Definition: Shock is a state in which there is failure of the circulatory system to maintain adequate cellular perfusion resulting in widespread reduction in delivery of oxygen & other nutrients to tissues. In shock, the mean arterial pressure is less than 60 mmHg or the systolic blood pressure is less than 90 mmHg.
• Regardless of the underlying pathology, shock constitutes systemic hypoperfusion
due to reduction either in cardiac out put or in the effective circulating blood volume. The end results are hypotension followed by impaired tissue perfusion and cellular hypoxia.
• Adequate organ perfusion depends on arterial blood pressure (BP) which, in turn, depends on: 1. Cardiac output (CO) 2. Peripheral vascular resistance (PVR)
• CO = stroke volume X heart rate
In turn, stroke volume depends on: a) Preload i.e. blood volume, b) Afterload i.e. arterial resistance, & c) Myocardial contractility.
• Therefore, shock (i.e. widespread decreased perfusion of tissues) occurs when the preload (i.e. the blood volume) is decreased, or when the afterload (the peripheral vascular resistance) is decreased, or when the myocardium fails to contract. These basic mechanisms of shock are used to classify it. Next, we will look at the classification of shock.
Classification of shock
Shock can be divided into:
A. Hypovolemic shock B. Cardiogenic shock C. Distributive shock
89 A. Hypovolemic shock
Definition: This is shock caused by reduced blood volume. Reduction in circulating blood volume results in the reduction of the preload which leads to inadequate left ventricular filling, reflected as decreased left & right ventricular end diastolic volume and pressure. The reduced preload culminates in decreased cardiac out put which leads to widespread tissue perfusion (shock).
Causes of hypovolumic shock include:
a) Haemorrhage b) Diarrhoea & vomiting c) Burns d) Trauma e) etc
The effect of haemorrhage depends on the rate and amount of blood loss. Hypovolumic shock is the most common type of shock in clinical medicine .A normal healthy adult can lose 550ml (10%of blood volume) without significant symptoms.
But loss of 25% or more of the blood volume (N=1250ml) results in significant hypovolemia. B. Cardiogenic shock
Definition: This is shock that results from severe depression of cardiac performance. It primarily results from pump failure [myocardial failure].
Cardiogenic shock is hemodynamically defined as:
o DBP<60mm Hg o Left ventricle filling pressure > 18mm Hg o Cardiac index< 1.8 l/min/m2 o Usually pulmonary oedema coexists.
Causes of cardiogenic shock can be divided into:
A. Myopathic B. Mechanical
90 A) Myopathic causes of cardiogenic shock include:
1. Acute myocardial infraction. Usually shock occurs in this conditioin if ≥ 40% of the left ventricular mass & more on the right ventricle is involved by infarction. 2. Mycocarditis 3. Dilated cardiomyopathy/hypertrophic cardiomyopathy 4. Myocardial depression in septic shock 5. Etc….
B) Mechanical
i) Intracardiac
a) Left ventricle outflow obstruction E.g.Aortic stenosis, hypertrophic cardiomyopathy
b) Reduction in forward cardiac output E.g. Aortic or mitral regurgitation
c) Arrhythmia
ii) Extracardiac
This can be called obstructive shock. The extracardiac causes of cardiogenic shock can be caused by:
a) Pericardial tamponade (gross fluid accumulation in the pericardial space) results in a
decreased ventricular diastolic filling → ↓CO b) Tension pneumothorax (gas accumulation in pleural space) This decreases the venous return by creating a positive pressure.
c) Acute massive pulumonary embolism occupying 50-60% of pulumonary vascular bed.
d) Severe pulumonary hypertension (10 pulmonary hypertension).
C. Distributive shock
Definition: Distributive shock refers to a group of shock subtypes caused by profound
peripheral vasodilatation despite normal or high cardiac output.
Causes of distributive shock
1) Septic shock – the commonest among the group & clinically very important.
2) Neurogenic shock
91 - Usually occurs in the setting of anaesthetic procedure [cephalo-caudal migration of anaesthetic agent] or spinal cord injury owing to loss of vascular tone & peripheral pooling of blood.
3) Anaphylactic shock
- Initiated by generalized IgE – mediated hypersensitivity response, associated with
- This is a type of shock that typically occurs in adrenal insufficiency.
Next, we will discuss septic shock in some detail. But before discussing septic shock in detail it would be useful to know some aspects of sepsis briefly. Bactermia is the presence of viable bacteria in the blood as evidenced by blood culture. Septicemia is systemic infection due the presence of microbes and their toxin the blood. Sepsis is a systemic response to severe infection mediated via macrophage-derived cytokines that target end organ receptors in response to infection. It is also called SIRS.
Septic shock
Definition: This is a kind of shock caused by systemic microbial infection, most commonly by gram – negative infection (endotoxic shock) but can also occur with gram – positive or fungal infections.
or
It can be defined as sepsis with
1. Hypotention, arterial blood pressure less than 90mmHg or 40mmHg less than the patient’s normal blood pressure,
2. Organ dysfunction, &
3. Unresponsiveness to fluid administration.
92 Pathogenesis of septic shock:
Septic shock has a mortality rate of over 50% ranking the first among the causes of death in intensive care units. It results from the spread & expansion of an initially localized infection like pneumonia into the blood stream.
Most causes of septic shock (~70%) are caused by endotoxin-producing gram-negative
bacilli, hence the term endotoxic shock. Endotoxins are bacterial wall lipopolyschardes (LPS) released when cell walls are degraded. Analogues molecules in the walls of gram- positive bacteria & fungi can also elicit septic shock. LPS bind with CD14 molecule on leucocytes, especially monocytes & macrophages, endothelial cells & others. Depending on the dosage of LPS – protein complex, initiation of a cascade of cytokine-mediated events take place.
The mononuclear phagocytes respond to LPS by producing TNF which, in turn, induces IL – 1 synthesis. TNF & IL-1 both act on endothelial cells to produce further cytokines like IL-6, IL-8, & secondary effectors like NO & PAF (platelet aggregating factor).
• High levels of the above molecules or mediators (TNF-α, IL-1, etc…) cause septic shock by acting on:
→ The heart – causing decreased myocardial contractility which results in low cardiac output,
→ Blood vessel – causing systemic vasodilation which decreases the peripheral arteries. The mediators also cause widespread endothelial injury & activation of the coagulation system resulting in DIC, &
Uncorrected shock passes through 3 important stages:
1) An initial nonprogressive phase
o It is also called a period of early compensatory period, during which compensatory
mechanisms are activated & perfusion of vital organs maintained.
Mechanisms
o A variety of neurohumoral mechanisms operate:
i) A decrease in cardiac output will stimulate peripheral & central baro receptors with subsequent intense sympatho-adrenal stimulation. This sometimes leads to up to 200 fold increase in plasma catecholamine level. The net effect is → Tachycardia, ↑ HR → ↑ CO → Peripheral vasoconstriction → ↑ BP. This is a major autocompensatory response.
ii) The fall in renal perfusion stimulates the renin – aldosterone secretion mechanism → renal conservation of fluid.
2. Progressive stage (Established shock)
• This is characterized by tissue hypoperfusion with onset of worsening circulatory &
metabolic imbalances including acidosis. • There is a widespread tissue hypoxia. • Anaerobic gycolysis results in excessive lactic acid production. The lactic acid reduces tissue PH & blunts vasomotor response. The hypoxic cells leak glucose leading to insulin-resistant hyperglycaemia and increased glycogenolysis. Impaired carbohydrate metabolism causes a fall in production of ATP, failure in function of Na+ - K+ ATPase, result in Na & water enterance into the cell, causing cellular swelling also called sick cell syndrome. Anoxic injury to endothelial cells results in DIC.
3. An irreversible stage
• A sage at which, even if hemodynamic disorders are corrected survival is not
possible. • Transition to irreversible damage is mediated via various mechanisms.
94 Morphology of septic shock:
• All organs are affected in severe shock. In shock, there is widespread tissue hypoperfusion involving various organs such as the heart, brain, & kidney. This leads to widespread hypoxic tissue necrosis. The widespread tissue necrosis manifests as multiple organ dysfunction [MODS]. Various organs may fail to perform their normal functions. And lungs may show ARDS or Shock lung.
Clinical course of shock
• Patient with shock may manifest as having a weak and rapid pulse, tachypenia, & cool, clammy, cyanotic skin. In septic shock, the skin will initially be warm & flushed because of peripheral vasodilation. The patient may present with confusion, restlessnes, decreased urine output, coma, and death.
