Myocardial oxygen demand

Increased oxygen demand secondary to increased heart rates and blood pressure has been hypothesized to lead to myocardial infarction (especially in patients with fixed coronary disease) and/or ventricular arrhythmias. In patients with no history of cardiac disease, cocaine is thought to induce acute isehemie complications via vasospasm of the coronaries (Ascher et al. 1988). In addition, Virmani et al. (1988) have reported a 20 percent incidence of myocarditis thought to be secondary to accumulated microvascular injuries. 

Another mechanism to maintain CO when contractility is low is to increase heart rate. This is achieved through sympathetic nervous system (SNS) activation and the agonist effect of norepinephrine on P-adrenergic receptors in the heart. Sympathetic activation also enhances contractility by increasing cytosolic calcium concentrations. SV is relatively fixed in HF, thus HR becomes the major determinant of CO. Although this mechanism increases CO acutely, the chronotropic and inotropic responses to sympathetic activation increase myocardial oxygen demand, worsen underlying ischemia, contribute to proarrhythmia, and further impair both systolic and diastolic function. 

Higher vasopressin concentrations are linked to dilutional hyponatremia and a poor prognosis in HF. Vasopressin exerts its effects through vasopressin type la (Vla) and vasopressin type 2 (V2) receptors.5,7 Vasopressin type la stimulation leads to vasoconstriction, while actions on the V2 receptor cause free water retention through aquaporin channels in the collecting duct. Vasopressin increases preload, afterload, and myocardial oxygen demand in the failing heart. 

There is a paucity of clinical trial evidence comparing the benefit of diuretics to other therapies for symptom relief or long-term outcomes. Additionally, excessive preload reduction can lead to a decrease in CO resulting in reflex increase in sympathetic activation, renin release, and the expected consequences of vasoconstriction, tachycardia, and increased myocardial oxygen demand. Careful use of diuretics is recommended to avoid overdiuresis. Monitor serum electrolytes such as potassium, sodium, and magnesium frequently to identify and correct imbalances. Monitor serum creatinine and blood urea nitrogen daily at a minimum to assess volume depletion and renal function. 

O Ischemic heart disease results from an imbalance between myocardial oxygen demand and oxygen supply that is most often due to coronary atherosclerosis. Common clinical manifestations of ischemic heart disease include chronic stable angina and the acute coronary syndromes of unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. 

Therapies to alleviate and prevent angina are aimed at improving the balance between myocardial oxygen demand and... 

TABLE 4-6. Effects of Anti-anginal Medications on Myocardial Oxygen Demand and Supply... 

Acute coronary syndromes is a term that includes all clinical syndromes compatible with acute myocardial ischemia resulting from an imbalance between myocardial oxygen demand and supply.3 In contrast to stable angina, an ACS results primarily from diminished myocardial blood flow secondary to an occlusive or partially occlusive coronary artery thrombus. Acute coronary syndromes are classified according to electrocardiogram (ECG) changes into STE ACS (STE MI) or NSTE ACS (NSTE MI and unstable angina) (Fig. 5-1). An STE MI, formerly... 

Intravenous or oral doses of a P-blocker should be administered early in the care of a patient with STE ACS, and then oral agents should be continued indefinitely. Early administration of a P-blocker to patients lacking a contraindication within the first 24 hours of hospitalization is a quality care indicator.2,3 In ACS the benefit of P-blockers mainly results from the competitive blockade of P,-adrenergic receptors located on the myocardium. Pi-Blockade produces a reduction in heart rate, myocardial contractility, and blood pressure, decreasing myocardial oxygen demand. As a result of these effects, P-blockers reduce the risk for recurrent ischemia, increase in infarct size and risk of reinfarction, and occurrence of ventricular arrhythmias in the hours and days following MI.39... 

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. 

Acute coronary syndromes (ACSs) include all clinical syndromes compatible with acute myocardial ischemia resulting from an imbalance between myocardial oxygen demand and supply. 

NTG causes venodilation, which lowers preload and myocardial oxygen demand. In addition, arterial vasodilation may lower BP, thereby reducing myocardial oxygen demand. Arterial dilation also relieves coronary artery vasospasm and improves myocardial blood flow and oxygenation. 

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. 

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. 

Dopamine produces dose-dependent hemodynamic effects because of its relative affinity for cq-, /Jr, /J2-, and Dr (vascular dopaminergic) receptors. Positive inotropic effects mediated primarily by / -receptors become more prominent with doses of 2 to 5 mcg/kg/min. At doses between 5 to 10 mcg/kg/min, chronotropic and -mediated vasoconstricting effects become more prominent. Especially at higher doses, dopamine alters several parameters that increase myocardial oxygen demand and potentially decrease myocardial blood flow, worsening ischemia in some patients with coronary artery disease. 

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