Cardiogenic shock pathophysiology

Cardiogenic Shock Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Cardiogenic shock from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Cardiogenic shock pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Cardiogenic shock pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Cardiogenic shock pathophysiology
CDC on Cardiogenic shock pathophysiology
Cardiogenic shock pathophysiology in the news
Blogs on Cardiogenic shock pathophysiology
Directions to Hospitals Treating Cardiogenic shock
Risk calculators and risk factors for Cardiogenic shock pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which results in the insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues. It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that do not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg. Despite the many possible causes for this cadiac failure, the most common is left ventricular failure in the setting of myocardial infarction. In the presence of cardiogenic shock develops a pathological cycle in which the ischemia, the initial aggression, leads to myocardial dysfunction. This will affect parameters like the cardiac output, stroke volume and myocardial perfusion thereby worsening the ischemia. The body will then initiate a series of compensatory mechanisms, such as heart sympathetic stimulation and activation of the renin/angiotensin/aldosterone system, trying to overcome the cardiac aggression, however, this will ultimately lead to a downward spiral worsening of the ischemia. Inflammatory mediators, originated in the infarcted area, will also intervene at some point causing myocardial muscle depression decreasing contractility and worsening hypotension. Lactic acidosis will also develop, resulting from the poor tissue perfusion, that causes a shift in the metabolism to glycolysis, which will also depress the myocardium, thereby worsening the clinical scenario.

Pathophysiology

The most common insult for cardiogenic shock is left ventricular pump failure in the setting of acute myocardial infarction. It usually takes a considerable area of infarcted myocardium (around 40%) to lead to cardiogenic shock, nevertheless, a smaller infarct may also originate this condition in a patient with a previously compromised ventricle function. However, there may also be other etiologies, other parts of the circulatory system may contribute, either alone or in combination, with inadequate compensation, or additional defects for this shock of cardiac origin, such as:

• Systolic Left Ventricular Dysfunction - acute myocardial infarction, CHF, Cardiomyopathy, Coronary artery bypass grafting, Myocarditis, Myocardial contusion and Hypophosphatemia
• Diastolic Left Ventricular Dysfunction - Ischemia
• Obstruction of Left Ventricular Outflow, with Increased Afterload - Aortic stenosis, Hypertrophic Cardiomyopathy, Coarctation of the Aorta and Malignant Hypertension
• Reversal of flow into the left ventricle - Acute aortic insufficiency and endocarditis
• Inadequate left ventricular filling due to mechanical causes - Tamponade and pulmonary embolism
• Inadequate left ventricular filling due to inadequate filling time - Tachycardia and tachycardia-mediated cardiomyopathy
• Conduction abnormalities - Atrioventricular block and sinus bradycardia
• Mechanical defect - VSD and left ventricle free wall rupture
• Right ventricular failure - Pulmonary embolism and hypoxic pulmonary vasoconstriction

Luckily many of these abnormalities are fully or partially reversible. This justifies the fact that most of the survivors have good chances of having a good outcome and living with considerable quality of life, assuming that they follow their physician's orders.

The Pathophysiologic "Spiral" of Cardiogenic shock

The pathologic process begins with myocardial ischemia leading to an abnormal function of the cardiac muscle. This abnormality worsens the initial ischemia, which then deteriorates even further the ventricular function, creating the so called downward spiral. When ischemia reaches a point that the left ventricle myocardium fails to pump properly, parameters like stroke volume and cardiac output will therefore decrease. The pressure gradient produced between the pressure within the coronary arteries and the left ventricle, along with the duration of the diastole, dictate myocardial perfusion. This will be compromised by the hypotension and the tachycardia, worsening the myocardial ischemia and the perfusion of other vital organs. The fact that the heart is the only organ that benefits from a low blood pressure, as afterload decreases, makes these hemodynamical changes both beneficial and detrimental. The pump failure will then decrease the ability to push the blood out of the ventricle, thereby increasing the ventricular diastolic pressures. This will not only reduce the coronary perfusion pressure, as it will also increase the ventricle wall stress, so that the myocardial oxygen requirements will also raise, consequently propagating the ischemia.

Other important reference to make in the setting of cardiac pump failure and hypoperfusion of the peripheral tissues is that this last one leads to the release of catecholamines. Catecholamines such as norepinephrine, will increase the heart's contractility and peripheral blood flow, by causing constriction of arterioles, together with angiotensin II, to maintain perfusion, however, this will also increase the heart's oxygen demand and have proarrhythmic and myocardiotoxic consequences. The increased SVR coupled with the low cardiac output will lead to an even more pronounced reduction in tissue perfusion.

The ischemia generated by all these processes increases the diastolic stiffness of the ventricle wall and this, along with the left ventricular dysfunction, will increase the left atrial pressure. The increased left atrial pressure will propagate through the pulmonary veins, generating pulmonary congestion, which by decreasing oxygen exchanges, leads to hypoxia. The hypoxia will further worsen the ischemia of the myocardium and the pulmonary congestion will propagate its effect through the pulmonary arteries to the right ventricle, hence jeopardizing its performance. Once myocardial function is affected, the body will put in motion compensatory mechanisms to try to increase the cardiac output. These include:

• Tachycardia and increased contractility through sympathetic stimulation
• Activation of the renin/angiotensin/aldosterone system, leading to fluid retention and consequently increased preload

However, these compensatory mechanisms eventually become maladaptive seeing that:

• Tachycardia and increased contractility will increase cardiac muscle oxygen demand, thereby exacerbating the initial ischemia;
• Vasoconstriction, as a response to impaired cardiac output, in order to try to maintain coronary artery perfusion and systemic blood pressure (SVR), increases myocardial afterload, leading to an impairment in myocardial performance and an increase in its oxygen demand, worsening ischemia;
• The activation of the neurohormonal cascade will promote retention of water and sodium, in order to compensate for the hypotension and improve perfusion, yet this will also exacerbate pulmonary edema.

The prolonged systemic hypoperfusion and hypoxia will cause a shift in cellular metabolism, prioritizing glycolysis, leading to a state of lactic acidosis, which jeopardizes contractility and systolic performance, thereby affecting the previously described system. All these factors affecting oxygen demand and cardiac performance create a vicious cycle that if not interrupted, may eventually lead to death. The therapeutic approach to cardiogenic shock focuses in disrupting this cycle.

References

Template:WikiDoc Sources