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![Cardiogenic shock /Acute circulatory Failure
• Is a state of end-organ hypoperfusion due to
cardiac failure.
• Cardiogenic shock
-systemic hypoperfusion due to severe
depression of the cardiac index (<2.2 [L/min]/m2)
- sustained systolic arterial hypotension (<90
mmHg) despite an elevated filling pressure
(pulmonary capillary wedge pressure [PCWP]
>18 mmHg)](https://image.slidesharecdn.com/shock-171013050847/85/Shock-12-320.jpg)
More Related Content
Shock
- 1. SHOCK Dr. S MSafayet Hosen MD-(Resident) Phase A
- 2. Definition Shock is theclinical syndrome Inadequate tissue perfusion The hypoperfusion-induced imbalance between the delivery & requirements for oxygen Substrate leads to cellular dysfunction
- 3. Types of Shock SHOCK Lowstroke volume Hypovolaemic Haemorrhage Burn Salt & water loss Cardiogenic MI acute mitral regurgitation Obstructive PE Cardiac Tamponade Tension pneumothorax Vasodilatation/ Distributive Sepsis/SIRS infection Anaphylactic Injection-penicillin Bee sting Anesthetics selfish Neurogenic Trauma to spinal cord Spinal anesthesia
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- 6. Hypovolaemic shock Due to a)Haemorrhage -External from wounds, open fractures -Internal from injury to spleen, liver, mesentery or pelvis b) Severe burn which result in loss of plasma C) intestinal obstruction c) Diarrhoea & vomiting of any cause
- 7. Hypovolaemic shock- Pathophysiology Dueto sudden loss blood volume or fluid from the vascular space. Loss of blood Filling of rt. Heart Filling of pulmonary vasculature Filling of left atrium & ventricle Stroke volume Arterial BP SHOCK
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- 9. Hypovolaemic shock- Management ABC(AIRWAY is always first) Control hemorrhage (splint the limb) Obtain IV access with wide bore cannula Resuscitate with fluids and blood - Isotonic saline/ ringer’s lactate solution - Blood transfusion if Hb <10g/dl **Supplemental oxygen should always be provided
- 10. Management goals AFTERsecuring the ABCs.. • STOP THE BLEEDING • RESTORE VOLUME • CORRECT ANY ELECTROLYTE/ACID-BASE DISTURBANCES Monitoring Urine output Vital signs Skin perfusion SP02 - Pulse Oximetry
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- 12. Cardiogenic shock /Acutecirculatory Failure • Is a state of end-organ hypoperfusion due to cardiac failure. • Cardiogenic shock -systemic hypoperfusion due to severe depression of the cardiac index (<2.2 [L/min]/m2) - sustained systolic arterial hypotension (<90 mmHg) despite an elevated filling pressure (pulmonary capillary wedge pressure [PCWP] >18 mmHg)
- 13. Causes of Cardiogenicshock Systolic dysfunction - CAD : Acute MI or ischemia (most common ) - Other conditions : severe myocarditis end stage cardiomyopathy Prolonged cardiopulmonary bypass Diastolic dysfunction - CAD - ventricular hypertrophy
- 14. Valvular orstructural abnormality (acute valve failure) Aortic Regurgitation -Aortic dissection -Infective endocarditis Mitral regurgitation -Papillary muscle rupture due to acute MI -Infective endocarditis Prosthetic valve failure -Mechanical valves: fracture , jamming, thrombosis -Biological valves: degeneration with cusp tear
- 15. Arrhythmia - VT/VF,bradycardia can cause shock - sinus tachycardia can aggravate shock Others Restrictive cardiomyopathy HOCM with Severe outflow obstruction Prolong hypovolemia or septic shock β-Blocker/CCB overdose
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- 17. Risk factors forCardiogenic Shock Older Age Prior MI Diabetes Mellitus HTN Anterior MI Extensive coronary artery stenosis History of HF STEMI New LBBB
- 18. Diagnosis • Proper history& clinical examination • ECG • Chest X-ray • Echocardiogram • Blood specimen for laboratory investigation ** Supportive therapy must be initiated simultaneously with diagnostic evaluation
- 19. Clinical findings SIGN SYMPTOMS Pulseweak , rapid (90-110BPM) / Severe bradycardia due to HB Systolic BP (<90mmHg) Narrow pulse pressure (<30 mmHg) Tachypnea JVP distention Soft s1 & an s3 gallop may found Systolic murmurs- Severe MR, VSR Crackles – LV failure Oliguria Chest pain Vomiting Palpitation Dyspnea Appear pale Altered mental state
- 21. A. General Measures •In addition to immediate treatment of acute MI initial therapy aimed • Maintaining systemic BP by Vasopressors • Ensure LV filling pressure by adjusting volume status • Correct hypoxemia & acidosis • May need ventilatory support • Negative ionotropics must stopped
- 22. B. Pharmacological support •VASOPRESSORS Norepinephrine -Potent vasoconstrictor & Inotropic stimulant -May cause arrhythmia -Can be used as initial vasopressor therapy -DOSE: 2-4µg/min to max. 15µg/min Dopamine -Dose depended hemodynamic effect -Better than Norepinephrine -DOSE: 2-5µg/kg/min to max. 20- 50µg/kg/min Dobutamine -Synthetic sympathomimetic amine -Positive inotropic action -DOSE: 10µg/kg/min
- 23. Inotropes and Vasopressors (ACC/AHAGuidelines) • SBP <70 mmHg Norepinephrine (2-4µg/min to max. 15µg/min) Switch to Dopamine (2-4µg/min to max. 15µg/min) once SBP ≥80 • SBP 70-100 mmHg Dopamine (2-4µg/min to max. 15µg/min) Add Dobutamine (2-20 g/kg/min) once SBP ≥90
- 24. C. Mechanical support IABP - Improve coronary & peripheral perfussion - Initiate as quick as possible - Higher rates of survival in high use centers Newer devices - LV, RV or BiV assist. Devices - Impella, tendem heart, Extarcorporeal life support (ECLS) - Trials have shown hemodynamic improvement but no survival benefit found
- 25. D. REPERFUSION-REVASCULARIZATION Early revascularizationwith PCI / CABG is recommended **from ACC/AHA guidelines. IRA, infarct-related artery , IABP- Intra-aortic balloon counterpulsation/pump
- 26. E. Treatment accordingto cause Shock due to RV infract -3% of cardiogenic shock due to RV infract & inf. Ischemia -Fluid resuscitation -Dopamine / Dobutamine -Early reestablishment of infract artery flow
- 27. MR -Severe MRdue to rupture papillary muscle -Diagnosis: Echo-Doppler -Rapid stabilization with IABP -Dopamine / Dobutamine VSR -Diagnosis: Echo-Doppler(Blood shunting Lt. to Rt. & open in interventricular septum) -Rapid stabilization with IABP -Dopamine / Dobutamine
- 28. AHA Guideline ClassI 1. Early revascularization (PCI/CABG) 2. Fibrinolysis in candidates unsuitable for ERV with no contraindications Class II a 1. Use of IABP can be useful in pt. with CS who don’t quickly stabilize with pharmacologic therapy Class II b Alternative LV assist device may be considered in pt with refractory CS
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- 30. Anaphylactic shock • Whatis anaphylaxis?? A manifestation of immediate hypersensitivity A sensitized individual to A specific antigen results in life-threatening respiratory distress followed by vascular collapse and shock accompanied by pruritis, urticaria, and angioedema
- 31. Etiology • Medications, includingantibiotics (especially penicillin and sulfa), vaccines, opiates, aspirin, NSAIDs, local anesthetics, intravenous fluids with dextran, and insulin • Foods, such as nuts, milk, eggs, soy, wheat, and seafood • Stings by fire ants and Hymenoptera species (eg, bees, wasps, yellow jackets, hornets) • Latex • Blood products, including plasma, immunoglobulin, cryoprecipitate, and whole blood • Idiopathic origins • Exercise causes
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- 36. Obstructive shock • Extra-cardiacobstruction to flow in the cardiovascular circuit • Either impairment of diastolic filling or excessive afterload Etiology - Tension pneumothorax - Pericardial tamponade -Massive Pulmonary embolus -IVC Obstruction DVT Gravid uterus on IVC Neoplasm -Increased intrathoracic pressure Excess positive end expiratory pressure neoplasm
- 37. • Develops whena lung or chest wall injury is such that it allows air into the pleural space but cannot out of it (a one way valve) • As a result - Air accumulation & compress the lung - Shifting the mediastinum - Compressing contralateral lung - Increasing intrathoracic pressure - Reduce Venus return to the heart - Causes shock Tension pneumothorax
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- 39. Tension pneumothorax (Management) 1.initial management– needle thoracostomy Convert the tension pneumothorax to a simple pneumothorax 2. Definitive management : Chest tube insertion 3. Supportive management: -Analgesia -Ventilatory support -CXR monitoring -Chest physiotherapy
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- 41. NEUROGENIC SHOCK • Atype of distributive shock that results from the loss or suppression of sympathetic tone • Causes massive vasodilatation in the venous vasculature → ↓venous return to heart → ↓cardiac output • Most common etiology: Spinal cord injury **Neurogenic shock is the rarest form of shock
- 42. Causes of NeurogenicShock The Common Causes Of Neurogenic Shock Include: • Blunt or penetrating injury to the spinal cord • Trauma to the spinal cord from motor vehicle accidents, sports injuries, falls, stab and gunshot wounds. • Improper administration of regional anesthesia can also cause neurogenic shock. • Devastating head injury • Drugs and medications which affect the autonomic nervous system can also cause neurogenic shock.
- 43. Pathophysiology of NeurogenicShock Disruption of sympathetic nervous system Loss of sympathetic tone Venous and arterial vasodilation ↓ venous return ↓ stroke volume ↓ cardiac output ↓ cellular oxygen supply ↓ tissue perfusion Impaired cellular metabolism
- 44. Assessment of NeurogenicShock • PATIENT ASSESSMENT -Hypotension -Bradycardia -Hypothermia -Warm, dry skin - ↓CO -Flaccid paralysis below level of the spinal lesion
- 45. Patient Also Experiences -SOB, rapid and deep shallow breathing. -Facial pallor, Dizziness, lightheadedness, fainting. -Nausea and vomiting. - weakness due to insufficient blood supply. -may changes in mental state or disorientation. -Has bluish discoloration of lips and fingers (cyanosis). -Decreased or absent urine output. -Sweats profusely. -Considerable chest pain -Loss of consciousness
- 46. Treatment For NeurogenicShock • Neurogenic shock is a serious condition • Requires emergent medical care • Airway, Breathing and Circulation (ABC) • Immobilize the patient, especially the spinal region to prevent any further damage to the spinal cord. • IV fluids to stabilize the patient's blood pressure • Inotropic agents, such as dopamine may be infused for fluid resuscitation, if needed. • Atropine is given intravenously to manage severe bradycardia. • Surgery is needed in case of accident/trauma/ injury/ to the patient
- 47. Spinal shock VsNeurogenic Acute spinal cord injury Hemodynamic phenomenon Loss of vasomotor tone & sympathetic tone Peripheral neurons become temporarily unresponsive to brain stimulation Disruption of autonomic pathways → Loss of sympathetic tone → vasodilatation C/F: Decreased reflexes Loss of sensation Flaccid paralysis below level of injury Hypotension Bradycardia Poikilothermia Last days to months (transient) May last up to 6wks