Shock

Question 1

What is shock and what causes it?

Answer 1

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

Question 2

What are the possible causes of reduced oxygen delivery to tissues?

Answer 2

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

Question 3

What is hypovolaemic shock?

Answer 3

condition of inadequate organ perfusion due to loss of intravascular volume, leading to decreased cardiac preload & impaired circulation

Question 4

What are the common causes of hypovolaemic shock?

Answer 4

Trauma, haemorrhage, fluid loss (e.g. severe vomiting/diarrhea or excessive urine production (polyuria)

Question 5

What are the clinical signs of hypovolaemic shock?

Answer 5

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

Question 6

How can hypovolaemic shock be diagnosed?

Answer 6

Clinical signs and history

Low blood pressure

Elevated Lactate

Point of care ultrasound:
- Collapsing caudal vena cava (flat)
- Poorly filling heart

Question 7

How can hypovolaemic shock be treated?

Answer 7

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

Question 8

What is distributive shock?

Answer 8

state of relative hypovolemia due to abnormal blood redistribution, caused by loss of vascular tone & increased permeability

Question 9

What are the causes of distributive shock?

Answer 9

Sepsis, systemic inflammatory response syndrome (SIRS) & conditions causing excessive vasodilation & vascular leakage (increased permeability)

Question 10

What are the clinical signs of distributive shock?

Answer 10

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.

Question 11

How is distributive shock diagnosed?

Answer 11

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)

Question 12

What is a bounding pulse, and how does it relate to distributive shock?

Answer 12

bounding pulse is strong but brief and easily collapses with light pressure.

In distributive shock:
- ↓ Diastolic BP due to loss of vascular tone
- Heart compensates with stronger contractions
- But low vascular resistance and poor volume → short, weak pulse
- Pulse collapses easily due to floppy vessels

Normal pulse = sustained and stable due to maintained systolic + diastolic pressure.

Question 13

What is the treatment approach for distributive shock?

Answer 13

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

Question 14

What is noradrenaline’s (norepinephrine) role in treating distributive shock?

Answer 14

Potent vasoconstrictor acting on alpha-1 receptors

Increases vascular tone and maintains blood pressure

Always start with lowest dose because can be dangerous

Question 15

What is dopamine’s role in treating distributive shock?

Answer 15

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

Question 16

How do you recognize a patient with both hypovolemic and distributive shock?

Answer 16

Signs may conflict due to opposing mechanisms:

Bounding pulse → vasodilation + heart compensation

Normal CRT & MM colour → perfusion appears normal due to pooling

Tachycardia (or bradycardia in cats)

Hypotension → from fluid loss + vasodilation

↑ Lactate → poor tissue perfusion

↑ RR → compensates for metabolic acidosis

Normal temp → sepsis raises, hypovolemia lowers

Mentation changes → most reliable indicator of deterioration

Question 17

How would you diagnose a patient with both hypovolaemic and distributive shock?

Answer 17

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

Question 18

How would you treat a patient with both hypovolaemic and distributive shock?

Answer 18

Give fluid boluses – To correct hypovolemia
Start vasopressor therapy – To restore vascular tone at same time

Question 19

What is cardiogenic shock

Answer 19

disorder of cardiac function causing critical reduction in heart’s pumping capacity due to systolic or diastolic dysfunction

Question 20

How is cardiogenic shock defined in terms of blood pressure?

Answer 20

SAP <90 mmHg or MAP 30 mmHg below baseline

Question 21

What are the common causes of cardiogenic shock?

Answer 21

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)

Question 22

What are the clinical signs of cardiogenic shock?

Answer 22

Poor pulses
Pale mucous membranes
Prolonged CRT
Reduced temperature!
Heart rate varies depending on cause

Question 23

How is cardiogenic shock diagnosed?

Answer 23

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

Question 24

How is cardiogenic shock treated?

Answer 24

Depends on cause

Hyperkalemia – Glucose, insulin, fluid therapy

Splenic disease – Splenectomy.

Hypoxia (secondary shock effects) – Treat underlying cause

Myocardial failure – Positive inotropes (dobutamine, pimobendan)

Question 25

How does dobutamine help in cardiogenic shock?

Answer 25

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.

Question 26

How does pimobendan work in cardiogenic shock?

Answer 26

Phosphodiesterase III inhibitor, increases calcium sensitivity for better contraction Does NOT increase myocardial oxygen demand, making it preferable in heart failure cases

Question 27

What is obstructive shock?

Answer 27

condition caused by physical obstruction of heart or great vessels, reducing venous return or cardiac output

Question 28

How is obstructive shock different from cardiogenic shock?

Answer 28

Cardiogenic shock is due to intrinsic heart failure, whereas obstructive shock is caused by external impediments to circulation

Question 29

What are the main causes of obstructive shock?

Answer 29

Right heart inflow obstruction (lesser circulation): - Cardiac tamponade – Pericardial effusion compresses heart - Pulmonary thromboembolism (PTE) – Blocks pulmonary flow - Mediastinal mass – Compresses pulmonary vessels Major vessel outflow obstruction (greater circulation): - Severe aortic stenosis – Limits blood ejection from heart Reduced preload (venous return): - Caval compression – From GDV, neoplasia, or tension pneumothorax

Question 30

What are the clinical signs of obstructive shock?

Answer 30

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)

Question 31

How is obstructive shock diagnosed?

Answer 31

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

Question 32

How is obstructive shock treated?

Answer 32

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

Question 33

What are the four main types of shock?

Answer 33

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)