Cardiogenic shock physical examination
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3] James Nasr[4]
Cardiogenic shock physical examination
Overview
The physical examination in cardiogenic shock should rapidly identify systemic tissue hypoperfusion, congestion, the likely shock phenotype, and clues to the underlying etiology. Bedside findings may include hypotension, narrow pulse pressure, cool or mottled extremities, delayed capillary refill, weak pulses, altered mentation, oliguria, elevated jugular venous pressure, pulmonary rales, respiratory distress, and new murmurs after myocardial infarction.[1][2]
Physical examination serves three practical functions: confirming the presence of hypoperfusion or congestion, identifying the likely hemodynamic phenotype, and monitoring the trajectory of shock severity over time. Examination findings should be interpreted serially because cardiogenic shock is dynamic and may progress rapidly from preshock to established or refractory shock.[3][4]
Role of physical examination
The 2025 ACC Expert Consensus Statement emphasizes that symptoms, physical examination, and vital signs form the initial diagnostic foundation for cardiogenic shock regardless of hospital setting or resource availability.[1] The physical examination should be used to assess:
- Presence and severity of hypoperfusion
- Presence and distribution of congestion
- LV-dominant, RV-dominant, biventricular, or mixed shock phenotype
- Evidence of mechanical complications after myocardial infarction
- Response to therapy or progression in shock severity
The SCAI shock staging system incorporates bedside findings into shock severity assessment. Findings progress from normal venous pressure, clear lungs, warm extremities, strong pulses, and normal mentation in stage A to elevated venous pressure and rales with preserved perfusion in stage B, and then to cold, ashen, or mottled skin, weak or nonpalpable pulses, altered mentation, decreased urine output, and respiratory distress in stage C through stage E.[2][3]
The Killip classification remains a rapid bedside tool for initial risk stratification in acute coronary syndrome. Killip class I indicates no heart failure; class II indicates rales, S3, or elevated jugular venous pressure; class III indicates pulmonary edema; and class IV indicates cardiogenic shock, typically with systolic blood pressure <90 mm Hg and peripheral vasoconstriction.[5][6]
Vital signs
| Vital sign | Findings in cardiogenic shock | Clinical interpretation |
|---|---|---|
| Blood pressure | Systolic blood pressure <90 mm Hg, mean arterial pressure <65 mm Hg, or >30 mm Hg decrease from baseline; may require vasopressor, inotrope, or mechanical circulatory support to maintain perfusion | Hypotension is common but is not required for diagnosis. The 2025 ACC Expert Consensus Statement uses mean arterial pressure <65 mm Hg in the SUSPECT CS mnemonic, while the 2022 AHA/ACC/HFSA SCAI table operationalizes lower mean arterial pressure ranges for SCAI stages B through E.[1][2] Normotensive cardiogenic shock should be suspected when hypoperfusion is present despite systolic blood pressure ≥90 mm Hg. |
| Pulse pressure | Narrow pulse pressure; pulse pressure less than 25% of systolic blood pressure suggests reduced stroke volume | Suggests low cardiac output and reduced forward flow in the appropriate clinical context.[7] |
| Heart rate | Tachycardia is common; bradycardia may occur with high-grade atrioventricular block, especially in inferior or right ventricular infarction | Tachycardia reflects sympathetic activation. Bradycardia with inferior myocardial infarction should raise suspicion for RV infarction or conduction system involvement. Diaphoresis may be prominent in RV infarction as part of vagotonic manifestations, including nausea, vomiting, and diaphoresis.[8] |
| Respiratory rate | Tachypnea; may progress to respiratory distress or respiratory failure | May reflect pulmonary edema, hypoxemia, metabolic acidosis compensation, or increased work of breathing. |
| Oxygen saturation | May be decreased with pulmonary edema, acute respiratory distress syndrome, right-to-left shunting, or respiratory failure | Hypoxemia worsens myocardial ischemia and systemic oxygen delivery. |
In the SHOCK trial registry, in-hospital mortality was 43% for normotensive cardiogenic shock, 66% for classic cardiogenic shock with hypotension and hypoperfusion, and 26% for isolated hypotension without hypoperfusion, underscoring that hypoperfusion is more prognostically important than hypotension alone.[9][7]
Peripheral perfusion assessment
Assessment of peripheral perfusion is central to the bedside evaluation of cardiogenic shock and may provide information about microcirculatory dysfunction not captured by blood pressure or cardiac index alone.[10]
| Finding | Examination description | Clinical implication |
|---|---|---|
| Skin temperature and moisture | Cold, clammy, sweaty, or cool extremities | Reflects sympathetically mediated vasoconstriction and low-output physiology. Cold and sweaty extremities should raise suspicion for cardiogenic shock even without hypotension.[1] |
| Skin mottling | Livedo or mottling pattern, often beginning around the knees | Marker of microcirculatory dysfunction. In the FRENSHOCK registry, mottling at admission was associated with higher 30-day mortality and 1-year mortality; new mottling during the first 24 hours carried the worst prognosis.[11] |
| Capillary refill time | Prolonged capillary refill; >2 seconds raises concern, while >3 seconds has been associated with adverse outcomes in cardiogenic shock studies | Provides information about microcirculatory perfusion. In a prospective multicenter study of 61 patients with cardiogenic shock, capillary refill time >3 seconds was associated with 90-day mortality or need for VA-ECMO.[12] |
| Pulse quality | Weak, thready, or nonpalpable distal pulses | Suggests markedly reduced stroke volume or severe vasoconstriction; weak or nonpalpable pulses are typical of established shock in SCAI staging.[2] |
A systematic review and meta-analysis across shock states found that capillary refill time had moderate specificity but limited sensitivity for mortality prediction, so it should be used as part of a structured perfusion assessment rather than as a standalone test.[13]
Neurologic examination
Altered mental status is a key bedside finding of systemic hypoperfusion. The spectrum ranges from subtle confusion, inattention, agitation, or lethargy to somnolence, obtundation, and coma.[1]
In patients with preceding cardiac arrest, neurologic examination helps assess the severity of hypoxic-ischemic brain injury. Persistent coma or absent brainstem reflexes after cardiac arrest are poor prognostic features and may influence decisions regarding escalation of invasive support.
Cardiovascular examination
| Finding | Examination description | Clinical implication |
|---|---|---|
| Jugular venous pressure | Elevated JVP or visible venous distension | Suggests elevated right atrial pressure, RV failure, biventricular failure, or tamponade. Markedly elevated JVP with clear lungs suggests RV-dominant shock.[14] |
| Abdominojugular reflux | Sustained rise in JVP during abdominal pressure | May unmask venous hypertension in right-sided or biventricular congestion.[14] |
| Heart sounds | Diminished heart sounds, S3, S4, or right-sided gallop | S3 suggests elevated filling pressures and ventricular dysfunction; globally diminished heart sounds may occur with severe low-output state or pericardial effusion. |
| New systolic murmur after myocardial infarction | Holosystolic murmur at lower left sternal border or apical systolic murmur | Should raise immediate suspicion for ventricular septal rupture or papillary muscle rupture with acute severe mitral regurgitation.[15] |
| Precordial impulse | RV heave, diffuse apical impulse, displaced impulse, or dyskinetic impulse | May suggest RV dilation, severe LV dysfunction, ventricular aneurysm, or cardiomyopathy. |
The absence of a murmur does not exclude a mechanical complication of myocardial infarction. Acute severe mitral regurgitation from papillary muscle rupture may have a soft or absent murmur because of rapid equalization of left atrial and left ventricular pressures.[15]
Pulmonary examination
| Finding | Interpretation |
|---|---|
| Bilateral rales or crackles | Suggest pulmonary edema from elevated left-sided filling pressures and are typical of LV-dominant cardiogenic shock with congestion. |
| Respiratory distress | Tachypnea, accessory muscle use, inability to speak in full sentences, or need for ventilatory support suggests severe pulmonary congestion, hypoxemia, respiratory failure, or metabolic acidosis compensation. |
| Clear lung fields | Does not exclude cardiogenic shock. Clear lungs with hypotension and elevated JVP suggest RV-dominant cardiogenic shock; cold-dry cardiogenic shock may also present without prominent pulmonary congestion.[8][16] |
Abdominal and renal examination
| Finding | Interpretation |
|---|---|
| Hepatomegaly or right upper quadrant tenderness | Suggests hepatic congestion from elevated right-sided filling pressures; pulsatile hepatomegaly may suggest severe tricuspid regurgitation.[14] |
| Abdominal distension or ascites | May occur in biventricular failure or acute-on-chronic RV failure. |
| Abdominal tenderness | May suggest splanchnic hypoperfusion or nonocclusive mesenteric ischemia, particularly in patients with low-flow states or vasopressor exposure. |
| Oliguria or anuria | Indicates renal hypoperfusion or acute kidney injury. Urine output should be monitored closely in suspected or confirmed cardiogenic shock.[1] |
Examination findings by hemodynamic profile
The warm/cold and wet/dry bedside profile can help categorize patients by perfusion and congestion. It should not replace echocardiography or invasive hemodynamic assessment when the phenotype is unclear.
| Profile | Examination findings | Clinical interpretation |
|---|---|---|
| Cold and wet | Cold, clammy extremities; weak pulses; altered mentation; oliguria; elevated JVP; rales; pulmonary edema; respiratory distress | Classic low-output cardiogenic shock with congestion; the most common cardiogenic shock phenotype, accounting for approximately 64% of patients with acute myocardial infarction-related cardiogenic shock in the SHOCK trial post-hoc analysis.[17][18] |
| Cold and dry | Cold extremities; weak pulses; altered mentation; oliguria; normal or low JVP; clear or minimal rales; no peripheral edema | Low-output state without overt congestion; accounted for approximately 28% of acute myocardial infarction-related cardiogenic shock in the SHOCK trial post-hoc analysis.[17][18] |
| Warm and wet | Warm extremities; bounding pulses; elevated JVP; rales; edema; fever, flushing, or systemic inflammatory features may coexist | Suggests congestion with inflammatory vasodilation, mixed cardiogenic-distributive physiology, or concomitant sepsis; accounted for approximately 5% of acute myocardial infarction-related cardiogenic shock in the SHOCK trial post-hoc analysis.[17][4] |
| Normotensive cardiogenic shock | Systolic blood pressure ≥90 mm Hg without vasopressor support; cold extremities, oliguria, altered mentation, prolonged capillary refill, or elevated lactate may be present | Hypoperfusion without hypotension; accounted for approximately 5% of acute myocardial infarction-related cardiogenic shock in the SHOCK trial post-hoc analysis and is easily missed if blood pressure is used as the sole screening criterion.[7][17] |
| RV-dominant shock | Elevated JVP, clear lung fields, hypotension, Kussmaul sign, RV heave, hepatomegaly, tricuspid regurgitation murmur, bradycardia or AV block in inferior MI | Suggests RV infarction, pulmonary embolism with RV failure, pulmonary hypertension, post-LVAD RV failure, or biventricular shock.[8] |
Right ventricular-dominant cardiogenic shock
Right ventricular-dominant cardiogenic shock has a distinct examination pattern because pulmonary congestion may be absent despite severe shock. The classical triad of RV infarction is hypotension, elevated jugular venous pressure, and clear lung fields.[8][16] Although virtually pathognomonic, this triad has a sensitivity of less than 25%. Distended neck veins alone have been shown to be 88% sensitive and 69% specific for RV infarction. Physical findings may be masked by volume depletion and may emerge only after volume loading.[19]
Kussmaul sign, defined as a paradoxical rise or failure of JVP to fall with inspiration, reflects impaired right ventricular filling. In a systematic review and meta-analysis of 8 studies including 469 patients with acute inferior myocardial infarction, Kussmaul sign had sensitivity of 62.5% and specificity of 90% for RV infarction.[20] In a prospective study of 53 consecutive patients with inferior myocardial infarction, absence of both elevated JVP of at least 8 cm H2O and Kussmaul sign made hemodynamically significant RV infarction highly unlikely; Kussmaul sign was present in all 8 patients with hemodynamic evidence of RV infarction and in none of the 45 without RV infarction.[21]
Additional findings suggesting RV-dominant shock include a right-sided S3 or S4, RV heave, tricuspid regurgitation murmur that increases with inspiration, hepatomegaly, hepatojugular reflux, right upper quadrant tenderness, peripheral edema, bradycardia, and atrioventricular block.[14][8]
Mechanical complications of myocardial infarction
Mechanical complications should be suspected when there is abrupt hemodynamic deterioration after myocardial infarction, particularly within the first week after the index event.[15]
| Complication | Key examination findings | Distinguishing features |
|---|---|---|
| Ventricular septal rupture | Loud, harsh holosystolic murmur at the lower left sternal border; palpable thrill in approximately 50% of cases; pulmonary edema and shock | Murmur is typically harsh; thrill is more common than in acute mitral regurgitation; echocardiography with color Doppler confirms left-to-right shunt.[22] |
| Papillary muscle rupture with acute mitral regurgitation | Soft or absent systolic murmur at the apex, acute pulmonary edema, respiratory distress, and shock | Murmur may be deceptively soft or absent because of rapid left atrial-left ventricular pressure equalization; urgent echocardiography is required when suspected.[15][23] |
| Free wall rupture | Jugular venous distension, muffled heart sounds, pulsus paradoxus, electromechanical dissociation, or sudden cardiovascular collapse | Presents as cardiac tamponade; rapid echocardiography is essential.[24] |
| Left ventricular pseudoaneurysm | Heart failure signs, chest pain, to-and-fro murmur, or persistent instability | May be contained rupture; diagnosis is confirmed by echocardiography, CT, or cardiac MRI.[24] |
Distinguishing cardiogenic shock from other shock types
| Feature | Cardiogenic shock | Septic or distributive shock | Hypovolemic shock | Obstructive shock from tamponade |
|---|---|---|---|---|
| Extremities | Cold, clammy, mottled in classic low-output shock | Warm and flushed early; cold late | Cold and pale | Cold |
| Jugular venous pressure | Elevated in LV-dominant congestion, RV-dominant shock, or biventricular shock | Low or normal unless mixed physiology | Low or flat | Markedly elevated |
| Lung examination | Rales with LV-dominant shock; clear lungs may occur in RV-dominant or cold-dry shock | May be clear or have ARDS findings | Usually clear | Usually clear |
| Heart sounds | S3, diminished S1, or new murmur if mechanical complication | Often hyperdynamic early | Tachycardia without new murmur | Muffled heart sounds; pulsus paradoxus |
| Pulse quality | Weak or thready | Bounding early; weak late | Weak or thready | Weak; pulsus paradoxus may be present |
| Skin | Cold, clammy, diaphoretic, mottled | Warm early; mottled late | Cool and dry | Cool |
Mixed cardiogenic-distributive shock may present with overlapping findings, such as cardiac dysfunction with warm extremities, low or normal systemic vascular resistance, fever, leukocytosis, or vasodilation. Mixed shock should be suspected when the bedside examination does not fit a pure cardiogenic pattern.[17][4]
Serial examination and monitoring trajectory
Physical examination should be repeated frequently, especially during the first 24 to 72 hours, because cardiogenic shock may improve or deteriorate rapidly. Key serial examination targets include:
- Mental status
- Extremity temperature and moisture
- Capillary refill time
- Mottling extent
- Pulse quality
- Urine output
- Respiratory rate, work of breathing, and oxygen requirement
- Jugular venous pressure
- New murmurs or changes in murmur intensity
- Peripheral edema and abdominal congestion
Improvement in peripheral perfusion, such as warming of extremities, normalization of capillary refill time, and resolution of mottling, may indicate therapeutic response and can complement laboratory and hemodynamic trends.[10]
Practical examination approach
- Assess vital signs, including systolic blood pressure, mean arterial pressure, heart rate, respiratory rate, oxygen saturation, and pulse pressure.
- Assess perfusion: mental status, extremity temperature, capillary refill time, mottling, pulse quality, and urine output.
- Assess congestion: JVP, lung rales, respiratory distress, peripheral edema, hepatomegaly, abdominal distension, and ascites.
- Assess for RV-dominant shock: elevated JVP, clear lung fields, Kussmaul sign, RV heave, hepatomegaly, and bradycardia or atrioventricular block in inferior myocardial infarction.
- Assess for mechanical complications after myocardial infarction: new murmur, thrill, pulmonary edema, muffled heart sounds, pulsus paradoxus, or sudden collapse.
- Repeat the examination serially and document trajectory.
Common pitfalls
- Relying on blood pressure alone and missing normotensive cardiogenic shock
- Assuming clear lungs exclude cardiogenic shock
- Missing RV-dominant shock in a patient with inferior myocardial infarction
- Failing to examine for new murmurs after myocardial infarction with abrupt deterioration
- Excluding papillary muscle rupture because the murmur is soft or absent
- Missing RV infarction when volume depletion masks elevated JVP and Kussmaul sign
- Treating peripheral perfusion findings as static rather than reassessing them serially
- Confusing mixed cardiogenic-distributive shock with isolated sepsis
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO (2025). "2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock". Journal of the American College of Cardiology. 85 (16): 1618–1641. doi:10.1016/j.jacc.2025.02.018.
- ↑ 2.0 2.1 2.2 2.3 Heidenreich PA, Bozkurt B, Aguilar D; et al. (2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure". Journal of the American College of Cardiology. 79 (17): e263–e421. doi:10.1016/j.jacc.2021.12.012.
- ↑ 3.0 3.1 Baran DA, Grines CL, Bailey S; et al. (2019). "SCAI Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock". Catheterization and Cardiovascular Interventions. 94 (1): 29–37. doi:10.1002/ccd.28329.
- ↑ 4.0 4.1 4.2 Lüsebrink E, Binzenhöfer L, Adamo M; et al. (2024). "Cardiogenic Shock". Lancet. 404 (10466): 2006–2020. doi:10.1016/S0140-6736(24)01818-X.
- ↑ Bergmark BA, Mathenge N, Merlini PA, Lawrence-Wright MB, Giugliano RP (2022). "Acute Coronary Syndromes". Lancet. 399 (10332): 1347–1358. doi:10.1016/S0140-6736(21)02391-6.
- ↑ Khot UN, Jia G, Moliterno DJ; et al. (2003). "Prognostic Importance of Physical Examination for Heart Failure in Non-ST-Elevation Acute Coronary Syndromes: The Enduring Value of Killip Classification". JAMA. 290 (16): 2174–2181. doi:10.1001/jama.290.16.2174.
- ↑ 7.0 7.1 7.2 Samsky MD, Morrow DA, Proudfoot AG; et al. (2021). "Cardiogenic Shock After Acute Myocardial Infarction: A Review". JAMA. 326 (18): 1840–1850. doi:10.1001/jama.2021.18323.
- ↑ 8.0 8.1 8.2 8.3 8.4 Goldstein JA, Lerakis S, Moreno PR (2024). "Right Ventricular Myocardial Infarction-a Tale of Two Ventricles: JACC Focus Seminar 1/5". Journal of the American College of Cardiology. 83 (18): 1779–1798. doi:10.1016/j.jacc.2023.09.839.
- ↑ Menon V, Slater JN, White HD; et al. (2000). "Acute Myocardial Infarction Complicated by Systemic Hypoperfusion Without Hypotension: Report of the SHOCK Trial Registry". The American Journal of Medicine. 108 (5): 374–380. doi:10.1016/S0002-9343(00)00310-7.
- ↑ 10.0 10.1 Kosyakovsky LB, Earle WB, Wichern C; et al. (2025). "Macrovascular Hemodynamics and Peripheral Perfusion in Cardiogenic Shock: Exploring Current Targets and Future Directions". JACC: Advances. 4 (10 Pt 1): 101964. doi:10.1016/j.jacadv.2025.101964.
- ↑ Merdji H, Bataille V, Curtiaud A; et al. (2023). "Mottling as a Prognosis Marker in Cardiogenic Shock". Annals of Intensive Care. 13 (1): 80. doi:10.1186/s13613-023-01175-0.
- ↑ Merdji H, Curtiaud A, Aheto A; et al. (2022). "Performance of Early Capillary Refill Time Measurement on Outcomes in Cardiogenic Shock: An Observational, Prospective Multicentric Study". American Journal of Respiratory and Critical Care Medicine. 206 (10): 1230–1238. doi:10.1164/rccm.202204-0687OC.
- ↑ Jacquet-Lagrèze M, Pernollet A, Kattan E; et al. (2023). "Prognostic Value of Capillary Refill Time in Adult Patients: A Systematic Review With Meta-Analysis". Critical Care. 27 (1): 473. doi:10.1186/s13054-023-04751-9.
- ↑ 14.0 14.1 14.2 14.3 Konstam MA, Kiernan MS, Bernstein D; et al. (2018). "Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association". Circulation. 137 (20): e578–e622. doi:10.1161/CIR.0000000000000560.
- ↑ 15.0 15.1 15.2 15.3 Damluji AA, van Diepen S, Katz JN; et al. (2021). "Mechanical Complications of Acute Myocardial Infarction: A Scientific Statement From the American Heart Association". Circulation. 144 (2): e16–e35. doi:10.1161/CIR.0000000000000985.
- ↑ 16.0 16.1 Houston BA, Brittain EL, Tedford RJ (2023). "Right Ventricular Failure". The New England Journal of Medicine. 388 (12): 1111–1125. doi:10.1056/NEJMra2207410.
- ↑ 17.0 17.1 17.2 17.3 17.4 van Diepen S, Katz JN, Albert NM; et al. (2017). "Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 136 (16): e232–e268. doi:10.1161/CIR.0000000000000525.
- ↑ 18.0 18.1 Bernhardt AM, Copeland H, Deswal A, Gluck J, Givertz MM (2023). "The International Society for Heart and Lung Transplantation/Heart Failure Society of America Guideline on Acute Mechanical Circulatory Support". Journal of Cardiac Failure. 29 (3): 304–374. doi:10.1016/j.cardfail.2022.11.003.
- ↑ Kinch JW, Ryan TJ (1994). "Right Ventricular Infarction". The New England Journal of Medicine. 330 (17): 1211–1217. doi:10.1056/NEJM199404283301707.
- ↑ Dubé E, Crozier M, Middleton A, Best B, Ohle R (2021). "Kussmaul's Sign for the Diagnosis of Right Ventricular Myocardial Infarction: A Systematic Review and Meta-Analysis of Diagnostic Test Accuracy Studies". CJEM. 23 (2): 185–194. doi:10.1007/s43678-020-00012-8.
- ↑ Dell'Italia LJ, Starling MR, O'Rourke RA (1983). "Physical Examination for Exclusion of Hemodynamically Important Right Ventricular Infarction". Annals of Internal Medicine. 99 (5): 608–611. doi:10.7326/0003-4819-99-5-608.
- ↑ Cubeddu RJ, Lorusso R, Ronco D; et al. (2024). "Ventricular Septal Rupture After Myocardial Infarction: JACC Focus Seminar 3/5". Journal of the American College of Cardiology. 83 (19): 1886–1901. doi:10.1016/j.jacc.2024.01.041.
- ↑ Gong FF, Vaitenas I, Malaisrie SC, Maganti K (2021). "Mechanical Complications of Acute Myocardial Infarction: A Review". JAMA Cardiology. 6 (3): 341–349. doi:10.1001/jamacardio.2020.3690.
- ↑ 24.0 24.1 Lorusso R, Cubeddu RJ, Matteucci M, Ronco D, Moreno PR (2024). "Ventricular Pseudoaneurysm and Free Wall Rupture After Acute Myocardial Infarction: JACC Focus Seminar 4/5". Journal of the American College of Cardiology. 83 (19): 1902–1916. doi:10.1016/j.jacc.2023.10.054.