Cardiac/Vascular Nurse Exam Secrets Study Guide (21 page)

Goals of treating of cardiogenic shock

Treatment of cardiogenic shock requires emergency and prompt attention to restore blood flow to various end organ systems. The goal of treatment is to initially treat the shock and then to treat the underlying cause of cardiogenic shock. Emergency life support treatment is required for cardiogenic shock, which aims to restore blood flow to brain, kidney, and other end organ systems. Patients experiencing cardiogenic shock will be given oxygen as well as fluids including blood products. The goal of pharmacologic treatment is to reduce mortality and morbidity as well as prevent further complications.

Pharmacologic and surgical interventions used for cardiogenic shock

Pharmacologic agents used to treat cardiogenic shock include vasopressors such as dopamine and dobutamine, phosphodiesterase enzyme inhibitors such as milrinone and inamrinone, vasodilators such as nitroglycerin, analgesics such as morphine sulfate, diuretics such as furosemide, and natriuretic peptides such as nesiritide.

More invasive surgical approaches used to treat cardiogenic shock include intra-aortic balloon pump and angioplasty. Other surgical approaches used to treat the underlying cause of cardiogenic shock include coronary artery bypass surgery, surgery to repair damaged cardiac valves, surgery to repair the wall between heart chambers, left ventricular assist device implantation, and heart transplant.

Prevention of cardiogenic shock

Although little can be done to prevent the onset of cardiogenic shock, patient education and increased awareness in individuals with a history of the condition or that have other comorbid cardiovascular or respiratory risk factors is important for prompt diagnosis and treatment. Prevention of cardiac disease and/or myocardial infarction is the best way to prevent the onset of cardiogenic shock. Prompt treatment of myocardial infarction and/or heart disease may prevent the onset of cardiogenic shock.

Patients should also maintain a diet low in sodium and saturated fats, increase potassium intake, increase exercise and physical activity, avoid smoking and tobacco use, get enough folic acid, manage stress, lose excess weight, avoid beta-blockers and illicit drug use, maintain proper lipid levels, maintain proper sugar levels, and maintain proper albumin excretion and creatinine levels.

Adrenergic group of drugs

The classes of agents included in the adrenergic group of drugs include sympathomimetics such as dobutamine, isoproterenol, dopamine, metaraminol, epinephrine, and norepinephrine; alpha-1 selective adrenergic agonists such as methoxamine, phenylephrine, and midodrine; alpha-2 selective adrenergic agonists such as clonidine, guanfacine, guanabenz, and methyldopa; alpha adrenergic antagonists such as doxazosin, prazosin, phenoxybenzamine, terazosin, phentolamine, and tolazoline; and beta-adrenergic antagonists such as acebutolol, atenolol, betaxolol, bisoprolol, carteolol, carvedilol, esmolol, labetalol, metoprolol, nadolol, penbutolol, pindolol, propranolol, sotalol, and timolol.

Sympathomimetic agents

Sympathomimetic agents stimulate both alpha and beta-adrenogenic receptors. Stimulation of alpha-adrenergic receptors induces vasoconstriction and stimulation of beta-adrenergic receptors increase cardiac contraction and heart rate. Sympathomimetic agents also target dopamine receptors, which also increases cardiac contraction and dilates renal blood vessels. Therapeutic uses of sympathomimetic agents include treatment of hypotension and cardiogenic shock associated with myocardial infarction.

Adverse events associated with sympathomimetic agents include gastrointestinal side effects such as nausea and vomiting, cardiovascular events such as tachycardia, dysrhythmia, hypertension, palpitations, and angina and central nervous system events such as throbbing headache and cerebral hemorrhage. Contraindications to sympathomimetic agents include tachydysrhythmia, ventricular fibrillation, and pheochromocytoma.

Alpha-1 selective adrenergic agents

The alpha-1 selective adrenergic agents stimulate vascular smooth muscle by targeting alpha-adrenergic receptors. Stimulation of alpha-adrenergic receptors increases peripheral vascular resistance and increase blood pressure through vasoconstriction. Therapeutic uses of alpha-1 selective adrenergic agents include the treatment of persistent hypotension, neurally mediated hypotension or orthostatic hypotension.

Adverse events associated with alpha-1 selective adrenergic agents include over stimulation that leads to high levels of blood pressure and profuse sweating. Contraindications of alpha-1 selective adrenergic agents include hypertension, tachycardia, vasospasm, and lactation.

These agents should not be stopped immediately, as sudden withdrawal could lead to reverse complications and sudden death. These agents should be tapered over a few days.

Alpha-2 selective adrenergic agents

The alpha-2 selective adrenergic agents stimulate the cardiovascular control centers of the central nervous system, activating alpha-2 receptors. Stimulation of alpha-2 receptors decreases blood pressure and heart rate. Therapeutically, alpha-2 selective adrenergic agents are used in the treatment of systemic hypertension.

Adverse events associated with alpha-2 selective adrenergic agents include central nervous system events such as depression, nightmares, sedation, drowsiness, fatigue, and headache, and cardiovascular events such as hypotension, congestive heart failure, and bradycardia. Other adverse events include dry mouth, sexual dysfunction, and decreased urinary output. Contraindications of alpha-2 selective adrenergic agents include severe coronary artery disease, vascular disease, and chronic renal failure. Sudden discontinuation of these agents could lead to withdrawal reactions, so practicing clinicians should titrate down dosages upon discontinuation.

Alpha-adrenergic antagonists

Alpha-adrenergic antagonists target both alpha-1 adrenergic and alpha-2 adrenergic receptors and block receptor action. Alpha-1 adrenergic receptors produce the effects of the sympathetic nervous system, while alpha-2 adrenergic receptors stimulate norepinephrine release. Drugs within this class of agents have different affinity for these receptors. Prazosin, terazosin, and doxazosin have more affinity for blocking alpha-1 receptors, while phenoxybenzamine and phentolamine have similar affinity for both alpha-1 and alpha-2 receptors.

Alpha-adrenergic antagonists decrease vascular tone, increase vasodilation and decrease blood pressure. Therapeutic uses of alpha-adrenergic antagonists include hypertension, pheochromocytoma, and extravasation of tissue-toxic agents.

Adverse events associated with alpha-adrenergic antagonists include cardiovascular events such as postural hypotension, dysrhythmia, edema, congestive heart failure, and angina; and central nervous system events such as dizziness, weakness, fatigue, drowsiness, and depression. Other adverse events include fainting and syncope up to 90 minutes post administration. Therefore, practicing clinicians should monitor patients starting treatment with these agents to assess side effects and titrate dose to get the desired effect with minimal adverse effects. Caution should be used when administrating these agents in patients with congestive heart failure, pregnancy, and renal failure.

Beta-adrenergic antagonists

Beta-receptor antagonists block beta-adrenergic receptor signaling. Beta-1 adrenergic receptors stimulate myocardial contraction and increase heart rate. Beta-2 receptors are found in vascular smooth muscle of lungs, blood vessels, and uterus and stimulate dilation and relaxation. Drugs within this class of agents have different affinity for these receptors, with most agents targeting both beta-1 and beta-2 receptors equally.

Beta-adrenergic antagonists decrease heart rate and blood pressure. Therapeutic uses include treatment of hypertension, ventricular dysrhythmia, chronic angina, prevention of reinfarction after myocardial infarction, congestive heart failure, supraventricular tachycardia, dysrhythmias, idiopathic hypertrophic subaortic stenosis, and pheochromocytoma.

Adverse events associated with beta-adrenergic antagonists include cardiovascular events such as bradycardia, heart block, congestive heart failure, hypotension and peripheral vascular insufficiency; pulmonary events such as shortness of breath, coughing, and bronchospasm; and central nervous system events such as fatigue, dizziness, depression, paresthesia, sleep disturbances, memory loss, and disorientation. Other adverse events include nausea, vomiting, diarrhea, colitis, decreased libido, sexual dysfunction, vomiting, slowed recovery from hypoglycemia, and decreased exercise dysfunction.

Contraindications include cardiovascular conditions such as bradycardia or heart block, pulmonary conditions such as bronchospasm, chronic obstructive pulmonary disease, or acute asthma. These agents should be used with caution in patients with heart failure and/or diabetes. Sudden discontinuation of these agents could lead to withdrawal reactions, so practicing clinicians should titrate down dosages over a 2-week period.

Ionotropic group of drugs

The classes of agents included in the ionotropic group of drugs include cardiac glycosides such as digitalis, digitoxin, and digoxin; phosphodiesterase inhibitors such as amrinone and milrinone; and sympathomimetics such as dopamine, dobutamine, isoproterenol, metaraminol, epinephrine and norepinephrine.

Sympathomimetic agents stimulate vasoconstriction and increase cardiac contraction. Sympathomimetic agents also target dopamine receptors, which also increases cardiac contraction and dilates renal blood vessels. Therapeutic uses of sympathomimetic agents include treatment of hypotension and cardiogenic shock associated with myocardial infarction.

Cardiac glycosides

Cardiac glycosides target the sodium/potassium pump, which maintains resting membrane potential of nerve and muscle cells of the heart. Cardiac glycosides allow for influx of calcium into myocardial cells during depolarization, which increases contraction of cardiac muscle, increases cardiac output, increases renal profusion, decreased heart rate, and decreased conduction velocity through the atrioventricular node. Therapeutically, cardiac glycosides are used to treat congestive heart failure, atrial flutter, atrial fibrillation, and paroxysmal atrial tachycardia.

Adverse events associated with cardiac glycosides include cardiovascular events such as premature ventricular contractions, dysrhythmia, and bradycardia; gastrointestinal events such as vomiting, anorexia, nausea and vomiting; central nervous system events such as changes to visual field, headaches, fatigue, confusion and depression.

Factors that can influence toxicity in patients undergoing treatment with cardiac glycosides include electrolyte imbalances such as decreased potassium levels as well as renal and hepatic insufficiency. Specifically, digitalis-related toxicities require treatment that includes decontamination, monitoring of plasma potassium levels, administration of anti-dysrhythmic agents, and digitalis antibodies.

Some drugs may decrease or increase the action of cardiac glycosides. Some specific examples include drugs that decrease effect of digoxin such as antacids, cholestyramine, neomycin, and sulfasalazine and drugs that increase effect of digoxin, such as albuterol, amiodarone, captopril, cyclosporine, diltiazem, erythromycin, nifedipine, omeprazole, tetracycline, and thyroxine.

Contraindications include ventricular tachycardia, ventricular fibrillation, atrioventricular block, idiopathic hypertrophic subaortic stenosis, myocardial infarction, and Wolff-Parkinson-White syndrome. Caution needs to be taken when administering cardiac glycosides, as their effective therapeutic dose is very close to their toxic dose.

Phosphodiesterase inhibitors

Phosphodiesterase inhibitors increase calcium levels within myocardial cells. These agents increase cardiac muscle contractions and cardiac output. However, these inhibitors have little impact on heart rate and blood pressure.

Phosphodiesterase inhibitors are typically prescribed over short periods due to a high degree of toxicity associated with these agents. They are used to treat decompensated congestive heart failure in patients who fail first line treatment approaches. Adverse events associated with phosphodiesterase inhibitors include cardiovascular events such as dysrhythmia and gastrointestinal events such as nausea, vomiting, and liver enzyme changes. Other adverse events include thrombocytopenia and bone marrow toxicity. Contraindications include aortic or pulmonary valvular disease, myocardial infarction, and ventricular dysrhythmia.

Anti-dysrhythmic group of drugs

The anti-dysrhythmic group of drugs includes 6 classes of agents and 2 additional agents. The 6 classes of agents include class IA, IB, IC, II, III and IV. Examples of class IA agents include quinidine, procainamide, moricizine, and disopyramide. Examples of class IB agents include lidocaine, tocainamide, mexiletine, and phenytoin. Examples of class IC agents include flecainide and propafenone. Examples of class II agents include propranolol, acebutolol and esmolol. Examples of class III agents include bretylium, amiodarone, ibutilide, dofetilide, and sotalol. Examples of class IV agents include verapamil and diltiazem. Other agents not categorized include digoxin and adenosine.

Adverse events associated with anti-dysrhythmic agents include cardiovascular events such as new dysrhythmia, heart block, hypotension, vasodilation, and cardiac arrest. Noncardiac events include nausea, vomiting, hypersensitivity, hemolytic anemia, tinnitus, headache, blurred vision, arthralgia, arthritis, dizziness, euphoria, perioral numbness, agitation, disorientation, paraesthesia, tremor, lightheadedness, slurred speech, seizures, bone marrow suppression, bronchospasm, photosensitivity, pulmonary fibrosis, liver enzyme dysfunction, thyroid dysfunction, constipation, lassitude, nervousness, peripheral edema, shortness of breath, flushing, and paresthesia. Specific agents within each class are more prone to certain adverse events than others, but all have potential for the above adverse events.