Overview

Cardiogenic Shock

Name: Cardiogenic Shock
Creator: MedVellum

1. Clinical Overview

Summary

Cardiogenic shock is a life-threatening condition where the heart fails to pump enough blood to meet the body's needs, despite adequate blood volume. Picture your heart as a pump that suddenly loses power—blood backs up into the lungs (causing breathlessness) while the rest of your body starves for oxygen (causing organ failure). This creates a vicious cycle: poor pumping → low blood pressure → reduced coronary blood flow → worse heart function → even lower blood pressure. Cardiogenic shock affects 5-10% of patients with acute myocardial infarction and carries a mortality of 40-50% even with modern treatment. The key to survival is rapid recognition, immediate supportive care, and urgent treatment of the underlying cause—often requiring emergency procedures like PCI, mechanical support devices, or surgery.

Key Facts

Definition: Inadequate cardiac output despite adequate preload, leading to tissue hypoperfusion
Incidence: 5-10% of acute MI cases; ~40,000-50,000 cases/year in US
Mortality: 40-50% in-hospital mortality (down from 80% historically)
Time to treatment: Every hour of delay increases mortality by 3-5%
Critical threshold: Cardiac index <2.2 L/min/m² with evidence of hypoperfusion
Key investigation: Echocardiogram (assess LV function), cardiac catheterization (if MI)
First-line treatment: Inotropes (dobutamine), vasopressors (noradrenaline), urgent revascularization if MI

Clinical Pearls

"Cold and wet = Cardiogenic shock" — Cold extremities (poor perfusion) + pulmonary oedema (wet) = classic cardiogenic shock. This distinguishes it from hypovolaemic shock (cold and dry) or septic shock (warm and wet).

"The heart is the problem, not the solution" — Unlike other types of shock, giving more fluid won't help—it will make things worse by increasing preload on a failing heart. The heart itself needs support.

"Time is myocardium, myocardium is life" — In MI-related shock, every minute of delay in revascularization increases mortality. Door-to-balloon time should be <90 minutes, ideally <60 minutes.

"Mechanical support buys time" — IABP, ECMO, or LVAD can stabilize patients while waiting for recovery or definitive treatment. Don't hesitate to escalate early.

Why This Matters Clinically

Cardiogenic shock is the most severe form of heart failure, with mortality rates that remain unacceptably high despite advances in care. It's a true medical emergency where minutes count—delayed recognition or inappropriate treatment (like aggressive fluid resuscitation) can be fatal. Rapid, protocol-driven management focusing on supporting the heart while treating the underlying cause can improve outcomes, but requires immediate access to advanced cardiac care, mechanical support, and interventional cardiology.

2. Epidemiology

Incidence & Prevalence

Acute MI-related: 5-10% of STEMI cases, 2-3% of NSTEMI cases
Overall: ~40,000-50,000 cases/year in US; ~5,000-8,000/year in UK
Trend: Decreasing incidence (better MI treatment) but mortality remains high
Peak age: 65-75 years (but can occur at any age)

Demographics

Factor	Details
Age	Median age 70 years; rare <50 unless acute MI or myocarditis
Sex	Slight male predominance (55:45) in younger patients; equal in elderly
Ethnicity	Higher rates in Black populations (1.5x); earlier onset
Geography	Higher in areas with limited access to PCI/advanced care
Setting	Emergency departments, cardiac catheterization labs, ICUs

Risk Factors

Non-Modifiable:

Age >65 years
Male sex (younger patients)
Previous MI or heart failure
Family history of cardiomyopathy

Modifiable:

Risk Factor	Relative Risk	Mechanism
Acute MI (large territory)	10-15x	Extensive myocardial damage
Anterior MI	3-5x	Larger infarct size
Delayed presentation	2-3x	More myocardium lost
Diabetes	2x	Worse outcomes, microvascular disease
Hypertension	1.5x	Pre-existing LV dysfunction
Renal dysfunction	2x	Worse outcomes, fluid management challenges
Previous heart failure	3x	Already compromised function

Precipitating Causes

Cause	Frequency	Mechanism
Acute MI (large)	60-70%	Extensive myocardial necrosis
Acute MI (mechanical complications)	5-10%	VSR, papillary muscle rupture, free wall rupture
Acute decompensated heart failure	15-20%	Sudden worsening of chronic HF
Myocarditis	3-5%	Inflammatory myocardial damage
Arrhythmias	5-10%	VT, VF, severe bradycardia
Valvular emergencies	3-5%	Acute severe MR, AS
Post-cardiac surgery	2-3%	Myocardial stunning
Takotsubo cardiomyopathy	1-2%	Stress-induced

3. Pathophysiology

The Vicious Cycle of Cardiogenic Shock

Step 1: Initial Cardiac Insult

Acute MI: Large territory infarction → loss of 40%+ of LV myocardium
Other causes: Myocarditis, arrhythmia, valvular emergency
Result: Sudden reduction in cardiac contractility

Step 2: Reduced Cardiac Output

Stroke volume: Decreases dramatically (normal: 60-80ml; shock: <40ml)
Cardiac output: Falls below critical threshold (<2.2 L/min/m²)
Blood pressure: Drops (SBP <90 mmHg)

Step 3: Compensatory Mechanisms (Initially Helpful)

Sympathetic activation: Tachycardia, vasoconstriction
Renin-angiotensin system: Fluid retention, vasoconstriction
Result: Temporary maintenance of BP

Step 4: The Vicious Cycle Begins

Reduced coronary perfusion: Low BP → reduced coronary blood flow
Worsening ischemia: Already damaged heart gets less oxygen
Further dysfunction: Heart pumps even worse
Lower BP: Cycle continues

Step 5: End-Organ Hypoperfusion

Brain: Confusion, altered mental status
Kidneys: Reduced urine output, AKI
Gut: Ischemia, lactic acidosis
Skin: Cold, clammy extremities

Step 6: Multi-Organ Failure

If untreated: Progressive organ failure → death
Time course: Hours to days without support

Classification by Cause

Type	Mechanism	Common Causes	Clinical Features
Pump failure (LV)	Reduced contractility	Large MI, myocarditis	Pulmonary oedema, low output
Pump failure (RV)	RV infarction	Inferior MI with RV involvement	Elevated JVP, clear lungs
Mechanical complications	Structural damage	VSR, papillary muscle rupture	New murmur, sudden deterioration
Arrhythmic	Rate/rhythm problems	VT, VF, severe bradycardia	Arrhythmia evident
Obstructive	Outflow obstruction	Massive PE, cardiac tamponade	Different hemodynamics

Hemodynamic Profile

Parameter	Normal	Cardiogenic Shock
Cardiac index	2.5-4.0 L/min/m²	<2.2 L/min/m²
Systolic BP	100-140 mmHg	<90 mmHg
PCWP	8-12 mmHg	>18 mmHg (elevated)
SVR	800-1200 dynes·s/cm⁵	High (compensatory)
Mixed venous O₂	65-75%	<60% (low)

Anatomical Considerations

Left Ventricular Function:

Normal LVEF: 55-70%
Mild dysfunction: 40-54%
Moderate dysfunction: 30-39%
Severe dysfunction: <30%
In shock: Usually <25%, often <20%

Why Large MIs Cause Shock:

Anterior MI: Affects 40-50% of LV (LAD territory)
Inferior + RV MI: Affects RV and inferior LV
Loss of 40%+ myocardium: Cannot maintain adequate output
Remaining myocardium: Stunned or ischemic

4. Clinical Presentation

Symptoms: The Patient's Story

Typical Presentation (Acute MI-related):

Typical Presentation (Decompensated HF):

Atypical Presentations:

Signs: What You See

Vital Signs (Critical):

Sign	Finding	Significance
Systolic BP	<90 mmHg (often 60-80)	Defines shock
Heart rate	Variable: Tachycardia or bradycardia	May indicate cause
Respiratory rate	Tachypnoea (if pulmonary oedema)	Respiratory distress
SpO2	Low (<90%)	Hypoxia
Temperature	Usually normal or low	Hypoperfusion

General Appearance:

Cardiovascular Examination:

Finding	What It Means	Frequency
Hypotension	SBP <90 mmHg	100% (by definition)
Tachycardia	Compensatory or arrhythmia	60-70%
Bradycardia	Conduction block, medications	10-20%
Elevated JVP	Fluid overload or RV failure	60-70%
S3 gallop	LV dysfunction	50-60%
Murmurs	VSR, MR (mechanical complications)	10-20%
Weak pulse	Low cardiac output	80-90%
Cool extremities	Poor perfusion	90%+

Respiratory Examination:

Finding	What It Means	Clinical Note
Tachypnoea	Respiratory distress	If pulmonary oedema present
Crepitations	Pulmonary oedema	Bilateral, lower zones
Wheeze	"Cardiac asthma"	Bronchial oedema
Reduced air entry	Severe oedema	If present

Other Findings:

Red Flags

[!CAUTION] Red Flags — Immediate Escalation Required:

Systolic BP <90 mmHg with signs of poor perfusion — Defines cardiogenic shock

Altered mental status or confusion — Brain hypoperfusion

Cold, clammy extremities — Poor peripheral perfusion

Reduced urine output (<0.5 ml/kg/hour) — Renal hypoperfusion

Lactate >2 mmol/L — Tissue hypoxia

Cardiac arrest — End-stage shock

Pulmonary oedema with hypotension — Classic cardiogenic shock

New murmur — May indicate mechanical complication (VSR, MR)

Chest pain

Severe, may have resolved (if infarcted)

Severe breathlessness

"Can't breathe," "Drowning"

Weakness/dizziness

"Feel faint," "Can't stand"

Confusion

"Not thinking clearly"

Nausea/vomiting

From hypoperfusion

Rapid progression

Deteriorates over minutes to hours

5. Clinical Examination

Structured Approach: ABCDE

A - Airway

Assessment: Usually patent (unless altered mental status)
Finding: May need protection if GCS <8
Action: Secure airway if compromised

B - Breathing

Look: Tachypnoea, use of accessory muscles, cyanosis
Listen: Crepitations (if pulmonary oedema), wheeze
Feel: Reduced chest expansion if severe oedema
Measure: SpO2 (low), respiratory rate (high)
Action: High-flow oxygen; consider CPAP/intubation if severe

C - Circulation

Look: Elevated JVP, pale/cyanotic, mottled skin
Feel: Weak pulse, cool extremities, hypotension
Listen: S3, murmurs, arrhythmias
Measure: BP (low), HR (variable), ECG
Action: IV access, inotropes, urgent echo

D - Disability

Assessment: GCS, pupil response, blood glucose
Finding: Often confused (hypoperfusion)
Action: Check glucose; consider if hypoperfusion causing confusion

E - Exposure

Look: Full body examination, look for wounds, signs of MI
Feel: Temperature (cool), pulses (weak)
Action: Keep warm, maintain dignity

Specific Examination Findings

Cardiovascular Assessment:

Inspection:

Elevated JVP (if RV failure or fluid overload)
Visible pulsations (if severe)

Palpation:

Pulse: Weak, thready, may be irregular
Apex beat: May be displaced, weak
Extremities: Cold, clammy

Auscultation:

S1: Usually soft (poor LV function)
S2: May be loud P2 (pulmonary hypertension)
S3: Pathognomonic of LV dysfunction
S4: Stiff, hypertrophied ventricle
Murmurs:
- VSR: Harsh pansystolic murmur, thrill
- MR: Pansystolic murmur (papillary muscle rupture)
- AS: Ejection systolic (if severe AS causing shock)

Respiratory Assessment:

If pulmonary oedema: Crepitations, wheeze, tachypnoea
If RV failure: May have clear lungs, elevated JVP

Renal Assessment:

Urine output: Reduced (<0.5 ml/kg/hour)
Urinalysis: May show protein, casts (renal hypoperfusion)

Special Tests

Test	Technique	Positive Finding	Clinical Use
Jugular venous pressure	Patient at 45°, observe JVP	Elevated	Indicates RV failure or fluid overload
Hepatojugular reflux	Firm pressure on liver	JVP rises	Confirms right heart failure
Pulsus alternans	Regular pulse with alternating strength	Alternating pulse volume	Severe LV dysfunction
Kussmaul's sign	JVP rises on inspiration	Paradoxical JVP rise	Constrictive pericarditis (rare)

6. Investigations

First-Line (Bedside) - Do Immediately

1. 12-Lead ECG

Purpose: Identify MI, arrhythmias, conduction blocks
Key Findings:
- STEMI: ST elevation (anterior = high risk)
- Arrhythmias: VT, VF, severe bradycardia
- Conduction blocks: AV block, bundle branch blocks
Action: Urgent if MI; treat arrhythmias immediately

2. Blood Pressure Measurement

Purpose: Confirm hypotension
Finding: SBP <90 mmHg
Action: Continuous monitoring; arterial line if unstable

3. Pulse Oximetry

Purpose: Assess oxygenation
Finding: Usually low (SpO2 <90%)
Action: High-flow oxygen; improves with treatment

4. Urine Output

Purpose: Assess renal perfusion
Finding: Reduced (<0.5 ml/kg/hour)
Action: Catheterize if not already; monitor hourly

Laboratory Tests

Test	Expected Finding	Purpose	Timing
Troponin	Markedly elevated	Confirm MI, assess extent	Immediate
BNP/NT-proBNP	Very elevated	Confirm heart failure	Within 1 hour
Lactate	Elevated (>2 mmol/L)	Assess tissue hypoxia	Immediate
Arterial Blood Gas	Metabolic acidosis, hypoxia	Assess acid-base, oxygenation	If SpO2 <90%
Urea & Creatinine	May be elevated	Assess renal function	Immediate
Full Blood Count	May show anaemia	Identify precipitant	Within 2 hours
Liver Function Tests	May be elevated	Assess hepatic congestion	Within 2 hours
Coagulation studies	May be abnormal	Assess bleeding risk	If procedures planned

Lactate Interpretation:

<2 mmol/L: Normal (good prognosis)
2-4 mmol/L: Moderate elevation (concerning)
>4 mmol/L: Severe (poor prognosis)
Trend: Improving = good; worsening = bad

Imaging

Chest X-Ray (Essential)

Finding	What It Shows	Clinical Note
Pulmonary oedema	Bilateral infiltrates	LV failure
Cardiomegaly	Enlarged heart	Chronic heart failure
Clear lungs	No oedema	RV failure or early shock
Pleural effusions	Bilateral effusions	Fluid overload

Echocardiogram (Urgent - Within Hours)

Finding	Significance	Clinical Impact
Severely reduced LVEF	<25%	Confirms pump failure
Regional wall motion abnormalities	Ischaemic	May need revascularization
Mechanical complications	VSR, MR, free wall rupture	Urgent surgery needed
RV dysfunction	RV failure	Different management
Valvular abnormalities	Severe AS, MR	May need valve surgery
Cardiac tamponade	Pericardial effusion	Needs pericardiocentesis

Cardiac Catheterization (If MI Suspected)

Finding	Significance	Clinical Impact
Coronary occlusion	Complete blockage	Needs urgent PCI
Multi-vessel disease	Extensive CAD	May need CABG
Mechanical complications	VSR, papillary muscle rupture	Needs surgery

Hemodynamic Monitoring

Arterial Line:

Purpose: Continuous BP monitoring
Indication: Unstable, requiring vasopressors
Benefit: Real-time BP, allows ABG sampling

Central Venous Pressure (CVP):

Purpose: Assess volume status
Finding: Usually elevated (>12 mmHg) in cardiogenic shock
Note: Less reliable than PCWP

Pulmonary Artery Catheter (Swan-Ganz):

Purpose: Detailed hemodynamics
Measurements: PCWP, cardiac output, SVR
Indication: Complex cases, unclear diagnosis
Note: Less commonly used now (echocardiogram preferred)

Cardiac Output Measurement:

Methods: Echocardiogram, PA catheter, non-invasive
Normal: 4-8 L/min (or 2.5-4.0 L/min/m² indexed)
Shock: <2.2 L/min/m²

Diagnostic Criteria

Cardiogenic Shock Definition:

Hypotension: SBP <90 mmHg (or >30 mmHg drop from baseline)
Evidence of hypoperfusion: At least one of:
- Altered mental status
- Cold, clammy extremities
- Reduced urine output (<0.5 ml/kg/hour)
- Lactate >2 mmol/L
Cardiac cause: Evidence of cardiac dysfunction (echo, ECG, clinical)

SHOCK Trial Criteria:

SBP <90 for >30 minutes
Cardiac index <2.2 L/min/m²
PCWP >15 mmHg
Evidence of end-organ hypoperfusion

7. Management

Management Algorithm

        CARDIOGENIC SHOCK PRESENTATION
    (Hypotension + signs of poor perfusion + cardiac cause)
                    ↓
┌─────────────────────────────────────────────────┐
│         IMMEDIATE ASSESSMENT (&lt;5 mins)          │
│  • ABCDE approach                                │
│  • High-flow oxygen                              │
│  • IV access (large bore x2)                     │
│  • Arterial line (if unstable)                   │
│  • 12-lead ECG                                   │
│  • Urgent echo                                   │
│  • Do NOT give large fluid boluses               │
└─────────────────────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────┐
│         IDENTIFY UNDERLYING CAUSE                │
├─────────────────────────────────────────────────┤
│  ACUTE MI                                       │
│  → Urgent cardiac catheterization                │
│  → Primary PCI (if STEMI)                        │
│  → Revascularization within 90 mins             │
│                                                  │
│  MECHANICAL COMPLICATION                        │
│  → Urgent echo to confirm                        │
│  → Surgical repair (VSR, papillary muscle)       │
│  → Bridge with IABP/ECMO if needed               │
│                                                  │
│  ARRHYTHMIA                                     │
│  → DC cardioversion if unstable                  │
│  → Antiarrhythmics                              │
│  → Pacing if bradycardia                         │
│                                                  │
│  OTHER (myocarditis, decompensated HF)          │
│  → Supportive care                               │
│  → Treat underlying cause                       │
└─────────────────────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────┐
│         SUPPORTIVE MANAGEMENT                    │
│  • Inotropes (dobutamine)                        │
│  • Vasopressors (noradrenaline) if needed        │
│  • Diuretics (if pulmonary oedema)               │
│  • Consider mechanical support (IABP/ECMO)      │
│  • Monitor closely (ICU/HDU)                    │
└─────────────────────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────┐
│         RESPONSE TO TREATMENT                    │
├─────────────────────────────────────────────────┤
│  Improving (BP ↑, lactate ↓, urine output ↑)   │
│  → Continue current therapy                      │
│  → Wean support gradually                        │
│  → Monitor for complications                     │
│                                                  │
│  Not improving or deteriorating                 │
│  → Escalate mechanical support                   │
│  → Consider ECMO                                │
│  → Consider LVAD or transplant evaluation       │
└─────────────────────────────────────────────────┘

Acute/Emergency Management - The First Hour

Immediate Actions (Do Simultaneously):

Recognize the Emergency
- Hypotension + signs of poor perfusion = shock
- Identify cardiac cause (ECG, echo, clinical)
- Do not delay—mortality increases with time
High-Flow Oxygen
- 15 L/min via non-rebreather mask
- Target SpO2 >90%
- Consider CPAP/intubation if severe pulmonary oedema
IV Access
- Large bore cannulae x2 (16-18G)
- Central line if vasopressors needed
- Arterial line for continuous BP monitoring
Do NOT Give Large Fluid Boluses
- Critical: Cardiogenic shock is NOT hypovolaemic
- Fluid will worsen pulmonary oedema
- Small boluses (250ml) only if truly hypovolaemic
- Monitor response carefully
Urgent Investigations
- 12-lead ECG (identify MI, arrhythmias)
- Echocardiogram (assess LV function, complications)
- Troponin, BNP, lactate
- CXR

Medical Management

Inotropes (First-Line Support):

Drug	Dose	Route	Mechanism	Notes
Dobutamine	2.5-15 mcg/kg/min	IV infusion	Increases contractility, mild vasodilation	First-line inotrope
Milrinone	0.375-0.75 mcg/kg/min	IV infusion	Phosphodiesterase inhibitor	Use if beta-blocker on board
Dopamine	2-20 mcg/kg/min	IV infusion	Inotrope + vasopressor	Less preferred (arrhythmogenic)

Mechanism: Increases myocardial contractility → improves cardiac output → improves BP and perfusion

Monitoring:

Continuous ECG (arrhythmia risk)
BP (should improve)
Lactate (should decrease)
Urine output (should increase)

Vasopressors (If Still Hypotensive):

Drug	Dose	Route	Mechanism	Notes
Noradrenaline	0.05-0.5 mcg/kg/min	IV infusion	Vasoconstriction	First-line vasopressor
Adrenaline	0.05-0.5 mcg/kg/min	IV infusion	Inotrope + vasopressor	Use if severe
Vasopressin	0.01-0.04 units/min	IV infusion	Vasoconstriction	Adjunctive therapy

Mechanism: Increases systemic vascular resistance → improves BP → improves coronary perfusion

Use Only If: Still hypotensive despite inotropes

Diuretics (If Pulmonary Oedema):

Drug	Dose	Route	Notes
Furosemide	20-40mg	IV	Cautious—may worsen renal function

Mechanism: Reduces preload → reduces pulmonary oedema

Caution: May worsen renal function; monitor closely

Mechanical Circulatory Support

Intra-Aortic Balloon Pump (IABP):

Indication	Mechanism	Duration	Notes
Bridge to revascularization	Reduces afterload, improves coronary perfusion	Days	Common in MI-related shock
Bridge to surgery	Stabilizes before operation	Days	For mechanical complications
Bridge to recovery	Supports while heart recovers	Days to weeks	For myocarditis, post-MI

Contraindications: Aortic regurgitation, aortic dissection, severe peripheral vascular disease

Extracorporeal Membrane Oxygenation (ECMO):

Type	Indication	Mechanism	Duration
VA-ECMO	Refractory cardiogenic shock	Complete circulatory + respiratory support	Days to weeks
VV-ECMO	Respiratory failure only	Respiratory support only	Days to weeks

Indications:

Refractory shock despite IABP and inotropes
Bridge to recovery, transplant, or LVAD
Post-cardiac arrest

Left Ventricular Assist Device (LVAD):

Indication	Type	Duration	Notes
Bridge to transplant	Temporary LVAD	Months	Awaiting heart transplant
Destination therapy	Permanent LVAD	Years	Not eligible for transplant
Bridge to recovery	Temporary LVAD	Months	May recover function

Revascularization (If Acute MI)

Primary PCI (If STEMI):

Timing: Within 90 minutes (ideally <60 minutes)
Goal: Restore coronary blood flow
Benefit: Can dramatically improve LV function
Outcome: Better if done early

CABG (If Multi-Vessel Disease):

Indication: Multi-vessel disease, not suitable for PCI
Timing: Urgent (within 24-48 hours)
Benefit: Complete revascularization

Surgical Management (If Mechanical Complications)

Ventricular Septal Rupture (VSR):

Indication: New harsh murmur, sudden deterioration
Procedure: Surgical repair
Timing: Urgent (within 24-48 hours)
Bridge: IABP or ECMO while waiting

Papillary Muscle Rupture:

Indication: Acute severe MR, sudden deterioration
Procedure: Mitral valve repair or replacement
Timing: Urgent

Free Wall Rupture:

Indication: Cardiac tamponade, sudden collapse
Procedure: Surgical repair (if survives)
Timing: Immediate
Prognosis: Usually fatal

Disposition

Admit to ICU/HDU (Always):

Requires continuous monitoring
Needs inotropes/vasopressors
May need mechanical support
High risk of complications

Monitoring:

Continuous ECG, BP, SpO2
Hourly urine output
Serial lactate
Daily echo (assess recovery)

Discharge Criteria (Rare in Acute Phase):

Stable off inotropes
Normal BP without support
Improving LV function
No complications
Clear plan for follow-up

Follow-Up:

Cardiology clinic: Within 1-2 weeks
Echocardiogram: Serial to assess recovery
Medication optimization: ACE inhibitor, beta-blocker once stable
Consider: Cardiac rehabilitation, device therapy (ICD, CRT)

8. Complications

Immediate (Hours)

Complication	Incidence	Presentation	Management
Cardiac arrest	20-30%	Loss of consciousness, VF/VT	CPR, defibrillation, ECMO
Arrhythmias	30-40%	VT, VF, AF, bradycardia	DC cardioversion, antiarrhythmics
Multi-organ failure	40-50%	AKI, liver failure, gut ischemia	Supportive care, may need dialysis
Mechanical complications	5-10%	VSR, papillary muscle rupture	Urgent surgery
Thromboembolism	5-10%	Stroke, PE, limb ischemia	Anticoagulation, consider

Cardiac Arrest:

Mechanism: Severe pump failure → VF/VT or asystole
Management: CPR, defibrillation, consider ECMO
Prognosis: Very poor (mortality 70-80%)

Multi-Organ Failure:

Kidneys: AKI from hypoperfusion
Liver: Ischemic hepatitis
Gut: Ischemia, risk of bacterial translocation
Brain: Hypoxic injury

Early (Days)

1. Acute Kidney Injury (40-50%)

Cause: Renal hypoperfusion
Management: Supportive, may need dialysis
Prevention: Maintain adequate BP, avoid nephrotoxins

2. Arrhythmias (30-40%)

VT/VF: High risk in first 48 hours
AF: Common, may need cardioversion
Bradycardia: Conduction blocks
Management: Antiarrhythmics, pacing if needed

3. Infection (20-30%)

Pneumonia: Ventilation, immobility
Line infections: Central lines, IABP
Management: Antibiotics, aseptic technique

4. Bleeding (10-20%)

Cause: Anticoagulation, procedures, coagulopathy
Management: Transfusion, reverse anticoagulation if needed

Late (Weeks-Months)

1. Persistent Heart Failure (30-40%)

Mechanism: Irreversible myocardial damage
Management: Long-term medications, consider device therapy
Prognosis: Poor long-term survival

2. Recurrent Shock (10-20%)

Cause: Underlying heart failure, new events
Management: Optimize medications, consider advanced therapies

3. Reduced Quality of Life

Symptoms: Persistent fatigue, breathlessness
Management: Cardiac rehabilitation, psychological support

4. End-Stage Heart Failure

Progression: Despite optimal therapy
Options: Heart transplantation, LVAD, palliative care

9. Prognosis & Outcomes

Natural History (Without Treatment)

Untreated Cardiogenic Shock:

Mortality: Near 100% within hours to days
Progression: Rapid deterioration → multi-organ failure → death
Time course: Death often within 24-48 hours if untreated

Outcomes with Treatment

Variable	Outcome	Notes
In-hospital mortality	40-50%	Improved from 80% historically
30-day mortality	45-55%	Higher in elderly, comorbidities
1-year survival	30-40%	Depends on cause and recovery
5-year survival	20-30%	Poor long-term prognosis
Need for advanced therapies	10-20%	LVAD or transplant

Factors Affecting Outcomes:

Good Prognosis:

Younger age (<65 years)
Reversible cause (arrhythmia, correctable)
Early revascularization (if MI, <90 minutes)
Rapid response to treatment (<6 hours)
No multi-organ failure
Good baseline function (before event)

Poor Prognosis:

Older age (>75 years)
Large MI (anterior, extensive)
Delayed presentation (>6 hours)
Multi-organ failure
Mechanical complications (VSR, rupture)
Previous heart failure
Multiple comorbidities

Prognostic Factors

Factor	Impact on Prognosis	Evidence Level
Age	Each decade increases mortality 1.5x	High
Time to revascularization	Each hour increases mortality 3-5%	High
Lactate level	>4 mmol/L = 2x mortality	High
Multi-organ failure	Each organ = 2x mortality	High
LVEF	<20% = worse prognosis	High
Mechanical complications	VSR/rupture = very poor	High

10. Evidence & Guidelines

Key Guidelines

1. ESC Heart Failure Guidelines (2021) — Comprehensive guidelines for acute and chronic heart failure. European Society of Cardiology

Key Recommendations:

Immediate inotropic support for cardiogenic shock
Urgent revascularization if MI-related (<90 minutes)
Consider mechanical support (IABP, ECMO) early
Evidence Level: 1A

2. AHA/ACC Heart Failure Guidelines (2022) — US guidelines for heart failure management. American Heart Association

Key Recommendations:

Rapid assessment and treatment
Inotropes + vasopressors as needed
Urgent revascularization for MI
Consider mechanical support
Evidence Level: 1A

3. SHOCK Trial Guidelines (1999) — Landmark trial establishing revascularization benefit. New England Journal of Medicine

Key Recommendations:

Early revascularization improves survival in MI-related shock
Evidence Level: 1A

Landmark Trials

SHOCK Trial (1999) — Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock

Patients: 302 patients with cardiogenic shock post-MI
Intervention: Early revascularization (PCI or CABG) vs. medical therapy
Key Finding: 6-month mortality 50% vs. 63% (absolute reduction 13%)
Clinical Impact: Established benefit of early revascularization
PMID: 10471456

IABP-SHOCK II Trial (2012) — Intra-Aortic Balloon Pump in Cardiogenic Shock

Patients: 600 patients with cardiogenic shock
Intervention: IABP vs. no IABP
Key Finding: No mortality benefit from IABP (39.7% vs. 41.3%)
Clinical Impact: IABP not routinely recommended (but still used as bridge)
PMID: 22920912

CULPRIT-SHOCK Trial (2017) — PCI Strategy in Cardiogenic Shock

Patients: 706 patients with MI and cardiogenic shock
Intervention: Complete revascularization vs. culprit-only PCI
Key Finding: Culprit-only PCI better (mortality 43.3% vs. 51.5%)
Clinical Impact: Don't do complete revascularization in shock
PMID: 29103656

Evidence Strength

Intervention	Level	Key Evidence	Clinical Recommendation
Early revascularization (MI)	1A	SHOCK Trial	Urgent PCI/CABG if MI-related
Inotropes	1B	Guidelines, observational	Dobutamine first-line
Vasopressors	1B	Guidelines	Noradrenaline if still hypotensive
IABP	2B	IABP-SHOCK II (no benefit)	Consider as bridge, not routine
ECMO	2B	Observational studies	Consider if refractory
Mechanical support	2B	Case series	Consider early if available

11. Patient/Layperson Explanation

What is Cardiogenic Shock?

Imagine your heart as a water pump that suddenly loses most of its power. In cardiogenic shock, your heart can't pump enough blood around your body, even though there's plenty of blood available. It's like a car engine that's lost most of its cylinders—it's running, but barely, and everything else in the car starts to fail because it's not getting enough power.

In simple terms: Your heart stops pumping effectively, so your body doesn't get enough oxygen and nutrients, causing your organs to start shutting down.

Why does it matter?

Cardiogenic shock is extremely serious and life-threatening. Without quick treatment, your organs (brain, kidneys, liver) don't get enough blood and start to fail. Even with the best treatment, about 4-5 out of 10 people don't survive. The good news? With rapid, expert care, many people do recover, especially if the cause can be fixed quickly (like opening a blocked artery in a heart attack).

Think of it like this: It's like a power outage—everything stops working. You need emergency power (medical support) while the main system (your heart) is being fixed.

How is it treated?

1. Supporting Your Heart: Doctors give you medicines (inotropes) that help your heart pump stronger, like giving a weak engine a boost. These are given through a drip in your arm.

2. Supporting Your Blood Pressure: If your blood pressure is still too low, other medicines (vasopressors) help tighten your blood vessels to keep blood pressure up.

3. Fixing the Cause:

If it's a heart attack: Doctors urgently open the blocked artery (angioplasty)
If it's a valve problem: May need urgent surgery
If it's an irregular heartbeat: Doctors fix the rhythm

4. Mechanical Support: Sometimes doctors use special machines to help your heart pump while it recovers:

IABP: A balloon in your aorta that helps your heart
ECMO: A machine that does the work of your heart and lungs temporarily

The goal: Support your heart and body while fixing the underlying problem, giving your heart time to recover.

What to expect

In the Hospital:

Intensive Care: You'll be in ICU, closely monitored 24/7
First few days: Most critical period—doctors will support your heart with medicines and machines
Days 3-7: If improving, doctors will gradually reduce support
Weeks 1-2: If stable, you'll move to a regular ward
Going home: Usually after 1-3 weeks if you're recovering well

After Going Home:

Medications: You'll need medicines every day to help your heart stay strong
Lifestyle changes: Less salt, fluid restriction, regular exercise (as able)
Follow-up: Regular doctor visits, tests to check your heart
Recovery: Can take weeks to months to feel back to normal

Recovery Time:

In hospital: 1-3 weeks typically
At home: 2-6 months to feel stronger
Long-term: Many people can live normal lives with the right medications and care

When to seek help

Call 999 (or your emergency number) immediately if:

You suddenly feel very weak or faint
You can't catch your breath
You feel confused or "not yourself"
Your chest hurts badly
You feel like something is very wrong

See your doctor urgently if:

You're more breathless than usual
Your ankles or legs are swelling
You're more tired than usual
You're gaining weight quickly
You feel dizzy or lightheaded

Remember: If you've had a heart attack or heart problems before and suddenly feel very unwell, don't wait—get help immediately. Cardiogenic shock can develop quickly.

12. References

Primary Guidelines

McDonagh TA, Metra M, Adamo M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599-3726. [PMID: 34447992]
Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032. [PMID: 35363499]

Key Trials

Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock (SHOCK Trial). N Engl J Med. 1999;341(9):625-634. [PMID: 10471456]
Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II). Lancet. 2013;382(9905):1638-1645. [PMID: 22920912]
Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock (CULPRIT-SHOCK). N Engl J Med. 2017;377(25):2419-2432. [PMID: 29103656]
Ponikowski P et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2016;37(27):2129-2200. [PMID: 27206819]
Mebazaa A et al. Short-term survival by treatment among patients hospitalized with acute heart failure: the global ALARM-HF registry. Intensive Care Med. 2011;37(2):290-301. [PMID: 21086121]
Thiele H et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012;367(14):1287-1296. [PMID: 22920912]
Ouweneel DM et al. Percutaneous mechanical circulatory support versus intra-aortic balloon pump in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017;69(3):278-287. [PMID: 27810347]
Baran DA et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv. 2019;94(1):29-37. [PMID: 30957961]
van Diepen S et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2017;136(16):e52-e68. [PMID: 28923988]
Hochman JS et al. One-year survival following early revascularization for cardiogenic shock. JAMA. 2001;285(2):190-192. [PMID: 11176812]
De Backer D et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-789. [PMID: 20200382]
Levy B et al. Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2018;72(2):173-182. [PMID: 29976291]
Jentzer JC et al. Contemporary management of severe acute kidney injury and refractory cardiogenic shock: SCAI SHOCK statement update. Catheter Cardiovasc Interv. 2020;96(7):1189-1200. [PMID: 32621614]
Tehrani BN et al. Standardized Team-Based Care for Cardiogenic Shock. J Am Coll Cardiol. 2019;73(13):1659-1669. [PMID: 30947916]

13. Examination Focus

Common Exam Questions

1. "What is the definition of cardiogenic shock?"

Answer: Cardiogenic shock is defined as persistent hypotension (SBP <90 mmHg or MAP <65 mmHg for >30 minutes) with evidence of end-organ hypoperfusion (altered mental status, cold extremities, oliguria, elevated lactate) due to primary cardiac dysfunction, despite adequate volume resuscitation.

2. "What are the haemodynamic criteria for cardiogenic shock?"

Answer: CI <2.2 L/min/m², PCWP >15 mmHg, elevated SVR, and low SBP. This distinguishes it from hypovolaemic shock (low PCWP) and septic shock (low SVR).

3. "What is the first-line vasopressor in cardiogenic shock?"

Answer: Noradrenaline. Dopamine is associated with higher arrhythmia rates per the De Backer trial. Dobutamine is an inotrope, not a vasopressor.

Common Mistakes

❌ Using Dopamine as first-line: De Backer trial showed higher mortality/arrhythmias with dopamine vs noradrenaline.
❌ Aggressive fluid resuscitation: Cardiogenic shock patients are already "wet". Fluids worsen pulmonary oedema. Exception: RV infarction.
❌ Delayed revascularization in AMI-CS: SHOCK trial showed early revascularization improves survival, despite initial no difference at 30 days.
❌ Complete revascularization acutely: CULPRIT-SHOCK showed culprit-only PCI is safer initially.
❌ Relying on IABP: IABP-SHOCK II showed no mortality benefit from IABP.

Viva Points

Scenario 1: The Post-MI Shock

"A 65-year-old male has anterior STEMI, BP 80/50, HR 110, cold peripheries, Lactate 5. How do you manage?" Answer: "This is cardiogenic shock post-MI. I would give Noradrenaline to maintain MAP >65. Arrange urgent coronary angiography with view to PCI (culprit-only). Consider IABP or Impella if haemodynamically unstable in cath lab. Avoid aggressive fluids. ICU admission."

Scenario 2: The IABP Question

"What is the evidence for IABP in cardiogenic shock?" Answer: "IABP-SHOCK II trial (2012) showed no mortality benefit from IABP in cardiogenic shock post-MI. Current guidelines suggest against routine use (Class III). However, it may still be used as a bridge or for mechanical complications."

Advanced MCQ Bank

Case 1: Culprit vs Complete A patient with cardiogenic shock from STEMI has 3-vessel disease on angiography. Question: What is the recommended revascularization strategy?

A) Complete revascularization of all vessels
B) Culprit lesion only PCI
C) CABG
D) Medical management Correct: B. CULPRIT-SHOCK trial showed culprit-only PCI reduces mortality vs complete revascularization in acute setting.

Case 2: The Cold Wet Patient A patient has BP 85/60, pulmonary oedema, cold hands, Lactate 4. Question: What is the haemodynamic profile?

A) Warm and Wet
B) Cold and Dry
C) Cold and Wet
D) Warm and Dry Correct: C. Cold (poor perfusion) + Wet (congested) = Cardiogenic shock.

Case 3: The RV Infarction Trap An inferior MI patient has hypotension, clear lungs, elevated JVP. Question: What is the management difference?

A) Give inotropes
B) Give fluids
C) Urgent dialysis
D) Pericardiocentesis Correct: B. RV infarction requires preload (fluids), unlike LV cardiogenic shock where fluids are harmful.

13. Differential Diagnosis

Conditions to Consider

Cardiogenic shock must be distinguished from other forms of shock and acute heart failure presentations:

Condition	Key Distinguishing Features	Investigation	Management Difference
Hypovolaemic shock	History of fluid loss, no pulmonary oedema, responds to fluids	CVP low, clear lungs on CXR	Give fluids (unlike cardiogenic)
Septic shock	Fever, infection source, warm peripheries initially	WCC high, lactate high, blood cultures	Antibiotics, fluids initially
Anaphylactic shock	Allergen exposure, urticaria, wheeze, rapid onset	Clinical diagnosis	Adrenaline IM, fluids
Pulmonary embolism	Sudden onset dyspnoea, chest pain, risk factors	CTPA shows clot, echo shows RV strain	Anticoagulation, thrombolysis
Cardiac tamponade	Raised JVP, muffled heart sounds, pulsus paradoxus	Echo shows pericardial effusion	Pericardiocentesis
Tension pneumothorax	Unilateral reduced air entry, tracheal deviation	Clinical + CXR	Needle decompression
Acute severe MR	New murmur, may not have hypotension initially	Echo shows regurgitation	Urgent valve surgery
Acute severe AS	Slow onset, elderly, history of AS	Echo shows severe stenosis	Urgent valve replacement
RV infarction	Inferior MI, elevated JVP, clear lungs, hypotension	ECG (RV leads), echo	Fluids (unlike LV shock)
Myocarditis	Younger patient, viral prodrome, troponin elevated	Echo, cardiac MRI, viral serology	Supportive, immunosuppression if severe

Clinical Differentiation

"Cold vs. Warm" and "Wet vs. Dry" Classification:

Type	Perfusion	Congestion	Clinical Features	Diagnosis
Cold & Wet	Poor	Yes	Hypotension, pulmonary oedema, poor perfusion	Cardiogenic shock
Cold & Dry	Poor	No	Hypotension, no oedema, poor perfusion	Hypovolaemic shock
Warm & Wet	Adequate	Yes	Normal BP, pulmonary oedema, warm peripheries	Acute decompensated HF
Warm & Dry	Adequate	No	Stable, compensated	Compensated HF

Hemodynamic Profiles:

Shock Type	Cardiac Output	SVR	PCWP	CVP	Treatment
Cardiogenic	Low	High	High	High	Inotropes, reduce preload
Hypovolaemic	Low	High	Low	Low	Fluids
Septic (early)	High	Low	Low	Low	Fluids, antibiotics
Septic (late)	Low	High	Variable	Variable	Inotropes, antibiotics
Obstructive	Low	High	Variable	High	Remove obstruction

Mimics & Pitfalls

1. RV Infarction Masquerading as Cardiogenic Shock:

Clue: Inferior MI + elevated JVP + clear lungs + hypotension
Key difference: Needs fluids (unlike LV shock)
Investigation: ECG (RV leads V3R-V4R), echo (RV dysfunction)
Management: Fluid challenge (unlike LV shock where fluids worsen)

2. Pulmonary Embolism:

Clue: Sudden dyspnoea, chest pain, RV strain on echo
Key difference: No LV dysfunction
Investigation: CTPA, D-dimer, echo
Management: Anticoagulation, thrombolysis if massive

3. Cardiac Tamponade:

Clue: Beck's triad (hypotension, raised JVP, muffled heart sounds)
Key difference: Pericardial effusion on echo
Investigation: Echo (effusion with RV collapse in diastole)
Management: Urgent pericardiocentesis

4. Septic Shock with Pre-existing Heart Disease:

Clue: Fever, infection source, may have cardiac history
Key difference: Responds to antibiotics + fluids
Investigation: Blood cultures, lactate, echo
Management: Antibiotics, fluids first (then inotropes if needed)

14. Prevention & Risk Reduction

Primary Prevention (Before First Event)

Cardiovascular Risk Factor Management:

Risk Factor	Target	Intervention	Evidence Level
Hypertension	BP less than 140/90 mmHg (less than 130/80 if high risk)	Lifestyle + antihypertensives	1A
Dyslipidaemia	LDL less than 1.8 mmol/L (high risk)	Statins	1A
Diabetes	HbA1c less than 53 mmol/mol (7%)	Lifestyle, metformin, newer agents	1A
Smoking	Complete cessation	Smoking cessation support	1A
Obesity	BMI 20-25 kg/m²	Diet, exercise, bariatric surgery if severe	1B
Physical inactivity	150 min moderate exercise/week	Structured exercise program	1A

Mechanism: Reduces risk of MI and heart failure, the two main causes of cardiogenic shock

Coronary Artery Disease Screening:

High-risk patients: Diabetes, family history, multiple risk factors
Tools: Stress testing, CT coronary angiogram
Action: Revascularization if significant disease

Secondary Prevention (After MI or Heart Event)

Post-MI Medications (Reduce Risk of Shock):

Drug Class	Example	Dose	Benefit	Evidence
Antiplatelet	Aspirin + Ticagrelor	75mg + 90mg BD	Prevents re-infarction	1A
Statin	Atorvastatin	80mg daily	Stabilizes plaques, reduces events	1A
ACE inhibitor	Ramipril	10mg daily	Prevents LV remodelling	1A
Beta-blocker	Bisoprolol	10mg daily	Reduces arrhythmias, improves LV function	1A
Mineralocorticoid antagonist	Eplerenone	50mg daily	If LVEF less than 40%	1A

Cardiac Rehabilitation:

Components: Exercise, education, psychological support
Benefit: Reduces mortality by 20-30%
Duration: 8-12 weeks typically
Evidence: 1A

Device Therapy (If LVEF less than 35%):

Device	Indication	Benefit	Evidence
ICD	LVEF less than 35% after 40 days post-MI	Prevents sudden cardiac death	1A
CRT	LVEF less than 35% + LBBB + symptomatic HF	Improves symptoms, reduces mortality	1A

Tertiary Prevention (Preventing Recurrence)

Heart Failure Optimization:

Guideline-directed medical therapy: ACE-I/ARB, beta-blocker, MRA, SGLT2 inhibitor
Regular monitoring: Echo, BNP, symptoms
Early escalation: If worsening symptoms

Lifestyle Modifications:

Modification	Target	Rationale	Evidence
Fluid restriction	1.5-2L/day if HF	Reduces congestion	1B
Salt restriction	less than 2g sodium/day	Reduces fluid retention	1B
Weight monitoring	Daily weight	Early detection of decompensation	1B
Alcohol limit	less than 14 units/week (or abstain if cardiomyopathy)	Reduces myocardial toxicity	1B
Smoking cessation	Complete	Reduces all cardiovascular events	1A

Patient Education:

Recognize warning signs (breathlessness, swelling, weight gain)
Medication adherence
When to seek help
Self-management strategies

Hospital Systems to Prevent Shock

Acute MI Pathways:

Door-to-balloon time less than 90 minutes: Reduces risk of shock developing
24/7 PCI availability: Immediate revascularization
Shock team: Early recognition and intervention

Heart Failure Clinics:

Regular follow-up for chronic HF patients
Optimization of medications
Early intervention if decompensating

15. Special Populations & Considerations

Elderly Patients (>75 Years)

Epidemiology:

Incidence: 2x higher than younger patients
Mortality: 60-70% (vs. 40-50% in younger)
Presentation: Atypical (confusion, falls, weakness)

Management Considerations:

Issue	Challenge	Approach
Polypharmacy	Drug interactions, side effects	Review all medications, stop non-essential
Renal dysfunction	Common, affects drug dosing	Dose adjust all medications
Cognitive impairment	Difficulty with consent, compliance	Involve family, simplified regimens
Frailty	Poor tolerance of invasive procedures	Consider risks vs. benefits carefully
Comorbidities	Multiple conditions affecting outcomes	Holistic approach

Treatment Adjustments:

Lower starting doses: Especially inotropes (increased sensitivity)
Careful fluid balance: Higher risk of overload
Consider goals of care: Early discussions about ceilings of treatment
Palliative approach: If very frail or multiple comorbidities

Prognosis:

Worse than younger patients
Consider quality of life vs. aggressive intervention
30-day mortality: 60-70%

Pregnancy & Peripartum

Causes of Cardiogenic Shock in Pregnancy:

Cause	Timing	Key Features	Management
Peripartum cardiomyopathy	Last month pregnancy to 5 months postpartum	New-onset HF, no prior heart disease	Supportive, bromocriptine, delivery if antenatal
Pre-eclampsia/Eclampsia	>20 weeks pregnancy	Hypertension, proteinuria, pulmonary oedema	Magnesium, antihypertensives, delivery
Amniotic fluid embolism	During/immediately after delivery	Sudden collapse, DIC, shock	Supportive, ICU care
Myocardial infarction	Any time	Rare, similar presentation to non-pregnant	PCI, medications (avoid ACE-I, ARB)

Management Principles:

Multidisciplinary team: Obstetrics, cardiology, anaesthetics, ICU
Fetal monitoring: If antenatally
Delivery considerations: May need urgent delivery if deteriorating
Medication safety: Avoid ACE-I, ARB, statins (teratogenic)
Safe drugs: Beta-blockers (labetalol), hydralazine, digoxin
Mechanical support: ECMO, IABP can be used if needed

Prognosis:

Depends on cause
Peripartum cardiomyopathy: 50% recover, 25% persistent dysfunction, 25% worsen
Multidisciplinary care improves outcomes

Renal Dysfunction & Dialysis Patients

Challenges:

Issue	Impact	Management
Fluid overload	Common, worsens pulmonary oedema	Dialysis/ultrafiltration
Drug dosing	Many drugs need adjustment	Dose reduction, avoid nephrotoxins
Contrast exposure	Risk of contrast-induced AKI	Minimize contrast, hydration protocols
Uraemic cardiomyopathy	Pre-existing LV dysfunction	Optimize dialysis

Management Approach:

Early dialysis: If fluid overload despite diuretics
Ultrafiltration: Can remove fluid without worsening electrolytes
Medication review: Adjust all doses for renal function
Nephrology involvement: Early consultation

Prognosis:

Worse than patients with normal renal function
Mortality: 60-70% (higher than general population)

Post-Cardiac Surgery

Causes:

Myocardial stunning: Temporary dysfunction post-bypass
Graft failure: Occluded graft or native vessel
Tamponade: Pericardial effusion
Bleeding: Hypovolaemia mimicking shock

Management:

High-dose inotropes: Often needed immediately post-op
Mechanical support: IABP, ECMO commonly used
Re-exploration: If bleeding or tamponade suspected
Time: Myocardial stunning usually improves over 24-48 hours

Prognosis:

If myocardial stunning: Usually recovers
If graft failure: May need re-operation or prolonged support
Mortality: 30-40% if true cardiogenic shock

Diabetes Mellitus

Special Considerations:

Issue	Impact	Management
Silent ischemia	May not feel chest pain	Lower threshold for investigation
Larger infarcts	Microvascular disease	More aggressive revascularization
Worse outcomes	1.5-2x mortality	Intensive glycaemic control, optimal therapy
Renal dysfunction	Common comorbidity	Careful dosing, avoid nephrotoxins

Management:

Glycaemic control: Target glucose 6-10 mmol/L (avoid hypo)
Continue diabetic medications: If tolerating (may need insulin if unwell)
Renal protection: Minimize contrast, maintain adequate BP
Aggressive risk factor modification: Post-discharge

Chronic Heart Failure Patients

Presentation:

Often acute-on-chronic deterioration
May have precipitant (infection, non-adherence, arrhythmia)
Baseline LV dysfunction already present

Management Differences:

Lower threshold for mechanical support: Already compromised
Home medications: Continue if stable, stop if hypotensive
Device therapy: May already have ICD/CRT (check functioning)
Advanced therapies: Earlier consideration of LVAD or transplant
Palliative care: Discuss goals of care if end-stage

Prognosis:

Worse than de novo cardiogenic shock
Higher risk of recurrence
May need advanced therapies (LVAD, transplant)

Last Reviewed: 2025-12-24 | MedVellum Editorial Team

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists. This information is not a substitute for professional medical advice, diagnosis, or treatment.

Overview

Cardiogenic Shock

1. Clinical Overview

Summary

Key Facts

Definition: Inadequate cardiac output despite adequate preload, leading to tissue hypoperfusion
Incidence: 5-10% of acute MI cases; ~40,000-50,000 cases/year in US
Mortality: 40-50% in-hospital mortality (down from 80% historically)
Time to treatment: Every hour of delay increases mortality by 3-5%
Critical threshold: Cardiac index <2.2 L/min/m² with evidence of hypoperfusion
Key investigation: Echocardiogram (assess LV function), cardiac catheterization (if MI)
First-line treatment: Inotropes (dobutamine), vasopressors (noradrenaline), urgent revascularization if MI

Clinical Pearls

"Cold and wet = Cardiogenic shock" — Cold extremities (poor perfusion) + pulmonary oedema (wet) = classic cardiogenic shock. This distinguishes it from hypovolaemic shock (cold and dry) or septic shock (warm and wet).

"The heart is the problem, not the solution" — Unlike other types of shock, giving more fluid won't help—it will make things worse by increasing preload on a failing heart. The heart itself needs support.

"Time is myocardium, myocardium is life" — In MI-related shock, every minute of delay in revascularization increases mortality. Door-to-balloon time should be <90 minutes, ideally <60 minutes.

"Mechanical support buys time" — IABP, ECMO, or LVAD can stabilize patients while waiting for recovery or definitive treatment. Don't hesitate to escalate early.

Why This Matters Clinically

2. Epidemiology

Incidence & Prevalence

Acute MI-related: 5-10% of STEMI cases, 2-3% of NSTEMI cases
Overall: ~40,000-50,000 cases/year in US; ~5,000-8,000/year in UK
Trend: Decreasing incidence (better MI treatment) but mortality remains high
Peak age: 65-75 years (but can occur at any age)

Demographics

Factor	Details
Age	Median age 70 years; rare <50 unless acute MI or myocarditis
Sex	Slight male predominance (55:45) in younger patients; equal in elderly
Ethnicity	Higher rates in Black populations (1.5x); earlier onset
Geography	Higher in areas with limited access to PCI/advanced care
Setting	Emergency departments, cardiac catheterization labs, ICUs

Risk Factors

Non-Modifiable:

Age >65 years
Male sex (younger patients)
Previous MI or heart failure
Family history of cardiomyopathy

Modifiable:

Risk Factor	Relative Risk	Mechanism
Acute MI (large territory)	10-15x	Extensive myocardial damage
Anterior MI	3-5x	Larger infarct size
Delayed presentation	2-3x	More myocardium lost
Diabetes	2x	Worse outcomes, microvascular disease
Hypertension	1.5x	Pre-existing LV dysfunction
Renal dysfunction	2x	Worse outcomes, fluid management challenges
Previous heart failure	3x	Already compromised function

Precipitating Causes

Cause	Frequency	Mechanism
Acute MI (large)	60-70%	Extensive myocardial necrosis
Acute MI (mechanical complications)	5-10%	VSR, papillary muscle rupture, free wall rupture
Acute decompensated heart failure	15-20%	Sudden worsening of chronic HF
Myocarditis	3-5%	Inflammatory myocardial damage
Arrhythmias	5-10%	VT, VF, severe bradycardia
Valvular emergencies	3-5%	Acute severe MR, AS
Post-cardiac surgery	2-3%	Myocardial stunning
Takotsubo cardiomyopathy	1-2%	Stress-induced

3. Pathophysiology

The Vicious Cycle of Cardiogenic Shock

Step 1: Initial Cardiac Insult

Acute MI: Large territory infarction → loss of 40%+ of LV myocardium
Other causes: Myocarditis, arrhythmia, valvular emergency
Result: Sudden reduction in cardiac contractility

Step 2: Reduced Cardiac Output

Stroke volume: Decreases dramatically (normal: 60-80ml; shock: <40ml)
Cardiac output: Falls below critical threshold (<2.2 L/min/m²)
Blood pressure: Drops (SBP <90 mmHg)

Step 3: Compensatory Mechanisms (Initially Helpful)

Sympathetic activation: Tachycardia, vasoconstriction
Renin-angiotensin system: Fluid retention, vasoconstriction
Result: Temporary maintenance of BP

Step 4: The Vicious Cycle Begins

Reduced coronary perfusion: Low BP → reduced coronary blood flow
Worsening ischemia: Already damaged heart gets less oxygen
Further dysfunction: Heart pumps even worse
Lower BP: Cycle continues

Step 5: End-Organ Hypoperfusion

Brain: Confusion, altered mental status
Kidneys: Reduced urine output, AKI
Gut: Ischemia, lactic acidosis
Skin: Cold, clammy extremities

Step 6: Multi-Organ Failure

If untreated: Progressive organ failure → death
Time course: Hours to days without support

Classification by Cause

Type	Mechanism	Common Causes	Clinical Features
Pump failure (LV)	Reduced contractility	Large MI, myocarditis	Pulmonary oedema, low output
Pump failure (RV)	RV infarction	Inferior MI with RV involvement	Elevated JVP, clear lungs
Mechanical complications	Structural damage	VSR, papillary muscle rupture	New murmur, sudden deterioration
Arrhythmic	Rate/rhythm problems	VT, VF, severe bradycardia	Arrhythmia evident
Obstructive	Outflow obstruction	Massive PE, cardiac tamponade	Different hemodynamics

Hemodynamic Profile

Parameter	Normal	Cardiogenic Shock
Cardiac index	2.5-4.0 L/min/m²	<2.2 L/min/m²
Systolic BP	100-140 mmHg	<90 mmHg
PCWP	8-12 mmHg	>18 mmHg (elevated)
SVR	800-1200 dynes·s/cm⁵	High (compensatory)
Mixed venous O₂	65-75%	<60% (low)

Anatomical Considerations

Left Ventricular Function:

Normal LVEF: 55-70%
Mild dysfunction: 40-54%
Moderate dysfunction: 30-39%
Severe dysfunction: <30%
In shock: Usually <25%, often <20%

Why Large MIs Cause Shock:

Anterior MI: Affects 40-50% of LV (LAD territory)
Inferior + RV MI: Affects RV and inferior LV
Loss of 40%+ myocardium: Cannot maintain adequate output
Remaining myocardium: Stunned or ischemic

4. Clinical Presentation

Symptoms: The Patient's Story

Typical Presentation (Acute MI-related):

Typical Presentation (Decompensated HF):

Atypical Presentations:

Signs: What You See

Vital Signs (Critical):

Sign	Finding	Significance
Systolic BP	<90 mmHg (often 60-80)	Defines shock
Heart rate	Variable: Tachycardia or bradycardia	May indicate cause
Respiratory rate	Tachypnoea (if pulmonary oedema)	Respiratory distress
SpO2	Low (<90%)	Hypoxia
Temperature	Usually normal or low	Hypoperfusion

General Appearance:

Cardiovascular Examination:

Finding	What It Means	Frequency
Hypotension	SBP <90 mmHg	100% (by definition)
Tachycardia	Compensatory or arrhythmia	60-70%
Bradycardia	Conduction block, medications	10-20%
Elevated JVP	Fluid overload or RV failure	60-70%
S3 gallop	LV dysfunction	50-60%
Murmurs	VSR, MR (mechanical complications)	10-20%
Weak pulse	Low cardiac output	80-90%
Cool extremities	Poor perfusion	90%+

Respiratory Examination:

Finding	What It Means	Clinical Note
Tachypnoea	Respiratory distress	If pulmonary oedema present
Crepitations	Pulmonary oedema	Bilateral, lower zones
Wheeze	"Cardiac asthma"	Bronchial oedema
Reduced air entry	Severe oedema	If present

Other Findings:

Red Flags

[!CAUTION] Red Flags — Immediate Escalation Required:

Systolic BP <90 mmHg with signs of poor perfusion — Defines cardiogenic shock

Altered mental status or confusion — Brain hypoperfusion

Cold, clammy extremities — Poor peripheral perfusion

Reduced urine output (<0.5 ml/kg/hour) — Renal hypoperfusion

Lactate >2 mmol/L — Tissue hypoxia

Cardiac arrest — End-stage shock

Pulmonary oedema with hypotension — Classic cardiogenic shock

New murmur — May indicate mechanical complication (VSR, MR)

Chest pain

Severe, may have resolved (if infarcted)

Severe breathlessness

"Can't breathe," "Drowning"

Weakness/dizziness

"Feel faint," "Can't stand"

Confusion

"Not thinking clearly"

Nausea/vomiting

From hypoperfusion

Rapid progression

Deteriorates over minutes to hours

5. Clinical Examination

Structured Approach: ABCDE

A - Airway

Assessment: Usually patent (unless altered mental status)
Finding: May need protection if GCS <8
Action: Secure airway if compromised

B - Breathing

Look: Tachypnoea, use of accessory muscles, cyanosis
Listen: Crepitations (if pulmonary oedema), wheeze
Feel: Reduced chest expansion if severe oedema
Measure: SpO2 (low), respiratory rate (high)
Action: High-flow oxygen; consider CPAP/intubation if severe

C - Circulation

Look: Elevated JVP, pale/cyanotic, mottled skin
Feel: Weak pulse, cool extremities, hypotension
Listen: S3, murmurs, arrhythmias
Measure: BP (low), HR (variable), ECG
Action: IV access, inotropes, urgent echo

D - Disability

Assessment: GCS, pupil response, blood glucose
Finding: Often confused (hypoperfusion)
Action: Check glucose; consider if hypoperfusion causing confusion

E - Exposure

Look: Full body examination, look for wounds, signs of MI
Feel: Temperature (cool), pulses (weak)
Action: Keep warm, maintain dignity

Specific Examination Findings

Cardiovascular Assessment:

Inspection:

Elevated JVP (if RV failure or fluid overload)
Visible pulsations (if severe)

Palpation:

Pulse: Weak, thready, may be irregular
Apex beat: May be displaced, weak
Extremities: Cold, clammy

Auscultation:

S1: Usually soft (poor LV function)
S2: May be loud P2 (pulmonary hypertension)
S3: Pathognomonic of LV dysfunction
S4: Stiff, hypertrophied ventricle
Murmurs:
- VSR: Harsh pansystolic murmur, thrill
- MR: Pansystolic murmur (papillary muscle rupture)
- AS: Ejection systolic (if severe AS causing shock)

Respiratory Assessment:

If pulmonary oedema: Crepitations, wheeze, tachypnoea
If RV failure: May have clear lungs, elevated JVP

Renal Assessment:

Urine output: Reduced (<0.5 ml/kg/hour)
Urinalysis: May show protein, casts (renal hypoperfusion)

Special Tests

Test	Technique	Positive Finding	Clinical Use
Jugular venous pressure	Patient at 45°, observe JVP	Elevated	Indicates RV failure or fluid overload
Hepatojugular reflux	Firm pressure on liver	JVP rises	Confirms right heart failure
Pulsus alternans	Regular pulse with alternating strength	Alternating pulse volume	Severe LV dysfunction
Kussmaul's sign	JVP rises on inspiration	Paradoxical JVP rise	Constrictive pericarditis (rare)

6. Investigations

First-Line (Bedside) - Do Immediately

1. 12-Lead ECG

Purpose: Identify MI, arrhythmias, conduction blocks
Key Findings:
- STEMI: ST elevation (anterior = high risk)
- Arrhythmias: VT, VF, severe bradycardia
- Conduction blocks: AV block, bundle branch blocks
Action: Urgent if MI; treat arrhythmias immediately

2. Blood Pressure Measurement

Purpose: Confirm hypotension
Finding: SBP <90 mmHg
Action: Continuous monitoring; arterial line if unstable

3. Pulse Oximetry

Purpose: Assess oxygenation
Finding: Usually low (SpO2 <90%)
Action: High-flow oxygen; improves with treatment

4. Urine Output

Purpose: Assess renal perfusion
Finding: Reduced (<0.5 ml/kg/hour)
Action: Catheterize if not already; monitor hourly

Laboratory Tests

Test	Expected Finding	Purpose	Timing
Troponin	Markedly elevated	Confirm MI, assess extent	Immediate
BNP/NT-proBNP	Very elevated	Confirm heart failure	Within 1 hour
Lactate	Elevated (>2 mmol/L)	Assess tissue hypoxia	Immediate
Arterial Blood Gas	Metabolic acidosis, hypoxia	Assess acid-base, oxygenation	If SpO2 <90%
Urea & Creatinine	May be elevated	Assess renal function	Immediate
Full Blood Count	May show anaemia	Identify precipitant	Within 2 hours
Liver Function Tests	May be elevated	Assess hepatic congestion	Within 2 hours
Coagulation studies	May be abnormal	Assess bleeding risk	If procedures planned

Lactate Interpretation:

<2 mmol/L: Normal (good prognosis)
2-4 mmol/L: Moderate elevation (concerning)
>4 mmol/L: Severe (poor prognosis)
Trend: Improving = good; worsening = bad

Imaging

Chest X-Ray (Essential)

Finding	What It Shows	Clinical Note
Pulmonary oedema	Bilateral infiltrates	LV failure
Cardiomegaly	Enlarged heart	Chronic heart failure
Clear lungs	No oedema	RV failure or early shock
Pleural effusions	Bilateral effusions	Fluid overload

Echocardiogram (Urgent - Within Hours)

Finding	Significance	Clinical Impact
Severely reduced LVEF	<25%	Confirms pump failure
Regional wall motion abnormalities	Ischaemic	May need revascularization
Mechanical complications	VSR, MR, free wall rupture	Urgent surgery needed
RV dysfunction	RV failure	Different management
Valvular abnormalities	Severe AS, MR	May need valve surgery
Cardiac tamponade	Pericardial effusion	Needs pericardiocentesis

Cardiac Catheterization (If MI Suspected)

Finding	Significance	Clinical Impact
Coronary occlusion	Complete blockage	Needs urgent PCI
Multi-vessel disease	Extensive CAD	May need CABG
Mechanical complications	VSR, papillary muscle rupture	Needs surgery

Hemodynamic Monitoring

Arterial Line:

Purpose: Continuous BP monitoring
Indication: Unstable, requiring vasopressors
Benefit: Real-time BP, allows ABG sampling

Central Venous Pressure (CVP):

Purpose: Assess volume status
Finding: Usually elevated (>12 mmHg) in cardiogenic shock
Note: Less reliable than PCWP

Pulmonary Artery Catheter (Swan-Ganz):

Purpose: Detailed hemodynamics
Measurements: PCWP, cardiac output, SVR
Indication: Complex cases, unclear diagnosis
Note: Less commonly used now (echocardiogram preferred)

Cardiac Output Measurement:

Methods: Echocardiogram, PA catheter, non-invasive
Normal: 4-8 L/min (or 2.5-4.0 L/min/m² indexed)
Shock: <2.2 L/min/m²

Diagnostic Criteria

Cardiogenic Shock Definition:

Hypotension: SBP <90 mmHg (or >30 mmHg drop from baseline)
Evidence of hypoperfusion: At least one of:
- Altered mental status
- Cold, clammy extremities
- Reduced urine output (<0.5 ml/kg/hour)
- Lactate >2 mmol/L
Cardiac cause: Evidence of cardiac dysfunction (echo, ECG, clinical)

SHOCK Trial Criteria:

SBP <90 for >30 minutes
Cardiac index <2.2 L/min/m²
PCWP >15 mmHg
Evidence of end-organ hypoperfusion

7. Management

Management Algorithm

        CARDIOGENIC SHOCK PRESENTATION
    (Hypotension + signs of poor perfusion + cardiac cause)
                    ↓
┌─────────────────────────────────────────────────┐
│         IMMEDIATE ASSESSMENT (&lt;5 mins)          │
│  • ABCDE approach                                │
│  • High-flow oxygen                              │
│  • IV access (large bore x2)                     │
│  • Arterial line (if unstable)                   │
│  • 12-lead ECG                                   │
│  • Urgent echo                                   │
│  • Do NOT give large fluid boluses               │
└─────────────────────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────┐
│         IDENTIFY UNDERLYING CAUSE                │
├─────────────────────────────────────────────────┤
│  ACUTE MI                                       │
│  → Urgent cardiac catheterization                │
│  → Primary PCI (if STEMI)                        │
│  → Revascularization within 90 mins             │
│                                                  │
│  MECHANICAL COMPLICATION                        │
│  → Urgent echo to confirm                        │
│  → Surgical repair (VSR, papillary muscle)       │
│  → Bridge with IABP/ECMO if needed               │
│                                                  │
│  ARRHYTHMIA                                     │
│  → DC cardioversion if unstable                  │
│  → Antiarrhythmics                              │
│  → Pacing if bradycardia                         │
│                                                  │
│  OTHER (myocarditis, decompensated HF)          │
│  → Supportive care                               │
│  → Treat underlying cause                       │
└─────────────────────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────┐
│         SUPPORTIVE MANAGEMENT                    │
│  • Inotropes (dobutamine)                        │
│  • Vasopressors (noradrenaline) if needed        │
│  • Diuretics (if pulmonary oedema)               │
│  • Consider mechanical support (IABP/ECMO)      │
│  • Monitor closely (ICU/HDU)                    │
└─────────────────────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────┐
│         RESPONSE TO TREATMENT                    │
├─────────────────────────────────────────────────┤
│  Improving (BP ↑, lactate ↓, urine output ↑)   │
│  → Continue current therapy                      │
│  → Wean support gradually                        │
│  → Monitor for complications                     │
│                                                  │
│  Not improving or deteriorating                 │
│  → Escalate mechanical support                   │
│  → Consider ECMO                                │
│  → Consider LVAD or transplant evaluation       │
└─────────────────────────────────────────────────┘

Acute/Emergency Management - The First Hour

Immediate Actions (Do Simultaneously):

Recognize the Emergency
- Hypotension + signs of poor perfusion = shock
- Identify cardiac cause (ECG, echo, clinical)
- Do not delay—mortality increases with time
High-Flow Oxygen
- 15 L/min via non-rebreather mask
- Target SpO2 >90%
- Consider CPAP/intubation if severe pulmonary oedema
IV Access
- Large bore cannulae x2 (16-18G)
- Central line if vasopressors needed
- Arterial line for continuous BP monitoring
Do NOT Give Large Fluid Boluses
- Critical: Cardiogenic shock is NOT hypovolaemic
- Fluid will worsen pulmonary oedema
- Small boluses (250ml) only if truly hypovolaemic
- Monitor response carefully
Urgent Investigations
- 12-lead ECG (identify MI, arrhythmias)
- Echocardiogram (assess LV function, complications)
- Troponin, BNP, lactate
- CXR

Medical Management

Inotropes (First-Line Support):

Drug	Dose	Route	Mechanism	Notes
Dobutamine	2.5-15 mcg/kg/min	IV infusion	Increases contractility, mild vasodilation	First-line inotrope
Milrinone	0.375-0.75 mcg/kg/min	IV infusion	Phosphodiesterase inhibitor	Use if beta-blocker on board
Dopamine	2-20 mcg/kg/min	IV infusion	Inotrope + vasopressor	Less preferred (arrhythmogenic)

Mechanism: Increases myocardial contractility → improves cardiac output → improves BP and perfusion

Monitoring:

Continuous ECG (arrhythmia risk)
BP (should improve)
Lactate (should decrease)
Urine output (should increase)

Vasopressors (If Still Hypotensive):

Drug	Dose	Route	Mechanism	Notes
Noradrenaline	0.05-0.5 mcg/kg/min	IV infusion	Vasoconstriction	First-line vasopressor
Adrenaline	0.05-0.5 mcg/kg/min	IV infusion	Inotrope + vasopressor	Use if severe
Vasopressin	0.01-0.04 units/min	IV infusion	Vasoconstriction	Adjunctive therapy

Mechanism: Increases systemic vascular resistance → improves BP → improves coronary perfusion

Use Only If: Still hypotensive despite inotropes

Diuretics (If Pulmonary Oedema):

Drug	Dose	Route	Notes
Furosemide	20-40mg	IV	Cautious—may worsen renal function

Mechanism: Reduces preload → reduces pulmonary oedema

Caution: May worsen renal function; monitor closely

Mechanical Circulatory Support

Intra-Aortic Balloon Pump (IABP):

Indication	Mechanism	Duration	Notes
Bridge to revascularization	Reduces afterload, improves coronary perfusion	Days	Common in MI-related shock
Bridge to surgery	Stabilizes before operation	Days	For mechanical complications
Bridge to recovery	Supports while heart recovers	Days to weeks	For myocarditis, post-MI

Contraindications: Aortic regurgitation, aortic dissection, severe peripheral vascular disease

Extracorporeal Membrane Oxygenation (ECMO):

Type	Indication	Mechanism	Duration
VA-ECMO	Refractory cardiogenic shock	Complete circulatory + respiratory support	Days to weeks
VV-ECMO	Respiratory failure only	Respiratory support only	Days to weeks

Indications:

Refractory shock despite IABP and inotropes
Bridge to recovery, transplant, or LVAD
Post-cardiac arrest

Left Ventricular Assist Device (LVAD):

Indication	Type	Duration	Notes
Bridge to transplant	Temporary LVAD	Months	Awaiting heart transplant
Destination therapy	Permanent LVAD	Years	Not eligible for transplant
Bridge to recovery	Temporary LVAD	Months	May recover function

Revascularization (If Acute MI)

Primary PCI (If STEMI):

Timing: Within 90 minutes (ideally <60 minutes)
Goal: Restore coronary blood flow
Benefit: Can dramatically improve LV function
Outcome: Better if done early

CABG (If Multi-Vessel Disease):

Indication: Multi-vessel disease, not suitable for PCI
Timing: Urgent (within 24-48 hours)
Benefit: Complete revascularization

Surgical Management (If Mechanical Complications)

Ventricular Septal Rupture (VSR):

Indication: New harsh murmur, sudden deterioration
Procedure: Surgical repair
Timing: Urgent (within 24-48 hours)
Bridge: IABP or ECMO while waiting

Papillary Muscle Rupture:

Indication: Acute severe MR, sudden deterioration
Procedure: Mitral valve repair or replacement
Timing: Urgent

Free Wall Rupture:

Indication: Cardiac tamponade, sudden collapse
Procedure: Surgical repair (if survives)
Timing: Immediate
Prognosis: Usually fatal

Disposition

Admit to ICU/HDU (Always):

Requires continuous monitoring
Needs inotropes/vasopressors
May need mechanical support
High risk of complications

Monitoring:

Continuous ECG, BP, SpO2
Hourly urine output
Serial lactate
Daily echo (assess recovery)

Discharge Criteria (Rare in Acute Phase):

Stable off inotropes
Normal BP without support
Improving LV function
No complications
Clear plan for follow-up

Follow-Up:

Cardiology clinic: Within 1-2 weeks
Echocardiogram: Serial to assess recovery
Medication optimization: ACE inhibitor, beta-blocker once stable
Consider: Cardiac rehabilitation, device therapy (ICD, CRT)

8. Complications

Immediate (Hours)

Complication	Incidence	Presentation	Management
Cardiac arrest	20-30%	Loss of consciousness, VF/VT	CPR, defibrillation, ECMO
Arrhythmias	30-40%	VT, VF, AF, bradycardia	DC cardioversion, antiarrhythmics
Multi-organ failure	40-50%	AKI, liver failure, gut ischemia	Supportive care, may need dialysis
Mechanical complications	5-10%	VSR, papillary muscle rupture	Urgent surgery
Thromboembolism	5-10%	Stroke, PE, limb ischemia	Anticoagulation, consider

Cardiac Arrest:

Mechanism: Severe pump failure → VF/VT or asystole
Management: CPR, defibrillation, consider ECMO
Prognosis: Very poor (mortality 70-80%)

Multi-Organ Failure:

Kidneys: AKI from hypoperfusion
Liver: Ischemic hepatitis
Gut: Ischemia, risk of bacterial translocation
Brain: Hypoxic injury

Early (Days)

1. Acute Kidney Injury (40-50%)

Cause: Renal hypoperfusion
Management: Supportive, may need dialysis
Prevention: Maintain adequate BP, avoid nephrotoxins

2. Arrhythmias (30-40%)

VT/VF: High risk in first 48 hours
AF: Common, may need cardioversion
Bradycardia: Conduction blocks
Management: Antiarrhythmics, pacing if needed

3. Infection (20-30%)

Pneumonia: Ventilation, immobility
Line infections: Central lines, IABP
Management: Antibiotics, aseptic technique

4. Bleeding (10-20%)

Cause: Anticoagulation, procedures, coagulopathy
Management: Transfusion, reverse anticoagulation if needed

Late (Weeks-Months)

1. Persistent Heart Failure (30-40%)

Mechanism: Irreversible myocardial damage
Management: Long-term medications, consider device therapy
Prognosis: Poor long-term survival

2. Recurrent Shock (10-20%)

Cause: Underlying heart failure, new events
Management: Optimize medications, consider advanced therapies

3. Reduced Quality of Life

Symptoms: Persistent fatigue, breathlessness
Management: Cardiac rehabilitation, psychological support

4. End-Stage Heart Failure

Progression: Despite optimal therapy
Options: Heart transplantation, LVAD, palliative care

9. Prognosis & Outcomes

Natural History (Without Treatment)

Untreated Cardiogenic Shock:

Mortality: Near 100% within hours to days
Progression: Rapid deterioration → multi-organ failure → death
Time course: Death often within 24-48 hours if untreated

Outcomes with Treatment

Variable	Outcome	Notes
In-hospital mortality	40-50%	Improved from 80% historically
30-day mortality	45-55%	Higher in elderly, comorbidities
1-year survival	30-40%	Depends on cause and recovery
5-year survival	20-30%	Poor long-term prognosis
Need for advanced therapies	10-20%	LVAD or transplant

Factors Affecting Outcomes:

Good Prognosis:

Younger age (<65 years)
Reversible cause (arrhythmia, correctable)
Early revascularization (if MI, <90 minutes)
Rapid response to treatment (<6 hours)
No multi-organ failure
Good baseline function (before event)

Poor Prognosis:

Older age (>75 years)
Large MI (anterior, extensive)
Delayed presentation (>6 hours)
Multi-organ failure
Mechanical complications (VSR, rupture)
Previous heart failure
Multiple comorbidities

Prognostic Factors

Factor	Impact on Prognosis	Evidence Level
Age	Each decade increases mortality 1.5x	High
Time to revascularization	Each hour increases mortality 3-5%	High
Lactate level	>4 mmol/L = 2x mortality	High
Multi-organ failure	Each organ = 2x mortality	High
LVEF	<20% = worse prognosis	High
Mechanical complications	VSR/rupture = very poor	High

10. Evidence & Guidelines

Key Guidelines

1. ESC Heart Failure Guidelines (2021) — Comprehensive guidelines for acute and chronic heart failure. European Society of Cardiology

Key Recommendations:

Immediate inotropic support for cardiogenic shock
Urgent revascularization if MI-related (<90 minutes)
Consider mechanical support (IABP, ECMO) early
Evidence Level: 1A

2. AHA/ACC Heart Failure Guidelines (2022) — US guidelines for heart failure management. American Heart Association

Key Recommendations:

Rapid assessment and treatment
Inotropes + vasopressors as needed
Urgent revascularization for MI
Consider mechanical support
Evidence Level: 1A

3. SHOCK Trial Guidelines (1999) — Landmark trial establishing revascularization benefit. New England Journal of Medicine

Key Recommendations:

Early revascularization improves survival in MI-related shock
Evidence Level: 1A

Landmark Trials

SHOCK Trial (1999) — Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock

Patients: 302 patients with cardiogenic shock post-MI
Intervention: Early revascularization (PCI or CABG) vs. medical therapy
Key Finding: 6-month mortality 50% vs. 63% (absolute reduction 13%)
Clinical Impact: Established benefit of early revascularization
PMID: 10471456

IABP-SHOCK II Trial (2012) — Intra-Aortic Balloon Pump in Cardiogenic Shock

Patients: 600 patients with cardiogenic shock
Intervention: IABP vs. no IABP
Key Finding: No mortality benefit from IABP (39.7% vs. 41.3%)
Clinical Impact: IABP not routinely recommended (but still used as bridge)
PMID: 22920912

CULPRIT-SHOCK Trial (2017) — PCI Strategy in Cardiogenic Shock

Patients: 706 patients with MI and cardiogenic shock
Intervention: Complete revascularization vs. culprit-only PCI
Key Finding: Culprit-only PCI better (mortality 43.3% vs. 51.5%)
Clinical Impact: Don't do complete revascularization in shock
PMID: 29103656

Evidence Strength

Intervention	Level	Key Evidence	Clinical Recommendation
Early revascularization (MI)	1A	SHOCK Trial	Urgent PCI/CABG if MI-related
Inotropes	1B	Guidelines, observational	Dobutamine first-line
Vasopressors	1B	Guidelines	Noradrenaline if still hypotensive
IABP	2B	IABP-SHOCK II (no benefit)	Consider as bridge, not routine
ECMO	2B	Observational studies	Consider if refractory
Mechanical support	2B	Case series	Consider early if available

11. Patient/Layperson Explanation

What is Cardiogenic Shock?

In simple terms: Your heart stops pumping effectively, so your body doesn't get enough oxygen and nutrients, causing your organs to start shutting down.

Why does it matter?

Think of it like this: It's like a power outage—everything stops working. You need emergency power (medical support) while the main system (your heart) is being fixed.

How is it treated?

1. Supporting Your Heart: Doctors give you medicines (inotropes) that help your heart pump stronger, like giving a weak engine a boost. These are given through a drip in your arm.

2. Supporting Your Blood Pressure: If your blood pressure is still too low, other medicines (vasopressors) help tighten your blood vessels to keep blood pressure up.

3. Fixing the Cause:

If it's a heart attack: Doctors urgently open the blocked artery (angioplasty)
If it's a valve problem: May need urgent surgery
If it's an irregular heartbeat: Doctors fix the rhythm

4. Mechanical Support: Sometimes doctors use special machines to help your heart pump while it recovers:

IABP: A balloon in your aorta that helps your heart
ECMO: A machine that does the work of your heart and lungs temporarily

The goal: Support your heart and body while fixing the underlying problem, giving your heart time to recover.

What to expect

In the Hospital:

Intensive Care: You'll be in ICU, closely monitored 24/7
First few days: Most critical period—doctors will support your heart with medicines and machines
Days 3-7: If improving, doctors will gradually reduce support
Weeks 1-2: If stable, you'll move to a regular ward
Going home: Usually after 1-3 weeks if you're recovering well

After Going Home:

Medications: You'll need medicines every day to help your heart stay strong
Lifestyle changes: Less salt, fluid restriction, regular exercise (as able)
Follow-up: Regular doctor visits, tests to check your heart
Recovery: Can take weeks to months to feel back to normal

Recovery Time:

In hospital: 1-3 weeks typically
At home: 2-6 months to feel stronger
Long-term: Many people can live normal lives with the right medications and care

When to seek help

Call 999 (or your emergency number) immediately if:

You suddenly feel very weak or faint
You can't catch your breath
You feel confused or "not yourself"
Your chest hurts badly
You feel like something is very wrong

See your doctor urgently if:

You're more breathless than usual
Your ankles or legs are swelling
You're more tired than usual
You're gaining weight quickly
You feel dizzy or lightheaded

Remember: If you've had a heart attack or heart problems before and suddenly feel very unwell, don't wait—get help immediately. Cardiogenic shock can develop quickly.

12. References

Primary Guidelines

McDonagh TA, Metra M, Adamo M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599-3726. [PMID: 34447992]
Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032. [PMID: 35363499]

Key Trials

Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock (SHOCK Trial). N Engl J Med. 1999;341(9):625-634. [PMID: 10471456]
Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II). Lancet. 2013;382(9905):1638-1645. [PMID: 22920912]
Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock (CULPRIT-SHOCK). N Engl J Med. 2017;377(25):2419-2432. [PMID: 29103656]
Ponikowski P et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2016;37(27):2129-2200. [PMID: 27206819]
Mebazaa A et al. Short-term survival by treatment among patients hospitalized with acute heart failure: the global ALARM-HF registry. Intensive Care Med. 2011;37(2):290-301. [PMID: 21086121]
Thiele H et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012;367(14):1287-1296. [PMID: 22920912]
Ouweneel DM et al. Percutaneous mechanical circulatory support versus intra-aortic balloon pump in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017;69(3):278-287. [PMID: 27810347]
Baran DA et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv. 2019;94(1):29-37. [PMID: 30957961]
van Diepen S et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2017;136(16):e52-e68. [PMID: 28923988]
Hochman JS et al. One-year survival following early revascularization for cardiogenic shock. JAMA. 2001;285(2):190-192. [PMID: 11176812]
De Backer D et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-789. [PMID: 20200382]
Levy B et al. Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2018;72(2):173-182. [PMID: 29976291]
Jentzer JC et al. Contemporary management of severe acute kidney injury and refractory cardiogenic shock: SCAI SHOCK statement update. Catheter Cardiovasc Interv. 2020;96(7):1189-1200. [PMID: 32621614]
Tehrani BN et al. Standardized Team-Based Care for Cardiogenic Shock. J Am Coll Cardiol. 2019;73(13):1659-1669. [PMID: 30947916]

13. Examination Focus

Common Exam Questions

1. "What is the definition of cardiogenic shock?"

Answer: Cardiogenic shock is defined as persistent hypotension (SBP <90 mmHg or MAP <65 mmHg for >30 minutes) with evidence of end-organ hypoperfusion (altered mental status, cold extremities, oliguria, elevated lactate) due to primary cardiac dysfunction, despite adequate volume resuscitation.

2. "What are the haemodynamic criteria for cardiogenic shock?"

Answer: CI <2.2 L/min/m², PCWP >15 mmHg, elevated SVR, and low SBP. This distinguishes it from hypovolaemic shock (low PCWP) and septic shock (low SVR).

3. "What is the first-line vasopressor in cardiogenic shock?"

Answer: Noradrenaline. Dopamine is associated with higher arrhythmia rates per the De Backer trial. Dobutamine is an inotrope, not a vasopressor.

Common Mistakes

❌ Using Dopamine as first-line: De Backer trial showed higher mortality/arrhythmias with dopamine vs noradrenaline.
❌ Aggressive fluid resuscitation: Cardiogenic shock patients are already "wet". Fluids worsen pulmonary oedema. Exception: RV infarction.
❌ Delayed revascularization in AMI-CS: SHOCK trial showed early revascularization improves survival, despite initial no difference at 30 days.
❌ Complete revascularization acutely: CULPRIT-SHOCK showed culprit-only PCI is safer initially.
❌ Relying on IABP: IABP-SHOCK II showed no mortality benefit from IABP.

Viva Points

Scenario 1: The Post-MI Shock

"A 65-year-old male has anterior STEMI, BP 80/50, HR 110, cold peripheries, Lactate 5. How do you manage?" Answer: "This is cardiogenic shock post-MI. I would give Noradrenaline to maintain MAP >65. Arrange urgent coronary angiography with view to PCI (culprit-only). Consider IABP or Impella if haemodynamically unstable in cath lab. Avoid aggressive fluids. ICU admission."

Scenario 2: The IABP Question

"What is the evidence for IABP in cardiogenic shock?" Answer: "IABP-SHOCK II trial (2012) showed no mortality benefit from IABP in cardiogenic shock post-MI. Current guidelines suggest against routine use (Class III). However, it may still be used as a bridge or for mechanical complications."

Advanced MCQ Bank

Case 1: Culprit vs Complete A patient with cardiogenic shock from STEMI has 3-vessel disease on angiography. Question: What is the recommended revascularization strategy?

A) Complete revascularization of all vessels
B) Culprit lesion only PCI
C) CABG
D) Medical management Correct: B. CULPRIT-SHOCK trial showed culprit-only PCI reduces mortality vs complete revascularization in acute setting.

Case 2: The Cold Wet Patient A patient has BP 85/60, pulmonary oedema, cold hands, Lactate 4. Question: What is the haemodynamic profile?

A) Warm and Wet
B) Cold and Dry
C) Cold and Wet
D) Warm and Dry Correct: C. Cold (poor perfusion) + Wet (congested) = Cardiogenic shock.

Case 3: The RV Infarction Trap An inferior MI patient has hypotension, clear lungs, elevated JVP. Question: What is the management difference?

A) Give inotropes
B) Give fluids
C) Urgent dialysis
D) Pericardiocentesis Correct: B. RV infarction requires preload (fluids), unlike LV cardiogenic shock where fluids are harmful.

13. Differential Diagnosis

Conditions to Consider

Cardiogenic shock must be distinguished from other forms of shock and acute heart failure presentations:

Condition	Key Distinguishing Features	Investigation	Management Difference
Hypovolaemic shock	History of fluid loss, no pulmonary oedema, responds to fluids	CVP low, clear lungs on CXR	Give fluids (unlike cardiogenic)
Septic shock	Fever, infection source, warm peripheries initially	WCC high, lactate high, blood cultures	Antibiotics, fluids initially
Anaphylactic shock	Allergen exposure, urticaria, wheeze, rapid onset	Clinical diagnosis	Adrenaline IM, fluids
Pulmonary embolism	Sudden onset dyspnoea, chest pain, risk factors	CTPA shows clot, echo shows RV strain	Anticoagulation, thrombolysis
Cardiac tamponade	Raised JVP, muffled heart sounds, pulsus paradoxus	Echo shows pericardial effusion	Pericardiocentesis
Tension pneumothorax	Unilateral reduced air entry, tracheal deviation	Clinical + CXR	Needle decompression
Acute severe MR	New murmur, may not have hypotension initially	Echo shows regurgitation	Urgent valve surgery
Acute severe AS	Slow onset, elderly, history of AS	Echo shows severe stenosis	Urgent valve replacement
RV infarction	Inferior MI, elevated JVP, clear lungs, hypotension	ECG (RV leads), echo	Fluids (unlike LV shock)
Myocarditis	Younger patient, viral prodrome, troponin elevated	Echo, cardiac MRI, viral serology	Supportive, immunosuppression if severe

Clinical Differentiation

"Cold vs. Warm" and "Wet vs. Dry" Classification:

Type	Perfusion	Congestion	Clinical Features	Diagnosis
Cold & Wet	Poor	Yes	Hypotension, pulmonary oedema, poor perfusion	Cardiogenic shock
Cold & Dry	Poor	No	Hypotension, no oedema, poor perfusion	Hypovolaemic shock
Warm & Wet	Adequate	Yes	Normal BP, pulmonary oedema, warm peripheries	Acute decompensated HF
Warm & Dry	Adequate	No	Stable, compensated	Compensated HF

Hemodynamic Profiles:

Shock Type	Cardiac Output	SVR	PCWP	CVP	Treatment
Cardiogenic	Low	High	High	High	Inotropes, reduce preload
Hypovolaemic	Low	High	Low	Low	Fluids
Septic (early)	High	Low	Low	Low	Fluids, antibiotics
Septic (late)	Low	High	Variable	Variable	Inotropes, antibiotics
Obstructive	Low	High	Variable	High	Remove obstruction

Mimics & Pitfalls

1. RV Infarction Masquerading as Cardiogenic Shock:

Clue: Inferior MI + elevated JVP + clear lungs + hypotension
Key difference: Needs fluids (unlike LV shock)
Investigation: ECG (RV leads V3R-V4R), echo (RV dysfunction)
Management: Fluid challenge (unlike LV shock where fluids worsen)

2. Pulmonary Embolism:

Clue: Sudden dyspnoea, chest pain, RV strain on echo
Key difference: No LV dysfunction
Investigation: CTPA, D-dimer, echo
Management: Anticoagulation, thrombolysis if massive

3. Cardiac Tamponade:

Clue: Beck's triad (hypotension, raised JVP, muffled heart sounds)
Key difference: Pericardial effusion on echo
Investigation: Echo (effusion with RV collapse in diastole)
Management: Urgent pericardiocentesis

4. Septic Shock with Pre-existing Heart Disease:

Clue: Fever, infection source, may have cardiac history
Key difference: Responds to antibiotics + fluids
Investigation: Blood cultures, lactate, echo
Management: Antibiotics, fluids first (then inotropes if needed)

14. Prevention & Risk Reduction

Primary Prevention (Before First Event)

Cardiovascular Risk Factor Management:

Risk Factor	Target	Intervention	Evidence Level
Hypertension	BP less than 140/90 mmHg (less than 130/80 if high risk)	Lifestyle + antihypertensives	1A
Dyslipidaemia	LDL less than 1.8 mmol/L (high risk)	Statins	1A
Diabetes	HbA1c less than 53 mmol/mol (7%)	Lifestyle, metformin, newer agents	1A
Smoking	Complete cessation	Smoking cessation support	1A
Obesity	BMI 20-25 kg/m²	Diet, exercise, bariatric surgery if severe	1B
Physical inactivity	150 min moderate exercise/week	Structured exercise program	1A

Mechanism: Reduces risk of MI and heart failure, the two main causes of cardiogenic shock

Coronary Artery Disease Screening:

High-risk patients: Diabetes, family history, multiple risk factors
Tools: Stress testing, CT coronary angiogram
Action: Revascularization if significant disease

Secondary Prevention (After MI or Heart Event)

Post-MI Medications (Reduce Risk of Shock):

Drug Class	Example	Dose	Benefit	Evidence
Antiplatelet	Aspirin + Ticagrelor	75mg + 90mg BD	Prevents re-infarction	1A
Statin	Atorvastatin	80mg daily	Stabilizes plaques, reduces events	1A
ACE inhibitor	Ramipril	10mg daily	Prevents LV remodelling	1A
Beta-blocker	Bisoprolol	10mg daily	Reduces arrhythmias, improves LV function	1A
Mineralocorticoid antagonist	Eplerenone	50mg daily	If LVEF less than 40%	1A

Cardiac Rehabilitation:

Components: Exercise, education, psychological support
Benefit: Reduces mortality by 20-30%
Duration: 8-12 weeks typically
Evidence: 1A

Device Therapy (If LVEF less than 35%):

Device	Indication	Benefit	Evidence
ICD	LVEF less than 35% after 40 days post-MI	Prevents sudden cardiac death	1A
CRT	LVEF less than 35% + LBBB + symptomatic HF	Improves symptoms, reduces mortality	1A

Tertiary Prevention (Preventing Recurrence)

Heart Failure Optimization:

Guideline-directed medical therapy: ACE-I/ARB, beta-blocker, MRA, SGLT2 inhibitor
Regular monitoring: Echo, BNP, symptoms
Early escalation: If worsening symptoms

Lifestyle Modifications:

Modification	Target	Rationale	Evidence
Fluid restriction	1.5-2L/day if HF	Reduces congestion	1B
Salt restriction	less than 2g sodium/day	Reduces fluid retention	1B
Weight monitoring	Daily weight	Early detection of decompensation	1B
Alcohol limit	less than 14 units/week (or abstain if cardiomyopathy)	Reduces myocardial toxicity	1B
Smoking cessation	Complete	Reduces all cardiovascular events	1A

Patient Education:

Recognize warning signs (breathlessness, swelling, weight gain)
Medication adherence
When to seek help
Self-management strategies

Hospital Systems to Prevent Shock

Acute MI Pathways:

Door-to-balloon time less than 90 minutes: Reduces risk of shock developing
24/7 PCI availability: Immediate revascularization
Shock team: Early recognition and intervention

Heart Failure Clinics:

Regular follow-up for chronic HF patients
Optimization of medications
Early intervention if decompensating

15. Special Populations & Considerations

Elderly Patients (>75 Years)

Epidemiology:

Incidence: 2x higher than younger patients
Mortality: 60-70% (vs. 40-50% in younger)
Presentation: Atypical (confusion, falls, weakness)

Management Considerations:

Issue	Challenge	Approach
Polypharmacy	Drug interactions, side effects	Review all medications, stop non-essential
Renal dysfunction	Common, affects drug dosing	Dose adjust all medications
Cognitive impairment	Difficulty with consent, compliance	Involve family, simplified regimens
Frailty	Poor tolerance of invasive procedures	Consider risks vs. benefits carefully
Comorbidities	Multiple conditions affecting outcomes	Holistic approach

Treatment Adjustments:

Lower starting doses: Especially inotropes (increased sensitivity)
Careful fluid balance: Higher risk of overload
Consider goals of care: Early discussions about ceilings of treatment
Palliative approach: If very frail or multiple comorbidities

Prognosis:

Worse than younger patients
Consider quality of life vs. aggressive intervention
30-day mortality: 60-70%

Pregnancy & Peripartum

Causes of Cardiogenic Shock in Pregnancy:

Cause	Timing	Key Features	Management
Peripartum cardiomyopathy	Last month pregnancy to 5 months postpartum	New-onset HF, no prior heart disease	Supportive, bromocriptine, delivery if antenatal
Pre-eclampsia/Eclampsia	>20 weeks pregnancy	Hypertension, proteinuria, pulmonary oedema	Magnesium, antihypertensives, delivery
Amniotic fluid embolism	During/immediately after delivery	Sudden collapse, DIC, shock	Supportive, ICU care
Myocardial infarction	Any time	Rare, similar presentation to non-pregnant	PCI, medications (avoid ACE-I, ARB)

Management Principles:

Multidisciplinary team: Obstetrics, cardiology, anaesthetics, ICU
Fetal monitoring: If antenatally
Delivery considerations: May need urgent delivery if deteriorating
Medication safety: Avoid ACE-I, ARB, statins (teratogenic)
Safe drugs: Beta-blockers (labetalol), hydralazine, digoxin
Mechanical support: ECMO, IABP can be used if needed

Prognosis:

Depends on cause
Peripartum cardiomyopathy: 50% recover, 25% persistent dysfunction, 25% worsen
Multidisciplinary care improves outcomes

Renal Dysfunction & Dialysis Patients

Challenges:

Issue	Impact	Management
Fluid overload	Common, worsens pulmonary oedema	Dialysis/ultrafiltration
Drug dosing	Many drugs need adjustment	Dose reduction, avoid nephrotoxins
Contrast exposure	Risk of contrast-induced AKI	Minimize contrast, hydration protocols
Uraemic cardiomyopathy	Pre-existing LV dysfunction	Optimize dialysis

Management Approach:

Early dialysis: If fluid overload despite diuretics
Ultrafiltration: Can remove fluid without worsening electrolytes
Medication review: Adjust all doses for renal function
Nephrology involvement: Early consultation

Prognosis:

Worse than patients with normal renal function
Mortality: 60-70% (higher than general population)

Post-Cardiac Surgery

Causes:

Myocardial stunning: Temporary dysfunction post-bypass
Graft failure: Occluded graft or native vessel
Tamponade: Pericardial effusion
Bleeding: Hypovolaemia mimicking shock

Management:

High-dose inotropes: Often needed immediately post-op
Mechanical support: IABP, ECMO commonly used
Re-exploration: If bleeding or tamponade suspected
Time: Myocardial stunning usually improves over 24-48 hours

Prognosis:

If myocardial stunning: Usually recovers
If graft failure: May need re-operation or prolonged support
Mortality: 30-40% if true cardiogenic shock

Diabetes Mellitus

Special Considerations:

Issue	Impact	Management
Silent ischemia	May not feel chest pain	Lower threshold for investigation
Larger infarcts	Microvascular disease	More aggressive revascularization
Worse outcomes	1.5-2x mortality	Intensive glycaemic control, optimal therapy
Renal dysfunction	Common comorbidity	Careful dosing, avoid nephrotoxins

Management:

Glycaemic control: Target glucose 6-10 mmol/L (avoid hypo)
Continue diabetic medications: If tolerating (may need insulin if unwell)
Renal protection: Minimize contrast, maintain adequate BP
Aggressive risk factor modification: Post-discharge

Chronic Heart Failure Patients

Presentation:

Often acute-on-chronic deterioration
May have precipitant (infection, non-adherence, arrhythmia)
Baseline LV dysfunction already present

Management Differences:

Lower threshold for mechanical support: Already compromised
Home medications: Continue if stable, stop if hypotensive
Device therapy: May already have ICD/CRT (check functioning)
Advanced therapies: Earlier consideration of LVAD or transplant
Palliative care: Discuss goals of care if end-stage

Prognosis:

Worse than de novo cardiogenic shock
Higher risk of recurrence
May need advanced therapies (LVAD, transplant)

Last Reviewed: 2025-12-24 | MedVellum Editorial Team

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists. This information is not a substitute for professional medical advice, diagnosis, or treatment.