CARDIOGENIC SHOCK can result when an acute myocardial infarction (MI)—usually an ST-elevation MI with left ventricular failure—damages more than 40% of the myocardium.1-3 Cardiogenic shock is a clinical condition of inadequate tissue perfusion because of cardiac dysfunction and occurs when either systolic or diastolic dysfunction of the heart's pumping action results in decreased cardiac output. Other causes of cardiogenic shock include myocarditis, endocarditis, cardiomyopathy, cardiac rupture, dysrhythmias, pulmonary embolism, cardiac tamponade, and drug overdoses or poisoning with substances that affect the heart's pumping ability.
The prevalence of cardiogenic shock in patients with an acute MI is 5% to 6%.4 A higher percentage of women with an acute MI develop cardiogenic shock compared with men.5 The prolonged deficits in oxygen utilization after cardiogenic shock may lead to tissue injury and multiple organ dysfunction syndrome (MODS), which can progress to irreversible organ failure and death. This article primarily addresses the definitions of primary and secondary MODS, as well as the pathophysiology, assessment, and management of patients with MODS, and concludes with a case study and discussion of cardiogenic shock with resultant MODS.
MODS is defined as a progressive physiologic failure of two or more organ systems in acutely ill patients.6 Additionally, according to The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3), organ dysfunction can be represented by an increase of at least two points in the Sequential Organ Failure Assessment (SOFA) score, which is associated with an in-hospital mortality of more than 10%.3 This physiologic dysfunction is so severe that homeostasis cannot be maintained without nursing and medical intervention. The inability to preserve end-organ oxygenation and perfusion because of any type of shock or systemic inflammatory response syndrome (SIRS) may result in MODS.7 MODS is at the severe end of the severity of illness spectrum of both infectious (sepsis, septic shock) and noninfectious conditions (such as SIRS from pancreatitis). It is important to note the current definitions of sepsis and septic shock as follows:3,8
- sepsis: a life-threatening organ dysfunction caused by a dysregulated host response to infection
- septic shock: a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.
Two forms of MODS have been identified. Primary MODS is the result of direct injury to an organ, which then leads to impaired perfusion or ischemia to tissues. Secondary MODS is organ failure attributable to the widespread systemic inflammation that causes dysfunction in organs not involved in the initial insult.9-13 Generally, any condition, situation, and/or treatment modality can result in tissue injury and lead to MODS. Examples include pancreatitis, burns, major trauma, aspiration syndromes, multiple blood transfusions, extracorporeal circulation (cardiac bypass), autoimmune disease, eclampsia, stretch injuries, anaphylaxis, and overdose.14-17
The pathophysiology of MODS is complex and multifaceted. Decreased tissue perfusion (shock) can be caused by decreased oxygen delivery, increased oxygen consumption, or decreased oxygen utilization. As noted previously, when a widespread inflammatory response is initiated, the release of mediators, direct insult to the endothelium, and hypermetabolism occur. In addition, vascular permeability accelerates. This increase in vascular permeability permits mediators and protein to seep from the endothelium into the interstitial space. White blood cells then start to digest the foreign debris, and the coagulation cascade is activated. As a result, organ perfusion is compromised related to the development of hypotension, decreased perfusion, microemboli, and redistributed or shunted blood flow. Pulmonary signs and symptoms typically appear first with the development of acute respiratory distress syndrome (ARDS). The organ systems that commonly follow, in sequential order, are the renal system, the hepatic system, and the gastrointestinal (GI) system.18
Early recognition and management of MODS is crucial to improving the possibility of survival. When caring for a patient with acute MI resulting in cardiogenic shock, assess tissue perfusion and oxygenation. Signs of cardiogenic shock include tachycardia, arterial hypotension (persistent systolic BP below 80 to 90 mm Hg or a mean BP 30 mm Hg lower than the patient's baseline level), tachypnea, cool or pale skin, dysrhythmias, decreased mentation, low oxygen saturation (SaO2), low cardiac output (CO) (<4 L/min; normal, 4 to 8 L/min), cardiac index (CI) (<1.8 L/min/m2 without support or <2.2 L/min/m2 with support; normal, 2.8 to 4.2 L/min/m2), decreased mixed venous oxygen saturation (SvO2) (<60%; normal, 65% to 75%), increased mean pulmonary artery occlusion pressure (PAOP) (>15 mm Hg; normal, 6 to 15 mm Hg), pulmonary artery diastolic pressure (>15 mm Hg; normal, 5 to 16 mm Hg), systemic vascular resistance (SVR) (>1,500 dynes/sec/cm-5; normal, 900 to 1400 dynes/sec/cm-5), and central venous pressure (>7 mm Hg; normal, 2 to 6 mm Hg).19 Additionally, observe the patient for signs and symptoms of SIRS, which can lead to MODS.
Cardiogenic shock can activate a massive systemic inflammatory response. The immune system and the body's response to stress can cause maldistribution of circulating volume, global tissue hypoxia, and metabolic alterations that damage organs. Recognition of these abnormal findings in all hospitalized patients, particularly those at risk for developing any type of shock or MODS, is imperative.7,20
In the clinical setting, progressive abnormalities of organ-specific parameters are frequently used to diagnose MODS. These parameters include respiratory (partial pressure of oxygen [PaO2]/fraction of inspired oxygen [FiO2] mm Hg), hematology (platelet count), renal (serum creatinine or urine output), liver (serum bilirubin), cardiovascular (hypotension and vasopressor requirement), and brain (Glasgow Coma Scale [GCS} score).8
The SOFA score generates a mortality estimation in patients with MODS. It incorporates all the previously noted organ-specific parameters. Specifically, the SOFA score uses simple measurements of major organ function to calculate a severity score. These measurements include:21
- respiratory (PaO2/FiO2, mm Hg)
- cardiovascular (mean arterial pressure [MAP]; the amount of vasoactive medication necessary to prevent hypotension)
- hepatic (bilirubin level)
- coagulation (platelet concentration)
- neurologic (GCS score)
- renal (serum creatinine).
The SOFA score is calculated in the ICU 24 hours after admission then every 48 hours.21 The mean and the highest scores are most predictive of mortality. As noted previously, MODS can be identified as an acute change in total SOFA score of at least 2 points consequent to the infection (a SOFA score of 2 or higher is indicative of an overall mortality risk of approximately 10% in a general hospital population with suspected infection). Further, scores that increase by 30% are associated with a mortality of 50%.22 Clinicians need to understand that patients who present with even mild organ dysfunction can deteriorate quickly. This fact emphasizes the seriousness of clinical findings and the need for rapid and appropriate interventions.3 The SOFA assessment can be accessed on the ClinCalc.com website (https://clincalc.com/IcuMortality/SOFA.aspx).
The goals of treating a patient in cardiogenic shock are to decrease preload and afterload, improve myocardial contractility with inotropic medications, treat dysrhythmias, deliver emergency revascularization, and provide needed mechanical support with intra-aortic balloon pump (IABP) counterpulsation, ventricular assist device therapy, and/or extracorporeal membrane oxygenation. The nursing care with any of these treatments for cardiogenic shock requires extensive training.20
Pharmacotherapy for the patient in cardiogenic shock usually starts with diuretics, such as furosemide, and venous vasodilators, such as morphine, nitroprusside, and nitroglycerin. These medications help decrease preload (measured by right atrial pressure [RAP]) and afterload (measured by SVR), as well as increase CI and contractility. Dobutamine is a positive inotropic medication commonly used for the treatment of cardiogenic shock. This will improve ventricular emptying, thus decreasing filling pressures (PAOP, RAP), which then cause increases in stroke volume and CI.23
With MODS, dysfunction and the inflammatory response in one organ could trigger dysfunction in another organ. ARDS can develop, which manifests with tachypnea, hypoxemia despite receiving high levels of supplemental oxygen, bilateral pulmonary infiltrates on chest X-rays, and dyspnea. Acute kidney injury will present itself as acute tubular necrosis (ATN) with oliguria to anuria, elevated serum creatinine and blood urea nitrogen (BUN), and urinary sodium levels over 20 mEq/L (normal, approximately 20 mEq/L).23 Liver failure/dysfunction presents with increased serum ammonia and bilirubin levels, jaundice, hepatomegaly, and elevated liver enzymes. Central nervous system failure presents with cerebral ischemia or infarction characterized by confusion, psychosis, lethargy, fever, and altered level of consciousness. Intestinal failure in MODS first presents with enteral feeding intolerance and abdominal distension.
Next, patients develop hypoactive to absent bowel sounds, indicating a paralytic ileus. The hematologic system can also be affected by inadequate perfusion and oxygenation caused by MODS. The patient will develop disseminated intravascular coagulation with thrombocytopenia, coagulopathy, prolonged prothrombin time (PT), activated partial thromboplastin times (aPTT), international normalized ratio (INR) greater than 1.5, petechiae, and bleeding. Finally, the endocrine system can be affected by MODS, causing hyperglycemia and lactic acidosis with increased serum lactate levels above 4 mmol/L (normal, 0.5 to 1.5 mmol/L).20,24 (See Manifestations of SIRS and MODS.)
Support must be provided to each organ demonstrating dysfunction or failure. For pulmonary failure, mechanical ventilation is instituted. Acute renal replacement therapy will treat the acute kidney injury. To support the endocrine system and intestinal system, begin enteral nutrition as early as possible. The cardiovascular support was already mentioned.20
Nursing has an important role in preventing MODS. Interventions include implementation of measures to prevent healthcare-associated infections (HAIs) and/or ventilator-associated pneumonia (VAP). Methods to prevent VAP include proper positioning (the head of the bed should be elevated to 30 to 45 degrees unless medically contraindicated), regular oral care, maintaining normal endotracheal tube (ETT) cuff pressures, and drainage of subglottic secretions that pool above the ETT cuff. In addition, sedation vacations (interrupting sedation daily to assess readiness to extubate) are used to decrease ventilator days and help decrease the risk of VAP. Other nursing interventions to prevent HAIs including central line-associated bloodstream infections, catheter-associated urinary tract infections, and surgical site infections, are also important.23,25,26
Unfortunately, there is no definitive treatment for MODS other than supportive care (increasing CO), as noted previously. Medical management focuses on correcting hemodynamic and metabolic derangements. Research has shown that MODS has a high mortality that appears to be decreasing. In general, the greater the number of organ failures, the higher the mortality, with the greatest risk being associated with respiratory failure requiring mechanical ventilation.8,27,28
Mortality from MODS with failure of two organ systems is approximately 54%, and compounds considerably to 100% when five or more organ systems have failed.27 This is thought to reflect the interdependence of organ systems and the systemic nature of MODS. However, research suggests that early identification of patients with a high probability of developing MODS and early normalization of lactate levels, SaO2, base deficit, and pH lead to decreased inpatient mortality.7,10,13,23,24,29
Case study and discussion
MK, a 92-year-old woman, arrived in the ED with ECG changes indicating an ST segment elevation anterior and lateral wall MI. Her symptoms began approximately 20 hours before coming to the hospital. She was taken to the cardiac catheterization lab for a percutaneous transluminal coronary angioplasty (PTCA) and stent placement to the left anterior descending and left circumflex artery. She was hypotensive at 82/45 mm Hg. As a result, IABP counterpulsation was initiated. On admission to the coronary care unit (CCU), her vital signs were: temperature, 98.6° F (37.0° C) orally; heart rate (HR), 136 beats/min; respiratory rate (RR), 30 breaths/min; and BP, 80/42 mm Hg. MK was started on dopamine and norepinephrine I.V. infusions to help maintain a MAP greater than 60 mm Hg. Additionally, she was started on a dobutamine infusion to increase myocardial contractility.
During her admission assessment, MK was asked if she wanted “full code status” with endotracheal intubation, cardiac compressions, dialysis, blood products, additional vasopressors, and more. She said, “I don't want to die. Do anything you need to do to save my life.” MK was never married, and her nephew held power of attorney for healthcare. She made it through the night, and the nurse who admitted her the evening before again asked if she wanted to be put on a ventilator in case she became hypoxemic and needed additional oxygen. MK's response was the same. IABP counterpulsation continued, and her dopamine and norepinephrine I.V. infusions were at the maximum rate advised. Her BP was 78/40 mm Hg and SaO2 87% on a 100% high-flow mask. The day-shift nurse called MK's nephew and informed him that his aunt needed to be placed on a mechanical ventilator. He responded that he knew his aunt wanted everything done to save her life. MK was endotracheally intubated and placed on mechanical ventilation on assist/control (AC) with RR, 16; tidal volume (TV), 560 cc; positive end-expiratory pressure (PEEP), 5 cm H2O; and FiO2, 60%. Her arterial blood gas results were pH 7.28; PaCO2, 60 mm Hg; HCO-3, 20 mEq/L; and PaO2, 58 mm Hg.
MK survived another night on enteral nutrition, vasopressors, IABP counterpulsation, and mechanical ventilation. Her urinary output was never adequate after she was placed on the ventilator. Her hourly urinary output was 10 to 15 mL on her third day in the CCU. MK's kidneys were failing with a BUN of 65 mg/dL and a creatinine of 8.3 mg/dL. She was then placed on continuous renal replacement therapy (CRRT) for anuria and acute kidney injury. MK's neurologic status was very poor because of her hypotension and inadequate cerebral perfusion. Without sedation, she had a GCS score of 3. Her pupils were dilated with a sluggish response to light. Her cardiac rhythm was now sinus bradycardia. An echocardiogram showed large areas of akinesis and an ejection fraction of 5% to 10% (normal, 55% to 70%). The nursing staff was unable to maintain a MAP of more than 60 mm Hg. Her ventilator setting on AC was now RR, 16; TV, 650 cc; PEEP, 10 cm H2O; and FiO2, 80%. On her fourth day in the CCU, MK's bloodwork showed evidence of liver dysfunction/failure with a high ammonia level, elevated liver enzymes, and abnormal coagulation profile.
MK's nephew had not been in to see her, so her changes in medical status were communicated to him via telephone. Again, he supported the wishes of his aunt in wanting to continue all medical interventions.
The next day, MK had no bowel sounds and over 250 mL of gastric residual. The resident was informed that her enteral nutrition was turned off as a result of her physical assessment by the CCU nurse. The resident ordered a portable abdominal flat plate. The radiologist called the resident and informed him that it appeared MK had free air in the abdomen and evidence of bowel infarction. The resident consulted a general surgeon to assess MK for abdominal surgery to remove the portion of infarcted bowel and assess and repair the bowel perforation. The general surgeon came to the CCU to assess MK for surgery. He refused to operate on her, stating that she was critically ill with MODS and surgery would result in an intraoperative death. With that information, the nurse caring for MK called her nephew and asked him to come see his aunt to discuss further treatment options.
The nephew arrived later that day and talked to the nurse, resident, and cardiologist about MK's condition. The nephew then gave consent to discontinue all supportive therapy. Upon stopping the vasopressors, IABP counterpulsation, CRRT, and mechanical ventilation, MK died within 4 minutes after being extubated. The nurse caring for MK provided emotional support to the nephew.
MK had cardiogenic shock that progressed to lung failure, kidney failure, neurologic failure, liver failure, and GI failure. The interprofessional team had done everything possible to save MK's life, but she was unable to survive MODS. When five or more organ systems fail, MODS has a mortality of 100%.29,30 MK's rapid decline in health status calls attention to the fact that nurses may be confronted with the fact that when treating a patient with MODS, implementing ongoing interventions may sometimes be futile. As such, it is important for the nurse to maintain communication between the interprofessional team and the patient's caregiver regarding realistic goals and likely patient outcomes. Withdrawal of life support and initiating end-of-life care may be the best option for some patients.
Nurses must realize that a patient with any type of shock is at risk for developing MODS. If MK had come to the ED sooner, she may have had a different outcome. Had she come to the hospital and been taken to the cardiac catheterization lab sooner and undergone percutaneous coronary intervention, the area of myocardial necrosis would have been less. She may have avoided developing cardiogenic shock altogether and never developed respiratory failure and the MODS cascade. Her advanced age and decreased function of her immune system were other challenges affecting the outcome.
The clinical sequence and development of MODS is contingent on a combination of genetic and acquired factors. There are numerous nonspecific therapies for the avoidance and resolution of MODS. However, the primary management for a patient with MODS is supportive until the organs begin to function again or organ failure causes the death of the patient.
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