CARDIOGENIC

SHOCK

Sparsh Goel
77
INTRODUCTION
The defining feature of ‘shock’ is a level of oxygen
delivery that fails to meet the metabolic requirements
of the tissues.

‘Shock’ is not synonymous with hypotension , which is

often a late manifestation.
WHAT IS CARDIOGENIC
SHOCK?
• Cardiogenic shock is defined as hypoperfusion
due to inadequate cardiac output or , more
technically , a cardiac index of <2.2 l/min/m2.

• Cardiac index is a haemodynamic parameter that relates

the cardiac output (CO) from left ventricle in one minute
to body surface area (BSA), thus relating heart
performance to the size of the individual. The unit of
measurement is litres per minute per square metre
(L/min/m2).
CAUSES
Common causes of cardiogenic shock :-

• Myocardial infarction
• Acute massive pulmonary embolism
• Acute valvular pathology
• Cardiac tamponade
• Ventricular septal defect
• Endocarditis of mitral valve
MYOCARDIAL INFARCTION
• Shock in acute MI is due to left ventricular dysfunction
in more than 70% of cases.
• Severe myocardial systolic dysfunction causes a fall in
cardiac output, BP and coronary perfusion pressure.
• Diastolic dysfunction causes a rise in left ventricular end-
diastolic pressure, pulmonary congestion and oedema,
leading to hypoxaemia that worsens myocardial
ischaemia.
• This is further exacerbated by peripheral
vasoconstriction. These factors combine to create the
downward spiral of cardiogenic shock.
Acute massive pulmonary
embolism
• This may complicate leg or pelvic vein thrombosis and
usually presents with sudden collapse.
• Bedside echocardiography may demonstrate a small,
underfilled , vigorous LV with a dilated RV; it is
sometimes possible to see thrombus in the right
ventricular outflow tract or main pulmonary artery.
• CT pulmonary angiography usually provides a
definitive diagnosis.
Cardiac Tamponade
• This is due to a
collection of fluid
or blood in the
pericardial sac,
compressing the
heart; the effusion
may be small and is
very occasionally
less than 100 mL.
Valvular Heart Disease
• The clinical diagnosis of
acute valvular
dysfunction is sometimes
difficult. Murmurs are
often unimpressive
because there is usually a
tachycardia and a low
cardiac output.
• Transthoracic
echocardiography will
establish the diagnosis in
most cases.
Patient presentation
• Cardiogenic shock is diagnosed after documentation of
myocardial dysfunction and exclusion of alternative
causes of hypotension, such as hypovolemia,
hemorrhage, sepsis, pulmonary embolism, pericardial
tamponade, aortic dissection, or preexisting valvular
disease.
• Shock is present if evidence of multisystem organ
hypoperfusion in the presence of hypotension is detected
upon physical examination (systolic blood pressure < 90
mm Hg, cardiac index < 2.2 L/min/m2, and  the
presence of normal or elevated pulmonary capillary
occlusion pressure [>15 mm Hg].
Characteristics of patients with
cardiogenic shock.
• Anxiety, restlessness, altered mental state due to
decreased blood flow to the brain and subsequent hypoxia.

• Low blood pressure due to decrease in cardiac output.

• A rapid, weak, thready pulse due to decreased

circulation combined with tachycardia.

• Cool, clammy, and mottled skin (cutis marmorata) due to

vasoconstriction and subsequent hypoperfusion of the skin.

• Distended jugular veins due to increased jugular venous

pressure.
• Oliguria (low urine output) due to inadequate blood
flow to the kidneys if the condition persists.

• Rapid and deeper respirations (hyperventilation) due to

sympathetic nervous system stimulation and acidosis.

• Fatigue due to hyperventilation and hypoxia.

• Absent pulse in fast and abnormal heart rhythms.
• Pulmonary edema, involving fluid back-up in the lungs
due to insufficient pumping of the heart.
• A systolic murmur is generally heard in patients with
acute mitral regurgitation or ventricular septal rupture.
The associated parasternal thrill indicates the presence of
a ventricular septal defect.

• The systolic murmur, which becomes louder upon

Valsalva and prompt standing, suggests hypertrophic
obstructive cardiomyopathy (idiopathic hypertropic
subaortic stenosis).
INVESTIGATIONS
• Complete blood count
• A complete blood count (CBC) is generally helpful to
exclude anemia. A high white blood cell (WBC) count
may indicate an underlying infection, and the platelet
count may be low because of coagulopathy related to
sepsis.
• Biochemical profile
• Measurement of routine biochemical parameters, such as
electrolytes, renal function (eg, urea and creatinine
levels), and liver function tests (eg, bilirubin, aspartate
aminotransferase [AST], alanine aminotransferase [ALT],
and lactate dehydrogenase [LDH]), are useful for
assessing proper functioning of vital organs.
Cardiac enzymes
• The diagnosis of acute myocardial infarction (MI) is
aided by a variety of serum markers, which include
creatine kinase (CK) and its subclasses, troponin,
myoglobin, and LDH.

Arterial blood gases

• Arterial blood gas values indicate overall acid-base
homeostasis and the level of arterial blood oxygenation.
(Acidosis can have a particularly deleterious effect on
myocardial function.)
Lactate
• An elevated serum lactate level is an indicator of shock.
Serial lactate measurements are useful markers of
hypoperfusion and are also used as indicators of
prognosis. Elevated lactate values in a patient with signs
of hypoperfusion indicate a poor prognosis; rising lactate
values during resuscitation portend a very high
mortality rate.
Electrocardiogram
An electrocardiogram helps establishing the exact diagnosis
and guides treatment, it may reveal:
• Abnormal heart rhythms, such as bradycardia (slowed
heart rate).
• Myocardial infarction (ST-elevation MI, STEMI, is
usually more dangerous).
• Signs of cardiomyopathy.
Echocardiography
• Echocardiography may show poor ventricular function,
signs of PED, rupture of the interventricular septum, an
obstructed outflow tract or cardiomyopathy.
MANAGEMENT
Circulatory support
The primary goals are to:
• Restore global oxygen delivery by ensuring adequate cardiac
output.
• Maintain an MAP that ensures adequate perfusion of vital
organs. The target pressure will be patient specific, depending
on pre-morbid factors (e.g. hypertension or coronary artery
disease), and may range from 60 to 90 mmHg.

• The first objective is to ensure that an ‘appropriate’

ventricular preload is restored, initially by adequate
volume resuscitation. Vasoactive drugs may then have to be
considered.
• Therapeutic options to optimise
cardiac function
If the cardiac output is inadequate and myocardial
contractility is poor, the available treatment options are to:

• Reduce afterload. Reduction can be achieved by using an

arteriolar dilator (e.g. nitrates).

• Increase preload. If there is significant impairment of

myocardial contractility, giving fluids to increase filling
pressures will only produce a small increase in stroke
volume and cardiac output, and risks precipitating
pulmonary oedema.
• Improve myocardial contractility. An inotrope may
be required to ensure adequate cardiac output and
peripheral blood flow sufficient to secure adequate
oxygen delivery.

• Control heart rate and rhythm.

PROGNOSIS
• If the precipitating cause and accompanying circulatory
failure are dealt with promptly, before significant organ
failure occurs (‘early’ shock), the prognosis is good. If
not, there is progressive deterioration in organ function
and MOF ensues (‘late’ shock).