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Flashcards in Shock Deck (26):

Types of shock



Definition of shock

Acute circulatory failure resulting in inadequate tissue perfusion and insufficient oxygen supply to the cells


Causes of hypovolemic shock

External blood loss
Hidden blood loss (intrathoracic/intrabdominal)

Diarrhoea and Vomiting
Cutaneous (burns)


Changes in the circulatiory system due to hypovolemic shock

Loss of circulating volume
Reduced venous return and cardiac fillinf

Therefore reduced SVand reduced CO

This reduces BP and oxygen delivery

Impaired cellular function


Neuroendocrine response to hypovolemic shock

Reduced blood volume and blood pressure reduces stretch of aortic and carotid baroreceptors, reduced blood flow to chemoreceptors.

Causes reflex increase in sympathetic tone and reduces parasympathetic input.

Results in increased heart rate (tachycardia)
Release of catecholamines from adrenals
Vasoconstriction (increased TPR to maintain bp, increased cardiac filling)

Activation of RAAS to incerase water retention

Produces increase in cardiac output and SVR. Blood flow re-distributed to vital organs


Clinical features of hypovolemic shock

Skin: cold, clammy, pale, slow capillary refill

Circulation: tachycardia, initially reduced pulse pressure (systolic maintained, diastolic rises), collapsed veins (severe)

Brain: confusion, restlessness, loss of consciousness

Respiration: tachypnoea

Altered brain and kidney function most significant


What are the metabolic changes that occur in hypovolemic shock

Increased anaerobic metabolism: Lactate and H+ production causing metabolic acidosis

Hyperglycaemia - glucagon and cortisol released in stress response

Lack of O2 reduces ATP production, leads to failure of Na/K+ pump. Cell swelling, release of K+, activation of lysomal enzymes, Ca2+ entery and cell death


Management of hypovolemic shock

High flow oxygen
Replacement of circulating volume (until bp is restored to normal limits)
Diagnosis and treatment of cause


Causes of cardiogenic shock

Acute MI
Heart failure (more common)


Clinical features of cardiogenic shock

Reduced contractility due to ischemia and infarction of the myocardium.

Low CO and high LVEDV

Results in pulmonary congestion - dyspnoea, crackles and wheeze, pulmonary oedema, pleural effusion

Eventually leads to RH failure - raised JVP, peripheral oedema


Management of cardiogenic shock

Diagnosis - from history (IHD, chest pain), ECG, troponin

Treat with thrombolytics, angiography (stenting), high flow oxygen, analgesia, diuretics, IV fluids if necessary


Causes of mechanical shock

Pulmonary embolism
Tension pneumothorax
Cardiac tamponade


Pulmonary embolism

A mass in the pulmonary vessels that travels from a distant site and causes obstruction of blood flow.

Causes acute overloading of the right ventricle and hypovolemia of the LA and LV


Diagnosis and treatment of PE

Pulmonary angiography
(V/Q scan, ECG)

Full resuscitation, anticoagulants, thrombolysis.


Clinical presentation of PE

Crushing central chest pain
High venous pressure
Increased SVR

(DVT may be present)


Tension pneumothorax

Abnormal collection of air in the pleural cavity that is markedly increased when a one-way valve is formed by an area of damaged tissue.

Increasing pressure collapses teh lung and pushes the mediastinum and heart to the other side.

Impairs respiration and circulation (raised intrathoracic pressure and deviated great vessels prevent cardiac filling)


Presentation of pneumothorax

hypoxia, hypercarbia, respiratory distress, hypotension and tachycardia

Examination shows poor chest expansion, mediastinal shift away from the side of the pneumothorax (deviated trachea, displaced apex beat) and a hyperresonant thorax


Treatment of tension pneumothorax

Immediate decompression and chest drain.

Tube inserted 2nd intercostal space, midclavicular line


Cardiac tamponade

Compression of the heart due to fluid accumulation in the pericardium. Compresses the heart.


Treatment of cardiac tamponade

Sub-xiphoid pericardiocentesis


Physiology of septic shock

Inflammatory mediators released in severe sepsis cause vasodilation, intravascular coagulation and loss of circulating volume through leaky capillaries

Blood pools in dilated peripheries, reducing venous return and CO.

Blood pressure is reduced (diastolic pressure falls, wider pulse pressure)


Clinical features of septic shock

Early: Vasodilation causes warm peripheries, low venous pressure (hypotension). bounding pulse, rapid capillary refill, (fever)

Late: cold peripheries, tachycardia, sweating


Mangement of septic shock

Sepsis 6

Oxygenation, fluid resusctation, inotropic agent, vasoconstrictor support

Bacterial cultures
Antibiotics and surgical drainage


Anaphylactic shock

Anaphylaxis is a serious allergic reaction that is rapid in onset (and may cause death)

Anaphylactic shock is associated with systemic vasodilation and increased capillary permeability that causes hypovolemia and low blood pressure


Presentation of anaphylaxis

Within 30min exposure...

Erythema, urticaria, oedema, palloe/cyanosis

Tachcardia, hypotension

Rhinitis, bronchospasm, laryngeal obstruction, pulmonary oedema

Vomiting, diarrhoea, cramps


Management of anaphylaxis

IM adrenaline asap
Fluid resuscitation
Steroids, antihistamines

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