Shock Flashcards
Circulatory shock definition
Abnormality of circulatory system that results in reduced organ perfusion and tissue oxygenation
Emotional shock definition
Acute stress reaction arising from a response to a traumatic event
Shock types
Reduced CO output
- Hypovolaemic
- Cardiogenic
- Obstructive
Reduced systematic vascular resistance
- Septic
- Anaphylactic
- Neurogenic
Hypovolaemic shock causes
Haemorrhage
- External vs internal
Vomiting
Diarrhoea
Diuresis
Burns
Cardiogenic shock causes
MI
Myocardial contusion
Myocarditis
Cardiac arrhythmia
Negatively inotropic drug overdose (beta blockers or CCB)
Cardiogenic shock causes
MI
Myocardial contusion
Myocarditis
Cardiac arrhythmia
Negatively inotropic drug overdose (beta blockers or CCB)
Cardiogenic shock causes
MI
Myocardial contusion
Myocarditis
Cardiac arrhythmia
Negatively inotropic drug overdose (beta blockers or CCB)
Cardiogenic shock causes
MI
Myocardial contusion
Myocarditis
Cardiac arrhythmia
Negatively inotropic drug overdose (beta blockers or CCB)
Obstructive shock causes
Tension pneumothorax
Massive PE
Cardiac tamponade
Pathophysiology of shock
BP = CO x SVR
CO = HR x SV (vol of blood pumped by heart per min)
SV = volume of blood pumped by heart per contraction
- Preload, myocardial contractibility, afterload
Preload = ventricular wall tension at end of diastole (degree of myocardial muscle stretch)
Blood pressure equation
BP = CO x SVR
Cardiac output equation
CO = HR x SV (vol of blood pumped by heart per min)
Stroke volume definition
SV = volume of blood pumped by heart per contraction
- Preload, myocardial contractibility, afterload
Preload definition
Preload = ventricular wall tension at end of diastole (degree of myocardial muscle stretch)
Determined by volume status, venous capacitance and difference between mean venous P and RA pressure
Frank-Starling mechanism
Increased fibre length (preload) leads to increased SV
Until certain point
Fibres are overstretched - further filling results in decreased SV
Eg in cardiac failure
Myocardial contractibility
Intrinsic ability of heart to work independently of preload and afterload
Positive inotropes increase this
Shifts Frank-Starling curve upwards
Afterload
Ventricular wall tension at end of systole
Resistance to anterograde blood flow
Shock pathophysiology
Cells switch to aerobic to anaerobic metabolism
Generates lactic acidosis
Causes myocardial depression
Shock presentation
SOB
Confusion
Drowsiness
Oliguria/anuria
Symptoms of cause
Kussmaul’s breathing = hyperventilation to compensate for metabolic acidosis
Hypotension
Prolonged CRT
Tachycardia
Investigation of shock
Blood gas - pH and lactate
ECG
CXR
Bloods
Echo
Trauma - pelvic XR, CT, FAST
Shock initial mangement
Maintain airway
High flow O2
Attach monitoring - pulse oximetry, BP, cardiac monitoring
Large-bore IV access
Fluid resuscitation IV
Urethral catheterisation and monitoring
Refer to HDU/ICU if BP falls for central line, arterial line or vasopressor/inotrope infusion
Treat cause
Type I haemorrhagic shock
Volume of blood loss > 750ml
Percentage blood loss < 15%
HR < 15bpm
BP and pulse pressure normal
RR 14-20
Urine output >30 ml/hr
Mental state: anxious
Type II hypovolaemic shock
750-1500ml blood loss (15-30%)
HR 100-120
BP normal
Pulse pressure decreased
RR 20-30
Urine output 20-30ml/hr
Mental state: anxious
Type III hypovolaemic shock
1500-2000ml blood loss (30-40%)
HR 120-140
BP and pulse pressure decreased
RR 30-40
Urine output 5-15
Mental state: confused
Type IV hypovolaemic shock
> 2000ml blood loss (>40%)
HR >140
BP and pulse pressure decreased
RR >35
Urine output nil
Mental state: lethargic
