Anesthesia in valvular heart disease

The article was written by MSc Ho Thi Xuan Nga - Anesthesiologist - Cardiovascular Center - Vinmec Central Park International General Hospital

Heart valves help direct blood flow into and out of the heart. Any problem with the heart valves is extremely dangerous for health. The following are the basic principles of valvular anesthesia.

Total blood volume is increased to maintain effective systemic flow, due to volume loss posterior to the ventricular and atrioventricular (T) narrowing site. Blood volume decreases due to more systemic flow than to the regurgitated portion, because atrioventricular valve leaks "steal" volume in the low-pressure system of the left atrium. Tolerance to hypovolaemia is low, and so during anesthesia, preload should be kept between normal to high.

The ventricle (T) acts as a chamber with two retrograde volume escape routes directly related to contractile function, the systemic vascular resistance must therefore be completely low. It is necessary to use anesthetic agents with vasodilator properties (isoflurane, nitroprusside, phentolamine).

It should be kept high to ensure presystolic flow. Therefore, only inotropes with no alpha effect (dobutamine, isoprenaline, amrinone, milrinone) should be used. In difficult cases, aortic balloon counterpulsation is very effective in providing ventricular (T) support, reducing mitral regurgitation, and improving coronary perfusion.

It is important to maintain a high level because bradycardia increases filling time and ventricular volume, thereby increasing the risk of acute ventricular dilatation (T). Since mitral regurgitation occurs during systole, the frequency variation does not change its duration much. Maintaining sinus rhythm is important as long as the atria (T) are not very dilated.

Pulmonary hypertension is frequent but generally moderate; Pulmonary vascular system is hyper-reactive; Avoid any pulmonary vasoconstriction (hypoxia, hypercarbia, acidosis, N 2 O) and maintain ventilation for a pH of 7.5 and a PaCO of 32-35 mmhg.

Helps improve left-sided flow because right-cardiac venous return is still well maintained, pre-mitral flow is increased, and trans-atrial pressure is reduced; reduce ventricular (T) load effectively.

It is necessary to keep the level high to ensure sufficient pressure gradient across the mitral valve, but the pulmonary vascular bed is not elastic because of chronic overload. In cases of hypovolemia or increased venous return (Trendelenburg position), there is an increased risk of acute pulmonary edema. Hypovolemia is very poorly tolerated because reduced mitral outflow is related to a decrease in atrial pressure (T) and cannot be compensated for by tachycardia.

Systemic vascular resistance should be kept high to compensate for the reduced systolic volume; The contractile function of the ventricles (T), which is usually preserved, supports the subsequent increase in load. Avoid any dilation of blood vessels. An alpha vasoconstrictor is the best way to maintain systemic pressure during surgery.

Ventricular (T) function is preserved; systolic volume is low and fixed. Beta-catecholamines are used only in relation to an excessive decrease in cardiac output (decrease in SvO2), as they are not beneficial for the ventricles (T) for two reasons: 1) tachycardia reduces ventricular filling (T) ) and 2) increased cardiac output increasing the pressure gradient across the mitral and atrial (T) valves.

It is essential to remain low to allow very slow ventricular filling.

Pre-capillary (arterial vasoconstriction) and post-capillary (venous hypertension) pulmonary hypertension. The risk of arterial vasoconstriction is increased in the presence of hypoxia, hypercapnia, acidosis or N20; Ventilation should be increased (PetCO2 30 mmHg), avoiding high ventilation pressure so as not to increase ventricular afterload (P). Pulmonary vasodilators are indicated if ventricular failure (P).

It is very beneficial for left-sided flow because venous return to the right heart is still well ensured and ventricular (P) is not impaired. Positive-pressure ventilation increases atrial return (T), reduces atrial infusion pressure, and improves valvular blood flow and reduces blood stasis.

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