High rate (90–100), especially SHF if not ischemic

Assuming that the appropriate diagnostic steps discussed above were taken, an arterial blood gas and basic metabolic panel should be analyzed for hypoxia, hypercarbia, acidosis, and hyperkalemia. These abnormalities will need to be reversed to create a favorable “metabolic milieu.” Next, ensure an adequate heart rate and rhythm; any bradycardia or tachycardia should be treated with the appropriate pharmacological or electrophysiological modality (i.e. pacing, cardioversion). Once rate and rhythm have been established, the adequacy of preload should be determined. In patients with existing invasive hemodynamic monitors, such as a central venous line or pulmonary artery (PA) catheter, this can be done by assessing central venous pressure (in the absence of significant structural heart or lung disease), pulmonary artery diastolic pressure, or pulmonary capillary wedge pressures. Calculated estimates of preload using arterial line tracings (i.e. pulse-pressure variability, stroke volume variability) can also be performed in select patients (intubated patients on positive pressure mechanical ventilation).^[17] If not already present, appropriate hemodynamic monitors and central vascular access should be obtained at this point (i.e. arterial line, central venous catheter, or PA catheter). If preload is determined to be inadequate, especially in diastolic HF, it should be optimized by administering appropriate crystalloid or preferably colloid (to minimize total fluid volume); if it is excessive, then it should be treated using diuretics, venodilators, or inotropes.

The next step is to increase contractility. However, choosing an appropriate inotrope can be difficult. The first step in choosing is to determine whether SVR is excessively high (hypertension, cool clammy extremities in the absence of hypovolemia) or inappropriately low (hypotension, warm flushed extremities; i.e. vasoplegia). Current SVR will establish whether a patient would benefit more from an inoconstrictor or an inodilator.

Adrenergic inoconstrictors include norepinephrine, epinephrine, and dopamine. These agents all cause an increase inotropy via β₁ mechanisms as well as vasoconstriction via α₁. Norepinephrine is most useful in states of vasodilatory or distributive shock requiring a strong vasoconstrictor effect. Epinephrine is a powerful inotrope that has mixed α₁ vasoconstrictor and β₂ vasodilator effects, therefore producing a more unpredictable effect on SVR. Dopamine is an indirect β₁ adrenergic agent with differing effects based on the dosing level used – primarily dopaminergic at low doses (<3 mcg/kg/min), β-adrenergic at moderate doses (3 to 10 mcg/kg/min), and α adrenergic at high doses (>10 mcg/kg/min).

Adrenergic inodilators, which are all synthetic derivatives of dopamine, include dobutamine and isoproterenol. All of these agents have positive inotropic effects via β₁, as well as β₂ vasodilatory effects. Dobutamine is a direct-acting β-adrenergic agent with a potent β₂-mediated dilatory effect; it even causes pulmonary artery dilation, which may be helpful in patients with a component of right ventricular HF. Isoproterenol has a potent positive chronotropic (i.e. heart rate increasing) effect that precedes its inotropic (contractility) effect and limits its usage to situations of profound bradycardia as a chemical pacemaker.

Other inotropic classes include the phosphodiesterase (PDE) inhibitors (i.e. milrinone). These agents work independently of the adrenergic receptor and thus are useful in patients with chronic HF and down-regulated β-receptors. PDE inhibitors are useful in both left- and right-sided HF, as well as diastolic dysfunction, because they enhance diastolic relaxation (known as a lusitropic effect).

Specialized afterload agents exist for use both in patients in whom contractility is adequate, but who have either an excessive or low SVR, and in patients on inotropes with persistently high or low SVR. Nitroglycerin and nitroprusside are two potent vasodilators with long-established use in management of HF. A newer agent, nesiritide (human recombinant B-type natriuretic peptide [BNP]) is a potent vasodilator with effects on reducing both afterload and preload, and relieving anasarca; its use has been limited primarily by cost.

The opposite situation may occur, in which SVR is inappropriately low, leading to a low perfusion state. This is typically seen in patients with an acute inflammatory syndrome (i.e. post-cardiopulmonary bypass, systemic inflammatory response syndrome, sepsis), which then leads to catecholamine (norepinephrine)-resistant vasodilatory shock. In these patients, low level infusions (1 to 4 units/hr) of arginine vasopressin (AVP) have been shown to reverse catecholamine-resistant vasoplegia.^[18] Consider adding AVP when increasing doses of traditional inotropes fail to improve low SVR states. Additionally, a single dose of methylene blue (2 mg/kg) has also been reported to reverse vasoplegia in patients with an acute inflammatory syndrome.^[19]

Most RV HF is due to LV dysfunction, but it can also be caused by either an increase in PVR or pure RV dysfunction because of myocardial ischemia. RV function could be improved by improving left-sided failure, lowering PVR (nitric oxide), and/or improving RV contractility (dobutamine, milrinone).

One final but critical point: HF or cardiogenic shock due to acute myocardial ischemia will likely not respond to standard inotropic agents (owing to worsening of the myocardial oxygen supply–demand balance). The most effective intervention for acute ischemic HF is insertion of an intra-aortic balloon pump (IABP). An IABP significantly improves the myocardial oxygen supply–demand balance via its counterpulsation mechanism – inflation during diastole and deflation during systole. Oxygen balance is improved by increasing coronary perfusion by forcing blood retrograde through the aorta during diastole (inflation) and decreasing afterload by creating a negative intra-aortic pressure during systole (deflation).^[20] Contraindications to IABP use include aortic insufficiency, aortic aneurysm or dissection, and severe peripheral vascular disease. It is important to remember that an IABP is not a ventricular assist device and therefore does not pump blood through the circulation; if IABP insertion does not reverse the ischemic shock, more invasive mechanical circulatory support should be pursued such as extracorporeal membrane oxygenation (ECMO), cardiopulmonary bypass, or a ventricular assist device.

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