Shock Flashcards
What is shock and what causes it?
Tissue Hypoxia (low oxygen)
can be due to:
- Reduced oxygen delivery to tissues!
- Excessive oxygen demand/usage by tissues
- Inadequate utilisation of oxygen by tissues
What are the possible causes of reduced oxygen delivery to tissues?
Pipes:
- Reduce the volume
- Increase the diameter
- Block them
Pump:
- Failure of the pump
- Block it working
These all reduce blood pressure and oxygen delivery
What is hypovolaemic shock?
condition of inadequate organ perfusion due to loss of intravascular volume, leading to decreased cardiac preload & impaired circulation
What are the common causes of hypovolaemic shock?
Trauma, haemorrhage, fluid loss (e.g. severe vomiting/diarrhea or excessive urine production (polyuria)
What are the clinical signs of hypovolaemic shock?
CS all relate to body’s compensatory mechanisms to try & restore blood pressure
Tachycardia (increase cardiac output)
Peripheral vasoconstriction (to prioritise vital organs)–> pale mucous membranes, prolonged CRT, poor pulse quality
Reduced mentation due to reduced cerebral oxygen supply
How can hypovolaemic shock be diagnosed?
Clinical signs and history
Low blood pressure
Elevated Lactate
Point of care ultrasound:
- Collapsing caudal vena cava (flat)
- Poorly filling heart
How can hypovolaemic shock be treated?
Depends on cause but fundamental same – restore volume
Fluid loss - > Isotonic Fluids
Blood/plasma loss - > Transfusion
Start with isotonic fluids in all circumstances & then transfusion if necessary
Speed is of essence – hypoxia leads to brain death rapidly – so bolus fluids
What is distributive shock?
state of relative hypovolemia due to abnormal blood redistribution, caused by loss of vascular tone & increased permeability
What are the causes of distributive shock?
Sepsis, systemic inflammatory response syndrome (SIRS) & conditions causing excessive vasodilation & vascular leakage (increased permeability)
What are the clinical signs of distributive shock?
Vasodilation - > injected mucous membranes, shortened CRT (pooling of blood in membrane capillaries), bounding/hyperdynamic pulse. Tachycardia due to hypotension.
Permeability - > peripheral oedema, pulmonary oedema, cavitatory effusions.
How is distributive shock diagnosed?
Clinical signs and history
Low blood pressure
Elevated Lactate
Point of care ultrasound:
- Collapsing caudal vena cava (flat)
- Poorly filling heart
- Septic focus e.g. septic abdomen (free fluid)
- Evidence of vascular leak e.g. pulmonary oedema, small effusions
- Gall bladder halo sign (oedema of the wall)
What is a bounding pulse, and how does it relate to distributive shock?
pulse that feels strong initially but is short-lived & easily compressed when pressure is applied.
In distributive shock, this occurs due to:
- Diastolic BP drop – baseline pressure lower because vascular tone is lost (“pipes aren’t working”).
- Heart compensates (pumps harder) to try & maintain circulation
- Despite strong initial beat, there isn’t enough volume to sustain full contraction, making pulse weak & low-pressure
- Since vessels lack normal tone, applying slight pressure collapses pulse easily
This contrasts with normal pulse, where both systolic & diastolic pressures are maintained, keeping pulse steady & well-sustained
What is the treatment approach for distributive shock?
Volume support – Fluid bolus
Vascular tone support – Vasopressors (e.g., noradrenaline, dopamine)
Permeability support – ensuring oncotic pressure is adequate
- Check albumin levels & consider plasma transfusion
- Nutritional support – Feeding tube if necessary
What is noradrenaline’s (norepinephrine) role in treating distributive shock?
Potent vasoconstrictor acting on alpha-1 receptors
Increases vascular tone and maintains blood pressure
Always start with lowest dose because can be dangerous
What is dopamine’s role in treating distributive shock?
Nor-adrenaline precursor (stimulates production of noradrenaline)
Low doses: Redirects blood to major organs
Higher doses:
Increases systemic vascular resistance (alpha-1)
Increases heart rate (beta-1)
Can cause tachy-arrythmias at high doses because heart works harder
Less effective in cats
How do you recognize a patient with both hypovolemic and distributive shock?
Can present with conflicting clinical signs because compensatory mechanisms from each type of shock counteract each other
Key Signs:
- Bounding pulse – Due to vasodilation & compensatory heart response
- Normal CRT – Vascular changes balance out CRT
- Tachycardia – Except cats, which may be bradycardic
- Elevated lactate – Indicates poor oxygen delivery to tissues
- Low blood pressure – Due to both volume loss & vasodilation
- Normal MM colour – Less blood available but pooling effect from distributive shock
- Respiratory rate elevated – compensation for metabolic acidosis
- Normal temperature – Hypovolemia lowers temp, sepsis raises it
- Mentation changes are critical – most reliable sign of patient deteriorating
How would you diagnose a patient with both hypovolaemic and distributive shock?
Perform POCUS (Point-of-Care Ultrasound) to confirm:
- Flat vena cava – Suggests volume depletion
- Collapsing heart – Reduced preload and contractility.
- Fluid in lungs – Possible vascular permeability issues.
- Gallbladder halo sign – Indicates vascular leak (sepsis).
- Free fluid in cavities
How would you treat a patient with both hypovolaemic and distributive shock?
Give fluid boluses – To correct hypovolemia
Start vasopressor therapy – To restore vascular tone at same time
What is cardiogenic shock
disorder of cardiac function causing critical reduction in heart’s pumping capacity due to systolic or diastolic dysfunction
How is cardiogenic shock defined in terms of blood pressure?
SAP <90 mmHg or MAP 30 mmHg below baseline
What are the common causes of cardiogenic shock?
Myocardial failure – End-stage DCM, or secondary to sepsis/SIRS
Arrhythmias – Primary cardiac disease or secondary to hyperkalemia, splenic disease, or hypoxia
Valvular disease – Severe failure preventing adequate cardiac output (less common)
What are the clinical signs of cardiogenic shock?
Poor pulses
Pale mucous membranes
Prolonged CRT
Reduced temperature!
Heart rate varies depending on cause
How is cardiogenic shock diagnosed?
Clinical signs & history
Low BP (<90 mmHg SAP)
Elevated lactate
POCUS:
- Poorly contracting heart
- evidence of cardiac disease.
ECG findings:
- Bradyarrhythmia – Atrial standstill or AV block.
- Tachyarrhythmia – Ventricular tachycardia, pulse deficits.
Blood tests – Electrolyte imbalances
How is cardiogenic shock treated?
Depends on cause
Hyperkalemia – Glucose, insulin, fluid therapy
Splenic disease – Splenectomy.
Hypoxia (secondary shock effects) – Treat underlying cause
Myocardial failure – Positive inotropes (dobutamine, pimobendan)
How does dobutamine help in cardiogenic shock?
Positive inotrope (Beta-1 agonist), increases myocardial contractility but also increases myocardial oxygen demand
Requires continuous infusion due to rapid metabolism
Used in equine anaesthesia for cardiovascular support.
How does pimobendan work in cardiogenic shock?
Phosphodiesterase III inhibitor, increases calcium sensitivity for better contraction
Does NOT increase myocardial oxygen demand, making it preferable in heart failure cases
What is obstructive shock?
condition caused by physical obstruction of heart or great vessels, reducing venous return or cardiac output
How is obstructive shock different from cardiogenic shock?
Cardiogenic shock is due to intrinsic heart failure, whereas obstructive shock is caused by external impediments to circulation
What are the main causes of obstructive shock?
Right heart filling obstruction (lesser circulation):
- Cardiac tamponade – Severe pericardial effusion compressing heart
- Pulmonary thromboembolism (PTE) – Clots blocking pulmonary circulation
- Mediastinal mass – Compressing pulmonary vasculature
Major vessel obstruction (greater circulation):
- Severe aortic stenosis – Narrowing of aorta impeding blood flow
Reduced preload (venous return blockage):
- Caval compression – Due to GDV, neoplasia, or tension pneumothorax
What are the clinical signs of obstructive shock?
Signs depend on location of obstruction, but include:
- Reduced cardiac output signs (like cardiogenic shock)
- Distended caudal vena cava (if downstream blockage).
- Respiratory distress (if affecting pulmonary circulation)
How is obstructive shock diagnosed?
Clinical signs & history
Elevated lactate (tissue hypoxia)
POCUS:
- Loss of glide sign → Tension pneumothorax
- Pericardial effusion & right-sided collapse → Cardiac tamponade
- Right ventricular enlargement → Pulmonary hypertension/PTE
- CVC distension → Downstream occlusion
- Aortic outflow obstruction → Neoplasia or stenosis
How is obstructive shock treated?
Relieve obstruction if possible:
- Cardiac tamponade → Pericardiocentesis.
- Tension pneumothorax → Thoracocentesis.
- GDV → Gastric decompression
If immediate removal isn’t possible, provide supportive care:
- Pulmonary thromboembolism (PTE) → Platelet inhibitors, oxygen therapy
- Neoplasia-related obstruction → Preload support with fluid bolus before surgery
What are the four main types of shock?
Hypovolemic shock – Due to fluid loss (e.g., hemorrhage, dehydration)
Distributive shock – Due to vasodilation (e.g., sepsis, anaphylaxis, neurogenic shock)
Cardiogenic shock – Due to heart failure (e.g., DCM, valvular disease, arrhythmias)
Obstructive shock – Due to vascular obstruction (e.g., cardiac tamponade, GDV, PTE)
