Ventricular arterial

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). 

Diuretics have become the cornerstone of all treatment regimens of CHF (III—II3). They can reheve symptoms of pulmonary and peripheral edema. In mild CHF, the thia2ide-type diuretics are adequate unless the GFR falls below 30 ml,/min, as compared to 120 ml,/min in normal subjects. Diuretics improve left ventricular function in CHF due in part to decrease of preload. Indapamide has been shown to cause reduction of pulmonary arterial pressure and pulmonary wedge pressure. 

Several clinical trials have been conducted with streptokinase adrninistered either intravenously or by direct infusion into a catheterized coronary artery. The results from 33 randomized trials conducted between 1959 and 1984 have been examined (75), and show a significant decrease in mortaUty rate (15.4%) in enzyme-treated patients vs matched controls (19.2%). These results correlate well with an ItaUan study encompassing 11,806 patients (76), in which the overall reduction in mortaUty was 19% in the streptokinase-treated group, ie, 1.5 million units adrninistered intravenously, compared with placebo-treated controls. The trial also shows that a delay in the initiation of treatment over six hours after the onset of symptoms nullifies any benefit from this type of thrombolytic therapy. Conversely, patients treated within one hour from the onset of symptoms had a remarkable decrease in mortaUty (47%). The benefits of streptokinase therapy, especially in the latter group of patients, was stiU evident in a one-year foUow-up (77). In addition to reducing mortahty rate, there was an improvement in left ventricular function and a reduction in the size of infarction. Thus early treatment with streptokinase is essential. 

Figure 4.2 Epicardial ECG recorded from an isolated blood-perfused rat heart at the moment of reperfusion. The heart was made regionally ischaemic by occluding a snare around the left anterior descending coronary artery and, after 10 min, reperfused by releasing the snare. Note the rapid onset of ventricular tachycardia (VT) and its subsequent degeneration into ventricular fibrillation (VF). Reproduced with permission from Lawson (1993).

CAD, coronary artery disease LVEF, left ventricular ejection fraction LVH, left ventricular hypertrophy. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE, Dunsworth TS, et al. (eds.) Pharmacotherapy Self-Assessment Program, 4th ed. Kansas City American College of Clinical Pharmacy 2001 217-267.)50... 

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-... 

Upon stabilization, placement of a pulmonary artery (PA) catheter may be indicated based on the need for more extensive cardiovascular monitoring than is available from non-invasive measurements such as vital signs, cardiac rhythm, and urine output.9,10 Key measured parameters that can be obtained from a PA catheter are the pulmonary artery occlusion pressure, which is a measure of preload, and CO. From these values and simultaneous measurement of HR and blood pressure (BP), one can calculate the left ventricular SV and SVR.10 Placement of a PA catheter should be reserved for patients at high risk of death due to the severity of shock or preexisting medical conditions such as heart failure.11 Use of PA catheters in broad populations of critically ill patients is somewhat controversial because clinical trials have not shown consistent benefits with their use.12-14 However, critically ill patients with a high severity of illness may have improved outcomes from PA catheter placement. It is not clear why this was... 

The answer is a. (Hardman, pp 762-764.) Experimentally, nitrates dilate coronary vessels. This occurs in normal subjects, resulting in an overall increase in coronary blood flow. In arteriosclerotic coronaries, the ability to dilate is lost, and the ischemic area may actually have less blood flow under the influence of nitrates. Improvement in the ischemic conditions is the result of decreased myocardial oxygen demand because of a reduction of preload and afterload. Nitrates dilate both arteries and veins and thereby reduce the work of the heart. Should systemic blood pressure fall, a reflex tachycardia will occur. In pure coronary spasm, such as Prinzmetal s angina, the effect of increased coronary blood flow is relevant, while in severe left ventricular hypertrophy with minimal obstruction, the effect on preload and afterload becomes important. 

The benefits result from blockade of //j receptors in the myocardium, which reduces heart rate, myocardial contractility, and BP, thereby decreasing myocardial oxygen demand. The reduced heart rate increases diastolic time, thus improving ventricular filling and coronary artery perfusion. 

Nesiritide is manufactured using recombinant techniques and is identical to the endogenous B-type natriuretic peptide secreted by the ventricular myocardium in response to volume overload. Consequently, nesiritide mimics the vasodilatory and natriuretic actions of the endogenous peptide, resulting in venous and arterial vasodilation increases in cardiac output natriuresis and diuresis and decreased cardiac filling pressures, sympathetic nervous system activity, and renin-angiotensin-aldosterone system activity. 

The action of nitrates appears to be mediated indirectly through reduction of MVo2 secondary to venodilation and arterial-arteriolar dilation, leading to a reduction in wall stress from reduced ventricular volume and pressure. Direct actions on the coronary circulation include dilation of large and small intramural coronary arteries, collateral dilation, coronary artery stenosis dilation, abolition of normal tone in narrowed vessels, and relief of spasm. 

CAD, coronary artery disease LDL, low-density lipoprotein LV, left ventricular Ml, myocardial infarction. 

A pulmonary artery (Swan-Ganz) catheter can be used to determine central venous pressure (CVP) pulmonary artery pressure CO and pulmonary artery occlusive pressure (PAOP), an approximate measure of the left ventricular end-diastolic volume and a major determinant of left ventricular preload. 

In the management of PE, thrombolytics restore pulmonary artery patency more rapidly when compared to UFH alone, but this early benefit does not improve long-term patient outcomes. Thrombolytic therapy has not been shown to improve morbidity or mortality and is associated with a substantial risk of hemorrhage. For these reasons, thrombolytics should be reserved for patients with PE who are most likely to benefit (e.g., those who present with shock, hypotension, right ventricular strain, or massive DVT with limb gangrene). 

Fig. 6.3 Hemodynamic profile of CAS 1609 on anesthetised dog (0.3mgkg 1 i.v.) systolic blood pressure (BPs), diastolic blood pressure (BPd), left ventricular end diastolic pressure (LVEDP), diastolic pulmonary artery pressure (PAPd), heart rate (HR), left ventricular...

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