Cardiogenic Shock Medication
- Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MD, MRCPI more...
Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated for persons with cardiogenic shock. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in patients with hypotension.
Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output.
Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values.
These agents augment coronary and cerebral blood flow during the low-flow state associated with cardiogenic shock. They also improve cardiac output in refractory hypotension and shock.
Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect depends on the dose. Lower doses primarily stimulate dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.
Dobutamine is a sympathomimetic amine with stronger beta effects than alpha effects. It produces systemic vasodilation and increases the inotropic state. Higher doses may cause an increase in heart rate, exacerbating myocardial ischemia.
Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia.
Norepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic blood pressure < 70 mm Hg) or hypotension unresponsive to other medication.
Milrinone is a selective phosphodiesterase inhibitor in cardiac and vascular tissue with positive inotropic and vasodilator effects; it has little chronotropic activity. This agent's mode of action differs from that of either digitalis glycosides or catecholamines.
Formerly known as amrinone, inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity. It produces vasodilation and increases the inotropic state. Inamrinone is more likely to cause tachycardia than is dobutamine, and it may exacerbate myocardial ischemia.
Vasodilators decrease preload and/or afterload.
This agent causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in preload and blood pressure (ie, afterload).
Antiplatelet Agents, Cardiovascular
Agents that irreversibly inhibit platelet aggregation may improve morbidity.
Aspirin is an odorless, white, powdery substance available in 81 mg, 325 mg, and 500 mg, for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids. It is a stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other salicylic acid derivatives. The acetyl group is responsible for inactivation of cyclo-oxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.
Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclo-oxygenase. This, in turn, inhibits the conversion of arachidonic acid to prostaglandin 12 (a potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (a potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for the life of the cell (approximately 10 d).
Aspirin may be used at a low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. It reduces the likelihood of myocardial infarction (MI) and is also very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute MI may reduce cardiac mortality in the first month.
Analgesics reduce pain, which decreases sympathetic stress and provides some preload reduction.
Morphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various intravenous doses are used; the drug is commonly titrated until the desired effect is achieved.
These drugs cause diuresis to decrease plasma volume and edema and thereby decrease cardiac output and, consequently, blood pressure. The initial decrease in cardiac output causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, extracellular fluid and plasma volumes return almost to pretreatment levels. Peripheral vascular resistance decreases below that of the pretreatment baseline.
Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.
Individualize the dose to the patient. Depending on the response, administer furosemide at increments of 20-40mg no sooner than 6-8 hours after the previous dose, until the desired diuresis occurs. When treating infants, titrate the drug in increments of 1mg/kg/dose until a satisfactory effect is achieved.
These drugs cause arterial and venous dilation by binding to the cyclic guanosine monophosphate (GMP) receptors on vascular smooth muscle, causing smooth muscle relaxation. Natriuretic peptides produce dose-dependent decreases in pulmonary capillary wedge pressure and systemic arterial pressure.
Nesiritide is a recombinant deoxyribonucleic acid (DNA) form of human B-type natriuretic peptide (hBNP), which dilates veins and arteries.
Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to the receptor causes an increase in cyclic GMP, which serves as a second messenger to dilate veins and arteries. Pulmonary capillary wedge pressure is reduced and dyspnea is improved in patients with acutely decompensated congestive heart failure.
Nesiritide may be considered in the treatment of patients with cardiogenic shock. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for acute congestive heart failure and currently retains US Food and Drug Administration (FDA) approval. However, it should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.
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