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Caring for Patients Receiving Vasopressors and Inotropes in the ICU

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Caring for Patients Receiving Vasopressors and Inotropes in the ICU Caring for patients receiving vasopressors and inotropes in the ICU Vigilant monitoring will maximize outcomes. By Sonya M. Grigsby, DNP, APRN, AGACNP-BC CNE 1.5 contact hours LEARNING O BJECTIVES 1. Identify receptors related to cardiovascular physiology. 2. Differentiate the effects of vasopressors and inotropes. 3. Discuss nursing care of patients receiving vasopressors and inotropes in the ICU. The authors and planners of this CNE activity have disclosed no relevant fi- nancial relationships with any commercial companies pertaining to this ac- tivity. See the last page of the article to learn how to earn CNE credit. Expiration: 2/1/24 SHOCK requires early recognition and quick peutic effect) these medications using the action to prevent organ failure. (See Types of lowest possible dose to avoid adverse effects. shock.) After initial I.V. fluid resuscitation, pharmacologic agents—such as vasopressors Cardiovascular physiology and inotropes—are used in critical care set- Shock disrupts cardiovascular physiology, par- tings as supportive therapies to improve my- ticularly blood pressure, so understanding ocardial contractility, heart rate, and vascular normal function is important. Short-term resistance in patients with low cardiac output. blood pressure (BP) regulation is controlled When critical care nurses understand shock by the autonomic nervous system (ANS) via pathophysiology and hemodynamic monitor- baroreceptors in the aortic arch and carotid si- ing, they can effectively and safely titrate (in- nus. The ANS regulates the heart, secretory crease or decrease an infusion rate for thera- glands, and smooth muscles via activation of MyAmericanNurse.com February 2021 American Nurse Journal 5 Types of shock Shock is a decline in tissue perfusion and oxygen delivery, leading to cellular dysfunction and death. Organ hypoperfusion results from decreased circulating volume (hypovolemic shock), decreased cardiac their physiologic response. Other receptors are output (cardiogenic and obstructive), and vasodilation (distributive). vasopressin (V1 and V2; this article focuses on V1) and dopamine. (See Receptor physiology.) Types of shock Common causes Adrenergic receptors. a1 receptors are Hypovolemic • Hemorrhage located within the veins, arterioles, and many • Emesis capillary beds. When stimulated, they pro- • Diarrhea duce vasoconstriction. a2 receptors also are lo - • Burns cated on the nerve terminals of the peripheral • Third spacing (too much fluid moving from the nervous system and function to inhibit trans- intravascular space into the interstitial space) mitter release. • Polyuria Beta receptors are found on the arterioles • of the heart, smooth muscle tissues, and the Cardiogenic Myocardial infarction lungs where they bind to circulating norepi- • Cardiomyopathy nephrine and epinephrine. b1, the dominant • Valvular diseases • Arrhythmias receptor found in the heart and kidney, en- • Myocarditis hances myocardial contractility and relaxation when it’s activated. It also increases heart rate Obstructive • Tension pneumothorax and cardiac output. Systemic vasodilation may • Pulmonary embolism offset increased cardiac output, resulting in • Air embolism decreased arterial pressures. b1 receptor acti- • Cardiac tamponade vation in the kidneys induces the release of • Aortic dissection renin into the blood, promoting angiotensin • synthesis and elevating BP. b2 receptors, Distributive Anaphylaxis which are located in the arterioles of the • Neurologic condition (such as spinal cord trauma) heart, smooth muscle tissues, and lungs, help • Sepsis mediate many essential processes. Although b2 receptors cause vasodilation, their effect on the parasympathetic and sympathetic systems. cardiac output is less than that of b1. In addi- Body processes activate the ANS in response tion, b2 receptors have a significant impact on to information produced by internal and ex- smooth muscles in the airway and cause bron- ternal stimuli, including blood pressure, body chodilation. temperature, heart rate, respiratory rate, me- Dopamine receptors. Site-specific dopa - tabolism, urination, defecation, digestion, and mine receptors also exert cardiovascular sexual response via chemical and neurotrans- actions. Small doses of dopamine result in mitter signaling. vasodilation. As activation increases, vaso- The sympathetic system prepares the body constriction occurs via stimulation of a1 re- for stressful or emergent situations, resulting ceptors and inhibition of norepinephrine re- in increased heart rate and contractility, vaso- lease. Dopamine receptor activation within constriction, and norepinephrine and epi- the kidney vasculature leads to enhanced re- nephrine release, which increase BP. The nal perfusion. parasympathetic system conserves and re- Vasopressin receptors. Arginine vaso- stores body processes during normal condi- pressin, an antidiuretic hormone, is synthe- tions, resulting in reduced heart rate, cardiac sized in the hypothalamus and controls the output, and BP. body’s osmotic balance, regulates BP, and in- fluences water reabsorption in the kidneys. V1 Receptors receptors are found in vascular smooth mus- Adrenergic receptors (which affect the sympa- cles. Their stimulation results in vasoconstric- thetic nervous system) within the heart and tion, primarily in the splanchnic, renal, and vascular system facilitate the hemodynamic ef- hepatic arteriole vasculature. Hypovolemia fects of vasopressors via the interaction of cat- and decreased arterial blood volume stimulate echolamines and synthetic medications such vasopressin release via baroreceptors in the as norepinephrine and epinephrine. Adrener- carotid sinuses and aortic arch, resulting in gic receptors are classified as alpha (a1, a2) or increased water retention that causes vascular beta (b1, b2), and their location determines smooth muscle constriction. 6 American Nurse Journal Volume 16, Number 2 MyAmericanNurse.com Receptor physiology Adrenergic (alpha and beta), dopamine, and vasopressin receptors exert actions on specific organs. Supportive pharmacologic therapies Vasopressors and inotropes are commonly Receptors Location Action used in the ICU to manage shock and support Adrenergic α1 • Smooth muscle • Vasoconstriction the cardiovascular system. (To view a detailed • Vascular walls • Increased force of list of common vasopressors and inotropes, • Heart heart contraction visit myamericannurse.com/?p=71893.) Vasopressors. Vasopressors are I.V. med- Adrenergic α2 • Central nervous system • Sedation ications that produce arteriole vasoconstric- • Arterioles • Analgesia tion via positive inotropic or chronotropic ef- • Pancreas • Vasodilation fects that lead to increased systemic vascular • Inhibition of insulin resistance and BP. Common vasopressors are release norepinephrine, epinephrine, phenylephrine, • • and vasopressin. Indications include a de- Adrenergic β1 Cardiac muscle Increased force and • Sinus node rate of heart crease in systolic pressure of more than 30 • Atrioventricular junction contraction mmHg from baseline or mean arterial pres- sure (MAP) less than 60 mmHg resulting in Adrenergic β2 • Skeletal vascular • Vasodilation end-organ dysfunction. (MAP, the average • Bronchial smooth muscle • Bronchodilation pressure in the arteries during one cardiac cy- • Liver • Hepatic cle, is the best indicator of organ perfusion.) • Cell membranes glycogenolysis Vasopressors work on specific adrenergic receptors by activating endogenous or syn- Dopamine • Kidney • Vasodilation thetic hormones to restore normal arterial • Splanchnic organs • Higher receptor • Heart activation causes pressure and organ perfusion during times of • physical or emotional stress. Cerebral vascular beds vasoconstriction by inhibiting Inotropes. Inotropes, which are crucial to norepinephrine resuscitating patients with cardiogenic shock release and heart failure, can exude positive or nega- tive effects on the heart. Positive inotropic Vasopressin • Vascular smooth muscle • Vasoconstriction agents, which include dopamine and dobuta- mine, increase myocardial contractility, boost- ing cardiac output. These agents have been electrocardiogram, temperature, respiratory used to treat heart failure, but variability in rate, pulse oximetry, and urine output. conditions and heart rate may alter their ef- Invasive monitoring includes inserting an fects. Adverse reactions associated with posi- arterial line for continuous BP measurement tive inotropic agents include arrhythmias, in- and arterial blood gas analysis, and central ve- duced myocardial ischemia, and hypotension. nous catheterization or pulmonary artery Negative inotropic agents, which include beta catheters (PACs) for advanced hemodynamic blockers and calcium blockers (such as meto- monitoring to guide fluid resuscitation and the prolol, diltiazem, and verapamil), decrease the need for vasopressors or inotropic infusions. heart’s workload by reducing the force of Both invasive and noninvasive monitoring muscle contraction; they are outside the scope are helpful for assessing patients’ responses to of this article. medications, so that titration is effective. Here is a closer look at invasive techniques used for Hemodynamic monitoring and monitoring and medication administration. medication administration Hemodynamic monitoring involves using in- Arterial catheterization vasive and noninvasive methods to gather in- Vasopressor and inotropic drugs act quickly, formation about a critically ill patient’s cardio- so invasive BP monitoring,
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