Medicine, via pristina

Medicine, via pristina

Cardiogenic Shock

1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
PMID: 31504439
DOI: https://doi.org/10.1093/eurheartj/ehz425


2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
DOI: https://doi.org/10.1016/j.jacc.2012.07.013


3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
PMID: 32742886
DOI: 10.7759/cureus.9349


4. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177.
PMID: 28886621
DOI: https://doi.org/10.1093/eurheartj/ehx393


5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
PMID: 25260716
DOI: https://doi.org/10.1016/j.jacc.2014.09.017

Background

Cardiogenic shock is a state of critical end-organ hypoperfusion due to a primary cardiac dysfunction, most commonly resulting from acute myocardial infarction. It is characterized by reduced cardiac output, elevated filling pressures, and systemic hypotension despite adequate intravascular volume. Without prompt intervention, it can lead to multiorgan failure and death. 


II) Classification or Types
 

By Etiology: 

  • Ischemic: Acute MI (most common) 
  • Mechanical: Papillary muscle rupture, ventricular septal defect, free wall rupture 
  • Arrhythmic: Severe bradycardia or tachyarrhythmias 
  • Myopathic: End-stage cardiomyopathy, myocarditis 
  • Valvular: Acute mitral or aortic regurgitation 

By Onset/Time Course: 

  • Acute: Sudden (e.g., MI, tamponade) 
  • Subacute: Progressive deterioration (e.g., decompensated heart failure) 


III) Epidemiology
 

  • Sex: Slight male predominance in ischemic cases 
  • Age: Incidence increases with age; highest in patients >65 
  • Incidence: Occurs in ~5–10% of ST-elevation myocardial infarctions (STEMIs) 
  • Mortality: Despite advances, in-hospital mortality remains high (~30–50%) 
  • Risk factors: Pre-existing CAD, diabetes, prior MI, LV dysfunction 

 


Etiology

I) What Causes It 

  • Acute MI (especially anterior STEMI) 
  • Severe left ventricular systolic dysfunction 
  • Mechanical complications post-MI (e.g., papillary muscle rupture → acute MR) 
  • Cardiomyopathy (dilated, stress-induced) 
  • Fulminant myocarditis 
  • Massive pulmonary embolism (RV shock) 
  • Severe aortic stenosis or regurgitation 
  • Cardiac tamponade 
  • Bradyarrhythmias (e.g., complete heart block) 
  • Tachyarrhythmias (e.g., ventricular tachycardia) 


II) Risk Factors
 

  • Prior myocardial infarction 
  • Left ventricular ejection fraction <40% 
  • Extensive coronary artery disease 
  • Diabetes mellitus 
  • Age >70 years 
  • Delay in reperfusion therapy 
  • Mechanical complications of MI 

 


Clinical Presentation

I) History (Symptoms) 

  • Chest pain (if ischemic) 
  • Dyspnea, orthopnea 
  • Profound fatigue or confusion 
  • Oliguria 
  • Syncope or presyncope 
  • Cold extremities 


II) Physical Exam (Signs)
 

Vital Signs: 

  • Hypotension (SBP <90 mmHg or MAP <65 mmHg) 
  • Tachycardia (or bradycardia in conduction blocks) 
  • Narrow pulse pressure 

Cardiac Exam: 

  • S3 or S4 gallop 
  • New murmur (e.g., mitral regurgitation from papillary rupture) 
  • Jugular venous distension 

Pulmonary Exam: 

  • Rales or crackles (pulmonary edema) 
  • Decreased breath sounds if pleural effusion present 

Peripheral: 

  • Cool, clammy extremities 
  • Delayed capillary refill 
  • Weak pulses 
  • Mottled skin 

 


Differential Diagnosis (DDx)

  • Hypovolemic shock 
  • Obstructive shock (e.g., PE, tamponade, tension pneumothorax) 
  • Distributive shock (e.g., septic shock) 
  • Acute decompensated heart failure without shock 
  • Takotsubo cardiomyopathy 
  • Drug overdose (e.g., beta-blockers, calcium channel blockers) 

 


Diagnostic Tests

Initial Tests: 

  • ECG: ST changes, arrhythmias, conduction blocks 
  • Cardiac biomarkers (Troponin): Elevation indicates MI 
  • BNP/NT-proBNP: Elevated in volume overload 
  • Chest X-ray: Pulmonary congestion, cardiomegaly 
  • ABG/Lactate: Metabolic acidosis, elevated lactate 
  • CBC, CMP: Assess end-organ perfusion and baseline function 


Cardiac Imaging:
 

  • Transthoracic Echocardiogram (TTE): 
  • Evaluates EF, wall motion, valve integrity 
  • Detects tamponade, VSD, MR, or thrombus 
  • Right heart catheterization (Swan-Ganz): 
  • Confirms elevated pulmonary capillary wedge pressure and low cardiac index 
  • Differentiates cardiogenic from other types of shock 
  • Coronary angiography: 
  • Urgent in suspected MI 
  • Guides revascularization 

 


Treatment

I) Medical Management 

Stabilization: 

  • Oxygen or mechanical ventilation if needed 
  • IV access and hemodynamic monitoring 
  • Vasopressors (e.g., norepinephrine) to maintain perfusion 
  • Inotropes (e.g., dobutamine, milrinone) for contractility 

Treat Underlying Cause: 

  • Acute MI: Emergent PCI or CABG 
  • Arrhythmia: Cardioversion, pacing, antiarrhythmic agents 
  • Mechanical complication: Surgical repair 
  • Severe MR: Afterload reduction ± urgent valve surgery 

Volume Management: 

  • Use diuretics cautiously if volume overloaded 
  • Avoid excess fluids in true cardiogenic shock 

Antiplatelets/Anticoagulation: 

  • In ACS or embolic risk 


II) Mechanical Circulatory Support (MCS)
 

  • Intra-aortic balloon pump (IABP): Temporizing support 
  • Impella or TandemHeart: For LV unloading 
  • VA-ECMO (veno-arterial extracorporeal membrane oxygenation): 
  • Used in refractory shock or cardiac arrest 
  • Requires specialized centers 

 


Patient Education, Screening, Vaccines

  • Education on early signs of ischemia or heart failure 
  • Adherence to medications (e.g., beta-blockers, antiplatelets) 
  • Smoking cessation, blood pressure, lipid, and glucose control 
  • Diet: Low sodium, fluid monitoring if CHF 
  • Avoid NSAIDs in heart failure 

Vaccinations: 

  • Annual influenza 
  • Pneumococcal (both PCV20 or PCV15 + PPSV23) 
  • COVID-19 

 


Consults

  • Cardiology: All patients; emergent in ACS 
  • Cardiothoracic Surgery: For mechanical complications, ECMO, valve repair 
  • Critical Care: ICU admission for advanced monitoring 
  • Electrophysiology: Recurrent arrhythmias or device placement 
  • Palliative Care: For end-stage heart failure or decision-making 
  • Primary Care: Risk factor modification post-discharge 

 


Follow-Up

  • Cardiac rehab after recovery from acute event 
  • Repeat echocardiogram to assess LV function post-stabilization 
  • Medication titration: ACEi/ARB, beta-blockers, aldosterone antagonists 
  • Close outpatient monitoring for signs of decompensation 
  • Assessment for advanced heart failure therapies: ICD, CRT, transplant 

 

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