Cardiac - Cardiogenic Shock

Question 2

Define cardiogenic shock (CS) following acute coronary syndrome (ACS).

Answer 2

CS is a clinical syndrome of end-organ hypoperfusion and tissue hypoxia caused by primary cardiac dysfunction, usually after AMI.

Question 3

What is the mortality rate range for CS following AMI?

Answer 3

40–70%

Question 4

What systemic vascular response is triggered by myocardial dysfunction in CS?

Answer 4

Compensatory vasoconstriction and sodium and water retention via RAAS and SNS activation.

Question 5

What are the two key neurohormonal activations in CS?

Answer 5

Renin-angiotensin-aldosterone system and sympathetic nervous system.

Question 6

How does high LV end-diastolic pressure worsen myocardial ischaemia?

Answer 6

It reduces coronary perfusion pressure and increases pulmonary congestion.

Question 7

What is the only intervention proven to improve mortality in CS-AMI?

Answer 7

Emergent myocardial revascularisation (PCI).

Question 8

What initial investigations are key in suspected CS?

Answer 8

Clinical examination, ECG, echocardiography, ABG (lactate), renal/liver function tests, and troponin.

Question 9

How does echocardiography assist in CS?

Answer 9

It assesses regional wall motion abnormalities, LV/RV function, mechanical complications, and predicts recovery potential.

Question 10

What classification stages cardiogenic shock severity?

Answer 10

SCAI shock stages (A to E).

Question 11

What defines SCAI Stage A?

Answer 11

At risk for CS but no hypoperfusion signs.

Question 12

What defines SCAI Stage C?

Answer 12

Classic CS with hypoperfusion requiring intervention beyond fluids.

Question 13

Name two common causes of mechanical CS after MI.

Answer 13

Ventricular septal rupture (VSR) and severe mitral regurgitation (MR).

Question 14

Describe the ‘cold and wet’ CS phenotype.

Answer 14

Reduced cardiac output, increased SVR, high filling pressures — classic CS presentation.

Question 15

What blood gas findings indicate severity in CS?

Answer 15

Metabolic acidaemia and hyperlactataemia.

Question 16

What is the first-line vasoactive agent typically used in CS-AMI?

Answer 16

Noradrenaline (norepinephrine).

Question 17

Why is fluid resuscitation hazardous in CS-AMI?

Answer 17

Patients are usually volume overloaded, not depleted.

Question 18

What is the role of pulmonary artery catheter (PAC) in CS?

Answer 18

Provides continuous monitoring of pressures, cardiac output, SVR, and guides therapy.

Question 19

Name two indications for mechanical circulatory support (MCS) in CS.

Answer 19

Failure of pharmacological therapy; preparation for surgery or recovery.

Question 20

Name two percutaneous MCS devices.

Answer 20

Intra-aortic balloon pump (IABP), Impella (microaxial LVAD).

Question 21

What is the maximum cardiac output augmentation achievable with IABP?

Answer 21

0.8–1.0 L/min.

Question 22

What is the main advantage of Impella over IABP?

Answer 22

Direct LV unloading with greater cardiac output support (up to 5 L/min).

Question 23

What are two major risks of VA-ECMO?

Answer 23

Increased LV afterload; systemic thromboembolism.

Question 24

What are complications of prolonged VA-ECMO without LV venting?

Answer 24

LV dilation, pulmonary edema, thrombus formation.

Question 25

When should surgical revascularisation be considered in CS?

Answer 25

Failed PCI, mechanical complications, coronary anatomy unsuitable for PCI.

Question 26

What are the potential renal complications of CS-AMI?

Answer 26

Acute kidney injury (AKI), requiring RRT.

Question 27

What blood management principle applies in CS-AMI?

Answer 27

Restrictive transfusion, but cardiac ICU may target Hb 9-10 g/dL.

Question 28

Why is sedation important in ventilated CS-AMI patients?

Answer 28

To optimize oxygen consumption and reduce catecholamine surge.

Question 29

What defines 'extremis' in SCAI shock staging?

Answer 29

Circulatory collapse with profound hypoperfusion despite maximal support.

Question 30

Name one important ventilator strategy in CS patients.

Answer 30

Use low tidal volume and low-pressure ventilation to protect lungs and right heart.

Question 31

What role does lactate monitoring play in CS-AMI?

Answer 31

Indicator of perfusion adequacy and therapeutic response.

Question 32

What is the significance of Q waves on ECG after AMI in CS?

Answer 32

Suggests transmural infarction and lower likelihood of LV recovery.

Question 33

Why is early specialist referral crucial in CS-AMI?

Answer 33

To access mechanical support, surgery, and advanced heart failure therapies.

Question 34

What ventilation mode may help in less severe CS without intubation?

Answer 34

Non-invasive ventilation (CPAP).

Question 35

What systemic vascular resistance (SVR) issue must be considered when using noradrenaline in CS-AMI?

Answer 35

Risk of excessive vasoconstriction increasing LV afterload.

Question 36

What is the goal MAP commonly targeted in CS management?

Answer 36

60–65 mmHg.

Question 37

What ECG features suggest proximal LAD or LMS occlusion?

Answer 37

Widespread ST elevation, significant anterior leads changes.

Question 38

What is the mechanism behind low urine output after IABP insertion?

Answer 38

Potential juxta-renal positioning causing renal artery compromise.

Question 39

What parameters are used to predict poor prognosis in CS?

Answer 39

High lactate, low cardiac index, high filling pressures, severe organ dysfunction.

Question 40

What role does pulmonary congestion play in CS pathophysiology?

Answer 40

Worsens hypoxaemia and myocardial ischaemia.

Question 41

In refractory shock, what defines appropriate escalation to MCS?

Answer 41

Failure to restore perfusion with pharmacological support alone.

Question 42

What is the first step if CS develops during an acute MI presentation?

Answer 42

Immediate preparation for emergent coronary angiography and PCI.