In this article, we will discuss the Clinical Features and Pathogenesis of Cardiogenic Shock. So, let’s get started.
Clinical Features and Pathogenesis
Irrespective of the cause of cardiogenic shock, it is characterized by a vicious circle of severe myocardial (systolic and diastolic) dysfunction. Systolic dysfunction results in fall in cardiac output, BP and thereby coronary perfusion pressure falls. Hypotension, oliguria, confusion or altered mental state, tachypnea, tachycardia and cold, clammy extremities are the manifestations of low output state or acute circulatory failure. Diastolic dysfunction on the other side of cycle causes a rise in CVP, left ventricular end-diastolic pressure, rise in PCWP, pulmonary congestion and edema, leading to hypoxia which further worsens the myocardial ischemia. Breathlessness, orthopnea, PND, cyanosis, cough, hemoptysis, hypoxia, perspiration and inspiratory crackles at the bases of the lungs, S3 and S4 gallops are features of acute pulmonary edema.
A systemic inflammatory response syndrome (SIRS) may accompany large infarction and shock. Inflammatory cytokines and excess nitric oxide may contribute to genesis of cardiogenic shock. Severe acidosis (lactic acidosis) reduces the efficacy of catecholamines and provoke arrhythmias. A Swan-Ganz catheter can be used to measure the pulmonary artery wedge pressure which is >18 mmHg.
Untreated or refractory shock leads to multiple organ dysfunction, e.g. heart, brain, lungs, kidney and liver.
Older patients mostly females, prior MI, diabetes and extensive anterior MI (EF<30%) are at increased risk of cardiogenic shock.
In this article, we will discuss various Causes of Cardiogenic Shock. So, let’s get started.
1. Following myocardial infarction
(a) Involvement of critical muscle mass (>40%) and/or refractory arrhythmias (80%)
(b) Mechanical complications of AMI (acute myocardial infarction)
- Acute mitral regurgitation due to rupture of papillary muscle or chordae tendineae of 6-7%
- Acquired Acquired ventricular septal defect (3-4%)
- Left ventricular free wall rupture/tamponade
- Ventricular aneurysm
2. Severe valvular lesions
- Severe aortic (stenosis/regurgitation) or mitral (stenosis/regurgitation) valve disease
- Left ventricular outflow tract obstruction
- Obstructive cardiomyopathy
3. Extracardiac obstructive causes
- Pericardial effusion with tamponade (1-1.5%)
- Massive pulmonary embolism
- Severe pulmonary hypertension (primary or Eisenmenger)
- Severe restrictive cardiomyopathy
4. Inflammatory/infectious myocardial disease
- Severe myocarditis
- Acute endocarditis with myopathic or valvular involvement
5. Severe myocardial depression
- Septic shock
- Acidosis or alkalosis
- Drugs, e.g. beta-blockers, calcium channel blockers, anaesthetics and anti-arrhythmics
- Post-cardiac arrest, post-cardiotomy
6. End stage of myocardial disease
7. Traumatic, e.g. pericardial, myocardial or valvular injuries.
In this article, we will discuss the Criteria of Cardiogenic Shock. So, let’s get started.
Criteria of Cardiogenic Shock
1. Systolic BP <90 mmHg or >60 mmHg fall below baseline level.
2. Cardiac index <2.2 L/min/m2. It is calculated by cardiac output divided by body surface area. Normal cardiac index is 2.6-4.2 (L/min/m2).
3. Left ventricular filling pressure or pulmonary capillary wedge pressure >18 mmHg; and pulmonary edema is usually present.
Transthoracic echocardiography (TTE): It is a non-invasive technique, provides same information as PCWP and CVP. It also differentiate hypovolemic shock (LV filling pressure is low but contractility is preserved) from cardiogenic shock (LV filling pressure is high but contractility is low/decreases). These hemodynamic parameters with clinical evidence of peripheral circulatory failure (e.g. altered mental state, cold clammy skin and oliguria with urine output <20 ml/hr) constitute clinical syndrome of cardiogenic shock.