Developinganaesthesia



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. 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

2. 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:

● Severe mitral regurgitation.

● Acute aortic regurgitation.

● Rupture of the interventricular septum.

● Large left ventricular aneurysm.

7. 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 |Mortality |

| | |(mmHg) | |

| | | | |

|I |>2 |2 |>18 |9% |

| | | | |

|III | ................
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