrine 10-1000 pg/minute Seconds Bradycardia, coronary vasoconstriction, decreased renal perfusion, metabolic acidosis Alpha-1, increased cardiac output (CO), decreased systemic vascular resistance (SVR)... 

BP, blood pressure CO, cardiac output HR, heart rate PCWP, pulmonary capillary wedge pressure SVR, systemic vascular resistance T, increase 4, decrease 0, no or little change. 

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... 

SVR Supraventricular rhythm systemic vascular resistance VTE Venous thromboembolism... 

Pulmonary artery catheter An invasive device used to measure hemodynamic parameters directly, including cardiac output and pulmonary artery occlusion pressure calculated parameters include stroke volume and systemic vascular resistance. 

Systemic vascular resistance The portion of resistance to blood flow leaving the heart that is determined by vascular tone (constriction or relaxation). Systemic vascular resistance = mean arterial blood pressure/cardiac output. 

NOx levels are increased in plasma and urine of septic animals. Many nonse-lective NO synthase inhibitors (e.g., L-NMMA) are used in several models with experimental induced sepsis (S40). In most studies it was shown that the cardiovascular abnormalities associated with sepsis were reversed, increasing blood pressure and systemic vascular resistance (F7, K9, M26, N5), together with a improvement in renal function (B42, H24). Also, selective inhibition of iNOS prolonged survival in septic rats (A7). 

Vasopressin is a potent vasoconstrictor that increases blood pressure and systemic vascular resistance. It may have several advantages over epinephrine. First, the metabolic acidosis that frequently accompanies cardiopulmonary arrest can blunt the vasoconstrictive effect of epinephrine this does not occur with vasopressin. Second, stimulation of P receptors by epinephrine can increase myocardial oxygen demand and complicate the postresuscitative phase of CPR. Vasopressin can also have a beneficial effect on renal blood flow in the kidney, causing vasodilation and increased water reabsorption. 

Nitrates (e.g., ISDN) and hydralazine were combined originally in the treatment of HF because of their complementary hemodynamic actions. Nitrates are primarily venodilators, producing reductions in preload. Hydralazine is a direct vasodilator that acts predominantly on arterial smooth muscle to reduce systemic vascular resistance (SVR) and increase stroke volume and cardiac output. Evidence also suggests that the combination may provide additional benefits by interfering with the biochemical processes associated with HF progression. 

The hallmark of the hemodynamic effect of sepsis is the hyperdynamic state characterized by high cardiac output and an abnormally low systemic vascular resistance. 

Administration by inhalation has been explored by Brilli [124], mentioned previously for his work with NONOates. Here he uses one of these same NONOates, DMAEP/NO (see Fig. 8.11), in aerosol form. When administered in an aerosolized state, DMAEP/NO again shows selective pulmonary vasodilation in a porcine model. This is achieved without affecting the systemic vascular resistance index (SVRI) or the cardiac index (Cl). Work from the same year by Adrie et al. [125] compared aerosolized DEA/NO with aerosolized SNP and inhaled NO, in sheep. As the NONOate has a short half-life (2.1 min), it was predicted that this would be a selective pulmonary vasodilator. However, compared with inhaled NO this was not observed, though SNP... 

Although not truly analogous, afterload is often clinically equated to the systemic vascular resistance (SVR). 

The relationship for pulmonary vascular resistance is very non-linear owing to the effect of recruitment and distension of vessels in the pulmonary vascular bed in response to increased pulmonary blood flow. The PVR is usually around 10 times lower than the systemic vascular resistance, at 50-150 dyne.s.cm-5. 

The integrated function of the vasculature and heart, as a closed circulatory system, supplies nutrients and oxygen to critical organs and removes metabolic wastes and carbon dioxide. This integrated system results from the careful control of cardiac output, arterial blood pressure (systolic and diastolic pressures integrated to derive mean arterial pressure), and systemic vascular resistance, thereby maintaining blood perfusion through... 

Hemodynamic effects - Digoxin produces hemodynamic improvement in patients with heart failure. Short- and long-term therapy with the drug increases cardiac output and lowers pulmonary artery pressure, pulmonary capillary wedge pressure, and systemic vascular resistance. 

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. 

Hemodynamic effects - Small decreases in cardiac output and increases in systemic vascular resistance have occurred, with no significant negative inotropic effect. Blood pressure and pulse rate remain essentially unchanged. Mild depression of myocardial function has been observed following IV mexiletine (dosage form not available in the US) in patients with cardiac disease. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

The prevalence of CHE increases and prognosis worsens with age. Some studies demonstrate that age markedly influences all follow-up events, including total mortality, and mortality or hospitalisation related to CHE. Some studies suggest that physiological changes occur in CHE with ageing with an age-related increase in systemic vascular resistance and circulating noradrenaline (norepinephrine) concentrations and a decrease in renal function. 

Dofetilide does not significantly alter the mean arterial blood pressure, cardiac output, cardiac index, stroke volume index, or systemic vascular resistance. There is a slight increase in the delta pressure/delta time (dP/dt) of ventricular myocytes. 

Anesthesia induction with propofol causes a significant reduction in blood pressure that is proportional to the severity of cardiovascular disease or the volume status of the patient, or both. However, even in healthy patients a significant reduction in systolic and mean arterial blood pressure occurs. The reduction in pressure appears to be associated with vasodilation and myocardial depression. Although propofol decreases systemic vascular resistance, reflex tachycardia is not observed. This is in contrast to the actions of thiopental. The heart rate stabilization produced by propofol relative to other agents is likely the result of either resetting or inhibiting the baroreflex, thus reducing the tachy-cardic response to hypotension. 

Halothane administration can result in a marked reduction in arterial blood pressure that is due primarily to direct myocardial depression, which reduces cardiac output. The fall in pressure is not opposed by reflex sympathetic activation, however, since halothane also blunts baroreceptor and carotid reflexes. Systemic vascular resistance is unchanged, although blood flow to various tissues is redistributed. Halothane also sensitizes the heart to the arrhythmogenic effect of catecholamines. Thus, maintenance of the patient s blood pressure with epinephrine must be done cautiously. 

Enflurane (Ethrane) depresses myocardial contractility and lowers systemic vascular resistance. In contrast to halothane, it does not block sympathetic reflexes, and therefore, its administration results in tachycardia. However, the increased heart rate is not sufficient to oppose enflurane s other cardiovascular actions, so cardiac output and blood pressure fall. In addition, enflurane sensitizes the myocardium to catecholamine-induced arrhythmias, although to a lesser extent than with halothane. Enflurane depresses respiration through mechanisms similar to halothane s and requires that the patient s ventilation be assisted. 

Mechanism of Action An antianginal and antihypertensive agent that inhibits calcium ion movement across cell membranes, depressing contraction of cardiac and vascular smooth muscle. Therapeutic Effect Increases heart rate and cardiac output. Decreases systemic vascular resistance and BP. 

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