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
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
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
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
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
(V/Q scan, ECG)
Full resuscitation, anticoagulants, thrombolysis.
Clinical presentation of PE
Crushing central chest pain
High venous pressure
(DVT may be present)
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
Compression of the heart due to fluid accumulation in the pericardium. Compresses the heart.
Treatment of cardiac tamponade
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
Oxygenation, fluid resusctation, inotropic agent, vasoconstrictor support
Antibiotics and surgical drainage
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
Rhinitis, bronchospasm, laryngeal obstruction, pulmonary oedema
Vomiting, diarrhoea, cramps