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CARDIOGENIC SHOCK
William Harvey demonstrating his theory of the circulation of the blood to King Charles I.
Oil on canvas, Robert Hannah, 1848, Royal College of Physicians, London.
“…And now I may be allowed to give in brief my view of the circulation of the blood, and
to propose it for general adoption.
Since all things, both argument and ocular demonstration, show that the blood passes
through the lungs, and heart by the force of the ventricles, and is sent for distribution to all
parts of the body, where it makes its way into the veins and porosities of the flesh, and then
flows by the veins from the circumference on every side to the centre, from the lesser to the
greater veins, and is by them finally discharged into the vena cava and right auricle of the
heart, and this in such a quantity or in such a flux and reflux thither by the arteries, hither
by the veins, as cannot possibly be supplied by the ingesta, and is much greater than can be
required for mere purposes of nutrition; it is absolutely necessary to conclude that the
blood in the animal body is impelled in a circle, and is in a state of ceaseless motion; that
this is the act or function which the heart performs by means of its pulse; and that it is the
sole and only end of the motion and contraction of the heart”.
William Harvey, Chapter XIV,
“On the Motion of the Heart and Blood in Animals”, 1628
William Harvey made one of medicine’s most important discoveries when he deduced the
circulation of the blood. For almost 1500 years, no one had challenged the doctrine
established by the Roman physician Galen that venous blood “somehow” proceeded from
the liver and that arterial blood “somehow” proceeded from the heart. Exactly were it was
going seemed to be anybody’s guess. There was certainly no thought of a circulatory
motion of the blood in Galen’s theory. In his Essay on “On The Motion of the Heart and
Blood in Animals” in 1628, Harvey rejected Galen’s theories and for the first time fully
explained the circulation of the blood and the central role played in this, by the heart.
Difficult as it is to imagine now his new theory was considered very controversial at the
time. His theory threw doubt onto the common practice of bloodletting (a “standard”
medical practice by doctors from ancient times through to as recently as the Eighteenth
century.) It was only after his death that his theory became widely accepted. Harvey would
have been one of very few in the 17th century capable of understanding the 21st century
concept of cardiogenic shock.
CARDIOGENIC SHOCK
Introduction
Clinical Definition:
Cardiogenic shock is an acute impairment of myocardial contractility presenting as a
clinical syndrome of: 1
1.
2.
A low systolic blood pressure:
●
< 90 mmHg, or a value of greater than 30 mmHg below normal levels in a
hypertensive patient
●
For a period of at least 30 minutes
Together with clinical evidence of decreased tissue perfusion, (such as peripheral
vasoconstriction, altered conscious state and urine output below 20 mls / hr)
Definition based on Hemodynamic Parameters:
Cardiogenic shock may also be defined by the acute presence of all three of:
1.
Systolic pressure less than 90 mmHg.
2.
A cardiac index of less than 2.2 L / min / M2.
3.
A pulmonary capillary wedge pressure of greater than 15 mmHg.
Pathophysiology
Causes:
1.
Myocardial infarction, this is by far the commonest cause.
●
Left ventricular, when there is critical loss (> 40%) of myocardium. The
effects of recent and old infarcts will be additive. This scenario is seen with
extensive anterior infarction.
●
Right ventricular infarction. This is much less common. It is seen in
association with inferior infarcts.
2.
Drug and poison overdose.
3.
Acute decompensation in patients with cardiomyopathies.
Other causes are less common, but may include the following:
4.
Severe myocarditis.
5.
Severe myocardial contusion.
6.
Myocardial failure secondary to acute structural lesions:
7.
●
Severe mitral regurgitation.
●
Acute aortic regurgitation.
●
Rupture of the interventricular septum.
●
Large left ventricular aneurysm.
Severe outflow obstruction:
●
Aortic stenosis.
●
HOCM
Note that there are many other cardiac causes of poor cardiac output and shock that are not
due to intrinsic contractility problems. By convention these are not included in the strict
definition of cardiogenic shock. These conditions include massive pulmonary embolism,
cardiac tamponade, tension pneumothorax and arrhythmias.
Reduced myocardial contractility due to severe sepsis is defined separately as septic shock.
Prognostic Features
1.
Worse with increasing age.
2.
Underlying type and extent of pathology.
3.
Associated medical problems.
4.
A number of classifications have been developed to correlate the extent of pump
failure with eventual mortality following an AMI. They include the Killip-Kimball
and the Forrester-Diamond-Swan classifications.
The Killip-Kimball Classification (based on clinical criteria)
CLASS I
No failure
5% mortality
CLASS II
Mild failure, basal creps &
S3
15-20% mortality
CLASS III
Frank Pulmonary Edema
40% mortality
CLASS IV
Cardiogenic Shock
80% mortality
The Forrester-Diamond-Swan classifications, (based on hemodynamic parameters):
GROUP
Cardiac Index
(L/min/M2)
PAWP
(mmHg)
Mortality
I
>2
<18
3%
II
>2
>18
9%
III
<2
<18
23%
IV
<2
>18
51%
Investigations
In patients with suspected cardiogenic shock, the following investigations will be needed:
Blood tests
●
FBE
●
U&Es and glucose
●
Troponin levels.
●
ABGs
CXR
To look for:
●
Associated pulmonary edema. If the lung fields are clear consider the possibility of
a RV infarction, especially in the setting of an inferior myocardial ischemia.
●
Other associated pathology.
ECG
To establish
●
The rhythm
●
The presence of any underlying ischemia or infarction.
A normal ECG will virtually exclude a diagnosis of cardiogenic shock due to myocardial
infarction.
Anterior infarctions are much more commonly associated with cardiogenic shock than are
inferior infarctions.
If a patient appears to be in cardiogenic shock and the ECG shows an inferior infarction,
then consider the possibility of RV infarction or other complicating pathology such as
cardiac tamponade.
Echocardiography
The most important investigation, if available, is bedside echocardiography. It should
ideally be done in all cases of suspected cardiogenic shock.
It will:
●
Confirm the diagnosis of cardiogenic shock.
●
Establish the type (left versus right sided, systolic versus diastolic) and the severity
of the myocardial failure.
●
Rule out the presence of any potentially reversible “structural” causes, such as
valvular lesions, free wall ruptures or interventricular septal ruptures.
●
Help rule out other pathologies such as aortic dissection, massive PE, or cardiac
tamponade.
Management
Management steps include the following:
1.
General measures.
2.
Optimizing fluid volume status.
3.
Inotropic drug support.
4.
Mechanical supports.
5.
Specific measures.
5.
Early consultation (ICU/ cardiology)
General measures:
1.
Immediate attention to any ABC issues, especially oxygenation.
2.
Pain relief
3.
Treat any arrhythmias.
4.
Treat hyperkalemia or hypokalemia.
5.
Continuous ECG monitoring and pulse oximetry.
Optimizing fluid volume status
1.
T o monitor volume status and “central” pressures insert an IDC and CVC.
●
Insertion of a CVC should not delay inotropic support. Inotropes can be
given via a cubital fossa vein in the first instance.
●
Femoral lines can be relatively quickly placed and will also give a
reasonable estimate of central pressures.
2.
Fluid boluses can be given (100 - 250 mls) to optimize central pressures to a CVC
of 10 cm water (15 mmHg PCWP)
3.
In cases of right ventricular infarction with cardiogenic shock, fluid therapy needs
to be somewhat more aggressive (up to 30 cms of water)
Inotropic Drug Support
Options for inotropic drug support include the following:
Most commonly:
1.
Adrenaline
2.
Milrinone
3.
Noradrenaline
Inotropes will improve contractility but with the following adverse effects:
●
Tachyarrhythmias.
●
Increased myocardial oxygen demand
●
Hyperglycemia and reduce glucose tolerance
●
Lactic acidosis
●
Vasocontriction-induced reduction in organ blood flow and ischaemia
●
Aggravation of hypotension with some agents, (isoprenaline, dobutamine)
Most commonly adrenaline will be the agent of choice for acute cardiogenic shock.
If this proves insufficient then the addition of the phosphodiesterase inhibitor
milrinone should be considered.
Milrinone as well as being a good positive inotropic agent will also cause
vasodilatation and so it is usually used in conjunction with noradreanaline. Therefore
if adrenaline is not successful, it may be replaced with milnirone and noradrenaline
infusions. Milrinone is primarily used in the ICU setting.
Note that milrinone should only be commenced in the ED after discussion with ICU/
ED consultant.
Less commonly other agents may be considered, (usually after cardiology consultation):
●
Dobutamine
●
Dopamine
●
Isoprenaline
Mechanical supports
When pharmacological measures are insufficient some patients may be suitable for
mechanical cardiac supports.
These may include:
●
The intraaortic balloon pump
●
ECMO.
Mechanical support devices, of which IABP is the most commonly used, have the major
advantage compared pharmacologic agents of being able to improve coronary perfusion
and cardiac performance, while at the same time reducing myocardial ischemia and cardiac
work
Indications for the Intraaortic balloon pump device include conditions that have a
potentially reversible problem, including:
●
Coronary occlusion.
●
Severe mitral regurgitation, (AI is contra-indicated)
●
Post trauma
●
Drug overdose
●
Patient’s on a wait list or those who may be suitable for cardiac transplantation.
Specific measures
1.
By far the commonest cause of cardiogenic shock is coronary artery occlusion and
the best chance of survival is procedural intervention.
●
Although not specifically contra-indicated, thrombolytic agents have not
been shown to improve outcome in cardiogenic shock from coronary artery
occlusion.
●
Emergency PTCA or CABG surgery offer the best prognosis in acute
cardiogenic shock due to myocardial infarction.
2.
In some patients there may be a surgically correctable lesion such as severe mitral
incompetence or septum rupture.
3.
If facilities are available some patients may be suitable for emergency cardiac
transplantation.
Disposition:
Early consultation should always be sought with:
●
ICU
♥
●
Any patient with cardiogenic shock should be referred early to ICU.
Cardiology
♥
Appendix 1
Any patient with cardiogenic shock due to myocardial infarction should be
referred early to the on call cardiologist in order to plan for a possible PCI
or emergency CABGs.
Inotropic Agents
Drug/Receptor
a-1
a-2
ß-1
ß-2
ß-3
Noradrenaline ++
++
++
+
+
Adrenaline
++
++
++
++
+
Dopamine
++
?
++
+
?
Dobutamine
++
+
?
Isoprenaline
++
++
++
-
Increase:
contractility,
HR, renin
&NA.
vasodilate
coronaries
Increase HR
contractility
vasodilation
bronchodilation
Metabolic
effects
brochodilation
vasodilation
contractility
fall
Inhibit Na
reabsorption
vasodilate:
renal,
cerebral,
splanchnic.
Actions:
Vasoconstriction,
increase
Postjunctional:
contractility,
vasoconstriction
(decrease HR)
prejunctional:
decrease NA
DA-1 & 2
++
Dobutamine
●
Useful in cases of mild hypotension (systolic pressures of 80-90 mmHg)
●
Improves contractility and may reduce afterload, however may worsen hypotension
Dopamine
●
Useful in moderate hypotension (systolic pressures of 60-80 mmHg)
●
Improves contractility and with alpha effects helps raise peripheral vascular
resistance, however tachycardia may be problematic.
Isoprenaline
●
This is most useful as a chronotropic agent for patients with severe
bradyarrhythmias.
●
It has significant beta 2 effects, however which may worsen hypotension.
Adrenaline
●
Useful in cases of severe hypotension, (systolic pressures less than 60 mmHg)
●
Improves contractility and maximally improves peripheral vascular resistance and
diverts blood to vital organs.
Milrinone
●
This is a phosphodiesterase inhibitor with positive inotropic effects.
●
It has some vasodilatory effects and so is usually used in conjunction with an agent
that gives some vasoconstriction such as noradrenaline.
References:
1.
Robert M. Califf, James R. Bengtson: Cardiogenic Shock NEJM, vol 3330 no. 24.
June 16 1994.
Dr J Hayes
Dr Graeme Duke
Dr John Green.
Reviewed 23 September 2006