What is the Killip Classification?
The Killip classification is a clinical tool used to stratify the severity of heart failure in patients with acute myocardial infarction (AMI). Developed in 1967 by Thomas Killip and John T. Kimball, it remains a valuable bedside assessment for predicting short-term mortality and guiding treatment decisions. Its simplicity, based on physical examination alone, allows for rapid risk assessment without requiring laboratory or imaging results.
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Table of Contents
Historical Background
Before the Killip classification, clinicians lacked a standardized way to evaluate the severity of cardiac decompensation during myocardial infarction. Killip and Kimball’s original study followed 250 AMI patients, classifying them into four categories based on signs of heart failure. They found a strong correlation between the Killip class and in-hospital mortality, which cemented its place in clinical cardiology.
Read more:
What is Acute Myocardial Infarction?
Classification Criteria
The classification is based on physical examination findings, specifically looking for signs of left ventricular failure and shock. It divides patients into four classes:
Killip Class I – No Signs of Heart Failure
1. Definition
Patients in Killip Class I present without any clinical evidence of heart failure following acute myocardial infarction (AMI).
2. Clinical Features
✔ Normal pulmonary exam – no rales or crackles heard on auscultation.
✔ No S3 gallop – extra heart sounds suggesting ventricular dysfunction are absent.
✔ Stable vital signs – no hypotension or tachycardia due to pump failure.
✔ No evidence of pulmonary congestion on chest X-ray.
3. Pathophysiology
✔ Left ventricular function is preserved enough to maintain cardiac output without fluid backing up into the lungs.
✔ Infarct size is generally smaller or compensated by the unaffected myocardium.
4. Prognosis
Historically: ~6% in-hospital mortality (much lower with modern treatment).
Best survival rate among Killip classes.
Killip Class II – Mild to Moderate Heart Failure
1. Definition
Patients in Class II show early signs of heart failure after AMI, but without frank pulmonary edema.
2. Clinical Features
✔ S3 gallop – a low-frequency extra heart sound indicating volume overload in the ventricle.
✔ Basal lung crackles – typically at the posterior lung bases, due to mild pulmonary congestion.
✔ Possible mild jugular venous distension (JVD).
✔ No severe respiratory distress.
3. Pathophysiology
✔ Infarction leads to partial impairment of left ventricular function, causing increased left atrial pressure and mild pulmonary venous congestion.
✔ The heart compensates via neurohormonal activation, preventing progression to severe failure—at least initially.
4. Prognosis
Historically: ~17% in-hospital mortality.
Higher complication rate (arrhythmias, worsening HF) than Class I.
Killip Class III – Severe Heart Failure (Pulmonary Edema)
1. Definition
Overt pulmonary edema with acute respiratory distress following AMI.
2. Clinical Features
✔ Widespread rales/crackles heard over most lung fields.
✔ Dyspnea and orthopnea (difficulty breathing when lying flat).
✔ Tachypnea and use of accessory respiratory muscles.
✔ Possible hypoxia and cyanosis.
✔ Pink, frothy sputum may be present in severe cases.
✔ S3 gallop is often present.
3. Pathophysiology
✔ Severe reduction in left ventricular contractility → markedly elevated left atrial and pulmonary venous pressures.
✔ Fluid shifts into alveoli cause alveolar flooding and impaired oxygen exchange.
4. Prognosis
Historically: ~38% mortality without aggressive treatment.
Requires urgent interventions (e.g., diuretics, vasodilators, oxygen, possibly noninvasive ventilation).
Killip Class IV – Cardiogenic Shock
1. Definition
Cardiogenic shock secondary to AMI, representing the most severe form of pump failure.
2. Clinical Features
✔ Systolic BP < 90 mmHg for >30 minutes or need for vasopressors to maintain BP.
✔ Signs of hypoperfusion:
- Cold, clammy skin
- Oliguria (< 30 mL/hour)
- Altered mental status
✔ Tachycardia (may also see bradycardia in advanced cases).
✔ Pulmonary findings may be variable — can coexist with pulmonary edema.
3. Pathophysiology
✔ Massive myocardial damage leads to a critical reduction in cardiac output.
✔ Hypoperfusion affects all major organs (kidneys, brain, liver), initiating a cascade of metabolic and inflammatory responses that worsen shock.
4. Prognosis
Historically: ~81% mortality before the reperfusion era.
Still carries a high risk despite PCI and advanced support (mortality ~40–50% today).
Requires ICU care, often with mechanical circulatory support (IABP, ECMO).
*Mortality rates are based on historical data; modern treatment has improved outcomes.
The Killip classification is still widely used today because it's a quick and reliable way to risk-stratify patients without needing advanced equipment. It helps guide immediate treatment decisions, such as the need for more aggressive supportive care or revascularization strategies.(alert-passed)
Table: Killip Classes; Definitions, Features, Pathophysiology, and Prognostic Values
| Killip Class | Clinical Findings | Approx. Mortality (%) |
|---|---|---|
| I | No clinical signs of heart failure | ~6% |
|
Definition: No evidence of heart failure after AMI. Features: Normal lung sounds, no S3 gallop, stable vitals. Pathophysiology: Preserved LV function, minimal myocardial damage. Prognosis: Best survival rate among all classes. |
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| II | S3 gallop and/or basal lung crackles, mild–moderate HF | ~17% |
|
Definition: Early signs of heart failure. Features: S3 gallop, mild crackles, possible mild JVD. Pathophysiology: LV dysfunction causing mild pulmonary venous congestion. Prognosis: Moderate increase in mortality and complications. |
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| III | Acute pulmonary edema | ~38% |
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Definition: Severe heart failure with pulmonary edema. Features: Widespread crackles, dyspnea, orthopnea, pink frothy sputum. Pathophysiology: Elevated LA and pulmonary venous pressures causing alveolar flooding. Prognosis: High mortality; urgent treatment required. |
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| IV | Cardiogenic shock | ~81% |
|
Definition: Cardiogenic shock after AMI. Features: Hypotension (<90 mmHg), hypoperfusion signs (cold skin, oliguria, confusion). Pathophysiology: Massive myocardial damage causing critically low cardiac output. Prognosis: Very high mortality even with advanced care. |
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* The above is an interactive table. Click/Touch the row to reveal its detailed explanation.
Clinical Assessment
The Killip class is determined entirely by physical examination:
✔ Auscultation for extra heart sounds (S3 gallop)
✔ Pulmonary exam for crackles or rales
✔ Vital signs to identify hypotension
✔ Signs of hypoperfusion, such as cold extremities, oliguria, or altered mental status
No laboratory test is required to assign a class, making it especially useful in resource-limited or pre-hospital settings.
Prognostic Value of Killip Classification
The Killip classification is a powerful, time-tested predictor of short-term mortality in patients with acute myocardial infarction (AMI). Developed in the pre-reperfusion era, it demonstrated a clear stepwise increase in in-hospital death rates with higher Killip classes: approximately 6% for Class I, 17% for Class II, 38% for Class III, and 81% for Class IV. Although modern therapies such as early reperfusion, advanced pharmacologic management, and mechanical circulatory support have significantly reduced these numbers, the relative risk gradient remains striking.
Even today, Killip class at presentation is incorporated into widely used risk stratification tools, including the TIMI and GRACE scores, because it independently predicts not only mortality but also the likelihood of complications such as arrhythmias, recurrent ischemia, and cardiogenic shock.
Its prognostic strength lies in its ability to rapidly and non-invasively capture the extent of hemodynamic compromise using only bedside clinical findings. Higher Killip classes indicate greater myocardial damage and reduced left ventricular function, translating to worse outcomes despite advances in treatment. As such, it remains a cornerstone of initial assessment, guiding the urgency and intensity of monitoring, intervention, and resource allocation in AMI care.
Integration into Clinical Practice
While echocardiography, BNP testing, and invasive hemodynamic monitoring provide more detailed information, the Killip classification remains a rapid and effective bedside tool. In modern practice, it helps determine:
✔ Need for intensive care unit (ICU) admission
✔ Use of aggressive therapies such as mechanical ventilation, vasopressors, or intra-aortic balloon pump
✔ Urgency of reperfusion therapy in AMI patients
Limitations of Killip Classification
Despite its utility, the Killip classification has limitations:
🗙 Subjectivity: Findings like rales or S3 can vary with examiner skill.
🗙 Overlap with other conditions: Pulmonary crackles may be caused by pneumonia, chronic lung disease, or ARDS.
🗙 Does not account for subclinical dysfunction: Patients with normal exam but reduced left ventricular function on echocardiography may still be at high risk.
The Killip classification remains an important, time-tested tool for the bedside assessment of heart failure severity in AMI. Its enduring relevance lies in its simplicity, prognostic accuracy, and integration into broader risk assessment systems.(alert-passed)
