Cardiogenic Shock: Hemodynamics and Physiology Explained in Clinical Practice

How low cardiac output, elevated central venous pressure, and compensatory vasoconstriction shape treatment decisions in cardiogenic shock.

(Part 2 in the Cardiogenic Shock series)

Why This Article Is Necessary

In Part 1, we demonstrated how cardiogenic shock is frequently overlooked - particularly when blood pressure and early warning scores provide false reassurance. Many patients are already severely circulatory compromised long before hypotension develops.

The goal of this article is different: to explain what actually happens hemodynamically in cardiogenic shock, and why seemingly intuitive treatment strategies may worsen the condition when pressure is prioritized over flow.

To ground the discussion in clinical reality, we use a real but anonymized patient case.

The Starting Point: The Patient Is in Cardiogenic Shock

The patient presents with:

• Severely reduced left ventricular systolic function (EF 10–15%)

• Low cardiac index (CI 1.1 L/min/m²)

• Elevated lactate

• Signs of multiorgan hypoperfusion

• Central venous pressure (CVP) of 19 mmHg

  
  

This represents cardiogenic shock in its purest form.

What Is Shock - Fundamentally?

Regardless of etiology, shock can be defined as:

A state in which tissues and organs do not receive sufficient oxygen delivery due to inadequate circulatory flow.

This distinction is essential:

• Shock is primarily a problem of flow and perfusion

• Not primarily a problem of blood pressure

In cardiogenic shock, the cause is straightforward:

→ The heart fails to generate adequate forward flow

The Central Hemodynamic Problem: Low Cardiac Output

Cardiac output (CO) is determined by:

CO = Heart rate × Stroke volume

In this patient:

• Stroke volume is profoundly reduced

• The ventricle is dilated and severely contractile impaired

  
  

The consequence is:

• Low cardiac output

• Low cardiac index

• Inadequate tissue perfusion

  
  

Cardiac Index

Cardiac index (CI) is cardiac output normalized to body surface area and provides a more accurate assessment of circulatory adequacy than CO alone, particularly in patients at the extremes of body size.

Why Blood Pressure May Appear Preserved

A falling cardiac output immediately activates powerful compensatory mechanisms:

• Sympathetic nervous system

• Renin–angiotensin–aldosterone system (RAAS)

• Antidiuretic hormone (ADH)

  
  

These responses produce:

• Intense systemic vasoconstriction

• Increased total peripheral resistance (TPR)

Mean arterial pressure can be approximated as:

MAP ≈ CO × TPR

As CO decreases, TPR rises. As a result, MAP may remain near-normal despite critically low flow.

This creates a dangerous clinical illusion: acceptable pressure with ongoing organ hypoperfusion.

When Compensation Becomes Maladaptive

Compensation has physiological limits.

As:

• Stroke volume continues to fall

• Afterload becomes excessive

• Hypoxia and metabolic acidosis worsen

…the compensatory mechanisms collapse.

Clinically, this manifests as:

• Hypotension

• Rapid lactate accumulation

• Progressive multiorgan dysfunction

  
  

Importantly, hypotension is often a late finding.

Vasoconstrictors: Why They Seem Logical - and Why They Can Be Harmful

When hypotension develops, vasopressors such as norepinephrine are often initiated reflexively.

Norepinephrine:

• Increases systemic vascular resistance

• Raises mean arterial pressure

  
  

However, this comes at a cost.

By increasing afterload, norepinephrine increases the resistance against which the failing ventricle must eject. In a severely impaired heart:

• Higher afterload → reduced stroke volume

• Reduced stroke volume → lower cardiac output

  
  

The result is often:

• Improved blood pressure

• Worsened circulatory flow and tissue perfusion

  
  

This illustrates a central principle of cardiogenic shock: pressure can improve while flow deteriorates.

Venous Return, Filling Pressures, and Congestion

Sympathetic activation affects not only arteries, but also veins.

This leads to:

• Venoconstriction

• Mobilization of blood from the venous reservoir

• Increased venous return and preload

  
  

The Venous Reservoir

The venous reservoir consists of a large proportion of circulating blood volume stored in the venous system, particularly the highly compliant splanchnic circulation (liver, spleen, intestines).

• In healthy hearts:

  • Mobilized venous blood → increased preload → increased stroke volume

• In failing hearts:

  • Mobilized venous blood → increased filling pressures → congestion

  • Little or no increase in cardiac output

The Frank-Starling curve. In the health heart and in a faling heart

Filling Pressures and the Frank–Starling Relationship

The Frank–Starling mechanism explains why increased filling normally augments stroke volume, and why this relationship fails in advanced heart failure.

Filling pressure describes the pressure within the cardiac chambers during diastolic filling and reflects the relationship between intraventricular volume and ventricular compliance.

• Often used as a surrogate for preload

• In heart failure, elevated filling pressures usually indicate:

  • Reduced ventricular compliance

  • Congestion

  • Not effective preload or improved forward flow

    
    

At advanced stages of ventricular dysfunction:

• The Frank–Starling curve is flattened

• Additional preload:

  • Does not increase stroke volume

  • Does increase filling pressures

    
    

In this patient:

• CVP ≈ 19 mmHg

• No meaningful increase in cardiac output

  
  

Why Elevated CVP Reduces Organ Perfusion

Organ perfusion pressure can be simplified as:

Perfusion pressure ≈ MAP − CVP

When CVP is elevated:

• Effective organ perfusion pressure falls

• Even if MAP appears acceptable

  
  

This explains:

• Oliguria

• Renal and hepatic dysfunction

• Persistently elevated lactate

Myocardial ischemia without coronary stenoses

Myocardial ischemia does not necessarily require obstructive coronary artery disease.

In cardiogenic shock, myocardial ischemia can occur as a consequence of hemodynamic stress rather than coronary obstruction. The combination of:

• increased wall stress due to ventricular dilation and elevated filling pressures,

• low cardiac output,

• and reduced coronary perfusion pressure

can be sufficient to cause ischemic myocardial injury, even when coronary angiography shows no significant stenoses.

Why the right ventricle is particularly vulnerable

The right ventricle is often more susceptible than the left ventricle in cardiogenic shock. This is largely because it:

• has limited contractile reserve,

• is highly sensitive to increases in afterload,

• and has a smaller metabolic reserve.

  
  

In the setting of cardiogenic shock, low diastolic blood pressure, elevated central venous pressure, and increased pulmonary vascular resistance can significantly impair coronary perfusion of the right ventricle. This may lead to RV ischemia and subsequent RV failure, even in the absence of coronary artery disease, further aggravating the overall hemodynamic compromise.

Improving Flow: Inotropy and Afterload Reduction

A critical concept:

• Improving cardiac output does not always require increased contractility

  
  

In many patients:

• Excessive vasoconstriction

• Markedly elevated afterload

are major contributors to low stroke volume.

In such cases:

• Afterload reduction alone may substantially increase forward flow

  
  

Vasodilation and Nitroprusside

Sodium nitroprusside is a potent arterial and venous vasodilator that:

• Reduces systemic vascular resistance

• Decreases ventricular wall stress

• Unloads the failing ventricle

  
  

In selected patients, this may result in:

• Increased cardiac output

• Reduced filling pressures

• Improved tissue perfusion without direct inotropic stimulation

  
  

Key physiological insight:

Cardiac output may increase simply by unloading the ventricle, even if contractility remains unchanged.

Dobutamine vs. Nitroprusside: Physiology Over Dogma

Dobutamine:

• Increases myocardial contractility

• Favored when:

  • Contractile failure is severe

  • Blood pressure is low or borderline

  • Vasodilation is not tolerated

    
    

Nitroprusside:

• Reduces afterload

• Favored when:

  • Blood pressure is preserved or elevated

  • Afterload is markedly increased

  • Low output is driven by vasoconstriction

    
    

Often, optimal therapy involves:

• Carefully balanced combinations

• Modest inotropy + controlled afterload reduction

  
  

Clinical Note

The selection of dobutamine versus nitroprusside in cardiogenic shock should be individualized and based on clinical judgment. No single therapeutic strategy is universally applicable, and treatment should be guided by the patient’s hemodynamic profile and blood pressure tolerance. Other inotropic agents, including milrinone, are used in clinical practice but are not discussed further in this article.

Mechanical Unloading: The Role of IABP

When pharmacological therapy is insufficient:

• Mechanical unloading may be required

Intra-aortic balloon pump (IABP):

• Deflation before systole → reduced afterload

• Inflation during diastole → improved coronary perfusion

  
  

Net effects:

• Reduced ventricular wall stress

• Lower myocardial oxygen demand

• Improved conditions for myocardial recovery

  
  

Key Hemodynamic Logic

• Cardiogenic shock is a low-flow state

• Vasoconstriction may preserve pressure but impair perfusion

• Elevated preload and afterload worsen ventricular failure

• High CVP reduces effective organ perfusion

• Vasopressors may improve pressure but may worsen flow

• Cardiac output can be improved by:

  • Inotropy

  • Afterload reduction

  • Mechanical unloading

• Treatment should address the physiology and should be individualized

Mechanical Circulatory Support – What Does the Evidence Show?

• Mortality in cardiogenic shock remains very high

• This applies even with mechanical circulatory support

  
  

Evidence from Randomized Trials

• IABP:

  • Has not demonstrated reduction in short- or long-term mortality

  • Shown in trials such as:

    • IABP-SHOCK II

  • Not recommended for routine use in infarct-related cardiogenic shock by ESC (Class III)

• Impella:

  • Randomized trials (ISAR-SHOCK, IMPRESS):

    • No reduction in short-term mortality compared with IABP or standard care

  • Reported 30-day mortality: ~46–50%

    
    

More Recent Data

• Meta-analysis (2024):

  • No difference in 30-day mortality

  • Possible reduction in 6-month mortality

  • At the cost of:

    • Increased risk of major complications

      • Bleeding

      • Limb ischemia

      • Sepsis

        
        

Practical Interpretation

• Mechanical circulatory support:

  • Is not mandatory

  • Has no proven short-term survival benefit in randomized trials

• May be considered:

  • Selectively

  • In patients judged likely to benefit based on physiology

Clinical Recommendation

• Patients with cardiogenic shock should:

  • Be closely monitored

  • Reassessed frequently

• If mechanical support is considered and:

  • Not available locally→ Early consultation with a center experienced in mechanical circulatory support is recommended

FAQ

1) What is cardiogenic shock?

Cardiogenic shock is a state of inadequate tissue oxygen delivery caused by critically reduced cardiac output (low flow), leading to organ hypoperfusion and rising lactate.

2) Can cardiogenic shock occur with normal blood pressure?

Yes. Compensatory vasoconstriction can maintain mean arterial pressure (MAP) despite severely reduced cardiac output, creating false reassurance.

3) Why is hypotension often a late finding?

Early neurohormonal compensation (sympathetic tone, RAAS, ADH) increases systemic vascular resistance and preserves MAP until the failing ventricle can no longer sustain forward flow.

4) What is the difference between cardiac output (CO) and cardiac index (CI)?

CO is total flow per minute, while CI is CO indexed to body surface area and better reflects adequacy of perfusion across different body sizes.

5) What do “filling pressures” mean in cardiogenic shock?

Filling pressures reflect diastolic chamber pressure and the interaction between volume and ventricular compliance; in heart failure they typically indicate congestion, not effective preload or improved forward flow.

6) Why does a high CVP worsen organ perfusion?

Organ perfusion pressure can be approximated as MAP − CVP; elevated CVP reduces the pressure gradient for organ blood flow even when MAP looks acceptable.

7) Why can norepinephrine worsen cardiogenic shock?

By increasing afterload, norepinephrine can reduce stroke volume and cardiac output in a failing ventricle—improving pressure but worsening flow and tissue perfusion.

8) When can vasodilation (e.g., nitroprusside) improve cardiac output?

If low output is strongly afterload-limited and blood pressure is preserved, controlled afterload reduction can increase stroke volume and cardiac output without directly increasing contractility.

9) How do you choose between dobutamine and nitroprusside?

Selection should be individualized. Dobutamine is typically favored when contractile failure is dominant and blood pressure is low/borderline; nitroprusside may be favored when blood pressure is preserved and excessive afterload is limiting forward flow.

10) What is the role of IABP in cardiogenic shock?

IABP provides mechanical unloading (reduced afterload) and improved coronary perfusion (diastolic augmentation), potentially reducing wall stress and myocardial oxygen demand when pharmacologic therapy is insufficient.