Shock and mods
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This document discusses shock, which is a profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate organ perfusion. There are four main types of shock: cardiogenic, hypovolemic, distributive, and obstructive. The document outlines the etiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of each type of shock. It emphasizes the importance of early goal-directed therapy and treatment of the underlying cause of shock to increase cardiac output and tissue perfusion in order to prevent multiple organ dysfunction.
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Shock and mods
- 2. Profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs
- 3. Cardiogenic (intrinsic vs compressive) Hypovolemic Distributive ◦ sepsis ◦ neurogenic (spinal shock) ◦ adrenal insufficiency ◦ anaphylaxis
- 5. Arterial hypotension associated with signs of altered tissue perfusion, visualized through three windows of body : Peripheral window: skin that is cold, clammy and blue ,pale or discolored. Renal window: decreased urine output :<0.5ml/kg/h. Neurological window : Altered mental state characterized by obtundation ,disorientation and confusion.
- 6. Usually not clinically apparent Metabolism changes from aerobic to anaerobic. ◦ Lactic acid accumulates -must be removed by blood and broken down by liver. usual cut-off value is 2mEq/L. but lactate level of >1.5mmol/L in patients with septic shock are associated with increased mortality.
- 7. Clinically apparent –Neural, Hormonal &Biochemical compensatory mechanisms Attempts aimed to overcome consequences of anaerobic metabolism and maintaining homeostasis.
- 8. 8 •Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP. •Vasoconstriction, while blood to vital organs maintained. •↓ blood to kidneys > activates renin– angiotensin system ↑ venous return to heart, CO, BP. •Impaired GI motility- Risk for paralytic ileus. •Cool, clammy skin . Except septic patient who is warm and flushed
- 9. Shunting of blood from lungs increases physiologic dead space. ↓ arterial O2 levels Increase in rate/depth of respirations V/Q mismatch SNS stimulation increases myocardial O2 demands. If perfusion deficit corrected, patient recovers with no residual sequelae . If deficit not corrected, patient enters progressive stage
- 10. Begins when compensatory mechanisms fail Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS) Hallmarks -↓ cellular perfusion & altered capillary permeability Leakage of protein into interstitial space ↑ systemic interstitial edema
- 11. Fluid leakage affects solid organs and peripheral tissues. • Anasarca Movement of fluid from pulmonary vasculature to interstitium(decreased blood flow to pulm.Cap.) Pulmonary edema Bronchoconstriction ↓ residual capacity Fluid moves into alveoli Edema-Red. surfactant Worsening V/Q mismatch Tachypnea, Crackles Incr.work of breathing
- 12. CO begins to fall Red. peripheral perfusion Hypotension Weak peripheral pulses Ischemia of distal extremities Myocardial dysfunction results in Dysrhythmias Ischemia; Myocardial infarction End result: complete deterioration of cardiovascular system
- 13. Liver fails to metabolize drugs and waste. Jaundice; Elevated enzymes Loss of immune function Risk for DIC and significant bleeding Mucosal barrier of GI system becomes ischemic Ulcers Bleeding Risk of translocation of bacteria Reduced ability to absorb nutrients
- 14. Exacerbation of anaerobic metabolism Accumulation of lactic acid ↑ capillary permeability Profound hypotension and hypoxia Tachycardia worsens. Failure of one organ system affects others. Recovery unlikely
- 15. Myocardial Injury or Obstruction to Flow ◦ Arrythymias ◦ valvular lesions ◦ AMI ◦ Severe CHF ◦ VSD ◦ Hypertrophic Cardiomyopathy
- 16. Pulmonary Edema Raised JVP Hypotension weak pulses oliguria
- 17. Pulmonary Embolism (obstructive) Cardiac Tamponade Tension Pneumothorax Presentation will be according to underlying disease process.
- 18. Reduced circulating blood volume with secondary decreased cardiac output ◦ Acute hemorrhage ◦ Vomiting/Diarrhea ◦ Dehydration ◦ Burns ◦ Peritonitis/Pancreatitis
- 19. Hypotensive collapsed neck veins clear lungs cool, cyanotic extremities evidence of bleeding? ◦ Anticoagulant use ◦ trauma, bruising oliguria
- 20. Peripheral Vasodilation secondary to disruption of cellular metabolism by the effects of inflammatory mediators. Gram negative or other overwhelming infection. Results in decreased Peripheral Vascular Resistance.
- 21. Febrile Tachycardia clear lungs, evidence of pneumonia warm extremities collapsed neck veins oliguria
- 22. Response to fluids Echo/ECG CXR Evidence of infection
- 23. Etiology CO PCWP SVR cardiogenic decreased increased increased hypovolemic decreased decreased increased distributive increased decreased decreased obstructive decreased Increased increased
- 24. Correct underlying disorder if possible and then direct efforts at increasing the blood pressure to increase oxygen delivery to the tissues. Maintain a mean arterial pressure of 65mmHg (1/3 systolic + 2/3 diastolic) Keep O2 sats >92%, intubate if neccesary
- 25. Normal Saline should be administered anytime a patient is hypotensive. If possible give colloid. Vasopressors specially for septic shock . Inotropic agents for cardiogenic shock Intra-aortic Balloon Pump for cardiogenic
- 26. Drugs Indication dose MOA Principle action Dopamine Hypotension 5- 10mcg/k g/min Beta1and dopaminergic Inotropic(+) Hypotension >10mcg /kg/min alpha1 Vasoconstri ction Dobutamine Cardiogenic shock 2.5- 25mcg/k g/min Selective beta1 Inotropic(+) Norephinephrine Hypotension 2- 4mcg/kg /min Alpha1and beta1 Vasoconstri ction Phenylephinphrine Hypotension 40- 180mcg/ kg/min Selective alha1 vasoconstri ction
- 27. Attempt to correct problem and increase cardiac output by diuresing and providing inotropic support. IABP is utilized if medical therapy is ineffective. Cardiac Catheterization if ongoing ischemia despite maximum medical therapy. Cardiogenic shock is the exception to the rule that NS is always given for hypotension NS will exacerbate cardiac shock.
- 28. Early goal directed therapy Identification of source of infection Broad Spectrum Antibiotics IV fluids Vasopressors Steroids ?? Recombinant human activated protein C ( Xygris) Bicarbonate if pH < 7.1
- 29. Correct bleeding abnormality If PT or PTT elevated then FFP Aggressive Fluid replacement with 2 large bore IV’s or central line. Pressors are last line, but commonly required.
- 30. HARRISON 18TH EDITION. Page no. 1689- 1695. Consensus on circulatory shock and hemodynamic monitoring. Task force of European society of Intensive care Medicine(Intensive care Med(2014)40:1795- 1815 DOI 10.1007/s00134-014-3525-z. The swan –Ganz catheter: past ,present and future(circulation .2009:119:147-152.)