Cardiogenic Shock

Cardiogenic Shock:



‘Shock’ is used to describe the clinical syndrome that
develops when there is critical impairment of tissue
perfusion
due to some form of acute circulatory failure.
There are numerous causes of shock,. The important features and causes  of acute heart failure or cardiogenic shock are described here.

Myocardial infarction
Shock in acute MI is due to left ventricular dysfunction
in more than 70% of cases. However, it may also be due
to infarction of the RV and a variety of mechanical complications,
including tamponade (due to infarction and
rupture of the free wall), an acquired ventricular septal
defect (due to infarction and rupture of the septum) and
acute mitral regurgitation (due to infarction or rupture
of the papillary muscles).
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.
Hypotension, oliguria, confusion and cold clammy
peripheries are the manifestations of a low cardiac output,
whereas breathlessness, hypoxaemia, cyanosis and
inspiratory crackles at the lung bases are typical features
of pulmonary oedema. A chest X-ray may reveal signs of pulmonary congestion when
clinical examination is normal. If necessary, a Swan–
Ganz catheter can be used to measure the pulmonary
artery wedge pressure to guide fluid replacement. The
findings can be used to categorise patients with acute
MI into four haemodynamic subsets. Those
with cardiogenic shock should be considered for immediate
intra-aortic balloon counterpulsation and coronary
revascularisation.
The viable myocardium surrounding a fresh infarct
may contract poorly for a few days and then recover.
This phenomenon is known as myocardial stunning and
means that acute heart failure should be treated intensively
because overall cardiac function may subsequently
improve.

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 sometimes < 100 mL. Sudden deterioration
 may be due to bleeding into the pericardial
space. Tamponade may complicate any form of pericarditis
but can be due to malignant disease. Other causes
include trauma and rupture of the free wall of the myocardium
following MI.
An ECG may show features of the underlying disease,
such as pericarditis or acute MI. When there is a large pericardial
effusion, the ECG complexes are small and there
may be electrical alternans: a changing axis with alternate
beats caused by the heart swinging from side to side
in the pericardial fluid. A chest X-ray shows an enlarged
globular heart but can look normal. Echocardiography
is the best way of confirming the diagnosis
and helps
to identify the optimum site for aspiration
of the fluid.

Prompt recognition of tamponade is important because
the patient usually responds dramatically to percutaneous
pericardiocentesis or surgical drainage.

Valvular heart disease:
Acute left ventricular failure and shock may be due to
the sudden onset of aortic regurgitation, mitral regurgitation
or prosthetic valve dysfunction.
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; however, transoesophageal
echocardiography is sometimes required, especially in
patients with prosthetic mitral valves.
Patients with acute valve failure usually require cardiac
surgery and should be referred for urgent assessment
in a cardiac centre.
Aortic dissection may lead to shock by causing aortic
regurgitation, coronary dissection, tamponade or blood
loss.

While hypotension is a sinister development and
requires urgent attention, it is often a late manifestation
of circulatory failure or shock, and also the cardiac
output and oxygen delivery may be critically low even
though the BP remains normal. The problem should
be identified and treated before the BP falls. Objective
markers of tissue oxygen delivery, such as base deficit,
blood lactate and urine output, may aid earlier identification
of shock.
The causes of circulatory failure or ‘shock’ may be categorised
as either low flow (reduced stroke volume)
or low
peripheral arteriolar resistance (vasodilatation), which are
the primary presenting circulatory abnormalities.
Low stroke volume
• Hypovolaemic: any condition provoking a major
reduction in blood volume, e.g. internal or external
haemorrhage, severe burns, salt and
water depletion.
• Cardiogenic: severe mechanical impairment, e.g.
myocardial infarction, acute mitral regurgitation.
• Obstructive: obstruction to blood flow around the
circulation, e.g. major pulmonary embolism, cardiac
tamponade, tension pneumothorax.
Vasodilatation
• Septic/SIRS: infection or other causes of a systemic
inflammatory response that produce widespread
endothelial damage with vasodilatation,
arteriovenous shunting, microvascular occlusion,
capillary leak and tissue oedema.
• Anaphylactic: inappropriate vasodilatation triggered
by an allergen (e.g. bee sting), often associated with
endothelial disruption and capillary leak.
• Neurogenic: caused by major brain or spinal
injury which disrupts brain-stem and neurogenic
vasomotor control.
Clinical assessment and complications
Clinical features depend upon the primary pathophysiological
abnormality (p. 178). Hypovolaemic,
cardiogenic and obstructive causes of circulatory failure
produce the ‘classical’ image of shock with cold
peripheries, reduced or absent peripheral pulses, weak
central pulses and evidence of a low cardiac output.
In early haemorrhagic shock, a narrowed pulse pressure,
i.e. a raised diastolic (DBP) and reduced systolic
(SBP) such as 105/95 mmHg, indicates the combination
of hypovolaemia (reduced stroke volume, hence
SBP) and activation of the sympathetic nervous system,
with noradrenaline (norepinephrine)-induced
vasoconstriction raising the DBP.
In contrast, septic shock and anaphylactic shock are
usually associated with warm peripheries, bounding
pulses and features of a high cardiac output. The BP
pattern is again distinctive. In the early stages, peripheral
vasodilatation results in a low DBP, but since the
left ventricular afterload is reduced, stroke volume and
hence systolic BP are maintained, e.g. 115/42 mmHg.
These patients are usually warm peripherally. However,
in more advanced septic or anaphylactic shock, SBP falls
and the peripheries become cool. This is usually due to
the hypovolaemia associated with capillary leak and
will respond to fluid resuscitation. If it does not, it is
possible that myocardial depression is present.
Neurogenic shock often results in vasodilated
hypotension with a paradoxically slow heart rate.

All forms of shock require early identification and
treatment because, if inadequate regional tissue perfusion
and cellular dysoxia persist, multiple organ
failure
(MOF) will develop. Early institution of invasive
haemodynamic
monitoring  is recommended.
Prognosis
If the precipitating cause and accompanying circulatory
failure (hypotension and frequently severe hypovolaemia
due to venodilatation and fluid loss through the
leaky vascular endothelium) 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).
The mortality of MOF is high and increases with the
number of organs that have failed, the duration of organ
failure and the patient’s age. Failure of four or more
organs is associated with a mortality > 80%.