Five to ten percent of patients who present with an acute myocardial infarction (MI) are in cardiogenic shock.1 Although the mortality from cardiogenic shock has decreased somewhat in the last decade, it is still greater than 50%.2 Despite the advantages of early percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG), half of the deaths occur within the first 48 hours.3 Cardiogenic shock is most often associated with a left ventricular MI and a loss of more than 40% of the myocardium. However, patients may also develop cardiogenic shock from right ventricular failure. What is cardiogenic shock? By definition, cardiogenic shock is decreased cardiac output and evidence of tissue hypoperfusion in the presence of adequate intravascular volume.1 The presence of adequate intravascular volume is important. This differentiates cardiogenic shock from other types of shock, which typically have a relative or an absolute volume deficit. With cardiogenic shock, the patient usually has enough intravascular volume it’s just not going to the right place(s) due to pump failure. These patients present with sustained hypotension defined by blood pressure less than 80 mmHg (or 90 mmHg if on pressors, inotropic agents or intraaortic balloon pump support) for greater than 30“60 minutes, a cardiac index under 1.8 liters/ minute, in the presence of a left ventricular end-diastolic pressure (LVEDP) or pulmonary capillary wedge pressure (PCWP) greater than or equal to 18 mmHg.4,5 When dealing with cardiogenic shock, think decreased forward flow because interventions must be aimed toward restoration of forward volume flow. We lose if we don’t perfuse! What causes cardiogenic shock? The major cause of cardiogenic shock is ischemic disease, both of the left and right ventricle. Valvular heart disease/dysfunction may also result in cardiogenic shock, a classic example being acute mitral insufficiency or regurgitation. Additional causes include: 1. Trauma from a myocardial contusion; 2. Cardiomyopathies: Hypertrophic, restricted, and dilated; 3. Infectious and inflammatory processes (viral myocarditis, infective endocarditis); 4. Pulmonary hypertension resulting in right ventricular failure; 5. Toxic drugs. The basic concept of cardiogenic shock is pump failure, not a surprise to anyone, but again, impaired forward flow is the key. When cardiac output decreases, the body responds with compensatory mechanisms. Catecholamines (norepinephrine and epinephrine), parasympathetic nervous stimulation, conduction disturbances, and dysrhythmias can all affect heart rate, but typically tachycardia is seen. Systemic vascular resistance (SVR) increases to tighten the arterial vascular circuit in an attempt to maintain blood pressure. But these are only temporizing measures. When caring for these patients, it helps to remember that cardiac output = stroke volume x heart rate. So unless immediate intervention is needed for a symptomatic rapid or relatively slow heart rate, efforts are aimed at increasing the stroke volume. Understanding the components of stroke volume helps direct patient management. Components of stroke volume: Preload, afterload, and contractility Preload is the amount of volume in the ventricle at end-diastolic filling.6 It is measured directly during heart catheterization via the LVEDP or indirectly measured by utilizing the PCWP. Think of preload as the end-diastolic stretch of the muscle determined by the volume of blood in the ventricle. Every heart has an optimal preload. Remember Starling’s Law: Increased stretch results in a more forceful contraction and greater stroke volume up to a physiologic limit. In other words, the muscle fiber can be stretched up to a point and result in a good contraction, but if overstretched, the contraction actually weakens and stroke volume decreases. Afterload is resistance to ventricular ejection. Increased afterload translates into increased work for the myocardium. Afterload for either ventricle is affected by several factors, the most important being vascular resistance.6 When the arterial vascular circuit constricts in an attempt to maintain pressure, afterload increases. More oxygen and energy is required for the heart to pump volume out against this increased resistance contributing to further problems for an ischemic ventricle. Afterload is clinically estimated for the right ventricle by calculating the pulmonary vascular resistance (PVR) and for the left ventricle, the systemic vascular resistance (SVR). Finally, there’s contractility. Contractility is the velocity of myocardial fiber shortening at the cellular level regardless of preload and afterload.6 It’s difficult to measure at the bedside, but one would hope to see evidence of increased contractility when adding an inotropic agent such as dopamine or dobutamine. When thinking about the hemodynamics of cardiogenic shock, keep it simple: The components of cardiac output are: Contractility, Rate, Afterload, and Preload, or CRAP. To manage these patients, you’ve got to know CRAP! (This acronym has long been passed down to many a critical care and cath lab staff and is helpful when managing cardiogenic shock). Every therapeutic intervention is aimed towards improving or altering a component of cardiac output or something in CRAP. The spiral of cardiogenic shock The underlying pathology of cardiogenic shock is profound depression of contractility resulting in a spiral of reduced CO, hypotension, further coronary insufficiency, and further reduction in contractility. Compensatory mechanisms of tachycardia and increased SVR are typically noted. However, a systemic inflammatory response (fever, elevated white count, low SVR) may also be seen.3 Patient Presentation In addition to tachycardia, patients often present with a narrow pulse pressure (PP). Pulse pressure is the difference between systolic and diastolic blood pressure and reflects stroke volume. Decreased stroke volume causes the pulse pressure to narrow (as is seen in cardiac tamponade). Signs and symptoms of hypotension are present: Weak or absent peripheral pulses; mottled extremities from low flow states; diaphoresis; and pallor. Patients may be restless with changes in level of consciousness. Remember that the kidneys are seeing a low flow state when not receiving adequate blood flow with a response of retaining volume and concentrating urine output. If left ventricular failure is present, pulmonary edema and dyspnea are hallmarks of cardiogenic shock. An extra heart sound, S-3 or a ventricular gallop, is an early sign of LV failure.5 A murmur may be appreciated as the ventricle dilates from volume overload, resulting in regurgitant flow. Murmurs may also occur with papillary muscle dysfunction from ischemia. Chest pain, which can be typical or atypical, might be present if the cause of failure is ischemic disease. If right ventricular failure is the culprit, the patient will present without pulmonary edema clear lungs and a normal to slightly raised PCWP. Persistent hypotension, elevated RA (CVP) pressure, and jugular vein distention are often noted as volume backs up from the right ventricle and forward flow declines. Suspect a right ventricular infarction in patients exhibiting these symptoms who present with an inferior wall MI. The reduction of preload (hypovolemia, diuretic use, nitroglycerin) intensifies hypotension in these individuals.5 Recording right-sided precordial leads and utilizing echocardiography assists in the diagnosis. Working the patient up (very quickly!) 1. ECG to rule out an ischemic event. If ischemic, revascularization is the key. 2. Cardiac enzymes, CBC, blood chemistries, ABGs, coagulation studies, liver function tests. 3. Correct magnesium and K levels. 4. If respiratory decompensation, intubate and support ventilations. 5. Lactate level a prognostic indicator for survival from cardiogenic shock.1 6. Echocardiogram for wall motion and valve function. 7. Hemodynamic monitoring to optimize the components of cardiac output and to obtain a mixed venous saturation. 8. Chest x-ray CRAP Optimizing Preload Does the patient have too much or too little preload? Higher filling pressures may actually be necessary in some patients, but typically those in cardiogenic shock have too much preload in the ventricle. The higher the PCWP (preload) and the lower the cardiac index, the higher the mortality.4 If too much volume is present for the heart to handle, there are the three well-recognized Ps for dealing with excessive preload: Pee the excess volume, park the excess volume, or pump it on forward! 1. Patients have pulmonary edema and high PCWP? Diurese them but avoid hypovolemia (may worsen blood pressureespecially with a RV MI). 2. Poor contractility and decreased forward flow? Pump it forward with inotropic support! 3. Pull extra volume off the heart (decrease venous return)i.e., nitroglycerin to dilate venous beds. Park the volume if blood pressure tolerates. Intravenous diuretics such as furosemide and bumetanide not only cause diuresis but also have an acute effect to increase venous capacity and decrease venous return to the heart. Morphine, in addition to decreasing pain and anxiety, also increases venous pooling.5 Even before there’s urine in the Foley bag (if you’re lucky enough to see any urine in cardiogenic shock), these drugs have already parked some excess volume. Now, pumping it forward usually means some inotropic help with dopamine, dobutamine, inamrinone, or milrinone (Inocor® and Primacor®, Sanofi-Synthelab Inc., New York, NY). CRAP Optimizing Contractility Inotropic support with a sympathomimetic agent is indicated. With low blood pressure less than 70 mmHg, norepinepherine 2 to 10 mg /kg/min would be considered.5 Norepinepherine is an alpha and beta-1 agonist, meaning it causes vasoconstriction and increases contractility and heart rate. Clinically, the alpha or vasoconstrictive properties (increases SVR) are greater than beta-1 effects, so its use should be limited for temporary stabilization if possible.4 Dopamine is a first-line inotropic agent in cardiogenic shock. It is usually initiated at 3-5 mg/kg/min and titrated up to 10 mcg/kg/min. At higher doses, dopamine provides vasopressor support. Doses greater than 10 mcg/kg/min may have undesirable effects such as tachycardia and increased pulmonary shunting along with the potential to decrease splanchnic perfusion and increase pulmonary arterial wedge pressure.1 Another inotropic agent, dobutamine, is a sympathomimetic amine with stronger beta effects than alpha effect, producing vasodilation (decreasing SVR) and increasing contractility. Dobutamine is initiated usually at 2.5-5mg /kg/min and titrated up to 10 mg/kg/min.4As it decreases SVR, it may also decrease blood pressure making it difficult to use in those with systolic pressures below 90 mmHg.5 Working via a different mechanism than dopamine and dobutamine are the phosphodiesterase inhibitors milrinone and inamrinone (formerly amrinone). These drugs have both inotropic and vasodilating effects, thus increasing stroke volume with both their contractile and afterload-reducing properties. These vasodilator effects may cause hypotensive episodes to develop and careful titration is needed. A loading dose may be given for both inamrinone and milrinone. The loading dose for inamrinone (Inocor®) is 0.75 mg/kg followed by an infusion of 5 to 10 mg/kg/min with total doses not to exceed 10 mg/kg/day.1 Milrinone (Primacor®) is approximately 15-20 times more potent than inamrinone. In addition, clinical studies have reported significantly less thrombocytopenia with milrinone as compared to inamrinone. Loading dose for milrinone is 50 mg/kg followed by a maintenance dose of 0.375-0.750 mg /kg/min.6 Careful dosing consideration of these drugs is required with hepatic and renal dysfunction. By increasing contractility, all inotropic agents increase myocardial workload and in addition, may cause tachyarrhythmias, exacerbating myocardial ischemia. CRAP Optimizing Heart Rate With cardiogenic shock, bradycardia is usually not the problem, but if present, a pacing wire may be necessary to sustain an adequate rate and output. Tachycardia is typically present and is related to sympathetic stimulation, a compensatory mechanism or may result from inotropic drug support. Increased heart rates not only decrease diastolic filling time, but also decrease coronary artery perfusion time. In addition myocardial workload is increased. Clearly, if the patient is in a lethal tachycardia or rapid supraventricular tachycardia (SVT), the rhythm will need termination. It is important to try to maintain the atrial contribution to stroke volume. Asynchrony between the atria and ventricles or the absence of atrial contraction (development of atrial fibrillation) may significantly reduce cardiac output. CRAP Optimizing Afterload It’s important to facilitate stroke volume ejection and forward flow by reducing the SVR if blood pressure permits. Some inotropic agents reduce SVR. Vasodilators such as nitroglycerin and sodium nitroprusside may also help. Intravenous nitroglycerin is a coronary vasodilator, but also tends to be at normal doses, a venodilator predominately dilating the venous bed. Nitroglycerin helps park volume. Nitroprusside, on the other hand, is a more balanced venous arterial vasodilator.6 It is often a challenge to add these drugs because of low blood pressure. As a result, these agents must be used cautiously, if at all, for besides hypotension, a reflex tachycardia may occur and coronary perfusion pressure can drop significantly. Vasodilator therapy should not be attempted in patients with systolic pressure below 90 mmHg.6 So use caution when reducing afterload in the presence of ischemic disease. Afterload reduction is also the mainstay of stabilization for acute mitral regurgitation (MR). In acute MR, blood flow is diverted back through the mitral valve. There is less resistance to flow into the lower pressure left atrium, verses forward flow out the aortic valve against arterial resistance (SVR). Forward flow out the front door (aortic valve) needs to be encouraged; therefore, therapies are targeted to reducing the SVR. The optimal mechanical afterload reducer is the intraaortic balloon pump, where a balloon is placed in the aorta distal to the subclavian artery and counterpulsates the heart. With the normal arterial waveform, the dicrotic notch signifies closure of the aortic valve closure and the beginning of diastole. Inflation of the balloon at this time augments diastolic pressure. This in turn increases coronary perfusion pressure. When the balloon deflates, aortic end-diastolic pressure decreases, making it easier for the next stroke volume to be ejected by the left ventricle. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; definitive diagnostic and therapeutic interventions (surgical repair of the valve or revascularization) need to be performed. Time is running out…. The clock is ticking when your patient is in cardiogenic shock. With a present mortality greater than 50%, there is hope it can be reduced as more patients receive early revascularization in the form of PCI or CABG. With rapid recognition of cardiogenic shock, prompt initiation of supportive measures, and immediate transport to a tertiary care center capable of intervention outcomes can be improved. Acknowledgement. Thank you to Deborah M. Winn RN, CCRN for her review of this article. Mary Dahling has over 17 years of experience in cardiovascular critical care nursing. She holds a specialty certification in critical care, and frequently lectures on cardiac topics, such as hemodynamics, 12-lead EKG interpretation, and cardiac pharmacology. She currently practices as a clinical nurse specialist for cardiac surgery for the Sentara Health System in Norfolk, Virginia. She would like to thank her numerous mentors in critical care for sharing their wisdom on CRAP and the 3 P’s. Mary can be contacted at email@example.com
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