SHOCK

JASHANPREET SINGH BALLAGAN

ROLL NO- 1437

MD-4

SHOCK Is generalized reduced perfusion ( hypoperfusion) of

tissues with blood - which results in impaired oxygenation of tissues.

Occurs due to: Reduced cardiac output Reduced blood volume Reduced vascular tone

Resulting in: hypotension impaired tissue perfusion cellular hypoxia multiple organ failure.

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SHOCK

Is final common pathway for many lethal conditions: Example:

Severe hemorrhage Large myocardial infarction Pulmonary embolism Sepsis (e.g.bacterial infection)

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TYPES OF SHOCK

1. Hypovolemic2. Cardiogenic3. Septic (endotoxic) shock4. Neurogenic5. Anaphylactic shock

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HYPOVOLEMIC SHOCK Due to excessive blood or fluid loss.

Hemorrhage: MCC of hopovolemic shock Loss of >20% of the blood volume (~1000 ml) results

in shock. Excessive fluid loss is seen in:

Excessive sweating, diarrhea, severe burns and excessive vomiting.

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PATHOGENESIS

1. Decreased Cardiac output (CO): Due to decreased volume of blood.

2. Increased total peripheral resistance (TPR): due to vasoconstriction of arterioles from catecholamines

and angiotensin II which are released in response to decreased CO.

3. Decreased left ventricular end diastolic volume (LVEDV).

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4.Decreased Mixed venous oxygen content: Best indicator of tissue hypoxia Indicates the degree of extraction of O2 from the blood

delivered to tissue In hypovolemic shock decreased blood flow through

microcirculation leads to increased extraction of O2 from the blood and a decreased MVO2

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Clinical findings: Cold clammy skin

from vasoconstriction of skin vessels Hypotension (decreased CO) Rapid, weak pulse (compensatory response to

decreased CO). Treatment:

IV fluids and whole blood.

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CARDIOGENIC SHOCK Due to myocardial pump failure, due either

to:1.damage to cardiac muscle2.extrinsic pressure3.obstruction to outflow.

Clinical examples Myocardial infarction Arrhythmia Cardiac tamponade Pulmonary embolism

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THROMBUS

Coronary artery

Heart: Gross changes

Area of INFARCTION

CARDIOGENIC SHOCK Most commonly after acute myocardial infarction. Findings:

Decreased CO : due to decreased force of contraction in LV.

Increased LVEDV**: blood accumulates in the left ventricle.

Increased PVR: same mechanism as in hypovolemic shock.

Decreased MVO2:Same mechanism as in hypovolemic shock

Clinical findings: similar to those in hypovolemic shock.

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NEUROGENIC SHOCK Due to sudden widespread loss of vasomotor

tone in venules and small veins (vasodilation) vessel volume increases pooling of blood

decreased venous return to heart decreased CO

Examples: Fainting Spinal cord injury

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ANAPHYLACTIC SHOCK IgE mediated type 1 hypersensitivity response Characterized by vasodilation & increased vascular

permeability due to release of histamine from mast cells.

Could be seen following a bee sting, hornet sting or intravenous administration of certain drugs.

SYMPTOMS- Difficulty breathing, Difficulty swallowing, anxiety, Nasal congestion, Nausea,itchiness, Swelling of the face, eyes, or tongue.

Treatment is subcutaneous injection of epinephrine.

SEPTIC SHOCK Most common type of shock with highest mortality.Due to overwhelming microbial infection

Gram negative septicemiaGram positive septicemiaFungal sepsis

Most cases caused by endotoxin producing gram-negative bacteria (usually E.coli) therefore, also k/a Endotoxic shock*

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SEPTIC SHOCK Common Causes of septic shock:

E.coli sepsis from indwelling urinary catheter most common cause

of septic shock. Urinary retention

secondary to prostate hyperplasia also common cause. Spread of localized infection to blood stream:

E.g. an abscess, pneumonia

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SEPTIC SHOCK

Pathogenesis Endotoxins are component of cell wall of gram negative

bacteria Are lipopolysacchrides (LPS) Released when bacterial cell wall is degraded. Endotoxins bind to CD14 receptor on WBC and endothelial

cells causing toxic shock syndrome.

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SEPTIC SHOCK : PATHOGENESIS

1. Activation of alternative complement pathway Result: release of C3a and C5a (vasodilation and

neutrophil chemotaxis)2. Direct injury to endothelial cells:

Result : release of chemical mediators NO (vasodilator) and PG I2 (vasodilator).

3. Macrophage release of IL-1/TNF: Result:

Fever, sleep, increased release of thromboplaastin and NO

Increased neutrophil adhesion to Endothelial cells (e.g. increased neutrophils in pulmonary capillaries) 17

PATHOPHYSIOLOGY Vasodilation results in

1. Initial increase in CO: Due to rapid flow through dilated arterioles

causing increased return to heart.2. Increased MVO2:

Tissue unable to remove oxygen because of increased blood flow through microcirculation tissue hypoxia

3. Decreased Peripheral vascular resistance (PVR): Due to vasodilation of peripheral arterioles

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SEPTIC SHOCK Clinical features

Warm skin: from vasodilation of skin vessels.

Bounding pulse due to Increased CO

Acute respiratory distress syndrome : due to neutrophil emigration into alveoli.

Disseminated intravascular coagulation: due to activation of intrinsic and extrinsic coagulation system.

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SEPTIC SHOCK: DIFFERENCES FROM OTHER TYPES

In septic shock patient has Warm rather than cold skin Increased CO Increased mixed venous oxygen content (MVO2):

tissue cannot extract oxygen from increased flow rate.

Decreased PVR

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SHOCK: RESULTS Multiple organs get damaged:

Kidney: acute tubular necrosis due to hypoxia causing renal failure.

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Pathogenesis of acute tubular necrosis

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SHOCK: RESULTS Brain:

Ischemia results in development of focal areas of necrosis.

GIT: Widespread mucosal ischemia results in multiple

hemorrhagic erosions or Gastric stress ulcers

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Sum

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SHOCK: RESULTS Lungs:

Show signs of diffuse alveolar damage (DAD) also k/a ARDS (Acute Respiratory Distress Syndrome)

Due to neutrophil mediated injury Endotoxic (septic) shock MCC of ARDS.

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SHOCK: RESULTS Others:

Metabolic acidosis: lactic acidosis due to tissue hypoxia

Severe absolute neutropenia : increased synthesis of adhesion molecule stimulated by endotoxin (in septic shock)

DIC: due to activation of coagulation cascade (in septic shock)

Multiorgan dysfunction: Most common cause of death

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STAGES OF SHOCK Stage I: stage of compensation

Perfusion to vital organs is maintained by reflex mechanismsIncreased sympathetic toneRelease of catecholaminesActivation of renin angiotensin mechanism

Stage II: stage of decompensationProgressive decrease in tissue perfusionPotentially reversible tissue injury occursDevelopment of metabolic acidosis, electrolyte

imbalances and renal insufficiency Stage III: irreversible shock

Irreversible tissue injury and organ failureUltimately resulting in death

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Stage I: stage of compensation: Clinical findings include:

tachycardia ( a heart rate of >100 beats /minute

skin pallor due to vasoconstriction , reduced urine output Stage II: stage of decompensation: clinical findings include:

hypotension , tachypnea and dyspnea

oliguria (urine output less than 500ml/day), acidosis Stage III: irreversible shock: clinical findings include:

marked hypotensionextreme tachycardia

respiratory distress not responding to oxygen therapy

loss of consciousness progressing to coma

gastrointestinal bleeding

anuria with elevated blood urea nitrogen and creatinine in bloodsevere acidosis

PREVENTION Learn ways to prevent heart deseases, falls,

injuries,dehydration , and other causes of shock.

If you have a known allergy (for example, to insect bites or stings), carry an epinephrine pen.

REFERENCES Hollenberg S. Cardiogenic shock. In: Goldman L, Schafer AI,

eds. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Saunders Elsevier; 2011:chap 107.

Tarrant AM, Ryan MF, Hamilton PA, Bejaminov O. A pictorial review of hypovolaemic shock in adults. Br J Radiol. 2008;81:252-257.

Jones AE, Kline JA. Shock. In: Marx JA, ,Hockberger RS, Walls RM, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, Pa: Mosby Elsevier; 2013:chap 6.

Rivers EP. Approach to the patient in shock. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 106.