Vol. 8 •Issue 10 • Page 21
The Learning Scope
Condition complicates up to 9 percent of acute MIs
This offering expires in 2 years: April 24, 2008
The goal of this continuing education offering is to provide nurses with information on cardiogenic shock. After reading this article, you will be able to:
1. Define cardiogenic shock.
2. Discuss the etiology of cardiogenic shock.
3. Describe the signs and symptoms of cardiogenic shock.
4. Describe collaborative treatment.
You can earn 1 contact hour of continuing education credit in three ways: 1) For immediate results and certificate, go to www.advanceweb.com/nurses. Grade and certificate are available immediately after taking the online test. 2) Send this answer sheet (or a photocopy) along with the $8 fee (check or credit card) to ADVANCE for Nurses, Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406. Make checks payable to Merion Publications Learning Scope (any checks returned for non-sufficient funds will be assessed a $25 service fee). 3) Fax the answer sheet (available with credit card payment only) to 610-278-1426. If faxing or mailing, allow 30 days to receive certificate or notice of failure. A certificate of credit will be awarded to participants who achieve a passing grade of 70 percent or better.
Merion Publications Inc. is an approved provider of continuing nursing education by the Pennsylvania State Nurses Association (No. 011-3-H-04), an accredited approver by the American Nurses Credentialing Center’s Commission on Accreditation. Merion Publications Inc. also is approved as a provider by the California Board of Registered Nursing (No. 13230) and by the Florida Board of Nursing (No. 3298).
There are three types of shock patients may experience: hypovolemic shock, cardiogenic shock and distributive shock. Distributive shock is a catchall term that includes septic, anaphylactic or neurogenic shock. This article will focus on cardiogenic shock and the nurse’s role when caring for a patient with cardiogenic shock.
Quite simply, shock occurs when the cardiovascular system is unable to oxygenate the body’s tissues. During cardiogenic shock the heart loses approximately 40 percent of its pumping ability.
The most common etiology for cardiogenic shock is acute myocardial infarction (MI) with left ventricular failure.1 According to the National Registry of Myocardial Infarction, of almost 300,000 MIs occurring in the U.S. between 1995 and 2004, cardiogenic shock was present in 8.6 percent of the cases and the incidence has remained stable over time.1 Six to 9 percent of acute MIs are complicated by cardiogenic shock.1
In the early 1990s, a research study called the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries trial studied 41,000 patients with acute MI who were treated with thrombolytic therapy. In that study, only 0.8 percent of the patients presented with shock, and 5.3 percent developed shock after admission.1 Fifty percent of individuals who developed shock after admission to the hospital did so within the first 24 hours.
Approximately 80 percent of cardiogenic shock cases are fatal, so it is important for nurses to recognize the early signs and symptoms of cardiogenic shock, be knowledgeable about potential complications and initiate emergency treatment to prevent profound hemodynamic compromise.2 The two most important predictors of survival are early detection and early intervention.
Other Physiologic Causes
In addition to acute MI, physiologic causes of cardiogenic shock may include the following:
• cardiac trauma;
• heart failure;
• chemical inhibition of function (e.g., drugs, hypoglycemia, acid-base, electrolyte disturbance);
• acute arrhythmias;
• cardiac tamponade;
• severe heart valve dysfunction;
• papillary muscle rupture;
• massive pulmonary embolism and tension pneumothorax;
• acute mitral regurgitation or ventricular septal defect; or
The etiology or the risks to developing cardiogenic shock may include the following:
• coronary artery disease;
• chest trauma;
• postoperative cardiac surgery;
• post-percutaneous transluminal coronary angioplasty;
• post-cardiopulmonary resuscitation;
• myocardial depressants (e.g., overdoses, toxins, drugs, disease); and
Sam Smith is a 50-year-old executive. He is five feet 10 inches tall and weighs 225 lbs. (102 kg). He takes a statin for his cholesterol and an occasional over-the-counter acid reducer for what he thinks is indigestion. He does not smoke and drinks occasionally while watching sports or entertaining clients. He does not exercise regularly because he is busy with family and work.
He recently experienced intermittent bouts of chest pressure while on a business trip, but these bouts always had resolved quickly, so he dismissed them as indigestion. At home one evening, he developed chest pain that did not resolve as it usually had. He began sweating, was flushed and short of breath. His wife called 911.
When the paramedics arrived, Mr. Smith’s vitals were BP = 160/86; HR = 122; Resp = 30; pulse oximetry = 88 percent. He was started on 4 L nasal cannula, given sublingual nitroglycerin and transferred to the hospital.
Mr. Smith arrived in the ED and a 12-lead ECG confirmed he had had an anterior wall MI. He had bilateral rales about halfway up. His BP was now 80/66; HR = 142; Resp = 36; pulse oximetry = 91 percent on 4 L. An arterial blood gas (ABG) revealed respiratory alkalosis: 7.67-28-80-40.
Mr. Smith was growing more anxious by the minute. These bouts of chest discomfort had always resolved quickly, but this time was different. Mr. Smith knew something “bad” was happening. A Foley catheter was inserted, which revealed minimum urine output.
The interventional cardiologist examined Mr. Smith in the ED. As arrangements were made for an emergency cardiac angiogram with possible angioplasty, the cardiologist ordered aspirin 325 mg to be chewed and Lopressor 5 mg IVP every 5 minutes for three doses, according to the Institute for Healthcare Improvement’s 100,000 Lives Campaign – Improved Care for Acute MI. The cardiologist also ordered dopamine 10 mcg/kg/min; dobutamine 10 mcg/kg/min IV, and milrinone 50 mcg/kg IV loading dose over 10 minutes followed by 0.5 mcg/kg/min continuous IV.
The cardiologist told the nurse to monitor Mr. Smith closely for worsening cardiogenic shock. Dopamine is a positive inotrope that stimulates adrenergic and dopaminergic receptors. Higher doses produce cardiac stimulation and vasoconstriction. Dobutamine is a positive inotrope and increases cardiac output by increasing the contractile force of the heart. The patient must be observed closely, as dopamine and dobutamine can cause an increase in heart rate (beta stimulation), which may increase myocardial oxygen demands. Milrinone is a phosphodiesterase enzyme inhibitor; thus, it improves cardiac output in patients with shock. Milrinone is both a positive inotrope and a vasodilator.
Links to Cardiogenic Shock
What clinical signs and symptoms did Mr. Smith display that led the cardiologist to suspect cardiogenic shock? An anterior wall MI may indicate severe dysfunction of the left ventricle, the most common type of cardiogenic shock. Severe ischemia also can result in shock with an infarct of any size. Clinical indicators of left ventricular failure will be present. Initially, Mr. Smith’s blood pressure was 160/86, and upon arrival to the ED it was 80/66. Chest pain and anxiety may cause hypertension, which will improve with the administration of nitroglycerin, but a dramatic drop in blood pressure would not be expected as a result of the nitroglycerin alone.
A telltale symptom of cardiogenic shock is a systolic blood pressure less than 90 mmHg. Orthostatic hypotension also is common. In cardiogenic shock, hypotension results from an acute decrease in stroke volume induced by an acute MI (stroke volume x heart rate = cardiac output). Guidelines published by the American Heart Association (AHA) and the American College of Cardiology (ACC) in 2004 recommend close, frequent monitoring of blood pressure, preferably with intrarterial pressure monitoring.
Another telltale sign of cardiogenic shock is a heart rate greater than 110 bpm. Mr. Smith’s heart rate was initially 122 and subsequently elevated to 142. There is an impaired ability of the ventricle to pump a sufficient amount of blood and the body is trying to compensate any way it can. Thus, more profound tachycardia occurs as the heart thinks, “If I pump faster, I can fix this.” Needless to say, the heart cannot fix this on its own. The more it tries, the more oxygen the compromised heart requires.
It is also important to note Mr. Smith’s respiratory rate. One may suspect a slightly elevated respiratory rate due to pain and anxiety. The physiologic reason for the tachypnea is that the body is trying to improve oxygenation. The initial ABG revealed respiratory alkalosis. As the shock progresses, the body will wear out and respiratory or metabolic acidosis will be present. Bradypnea may be seen as cardiogenic shock progresses. In addition, Mr. Smith had minimum urine output, another indication of cardiogenic shock. There is decreased cardiac perfusion to the kidneys, causing increased sodium and water retention, decreased renal blood flow and decreased urine output.
In cardiogenic shock, the early clinical presentation is similar to that of acute heart failure. Patients with cardiogenic shock will have tachycardia, hypotension and a narrowed pulse pressure. Heart sounds are usually distant and a third or fourth sound may be present.
Guidelines published by the AHA and the ACC in 2004 state pulmonary artery catheterization (Swan-Ganz catheter) should be performed in patients with cardiogenic shock. The catheter will measure cardiac output, cardiac index, central venous pressure, pulmonary wedge pressure and systemic vascular resistance. In cardiogenic shock, the cardiac output will be low, less than 4 L/min. The body tries to compensate for this hypotension by increasing systemic vascular resistance to greater than 1,800 dynes/sec/cm-5, which in turn increases myocardial oxygen consumption. A Swan will reveal a low cardiac index (less than 2.1 L/min/m2) and a wedge pressure of >20 mmHg.
Patients with cardiogenic shock also exhibit tachypnea, cyanosis (late sign) and rales, which are indications blood is backing up into the lungs. Jugular vein distention also may be present if the right ventricle is compromised (e.g., inferior wall MI). A chest X-ray is likely to reveal pulmonary infiltrates. Patients will have pallor and cool, clammy extremities as blood is shunted to the vital organs. There may be decreased cerebral perfusion, which may manifest as anxiety, confusion and agitation. Physical examination will reveal decreased bowel sounds, again due to blood being shunted to the vital organs, and patients may complain of nausea or vomiting.
If the underlying reason for the cardiogenic shock is not corrected, cardiogenic shock may lead to hypovolemic shock. The goals in cardiogenic shock are to correct the underlying cause of the pump failure, increase myocardial oxygen supply, decrease myocardial oxygen demand and restore tissue perfusion.
Into the Cath Lab
Mr. Smith was taken to the cath lab for an emergency cardiac angiogram with possible angioplasty. The angiogram revealed a 90 percent occluded right coronary artery, a 90 percent left main and a 90 percent left anterior descending. During attempts at revascularization, Mr. Smith experienced profound chest pain and hypotension. An intra-aortic balloon pump (IABP) was emergently inserted and the cardiothoracic surgery team was notified of an impending emergency coronary artery bypass graft (CABG). An IABP will increase myocardial oxygen supply, decrease myocardial oxygen demand, increase blood flow to the renal arteries and lower extremities, and decrease afterload. Afterload is the pressure the heart must pump against to open the semilunar valve.
Mr. Smith was intubated and ventilated and had a three-vessel CABG. AHA and ACC guidelines of 2004 recommend CABG for patients younger than age 75 who have had an acute MI and can be treated within 18 hours of onset of shock.
Mr. Smith spent 5 days in the hospital post CABG and was discharged. He has lost weight, gets regular exercise and takes his prescribed medications. He knows he was in bad shape that fateful evening. Due to the quick action of the medical team, his outcome was positive.
Collaborative management for Mr. Smith may include:
• Maximizing oxygen delivery to the tissues. Oxygen delivery can be measured by monitoring ABGs, hemoglobin and cardiac output. Normal hemoglobin and vascular volume should be maintained. Oxygen is administered as needed and patients may need intubation and mechanical ventilation to maintain adequate oxygenation and acid-base balance.
• Optimizing cardiac contractility and cardiac output. Pulmonary artery catheter readings, ECGs and neurologic assessment can provide information about cardiac function.
• Recognizing the risks and benefits of commonly used medications such as inotropes, vasopressors, phosphodiesterase enzyme inhibitors, vasodilators, analgesics and diuretics.
• Maintaining bed rest to minimize oxygen consumption.
• Administering deep vein thrombosis/pulmonary embolism prophylaxis.
• Avoiding overheating, which may cause vasodilation.
• Correct the metabolic acidosis to improve cardiac contractility. Improving oxygenation and perfusion is the best way to treat metabolic acidosis. Sodium bicarbonate should be used sparingly.
• Treating pain and anxiety.
• Providing patient and family support.
• Attending to nutritional needs. Enteral feedings may be necessary if patient is ventilated, parenteral feedings may be necessary if enteral feedings are contraindicated (e.g., pancreatitis).
• Maintaining renal perfusion. Monitor lab work (BUN, creatinine, urine sodium, creatinine clearance); replace volume as indicated by central venous pressure.
• Recognizing and understanding the care of the patient with an IABP.
• Optimizing the care of the patient pre- and postangiogram.
• Optimizing the care of the patient pre- and post-CABG.
As the staff becomes familiar and comfortable with the complex care of the patient with cardiogenic shock, the staff can anticipate patient needs and provide early intervention, which may improve patient outcomes.
1. Menon, V., & Hochman, J. Treatment of cardiogenic shock complicating acute myocardial infarction. Retrieved April 12, 2006 from the World Wide Web: http://www.patients.uptodate.com/topic.asp?file=chd/19259
2. Medline Plus. (2004, April 30). Medical encyclopedia: Cardiogenic shock. Retrieved April 12, 2006 from the World Wide Web: http://www.nlm.nih.gov/medlineplus/print/ency/article/000185.htm
Holcomb, S.S. (2002). Helping your patient conquer cardiogenic shock. Nursing, 32(9), 32cc1-32cc6.
Mower-Wade, D.M, Bartley, M.K., & Chiari-Allwein, J.L. (2001). How to respond to shock. Dimensions of Critical Care Nursing, 20(2), 22-27.
Sharma, S. (2005). Cardiogenic shock. Retrieved April 12, 2006 from the World Wide Web: http://www.emedicine.com/med/topic285.htm
Liz Farwell is care manager and advanced practice nurse for the vascular clinic at Advocate Lutheran General Hospital, Park Ridge, IL.