Cardiogenic Shock


Article Author:
Ateet Kosaraju


Article Editor:
Ofek Hai


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
1/25/2019 11:07:30 PM

Introduction

Cardiogenic shock is defined as a primary cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion. Clinical criteria include a systolic blood pressure of less than or equal to 90 mm Hg for greater than or equal to 30 minutes or support to maintain systolic blood pressure less than or equal to 90 mm Hg and urine output less than or equal to  30 mL/hr or cool extremities. Hemodynamic criteria include a depressed cardiac index (less than or equal to 2.2 liters per minute per square meter of body surface area) and an elevated pulmonary-capillary wedge pressure (greater than 15 mm Hg).

Cardiogenic shock is a clinical entity characterized by a low cardiac output state of circulatory failure that results in end-organ hypoperfusion and tissue hypoxia. The most common cause of cardiogenic shock is acute myocardial infarction, though other disorders leading to impairment of the myocardium, valves, conduction system or pericardium also can result in cardiogenic shock. Despite advances in reperfusion therapy and mechanical circulatory support treatments, morbidity and mortality among patients with cardiogenic shock remain high.[1][2][3]

Etiology

Cardiogenic shock can be caused by various forms of cardiac dysfunction. [4][5]

The most common causes of cardiogenic shock include:

  • Acute myocardial ischemia 
  • Mechanical defect: Acute mitral regurgitation (papillary muscle rupture), ventricular wall rupture (septal or free wall), cardiac tamponade, left ventricular outflow obstruction (hypertrophic obstructive cardiomyopathy [HOCM], aortic stenosis [AS]), Left ventricular inflow obstruction (MS, atrial myxoma)
  • Contractility defect: Ischemic and non-ischemic cardiomyopathy, arrhythmias, septic shock with myocardial depression, myocarditis
  • Pulmonary embolus (right ventricular with or without left ventricular failure)
  • Right ventricular failure
  • Aortic dissection
  • Other causes include cardiotoxic drugs (doxorubicin), medication overdose (beta/calcium channel blockers), metabolic derangements (acidosis), electrolyte abnormalities (calcium or phosphate)

Epidemiology

The incidence of cardiogenic shock is in decline which can be attributed to increased rates of use of primary PCI for acute MI. However, approximately 5% to 8% of STEMI and 2% to 3% of NON-STEMI cases can result in cardiogenic shock. This can translate to 40,000 to 50,000 cases per year in the United States.[6][7]

Cardiogenic shock has a higher incidence in the following classes of patients:

  • Elderly population
  • Patient population with diabetes
  • Prior history of left ventricular injury
  • Female gender

Pathophysiology

The pathophysiology of cardiogenic shock is complex and not fully understood. Ischemia to the myocardium causes derangement to both systolic and diastolic left ventricular function, resulting in a profound depression of myocardial contractility. This, in turn, leads to a potentially catastrophic and vicious spiral of reduced cardiac output and low blood pressure perpetuating further coronary ischemia and impairment of contractility. Several physiologic compensatory processes ensue. These include:

  • The activation of the sympathetic system leading to peripheral vasoconstriction which may improve coronary perfusion at the cost of increased afterload, and
  • Tachycardia which increases myocardial oxygen demand and subsequently worsens myocardial ischemia.

These compensatory mechanisms are subsequently counteracted by pathologic vasodilation that occurs from the release of potent systemic inflammatory markers such as interleukin-1, tumor necrosis factor a, and interleukin-6. Additionally, higher levels of nitric oxide and peroxynitrite are released, which also contribute to pathologic vasodilation and are known to be cardiotoxic. Unless interrupted by adequate treatment measures, this self-perpetuating cycle leads to global hypoperfusion and the inability effectively meet the metabolic demands of the tissues, progressing to multiorgan failure and eventually death.

History and Physical

The presenting symptoms of cardiogenic shock are variable. The most common clinical manifestations of shock such as hypotension, altered mental status, oliguria and cold, clammy skin can be seen in patients with cardiogenic shock.

History plays a very important role in understanding the etiology of the shock and thus helps in the management of the cardiogenic shock.

The patient should also be assessed for cardiac risk factors:

  • Diabetes mellitus
  • Tobacco smoking
  • Hypertension
  • Hyperlipidemia
  • A family history of premature coronary artery disease
  • Age older than 45 in men and older than 55 in women
  • Physical inactivity

Physical examination findings in patients with cardiogenic shock include the following:

  • Altered mental status, cyanosis, cold and clammy skin, mottled extremities
  • Peripheral pulses are faint, rapid and sometimes irregular if there is an underlying arrhythmia
  • Jugular venous distension
  • Diminished heart sounds, S3 or S4, may be present, murmurs in the presence of valvular disorders such as mitral regurgitation or aortic stenosis
  • Pulmonary vascular congestion may be associated with rales 
  • Peripheral edema may be present in the setting of fluid overload

Evaluation

Rapid diagnosis with prompt supportive therapy and coronary artery revascularization plays a vital role in achieving good outcomes in patients with cardiogenic shock.[8][9]

Diagnostic evaluation of cardiogenic shock includes the following:

  • Complete blood picture, comprehensive metabolic panel, magnesium, phosphorous, coagulation profile, thyroid-stimulating hormone
  • Arterial blood gas
  • Lactate
  • Brain natriuretic peptide
  • Cardiac enzyme test
  • Chest x-ray
  • Electrocardiogram
  • Two-dimensional Echocardiography
  • Ultrasonography to guide fluid management
  • Coronary angiography

Treatment / Management

Cardiogenic shock is an emergency requiring immediate resuscitative therapy before the irreversible damage of vital organs. Rapid diagnosis with prompt initiation of pharmacological therapy to maintain blood pressure and to maintain respiratory support along with reversal of underlying cause plays a vital role in the prognosis of patients with cardiogenic shock.[10][4][11]

Early restoration of coronary blood is the most important intervention and is the standard therapy for patients with cardiogenic shock due to myocardial infarction.

The management of the cardiogenic shock involves the following:

Medical Management

The goal of medical management is to restore cardiac output and prevent irreversible end-organ damage rapidly.

  • The optimal choice of vasoactive agent in cardiogenic shock is unclear.
  • Norepinephrine is preferred over dopamine in patients with severe hypotension (systolic blood pressure less than 70 mm Hg) or hypotension unresponsive to other medication as dopamine has been associated with higher rates of arrhythmias and a higher risk of mortality in this patient population. However, norepinephrine should be used with caution as it can cause tachycardia and increased myocardial oxygen demand in patients with recent myocardial infarctions.  
  • Dobutamine is widely used, has beta-1 and beta-2 agonist properties, which can improve myocardial contractility, lower left ventricular end-diastolic pressure and increased cardiac output
  • Milrinone, also a widely used inotrope, has been shown to reduce left ventricular filling pressures,  
  • Saline or lactated ringer solution greater than 200 ml per 15 to 30 minutes is indicated in patients with no signs of fluid overload.
  • Fibrinolytic therapy should be administered to patients who are unsuitable candidates for either percutaneous coronary intervention or coronary artery bypass graft, if there are no contraindications. 
  • Patients with myocardial infarction or acute coronary syndrome are given aspirin and heparin. They have been shown to be effective in reducing mortality.
  • Diuretics such furosemide play a role in decreasing plasma volume and edema and thereby decreasing cardiac output and blood pressure. This is associated with a compensatory increase in peripheral vascular resistance. With continuous therapy, extracellular fluid and plasma volumes return almost to pretreatment levels.
  • Therapeutic hypothermia is established for out-of-hospital cardiac arrest patients with shockable rhythm to prevent brain injury and improve survival.

Procedures

  • Central line placement plays a role in fluid resuscitation, access for multiple infusions, and allows invasive monitoring of central venous pressure.
  • Arterial line placement is useful in providing continuous blood pressure monitoring especially in patients requiring inotropic agents
  • Mechanical ventilation is indicated in patients with cardiogenic shock for oxygenation and airway protection.

Percutaneous Coronary Intervention and Coronary Artery Bypass

  • Primary percutaneous coronary intervention (PCI) should be performed, irrespective of time delay from the onset of myocardial infarction
  • Urgent coronary artery bypass grafting is indicated in patients with coronary anatomy not amenable to PCI.

SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial data confirmed an approach that combines early revascularization with medical management in patients with cardiogenic shock is optimal.

Mechanical Circulatory Support

Due to poor prognosis associated with cardiogenic shock, medical therapy is often inadequate and mechanical circulatory support (MCS) therapy to improve end-organ perfusion may be required. Evaluation for MCS should be performed by an experienced multidisciplinary team.

  • Percutaneous circulatory assist devices provide superior hemodynamic support compared with pharmacologic therapy; this is particularly apparent for the Impella and Tandem-Heart devices.
  • Intra-aortic balloon pumps can be considered but are less likely to provide benefit compared to other MCS devices and should not be routinely used but may still play an important role in patients with acute severe mitral regurgitation, ventricular septal defects, or when other MCS devices cannot be placed.
  • Extracorporeal membrane oxygenation (ECMO) is indicated in patients with poor oxygenation not expected to rapidly improve with alternative temporary mechanical support devices.
  • In appropriately selected patients not likely to recover from cardiogenic shock without long-term MCS support, a ventricular assist device can be implanted as a bridge to recovery, bridge to bridge, bridge to transplant, or destination therapy.
  • Cardiac transplantation may be performed in suitable candidates not expected to recover after MCS device implantation and may be the only hope for meaningful long-term recovery. However, it remains a very limited option owing to the low number of available hearts.

Palliative Care in Cardiogenic shock

  • Early referral to a palliative care specialist is recommended as a strategy to reduce physical and emotional distress, optimize symptom control and improve quality of life.

Differential Diagnosis

  • Septic shock
  • Shock due to hemorrhage
  • Myocarditis
  • Pulmonary embolism

Enhancing Healthcare Team Outcomes

Cardiogenic shock is a life-threatening disorder and is the main cause of death after an acute MI. Even in the best of hands and the latest treatment, the condition carries a mortality rate in excess of 30%. The key to survival is to have prompt resuscitation with coronary artery revascularization. Unfortunately, even with revascularization, multiorgan failure is common, and the long-term survival is not guaranteed. Because cardiogenic shock affects almost every other organ in the body, the condition is best managed by a multidisciplinary team that also includes ICU nurses. Even though cardiogenic shock cannot be entirely prevented, patients must be educated on reducing risk factors for heart disease. Patients should be urged not to smoke, lower the lipids and ensure better control of blood sugars. In addition, enrollment in an exercise program can help lower body weight and help achieve better control of the blood pressure.[12][13] (Level V)


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Cardiogenic Shock - Questions

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Which is false about cardiogenic shock?



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A 72-year-old male is admitted to the intensive care unit with dyspnea, crackles, and chest pain. His blood pressure is 70/40 mmHg, and he has a third heart sound. His cardiac enzymes are elevated. Which is not true of this disorder?



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A 73 year old is seen in the ER with chest pain. After insertion of a pulmonary catheter, the following parameters are obtained. Blood pressure 75/45, Pulse 120, Pulmonary Capillary Wedge Pressure 27, Systemic Vascular Resistance 1900 dynes sec cm and a central venous pressure of 13. What would the shock be categorized as?



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A 63-year-old is seen in the emergency department with chest pain. After placement of a Swan-Ganz catheter, the following parameters are obtained. The blood pressure is 70/40, Pulse 125, Pulmonary Capillary Wedge Pressure 28 (H, normal is 10-14), Systemic Vascular Resistance 2000 dynes sec cm (normal is 800-900) and a central venous pressure of 12. How would the shock would be categorized?



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Which statement is false regarding the treatment of cardiogenic shock?



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A patient who develops cardiogenic shock must have at least what percentage of his left ventricle infarcted?



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A patient in the intensive care unit has a mixed venous oxygen saturation of 55%. His hemodynamics reveal a cardiac index of less than 1.7, a blood pressure of 100/64 mm Hg, and a heart rate of 110 beats per minute. His Pa02 is 90 on an FIO2 of 50%. His hematocrit is 31%. Which of the following is most appropriate next step in this patient's management?



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A patient presents with a blood pressure of 70/40, a pulse of 135, a pulmonary capillary wedge pressure of 27, a CVP of 11, and a systemic vascular resistance of 2000 dynes sec cm. The hemodynamic profile of the patient suggests which of the following shock states?



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Which of the following agents may have some usefulness in the setting of cardiogenic shock?



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What is the most common cause of cardiogenic shock?



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What kind of shock is most likely seen in a 67-year-old with a myocardial infarction?



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Which of following is commonly seen in cardiogenic shock?



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What is the approximate mortality rate of cardiogenic shock associated with an acute myocardial infarction?



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Why is dopamine preferred over dobutamine for the treatment of post-myocardial infarction cardiogenic shock?



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A previously healthy 37-year-old male develops acute chest pain associated with dyspnea. He has no cardiac risk factors and denies illicit drug use. His condition deteriorates, and he develops cardiogenic shock. Electrocardiogram demonstrates ST elevation in the lateral leads and repolarization abnormalities. Cardiac enzymes are elevated. Select the most important diagnostic test.



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What is the first-line agent used to treat hypotension secondary to cardiogenic shock?



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Which of the following is an inotropic agent used in the treatment of cardiogenic shock?



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Which is used for a patient in cardiogenic shock?



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Cardiogenic shock is the most common complication of which of the following?



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Which of the following are causes of cardiogenic shock?



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Which test is most helpful in diagnosing the cause of cardiogenic shock in neonates?



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What management is inappropriate for patients who develop acute onset of pulmonary edema status post myocardial infarction 12 hours ago?



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A 62-year-old smoker presents with severe chest pain. He is vomiting, tachypneic, and diaphoretic. His vitals are HR 110, RR 32, Sp02 78%, BP 80/40 mmHg, and temperature 98.6 degrees Fahrenheit. An EKG shows an anterior wall STEMI. On bedside echo, he has an estimated EF < 15%. Which of the following therapies would be contraindicated?



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What is the advantage of using dopamine to treat cardiogenic shock?



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A patient with cardiogenic shock has an intra-aortic balloon placed. The transthoracic echocardiogram reveals an akinetic lateral wall. A dobutamine echocardiogram shows an increase in regional wall thickness. What is the best management for this patient?



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A 65-year old is in the ICU following a myocardial infarct. The next day his urine output and blood pressure drop significantly and he is requiring massive doses of inotropes. To develop cardiogenic shock, a patient must have at least what percent of his left ventricle infarcted?



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Which is not involved in the definition of cardiogenic shock?



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Cardiogenic Shock - References

References

Rab T,Ratanapo S,Kern KB,Basir MB,McDaniel M,Meraj P,King SB 3rd,O'Neill W, Cardiac Shock Care Centers: JACC Review Topic of the Week. Journal of the American College of Cardiology. 2018 Oct 16     [PubMed]
Maeda K,Takanashi S,Saiki Y, Perioperative use of the intra-aortic balloon pump: where do we stand in 2018? Current opinion in cardiology. 2018 Nov     [PubMed]
Kalmanovich E,Audurier Y,Akodad M,Mourad M,Battistella P,Agullo A,Gaudard P,Colson P,Rouviere P,Albat B,Ricci JE,Roubille F, Management of advanced heart failure: a review. Expert review of cardiovascular therapy. 2018 Oct 3     [PubMed]
Ginwalla M,Tofovic DS, Current Status of Inotropes in Heart Failure. Heart failure clinics. 2018 Oct     [PubMed]
Saleh M,Ambrose JA, Understanding myocardial infarction. F1000Research. 2018     [PubMed]
El Sibai R,Bachir R,El Sayed M, Outcomes in Cardiogenic Shock Patients with Extracorporeal Membrane Oxygenation Use: A Matched Cohort Study in Hospitals across the United States. BioMed research international. 2018     [PubMed]
Mohananey D,Smilowitz N,Villablanca PA,Bhatia N,Agrawal S,Baruah A,Ali MS,Bangalore S,Ramakrishna H, Trends in the Incidence and In-Hospital Outcomes of Cardiogenic Shock Complicating Thyroid Storm. The American journal of the medical sciences. 2017 Aug     [PubMed]
Gaubert M,Resseguier N,Thuny F,Paganelli F,Cautela J,Pinto J,Ammar C,Laine M,Bonello L, Doppler echocardiography for assessment of systemic vascular resistances in cardiogenic shock patients. European heart journal. Acute cardiovascular care. 2018 Aug 20     [PubMed]
Braile-Sternieri MCVB,Mustafa EM,Ferreira VRR,Braile Sabino S,Braile Sternieri G,Buffulin de Faria LA,Sbardellini BC,Vianna Queiroz CO,Braile DM,Zotarelli Filho IJ, Main Considerations of Cardiogenic Shock and Its Predictors: Systematic Review. Cardiology research. 2018 Apr     [PubMed]
Santucci A,Cavallini C, [Which role today for intra-aortic balloon counterpulsation?] Giornale italiano di cardiologia (2006). 2018 Oct     [PubMed]
Bonello L,Delmas C,Schurtz G,Leurent G,Bonnefoy E,Aissaoui N,Henry P, Mechanical circulatory support in patients with cardiogenic shock in intensive care units: A position paper of the     [PubMed]
Singh P,Lima FV,Parikh P,Zhu C,Lawson W,Mani A,Jeremias A,Yang J,Gruberg L, Impact of prior revascularization on the outcomes of patients presenting with ST-elevation myocardial infarction and cardiogenic shock. Cardiovascular revascularization medicine : including molecular interventions. 2018 Oct 15     [PubMed]
Garan AR,Malick WA,Habal M,Topkara VK,Fried J,Masoumi A,Hasan AK,Karmpaliotis D,Kirtane A,Yuzefpolskaya M,Farr M,Naka Y,Burkhoff D,Colombo PC,Kurlansky P,Takayama H,Takeda K, Predictors of Survival for Patients with Acute Decompensated Heart Failure Requiring Extra-Corporeal Membrane Oxygenation Therapy. ASAIO journal (American Society for Artificial Internal Organs : 1992). 2018 Oct 9     [PubMed]

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