Cardiogenic Shock

Introduction

Cardiogenic Shock (CS) is a type of shock identified by inadequate cardiac output to meet the tissue oxygen delivery requirements.
CS is associated with high rates of morbidity and mortality
CS is very challenging to identify and treat because presentation and treatment is different from other forms of shock (i.e. septic shock).
AMI --> accounts for 81% of cases

Abbreviations

CS - Cardiogenic Shock
Items in pink are key learning points that are often the subject of questions on the quiz.

Assessment of a patient with CS

Phenotypic Classification of CS

Invasive Hemodynamics

Definitions

"CS is a low-cardiac-output (CO) state resulting in life-threatening end-organ hypoperfusion and hypoxia"
Overall, "leads to a state in which ineffective CO caused by primary cardiac disorder results in both clinical and biochemical manifestations of inadequate tissue perfusion"
No standard diagnostic criteria, but various trials used variations of criteria (see image on the right).

Definitions of cardiogenic shock published in literature.

Causes

Any condition that decreases cardiac output can cause CS:

Myocardial
- **Ischemic heart disease** (i.e. Acute myocardial infarction, or chronic deteriorating heart failure)
- Acute inflammation (sarcoidosis, myocarditis)
Valves - Acute/chronic valve dysfunction
Pericardium - Pericardial tamponade/constriction
NOTE: PE must be ruled out

Hemodynamics

When the patient develops acute CS, cardiac output drops, resulting in reduced tissue perfusion. This activates compensatory mechanisms resulting in:
- - Hypotension
  - Vasoconstriction (increased catecholamines)
  - Salt/water retention (renal/adrenergic activation of Renin-Angiotensin System).
  - Sharp rise in preload
Preload is initially beneficial because it increases cardiac output to a certain extent. An increase in preload has diminishing returns - see Frank Starling Curve.
- However, the downside of preload is venous congestion:
  - Left-sided venous congestion --> Pulmonary edema --> Hypoxemia
  - Right-sided venous congestion --> End-organ high venous pressure --> reduction of end organ perfusion due to a drop in tissue perfusion pressure (MAP - CVP)

SVR and MAP Relationship; MAP - mean arterial pressure; CVP - central venous pressure; SVR - systemic vascular resistance

Tissue oxygen delivery is not directly related to blood pressure (see formula on the right).
Blood pressure is inversely correlated to systemic vascular resistance (SVR)
In patients with CS, cardiac output is generally fixed. Tissue perfusion is reduced, leading to compensatory vasoconstriction. This increases systemic vascular resistance (SVR), resulting in increased BP.
NOTE: Although BP is reduced in most patients with CS, a subset of patients with CS experience significant vasoconstriction (rise in SVR), which increases blood pressure to a normal level. This "normotensive CS" is commonly seen in patients with bradycardia, and can lead to false reassurance.
When managing CS, clinicians need to look for markers of perfusion in addition to patient's BP because BP can be misleading.

Assessment of a patient with CS

Approach to patient with suspected CS:
1. Evaluate for markers of reduced forward flow (reduced perfusion / ischemia)
2. Assess for R-sided and L-sided congestion
3. Identify causes of CS

Identify end-organ malperfusion and vasoconstriction
- Physical exam:
  (NOTE: these are features of adrenergic vasoconstriction!)
  - Tachycardia, hypotension, reduced pulse pressure
  - Cold/clammy extremities, reduced capillary refill, altered mental state
  - **Reduced urine output** (directly related to renal perfusion and cardiac output)
    - < 30ml/min is concerning, but usually CS patients are anuric.
- Laboratory Markers of Malperfusion:
  - Elevated Lactate
  - Elevated Liver Enzymes (liver congestion/malperfusion)
  - Elevated Troponin (reduced coronary perfusion)
  - Elevated CK (poor muscle perfusion)
  - **Reduced Central Venous Oxygenation (CvO2) < 70%**
    (increased O2 extraction by tissues)
    - CvO2 is obtained from a blood gas drawn from a central line, and is very helpful in diagnosis of CS. Patients with sepsis have reduced tissue O2 extraction and should have an elevated or normal CvO2.
  - Elevated Creatinine (late finding - may take days to rise)
- Invasive hemodynamics
  - Reduced Cardiac Output (CO) < ~4 L/min (Cardiac Index (CI) < 2.2 L/min/m^2)
  - High systemic vascular resistance (SVR)
    - NOTE: Low SVR is not compatible with CS, and suggests vasodilatory shock (i.e. sepsis)
Identify markers of congestion
- Physical Exam:
  - R-sided --> Peripheral edema, Ascites, Pulsatile Liver
  - L-sided --> Pulmonary Rales / Effusions
- Laboratory:
  - BNP is helpful for risk-stratification, but is non-specific in CS. Although, low BNP suggests an alternative diagnosis.
- Chest Xray: Pulmonary edema/Effusions
- Invasive Hemodynamics
  - Elevated right atrial pressure (RAP)
  - Elevated left atrial pressure - (surrogate is Pulmonary Capillary Wedge Pressure PCWP)
  - Elevated left ventricular end-diastolic pressure (LVEDP) > 15 mmHg
    - Practical Tip: **LVEDP is often available in the cardiac angiogram report** if the interventional cardiologist enters the LV cavity.
Identify Causes of CS
- Physical Exam:
  - New murmur? (Acute MR/AR)
  - Arrhythmias
  - Signs of tamponade (muffled sounds, pulsus paradoxus)
- Laboratory: Troponin is non-specific.
- ECG: Acute STEMI? Arrhythmia? (everything else is non-specific)
- Echocardiogram:
  - An urgent echocardiogram is indicated since it identifies most causes and can reveal urgent treatment options.

Phenotypic Classification of CS

Phenotypes of cardiogenic shock, which directs types of treatment. NOTE: Most patients present in cold and wet phenotypes

Treatment must be tailored to each CS presentation. Your assessment of a CS patient should place the patient into one of 4 categories:

NOTE: Warm/Cold is related to vasoconstriction/dilation, and wet/dry refers to venous/filling pressures (preload).

Cold + Wet --> Most CS patients with congestion and poor perfusion
- Management includes decongestion.
Cold + Dry --> Reduced cardiac output + normal/reduced filling pressures (preload).
- Seen in patients with CS who are decongested (i.e. diuresis)
- Further decongestion may worsen hemodynamics. Management must focus on increasing CO.
Warm + Wet --> Cardiogenic shock with vasodilation / mixed shock (commonly seen in CS patients with overlying sepsis).
Warm + Dry --> Classic vasodilatory shock (not CS).

Invasive Hemodynamics

Swan-Ganz catheter used to objectively measure hemodynamic parameters, which can be used to:
1. Confirm diagnosis of CS.
2. Determine hemodynamic response and guide titration of supportive medical therapy.
3. Risk stratify CS patients and determine eligibility and type of advanced heart failure therapy (i.e. cardiac transplantation, mechanical ventricular support, and palliative care).
Practical Tip: #3 is the most important reason for Swan-Ganz Catheterization. A patient in CS may be temporarily supported by altering hemodynamics with diuretics, vasopressors, and inotropes. However, identifying and delivering definitive advanced therapy is the only long-term solution.
In patients with cardiogenic shock the use of balloon flotation catheters to determine the hemodynamic response to supportive therapy is still necessary and strongly recommended.

Authors

Authors: Dr. Pavel Antiperovitch (MD, FRCPC[Cardiology])
Reviewer: Atul Jaidka (MD, FRCPC, Cardiology Fellow)
Staff Reviewer: Pending (MD, FRCPC[Cardiology])
Last Updated: April 7, 2022
Comments or questions please email feedback@cardioguide.ca

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Cardiogenic Shock

Introduction

Abbreviations

Table of Contents

Definitions

Causes

Hemodynamics

Assessment of a patient with CS

Phenotypic Classification of CS

Invasive Hemodynamics

Further Reading

Authors