CARDIOGENIC SHOCK-Approach to Nontraumatic Shock .pptx

CARDIOGENIC SHOCK-Approach to Nontraumatic Shock- Case,SHOCK,Hemodynamic profiles of the types of shock,Hemodynamic Principles,Risk Factors for Cardiogenic Shock,Pathophysiology,Approach to patient with cardiogenic shock ,CLINICAL FEATURES,Causes of cardiogenic shock,ED TREATMENT AND STABILIZATION

1. CARDIOGENIC SHOCK Approach to Nontraumatic Shock DR PANKAJ PARMAR JR2 EMERGENCY MEDICINE DEPARTMENT

2. PREV. QUE Discuss the ED management of: a) Distributive shock. [5] b) Cardiogenic shock.

3. Case A 65-year-old male patient, Mr. suresh , presents to the emergency department with severe chest pain and shortness of breath since 3 hr ago. He has a history of hypertension, hyperlipidemia , and smoking. PRIMARY SURVEY - Blood pressure: 80/50 mmHg- Heart rate: 110 beats per minute - Respiratory rate: 24 breaths per minute - Oxygen saturation: 88% on room air GSC 15/15,AFEBRILE, RBS 110mg/dl SECONDRY SURVEY HEENT- normal – Cool, clammy skin Jugular venous distension Bilateral lung crackles Decreased peripheral pulses CRT >3 SEC.

4. SHOCK Shock is a state of circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and demand (consumption), resulting in end-organ dysfunction. TYPE Hypovolemic- occurs when decreased intravascular fluid or decreased blood volume causes decreased preload, stroke volume, and cardiac output (CO). Distributive- there is relative intravascular volume depletion due to marked systemic vasodilatation. Anaphylaxis, adrenal insufficiency, and neurogenic shock are additional causes of distributive shock. Cardiogenic- the left ventricle fails to deliver oxygenated blood to peripheral tissues due to variances in contractility, as well as preload, afterload, and right ventricular function. Obstructive- uncommon (1%) and is due to a decrease in venous return or cardiac compliance due to an increased left ventricular outflow obstruction or marked preload decrease

5. Hemodynamic profiles of the types of shock

6. Hemodynamic Principles Cardiac Output (CO): Determined by heart rate (HR) and stroke volume (SV). Stroke Volume is influenced by preload, afterload, and contractility. Mean Arterial Pressure (MAP): Calculated as MAP = CO × SVR. There is a critical MAP threshold below which tissue oxygen delivery is compromised. In shock, despite sometimes normal blood pressure ("cryptic shock"), inadequate CO or abnormal SVR may impair tissue oxygenation.

7. Risk Factors for Cardiogenic Shock Elderly Female Acute or prior ischemic event associated with the following • Impaired ejection fraction • Extensive infarct (evidence of large myocellular leak) • Proximal left anterior descending coronary artery occlusion • Anterior myocardial infarction • Multivessel coronary artery disease Prior medical history • Previous myocardial infarction • Congestive heart failure • Diabetes

8. Pathophysiology Primary cause: Extensive myocardial infarction (MI) leading to pump failure . ↓ Cardiac Output (CO) → ↓ BP → Hypoperfusion → Organ Dysfunction . Diastolic BP ↓ ( due to lack of compensatory SVR increase) → Coronary hypoperfusion → Ischemia worsening . Cycle of ischemia → LV dysfunction → Pulmonary edema → Hypoxia → More dysfunction . Peripheral vasoconstriction may help perfusion but increases afterload , worsening CO. Systemic inflammatory response (NO, cytokines) → Vasodilation & Negative inotropic effect .

9. The pathophysiology of shock, the inflammatory response, and multiorgan dysfunction.

10. Approach to patient with cardiogenic shock

11. CLINICAL FEATURES PHYSICAL EXAMINATION 🔹 Hemodynamic Features ↓ Cardiac Index (CI) < 2.2 L/min/m² → Hypoperfusion (may not always have hypotension). SBP < 90 mmHg (but can be higher in hypertensive patients). Pulse Pressure < 20 mmHg if SVR is maintained. Sinus Tachycardia common (except if on β- blockers). 🔹 Systemic Hypoperfusion Signs Pale, cyanotic, cool, mottled extremities . Diaphoresis (sympathetic activation). Altered Mental Status (cerebral hypoperfusion). Low Urine Output (renal hypoperfusion). 🔹 Right Ventricular (RV) Infarction Signs Clear lungs (no pulmonary edema ). Venous Congestion: ↑ JVP Kussmaul Sign (rise in JVP with inspiration). Hepatojugular Reflux (JVP rise on liver compression). Peripheral Edema , Enlarged Liver . S3 (RV origin) . 🔹 Respiratory Signs Tachypnea (until respiratory fatigue sets in). Pulmonary Edema (LV failure) → Rales on auscultation. HISTORY - shortness of breath, chest pain, or weakness

12. 🔹 Mechanical Complications (~10% Post-MI Cardiogenic Shock) 1️⃣ Acute Mitral Regurgitation Soft holosystolic murmur (apex → axilla) . Causes: Chordae tendineae rupture, papillary muscle dysfunction. 2️⃣ Acute Ventricular Septal Defect (VSD) Loud holosystolic murmur (left parasternal). Palpable thrill. Murmur ↓ as intraventricular pressures equalize. 3️⃣ Acute Aortic Insufficiency Soft diastolic murmur, soft S1 sound.

13. Causes of cardiogenic shock Mechanical obstruction to forward blood flow • Aortic stenosis • Hypertrophic cardiomyopathy • Mitral stenosis • Left atrial myxoma • Pericardial tamponade Mechanical complications • Acute mitral regurgitation secondary to papillary muscle dysfunction or chordal rupture • Ventricular septal defect • Free wall rupture • Right ventricular infarction • Acute aortic insufficiency (aortic dissection) Severe depression of cardiac contractility • Acute myocardial infarction • Sepsis • Myocarditis • Myocardial contusion • Cardiomyopathy • Medication toxicity (e.g., β- blocker overdose, calcium channel–blocker overdose) • Unstable dysrhythmia

14. RTA with CARDIAC TAMPONADE AORTIC DISSECTION

15. MR

16. DIAGNOSIS LABORATORY TESTING Cardiac biomarkers CBC identifies anemia serum lactate serum electrolytes ,RFT/LFT Serum B-type natriuretic peptide Blood gas measurements Electrocardiogram Bedside Point of Care Ultrasound Hemodynamic Monitoring

17. ED TREATMENT AND STABILIZATION Initial ED management focuses on airway stability and improving myocardial pump function to maintain end-organ perfusion while arranging definitive care. AIRWAY STABILIZATION HYPOTENSION Guide initial therapy by the clinical findings. Give crystalloid fluid boluses (250 to 500 mL, and repeat after assessing benefit or harm) if pulmonary congestion is absent or for an RV infarct with hypotension D RUG Dobutamine- increases cardiac contractility and is most effective WHEN systolic blood pressure is ≥90 mm Hg . Avoid when SBP <90 mmhg Dopamine - vasopressor with some inotropic effect, but it may increase cardiac work by increasing heart rate and may also increase LVEDP by its β-agonist effect. Norepinephrine - potent vasoconstrictor use alone or wi th combination

18. Epinephrine is associated with more systemic acidosis, tachycardia, and dysrhythmias Milrinone (a selective phosphodiesterase-3 inhibitor ) can be substituted for the catecholamine if dobutamine is ineffective. In case Patients on β- blocker therapy If shock persists despite use of these agents, consider an intra-aortic balloon pump or other assist device DONOT USE

19. DEFINITIVE MANAGEMENT EARLY REVASCULARIZATION THROMBOLYTIC THERAPY INTRA-AORTIC BALLOON PUMP COUNTERPULSATION VENTRICULAR ASSIST DEVICES EXTRACORPOREAL MEMBRANE OXYGENATION - Veno-arterial Extracorporeal Membrane

20. THANK YOU