Which Product Is Ideal for You?

Summary

Right ventricle (RV) anatomy and physiology: the RV has a higher volume than the left ventricle (LV) but the muscle mass is about one-sixth of the LV; the ventricles are also shaped differently; internally, the RV can be divided into the 1) inlet, the 2) apical trabeculated myocardium, and the 3) smooth infundibulum (aka, the outlet); the inlet contains the tricuspid valve, chordae, and papillae; the trabeculated apex has 3 muscle bands; unlike in the LV, the inlet valve is not connected by collagen to the pulmonary valve; most of the contraction in the RV results from deep longitudinal fibers moving the tricuspid valve downward; superficial circumferential fibers pull the free wall toward the middle of the heart; 20% to 40% of the contraction comes from LV traction; the LV also has oblique fibers and contracts in a wringing fashion; the RV is connected to the LV in series and must pump approximately the same stroke volume as the LV; hemodynamic function — determinants include the preload (venous return), lung interactions, afterload, contractility, contraction synchrony, and ventricular interdependence

Preload: the RV is very compliant and functions well with more preload, unlike the LV; most of the preload is dependent on venous return; the intrathoracic pressure that occurs with each breath is largely responsible for increasing the preload and for waxing and waning venous return by affecting right atrial pressure (decreased with inspiration); rate, rhythm, and pericardial constraint are also very important; LV overload can push into the RV and decrease preload

Afterload: the RV is highly sensitive to downstream pressure; pulmonary vascular resistance (PVR) is used as a proxy for afterload; the RV compensates briefly for increased afterload before function or stroke volume drops; unlike the LV, the RV is highly volume tolerant but pressure intolerant; respiratory effects also have an impact on RV afterload; when the lungs inflate, preload increases as a result of the small alveolar vessels being squeezed; when the lungs collapse, afterload increases as the bigger vessels are squeezed

Contractility: is largely dependent on proper preload; other determinants of contractility are the sympathetic and parasympathetic output; the muscle fibers have a faster twitch velocity; the thinner RV is more resistant to ischemia than the LV

Ultrasonographic assessment of the RV: qualitative — the size of the RV can be easily determined by comparing it to the LV; a normal RV on the 4-chamber view is <66% of the LV; the RV is mildly dilated if it is exactly 66% of the LV size, moderately dilated if it is equal to the LV, and severely dilated if it is greater than the LV; a visible moderator band also indicates RV enlargement; the potential cause of RV dysfunction can be assessed by observing the timing of septum flattening in the cardiac cycle; if it flattens during diastole, the RV is volume overloaded; if it flattens during systole, the RV is pressure overloaded; if it flattens during both, there is volume and pressure overload; brisk vertical movement of the lateral tricuspid annulus indicates good systolic RV function; quantitative — abnormal values are a base (site of the tricuspid annulus) >41 mm, a midchamber measurement >35 mm, fractional area change (FAC) between systole and diastole <35%, RV ejection fraction (EF) <45%, tricuspid annular plane systolic excursion (TAPSE; vertical movement of the lateral tricuspid annulus) <17 mm, and velocity of the lateral annulus (S’) <9.5 cm/sec; a more negative strain value (ie, -30 vs -15) indicates better RV function

Causes of perioperative RV dysfunction: pressure overload — any process impairing the flow of blood from the RV to the LV, eg, increased PVR, pulmonary and mitral stenosis; volume overload — eg, tricuspid regurgitation, atrial septal defect (ASD), and rarely acute rupture of a sinus of Valsalva aneurysm; impaired contractility — happens with myocardial infarction or when cardiac function is compromised after bypass

Pulmonary hypertension (increased PVR): Group 1 — includes pulmonary artery hypertension (PAH; idiopathic, genetic, connective tissue diseases, and HIV); Group 2 — left heart disease; Group 3 — includes chronic obstructive pulmonary disease (obtain echocardiography in end-stage disease); Group 4 — pulmonary emboli; Group 5 — includes other pulmonary vasculature pathology

Treprostinil: must be weaned slowly (do not discontinue abruptly); it is a synthetic analogue of prostacyclin available in oral and inhaled forms; it inhibits platelets and can cause systemic vasodilation

Chronic RV dysfunction: outflow thickens and the heart beats against the increased PVR; chronically elevated PVR causes generalized hypertrophy, an increased heart rate, and elevated right atrial pressure; RV outflow hypertrophy is associated with normal central venous pressure (CVP); the end result is dilated cardiomyopathy with decreased cardiac output; a chronically compromised RV can work normally for some time, then the pulmonary artery pressure, cardiac index, and stroke volume drop while CVP and RV volume increase; patients with PAH and RV dysfunction have a higher risk for mortality

Acute RV dysfunction: an acute increase in PVR (eg, a pulmonary embolism) causes rapid RV dilation and dysfunction; the dilation causes the septum to bow into the LV, reducing LV stroke volume and causing hypotension, which then causes hypoperfusion of the already failing RV, leading to decreased RV output (the “circle of death”)

Assessing RV function: decreasing cardiac output, cardiac index, and pulmonary artery pressures with increasing CVP correlates well with right-heart failure; ratio of CVP to pulmonary capillary wedge pressure (PCWP) >0.8 has been associated with RV failure in cardiogenic shock and >0.54 is RV failure in patients with a left ventricular assist device (LVAD); the pulmonary artery pulsatility index (PAPi) is (PA systolic minus PA diastolic pressure) divided by CVP; a PAPi ≤0.9 in a patient with an MI indicates higher risk for mortality or ionotropic support requirement; <1.85 with an LVAD has a higher risk postoperative RV failure

Factors that compromise the RV: include acidosis, hypercarbia, hypoxemia, hypothermia, pain (sympathetic stimulation increases RV afterload), large pleural effusions, and overdistension of the lungs; never use β blockers or calcium-channel blockers in a patient with a failing RV; perform cardioversion for atrial fibrillation

Intraoperative care: optimize preload, afterload, contractility, heart rate, and ventricular interdependence; epinephrine boluses are useful for hypotension or cardiac arrest (10 μg/mL), then start dobutamine (the best inotrope according to speaker); vasodilate the pulmonary vessels with inhaled epoprostenol or nitric oxide; extracorporeal membrane oxygenation (ECMO) can be used for significant RV failure; while providing mechanical ventilation, decrease positive end-expiratory pressure (PEEP) and tidal volumes and keep plateau pressure <25 mm Hg