Perfusion coronary

Modern representations of the virtual heart, therefore, describe structural aspects like fibre orientation in cardiac muscle, together with the distribution of various cell types, active and passive electrical and mechanical properties, as well as the coupling between cells. This then allows accurate reproduction of the spread of the electrical wave, subsequent contraction of the heart, and effects on blood pressure, coronary perfusion, etc. It is important to point out, here, that all these parameters are closely interrelated, and changes in any one of them influence the behaviour of all others. This makes for an exceedingly complex system. 

The individual modules of the in situ heart can be coupled together to compute a whole sequence from ventricular pressure development, coronary perfusion, tissue supply of metabolites, cell energy consumption, and electrophysiology, to contractile activity and ventricular pressure development in the subsequent beat. The starting point (here chosen as ventricular pressure development) can be freely selected, and drug effects on the system can be simulated. Inserted into a virtual torso, these models allow one to compute the spread of excitation, its cellular basis, and the consequences for an ECG under normal and pathological conditions. 

Because risk varies and resources are limited, it is important to triage and treat patients according to their risk category. Initial approaches to treatment of STE and NSTE ACS patients are outlined in Fig. 5-1. Patients with STE are at high risk of death, and efforts to re-establish coronary perfusion,... 

Patients with STE ACS are at high risk of death, and efforts to reestablish coronary perfusion should be initiated immediately (without evaluation of biochemical markers). 

Coronary perfusion pressure should be assessed in patients for whom intraarterial monitoring is in place. 

Nitroprusside is effective in the short-term management of severe HF in a variety of settings (e.g., acute MI, valvular regurgitation, after coronary bypass surgery, decompensated HF). Generally, it will not worsen, and may improve, the balance between myocardial oxygen demand and supply. However, an excessive decrease in systemic arterial pressure can decrease coronary perfusion and worsen ischemia. 

Successful fluid resuscitation should increase SBP (greater than 90 mm Hg), Cl (greater than 2.2 L/min/m2), and urine output (0.5 to 1 mL/kg/hour) while decreasing SVR to the normal range. MAP greater than 60 mm Hg should be achieved to ensure adequate cerebral and coronary perfusion pressure. 

CPP is coronary perfusion pressure and ADP is aortic diastolic pressure. 

Hyperkaiemia Elevated serum potassium (at least 0.5 mEq/L greater than the upper limit of normal) was observed in 0.4% of hypertensive patients given trandolapril, approximately 1% of hypertensive patients given benazepril, enalapril, ramipril, or moexipril approximately 2% of patients receiving quinapril or lisinopril, approximately 2.6% of hypertensive patients given fosinopril, and approximately 4.8% of CHF patients given lisinopril. Hyperkalemia also occurred with captopril. Vaivuiar stenosis Theoretically, patients with aortic stenosis might be at risk of decreased coronary perfusion when treated with vasodilators, because they do not develop as much afterload reduction as others. 

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]. 

Murad-Netto S, Moura R, Romeo LJ, Manoel Neto A, Duarte N, Barreto F, Jensen A, Vina RE, Vraslovik F, Oberdan A, Benetti F, Saslavsky J, Vina ME, Amino JG. Stem cell therapy with retrograde coronary perfusion in acute myocardial infarction. A new technique. Arq Bras Cardiol 2004 S3 352-254 349-351. 

Isoprenaline stimulates pi and 32 adrenoceptors (pi>32) resulting in increased myocardial contractility and reduced peripheral vascular resistance. It does not act on a adrenoceptors. Cardiac output increases partly due to reduced afterload and an increase in heart rate. There is a diversion of blood to non-essential tissues, e.g. skeletal muscle and skin. Because of the decrease in peripheral vascular resistance arterial blood pressure and coronary perfusion pressure may decrease, which may predispose to myocardial ischaemia. 

Unfortunately, the patient with shock may not respond to any of these therapeutic maneuvers the temptation is then to use vasoconstrictors to maintain blood pressure. Coronary perfusion may be improved, but this gain may be offset by increased myocardial oxygen demands as well as more severe vasoconstriction in blood vessels to the abdominal viscera. Therefore, the goal of therapy in shock should be to optimize tissue perfusion, not blood pressure. 

Decreased diastolic perfusion time due to tachycardia Decreased coronary perfusion... 

Pretreatment with G115 reduces by 30% coronary perfusion pressure... 

For the vascular system, Lagana et al. [261] employed a hierarchical methodology for multiscale modeling of pulmonary and coronary perfusions in the cardiovascular system. Essentially, they studied different shunt size effect on the pressure of blood within the vessels. 

K. Lagana et al Multiscale modeling of the cardiovascular system application to the study of pulmonary and coronary perfusions in the univentricular circulation. J. Biomech. 38, 1129-141 (2004)... 

Adverse effects Phenoxybenzamine can cause postural hypotension, nasal stuffiness, and nausea and vomiting. It can inhibit ejaculation. The drug also may induce tachycardia, mediated by the baroreceptor reflex and is contraindicated in patients with decreased coronary perfusion. 

In contrast to phenoxybenzamine, phentolamine [fen TOLE a meen] produces a competitive block of ai and a2 receptors. The drug s action lasts for approximately 4 hours after a single administration. Like phenoxybenzamine, it produces postural hypotension and causes epinephrine reversal. Phentolamine had been used in the diagnosis of pheochromocytoma and in other clinical situations associated with excess release of catecholamines. Phentolamine-induced reflex cardiac stimulation and tachycardia are mediated by the baroreceptor reflex and by blocking the a2 receptors of the cardiac sympathetic nerves. The drug can also trigger arrhythmias and anginal pain and is contraindicated in patients with decreased coronary perfusion. 

Langendorff-perfused rat heart have been investigated and compared to that of nifedipine. Nifedipine decreased concentration-dependent (IC50 = 8.89 1.09 x 10-8 M) left ventricular pressure leaving unaltered coronary perfusion pressure, whereas DP7 did not affect these parameters. Nifedipine did not modify QRS and QT intervals of ECG [112], It has also been investigated that neither pyruvate kinase nor lactate dehydrogenase was inhibited by DP7... 

Cardiac muscle has a large oxygen requirement, and extraction of oxygen from coronary blood is high. The coronary arteries are compressed in systole, particularly in the left ventricle. Sympathetic stimulation, which increases heart rate and force, reduces the duration of diastole and increases myocardial oxygen consumption. A slow heart rate improves coronary perfusion, reduces oxygen demand and is beneficial for coronary perfusion. 

Digoxin is a cardiotonic agent with a narrow therapeutic index which is used to treat atrial fibrillation since it not only increases cardiac contractility but also acts on vagal centres in the brain and beneficially slows the heart. A slow heart facilitates coronary perfusion and ventricular filling, which improves cardiac output. 

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