Cardiogenic shock patients are brought to the emergency room presenting with a spectrum of signs and symptoms that represents a different phase of the clinical condition, from inciting event to end stage organ failure.

The following system wise presentation of signs and symptoms are commonly seen in cardiogenic shock and its inciting events:

• General Appearance: Patients in shock usually appears ashen or cyanotic because of the progressive hypoperfussion state of the tissues. 
• Integumentary: The skin will appear cold to touch because of peripheral tissue hypoperfusion. 
• Head and Neck: Jugular venous distention may be evident due to the increased a cardiac compliance. 
• Chest and heart: Complains of chest heaviness of pain may herald the inciting event of MI. Heart sounds will appear distant and fast (tachycardia) upon auscultation due to cardiac tamponade or overload. The presence of the 3rd and 4th heart sounds due to valvular dysfunction may also be heard. Heavy breathing may also ensue as a compensatory mechanism to overcome the hypoxemia. 
• Abdomen: The urine output will be low because of renal hypoperfusion during shock.
• Extremities: The peripheral pulses will appear rapid or faint due to the drop of blood pressure. Irregular pulses may also be felt with arrhythmias. 
• Neurologic: Patients may also present with altered mental status due the brain’s hypoxic states.

Cardiogenic shock often presents as an emergency and they are diagnosed clinically by their characteristic sign and symptoms. The following diagnostic tests are also performed with patients suffering of cardiogenic shock:

• Blood Pressure Monitoring: Patients in frank shock will present with very low blood pressure reading. 
• Electrocardiogram (ECG): This test makes use of electrodes that are attached to the chest to determine the electrical activity of the heart. Ischemic heart muscle does not conduct electrical impulse thus acute heart attacks can be diagnosed using this test.
• Chest X-ray: Imaging will reveal the size of the heart and its vessels. This will also show lung congestion in patients with heart attacks.
• Blood tests: This tests will evaluate the kidneys and the liver status of the patient. This can also check for possible infections of the heart. Arterial blood gas can demonstrate acidosis and hypoxemia states.
• Echocardiogram: This imaging modality makes use of sound waves to scan the heart walls and point out which part of the heart wall is no longer pumping.
• Coronary angiogram (catheterization) – This is an invasive technique that makes use of a long slender tube inserted in the femoral arteries where a dye is injected to exactly show which cardiac artery is blocked during the attack. Cardiac catheterization can be used to repair the vessel using inset balloons or mesh in a procedure called angioplasty. 

Patients in cardiogenic shock usually come in the emergency room illegible for advanced life support like ventilators, continuous oxygenation and intravenous access for medications. Some patients may require medications to increase blood flow through the heart and improve the heart pump muscles. The following medications are usually used in cardiogenic shock and heart attacks:

• Aspirin
• Thrombolytic
• Anti-platelets
• Anti-coagulants
• Inotropic agents
• Beta-blockers and renin-angiotensin-aldosterone inhibitors [7]

Invasive medical approach to cardiogenic shock includes: Angioplasty, stenting, and balloon pumps [8]. Where medical approach are futile, the following cardiovascular procedures may be done in cardiogenic shock:

•  Coronary Artery Bypass Graft (CABG) surgery [9]
•  Surgical repair of the heart
•  Heart pumps – Ventricular assist devices (VAD) [10]
•  Heart transplant

The mortality rate of patients with cardiogenic shock among myocardial infarction patients is very high and despite expert medical care at 50-60% [4].

The key to the survival of cardiogenic shock patients in ischemia or infarction of the heart is the rapid identification of the clinical disease, prompt fluid resuscitation, and immediate coronary artery revascularization [5]. The demonstration of a right ventricular dilatation and infarction by voltage in an electrocardiogram confers a poor outcome among patients [6].

Complications

When cardiogenic shock is left unmitigated, the following complications may arise as a result:

• Liver damage
• Kidney failure
• Brain damage
• Cardiac damage
• Cardio-pulmonary arrest
• Cardiac dysrhythmia
• Ventricular aneurysm
• Thromboembolic problems
• Death

Cardiogenic shock occurs when the heart becomes dysfunctional and is unable to keep up with the body’s needs. The most common causes are serious cardiac complications that occur during a myocardial infarction, the most common etiology includes:

• Cardiac standstill where a large section of the cardiac wall is unable to move
• Cardiac rupture due to increased myocardial damage
• Heart dysrhythmias like ventricular tachycardia and ventricular fibrillation
• Pericardial tamponade
• Cardiac valve prolapse
• Cardiac septal tear
• Symptomatic bradycardia 
• Systolic dysfunction
• Diastolic dysfunction
• Coronary artery disease
• Acute coronary syndromes due to beta-blockers and angiotensin-converting enzyme inhibitors [2] 

In the United States, the incidence of cardiogenic shock among heart attack patients ranges from 5% to 10%. Although, a community-wide analysis done in the Worcester Heart Attack study conveyed an average of 7.5% incidence of cardiogenic shock during heart attacks [3].

In ST-elevation myocardial infarction (STEMI), cardiogenic shock occurs in 8.6% of patients. In Europe, relative incidence of cardiogenic shock averages at 7% among MI cases. The Hispanic race has the highest mortality rate for cardiogenic shock reaching a 74% level. There is a male predisposition of cardiogenic shock mortality of up to 58%.

Cardiogenic shock represents an acute deterioration of the heart pump muscle affecting up to 40% of the left ventricular muscle function. Heart conditions that leads to this state includes myocardial infarction, myocardial ischemia, advanced cardiomyopathy, acute myocarditis, uncontrolled arrhythmia, and valvular dysfunction.

The cardiac muscle pathophysiology is based on the hypoperfusion state of the heart muscle causing an increased cardiac demand but poor cardiac output. This vicious cycle pattern leads to cardiogenic shock and gives rise to its characteristic symptoms. The prolonged tissue hypoperfusion will lead to anaerobic glycolysis and the accumulation of lactic acid which results in intracellular acidosis.

The acidotic state will breakdown the lysosomes and cause myonecrosis of the heart muscles at the site of ischemia or infarction. In some cases of myocardial hypoperfusion, the heart muscle becomes stunned or hibernates into a reversible state of functionality where it may resume to function normally after adequate revascularization to the heart muscle happens.

The dysfunctional left ventricle in the myocardial infarction or ischemia will increase its diastolic filling end-pressure, the diminished state of cardiac compliance will lead to the accumulation of the blood in the lungs and presents with pulmonary congestion. The diminished blood flow to the brain may lead to cortical signs of confusion, altered state of sensorium, agitation and flaccid coma.

The most effective way to prevent the occurrence of a cardiogenic shock is to directly prevent the occurrence of a heart attack that causes it. The following lifestyle modifications are done to prevent a heart attack:

• Active control of hypertension
• Watch your weight
• Quit smoking
• Regular cardio exercises
• Healthy eating
• Lower daily stress

Cardiogenic shock is a clinical condition where the heart as a pump is no longer able to perfuse the tissues adequately which causes significant hypoxia in the presence of adequate blood volume. Cardiogenic shock is the most common cause of death in acute myocardial infarction (MI) despite advances in medical care [1].

Cardiogenic shock is considered as a rare and fatal physiologic state caused by heart dysfunction at systole. There is usually a sustained form of hypotension occurring below 90 mmHg for at least 30 minutes, a reduced cardiac index of less than 2.2 l/min/m2, and increase in capillary wedge pressure of more than 15 mmHg. Tissue hypoxemia is clinical seen as cyanosis, oliguria, altered sensorium and cool extremities.

Definition

Cardiogenic shock is a medical condition wherein the heart is no longer capable to pump effectively and preserve adequate tissue perfusion.

Cause

Cardiac standstill, cardiac rupture, tamponade, dysrhythmias, Valvular diseases, and ventricular septal defects may cause cardiogenic shock.

Symptoms

Patients may appear with altered mental state, blue or purple coloration of the skin or mucous membranes, chest pain, low output of urine and thread-like pulses. 

Diagnosis

History and physical examination is the mainstay in emergency diagnosis. This may be augmented with ECG, Chest X-ray and Echocardiogram.

Treatment and follow-up

Advanced cardiac life support, blood thinning medications, inotropic agents. Surgical options include coronary artery by-pass surgery and heart transplant surgery.

1. Dubey L, Sharma S, Gautam M, Gautam S, Guruprasad S, Subramanyam G. Cardiogenic shock complicating acute myocardial infarction. Acta Cardiol. 2011; 66(6):691-9 (ISSN: 0001-5385)
2. Al-Reesi A, Al-Zadjali N, Perry J, Fergusson D, Al-Shamsi M, Al-Thagafi M, et al. Do beta-blockers reduce short-term mortality following acute myocardial infarction? A systematic review and meta-analysis. CJEM. May 2008; 10(3):215-23.
3. Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. Apr 15 1999; 340(15):1162-8.
4. Buerke M, Lemm H, Dietz S, Werdan K. Pathophysiology, diagnosis, and treatment of infarction-related cardiogenic shock. Herz. 2011; 36(2):73-83 (ISSN: 1615-6692)
5. Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA. Jul 27 2005; 294(4):448-54
6. Hamon M, Agostini D, Le Page O, Riddell JW, Hamon M. Prognostic impact of right ventricular involvement in patients with acute myocardial infarction: meta-analysis. Crit Care Med. Jul 2008; 36(7):2023-33.
7. van Diepen S, Reynolds HR, Stebbins A, Lopes RD, Džavík V, Ruzyllo W, Geppert A, Widimsky P, Ohman EM. Incidence and outcomes associated with early heart failure pharmacotherapy in patients with ongoing cardiogenic shock. Crit Care Med. 2014; 42(2):281-8 (ISSN: 1530-0293)
8. Thiele H, Schuler G, Neumann FJ, Hausleiter J, Olbrich HG, Schwarz B, Hennersdorf M, Empen K, Fuernau G. Intraaortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock: design and rationale of the Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial. Am Heart J. 2012; 163(6):938-45 (ISSN: 1097-6744)
9. Hochman JS, Sleeper LA, White HD, Dzavik V, Wong SC, Menon V, et al. One-year survival following early revascularization for cardiogenic shock. JAMA. Jan 10 2001; 285(2):190-2.
10. Basra SS, Loyalka P, Kar B. Current status of percutaneous ventricular assist devices for cardiogenic shock. Curr Opin Cardiol. 2011; 26(6):548-54 (ISSN: 1531-7080)