JC 11 (Surgery) - Shock Flashcards
Define Shock
state of cellular and tissue hypoxia due to reduced O2 delivery, increased O2 consumption or inadequate O2 utilization
inadequate oxygen delivery (DO2) to meet cellular metabolic demands
3 methods to assess for tissue hypoperfusion clinically
o Skin: Decreased capillary refill/ Cool and pale skin
o Renal: Decreased urine output < 0.5 mL/kg/hr
o CNS: Anxiety/ Lethargy/ Confusion
Equations for oxygen delivery and oxygen content
□ Oxygen delivery (DO2) = CO × CaO2
□ Oxygen content (CaO2) = Hb × SaO2 × 1.34 + PaO2 × 0.027
Hypotension is a pre-requisite to shock
True or False, explain
Circulatory failure may not present as occult hypotension
o Patients in the early stages of shock can be normotensive or hypertensive
o Patients who have hypotension does NOT necessarily have shock:
chronic hypotension, drug-induced hypotension, autonomic dysfunction, vasovagal syncope and peripheral artery disease
Define absolute, relative and orthostatic hypotension
- Absolute = SBP < 90 mmHg (OR) MAP < 65 mmHg
- Relative = Reduction in SBP > 40 mmHg from baseline
- Orthostatic = Reduction in SBP > 20 mmHg (OR) DBP > 10 mmHg on standing
Stages of shock
□ Pre-shock: compensated shock to tissue hypoperfusion
→ tachycardia, modest increase BP, low urine output, mild lactate
□ Shock: compensatory changes overwhelmed
→ Low BP and S/S of tissue hypoperfusion, eg. oliguria, cold and clammy skin
□ End-organ dysfunction: multiorgan failure and death
→ acute renal failure, severe hypotension, mental obtundation and coma
4 severities of hypovolemic shock and associated volume blood loss
Compare the HR, BP and RR response in 4 severities of shock
List all assessments for severity of shock
- Volume of blood loss
- HR
- BP
- RR
- Mental status
- Capillary refill
- Bowel sounds
- Urine output
Compare the Mental status between 4 severities of shock
Compare capillary refill time, bowel sounds and urine output for 4 severities of shock
4 classes of shock
Hypovolemic
Cardiogenic
Obstructive
Distributive: Sepsis, anaphylaxis, Neurogenic
Causes of hypovolemic shock
Causes:
haemorrhagic
- trauma, GI bleed
non-haemorrhagic
- excessive vomiting and diarrhea,
- skin burns,
- 3rd space loss,
- dehydration
Causes of cardiogenic shock
Causes:
- cardiomyopathic (eg. MI, severe dilated cardiomyopathy, myocarditis),
- arrhythmogenic,
- mechanical (eg. severe valvular heart disease, ruptured LV aneurysm, atrial myxoma)
Causes of obstructive shock
Cardiac tamponade
Pulmonary embolism
Tension pneumothorax
Causes of distributive shock
Sepsis
Anaphylaxis: severe systemic allergic reaction to an antigen precipitated by abrupt release of chemical mediators in a previously sensitized patient
Neurogenic: traumatic brain injury or spinal cord injury, Interruption of autonomic pathways leading to loss of sympathetic tone and unopposed vagal tone
Compare anaphylaxis reaction to anaphylactoid reaction
Anaphylaxis refers severe systemic allergic reaction to an antigen precipitated by abrupt release of chemical mediators in a previously sensitized patient
Anaphylactoid reaction refers to direct histamine release from mast cells without need for prior sensitization
Common causes of anaphylactic shock
Common causes for anaphylactic shock
o Drugs: Penicillin/ Aspirin/ NSAIDs/ Colloids/ TCM
o Food: Peanuts/ Egg/ Shellfish
o Venoms: Bees/ Wasp/ Hornets
o Environment: Latex/ Dust/ Pollen grains
o Infections: EBV/ HBV/ Coxsackie virus/ Parasites
Pathophysiology of hypovolemic shock
Pathophysiology - Intravascular blood volume depletion
↓ Preload (e.g. due to blood loss)
↓ SV (Frank-Starling curve: Decrease preload = Decrease stroke volume)
↓ CO, BP and LV filling pressure
↑ Sympathetic compensation to increase HR and Total Peripheral resistance
>> Increase HR
>> Increase Systemic vascular resistance
>> Decrease JVP
Pathophysiology of cardiogenic shock
Pathophysiology
↓ Blood flow to heart due to intrinsic cardiac function deficit
↓ Contractility
↓ SV + Increase LV filling pressure (Backward failure - pulmonary edema)
↓ CO
↑ Sympathetic compensation to increase HR and Total Peripheral resistance
Increase HR, Systemic vascular resistance, JVP
Pathophysiology of obstructive shock
Triad of symptoms
Mechanical obstruction to cardiac filling > Low LV filling > ↓CO and BP + Backward failure of right heart (Increase JVP)
Beck’s triad of cardiac tamponade
• Hypotension (Low BP)
• Distended neck veins (High CVP)
• Muffled heart sounds
Pathophysiology of Distributive shock
Peripheral vascular dilatation > Increase CO (opposite to hypovolemic and cardiogenic shock), but perfusion of vital organ remains compromised as the body lose ability to distribute blood properly
- Hypotension with wide BP (↓DBP due to peripheral vasodilatation)
- Compensatory tachycardia and tachypnoea
- Warm peripheries
- Bounding peripheral pulses
-
Features of hypoperfusion
Hyperlactataemia and lactic acidosis
Oliguria
Mental status changes
>> Increase HR (except neurogenic shock with low HR)
>> Decrease systemic vascular resistance
>> Decrease JVP
Pathophysiology of Neurogenic shock
Neurogenic shock
Due to interruption of neurogenic vasomotor control → inappropriate ↓HR, ↓SVR
>> Paradoxically slow HR due to loss of SN control
>> Decrease systemic vascular resistance
>> Decrease JVP
Features of anaphylactic shock
Due to severe type I hypersensitivity reaction
Anaphylactic S/S
□ Severe bronchospasm and angioedema
□ Urticaria, widespread flushing and pruritus
Airway protective measures
→ Airway management measures as required: Head-tilt, chin lift, jaw thrust (for suspected C-spine injury), remove foreign bodies…etc
→ Rapid sequence intubation
Breathing protective measures
→ High flow O2 (15L/min) using face-mask and reservoir for ALL pt
→ Mechanical ventilation if intractable hypoxaemia/hypercapnia, resp distress or ↓consciousness
Circulation protective measures
- Hypovolemia (2)
- Cardiogenic (3)
- Distributive (3))
Hypovolemia:
- Optimize preload by volume resuscitation ± short-term vasopressors (adrenaline, noradrenaline)
- Secure large-bore IV access (14-18G)
Cardiogenic
- Optimize afterload by vasodilators and intra-aortic balloon pump (IABP)
- Optimize contractility by inotrope (dobutamine) or antiarrhythmics (if in arrhythmia)
- Optimize Hb by RBC transfusion to keep Hb 7-9mg/dL
Distributive
- As above
- Optimize MABP by vasopressors
- eradicate infective focus
First-line monitoring for suspected shock
Clinical evaluation for type of shock and aetiology
Clinical monitoring: BP/P, UO, fluid balance charts, cardiac monitor
First-line tests/ investigations for suspected shock with rationale (7)
Cardiogenic: ECG, Cardiac enzymes/BNP
CBC/D: anaemia w/ bleeding (haemorrhagic shock), ↑eosinophil (anaphylaxis), ↑/↓WBC (sepsis or stress response), ↓PLT (bleeding tendency)
L/RFT: ↑U/Cr (shock-induced AKI), ↑ALT/AST (shock liver), electrolyte disturbance, dehydration (hypovolemia)
V/ABG + lactate: lactic acidosis (poor tissue perfusion), assess need for ventilation
Clotting + D-dimer: ↑PT/INR (haemorrhagic shock, septic APR), ↑D-dimer (PE, DIC)
- *CXR:** pneumonia, pneumothorax, pulmonary oedema, widened mediastinum (obstructive
shock) , aortic dissection…
Acute management of Cardiac arrest
- CPR with 30:2 compression -ventilation ratio
- Shock for Ventricular defibrillation
- Adrenaline (or amiodarone/ Lidocaine for refractory)
- Airway: ET tube or supraglottic advanced airway
- Monitor return of spontaneous circulation: Pulse, BP, ECG
Acute assessment of hypovolemia
Straight leg raise if unsure of hypovolemic shock
- If BP goes up > hypovolemic shock
Fluid challenge: 100-500mL of fluid infusion to see If BP goes up
Acronym for causes of traumatic cardiac arrest
HOTT
Hypovolemia
Oxygen
Tension pneumothroax
Tamponade
