2 shock 1
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Shock is defined as failure to meet the metabolic demands of tissues due to decreased systemic tissue perfusion. There are several stages and types of shock. The pathophysiology involves cellular hypoxia leading to metabolic acidosis, endothelial injury, and organ dysfunction. Management involves addressing airway, breathing, circulation, and the underlying cause of shock. Fluid resuscitation is initially used but vasopressors may be needed. Complications can include acute renal failure, acute respiratory distress syndrome, and multi-organ failure if shock is not promptly recognized and treated.
2 shock 1
- 2. outlines • Definition • Pathophysiology • Stages of shock • Classification • Management • Complications shock 2
- 3. Definition Shock - is failure to meet the metabolic demands of the cells & tissues and the consequence that follows. -The centeral component of shock is decreased systemic tissue perfusion. -This may be the direct consequence of the etiology of shock like hypovolumic,cardiogenic,obstructive,or secondary to released molecules or cellular products that result in endothelial activation like in septic and traumatic shock. This creates an imbalance between oxygen delivery and oxygen consumption. shock 3
- 4. • It is reversible at early stages but prolonged tissue hypo perfusion leads to irreversible shock. • Clinical parameters like BP & HR are insensitive and Dx needs additional parameters. • This is b/c vital sign derangement is noticed after significant hemodynamic disturbance. shock 4
- 5. PATHOPHYSIOLOY • Regardless of the etiology the physiologic response in shock is driven by tissue hypo perfusion and developing cellular energy deficit. • The mechanism is mainly by; -Deacreasing intravascular fluid or -Causing vasodilation. .The circulatory response is to keep perfusion to vital organs at expense of other tissue. shock 5
- 6. • Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. • Decreased tissue perfusion and shock results in a feed forward loop that can exacerbate cellular injury & tissue dysfunction Vicious cycle. shock 6
- 8. Cellular hypo perfusion • Prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes at the cellular level, which can progress to the systemic level. • Oxygen deficit leads to lactic acidosis accumulation and metabolic acidosis. shock 8
- 9. Microcirculation • Hypoxia & acidosis activates complement system. This results in release of o2 free radicals & cytokines capillary endothelial cell injury. Endothelium becomes leaky, tissue edema. This exacerbates cellular hypoxia. shock 9
- 10. • Systemic effects Respiratory –metabolic acidosis causes tachypnea. Renal- ed renal perfusion ed UOP act ivation of RAAS water & sodium retention. shock 10
- 11. Cvs-as prelaod and afterload decreases there will be compensatory baroreceptor response which causes sympathetic activation. This results in tachycardia and vasoconstriction (except sepsis). shock 11
- 12. • Ischemia-reperfusion injury When the normal tissue perfusion is restored, cellular and humeral elements activated by hypoxia (complement, neutrophil, microvascular thrombi) will be flushed back into the circulation where they cause endothelial injury to organs like lung and kidney. This leads to acute lung injury, ARI, MOF & death. shock 12
- 13. STAGES OF SHOCK Regardless of the type of shock there is a physiologic continuum. A)Preshock or compensated shock Characterized by rapid compensation for diminished tissue perfusion by various mechanisms. Blood flow to vital organs like heart and brain will be maintained by reducing flow to the skin, muscle and GIT. Tachycardia and peripheral vasoconstriction my be the only signs. shock 13
- 14. B) Decompensation Mild shock-tachycardia, tachypnea and mild reduction in urine output. Bp is maintained. Cold extremities with prolonged capillary refill(except in septic shock). Moderate shock- renal perfusion falls and urine output dips below 0.5 ml/kg/hr. Tachycardia increases & BP starts to falls. Severe shock- profound tachycardia and hypotension.UOP falls to zero & patient becomes unconscious. If not corrected patient will develop MOF. shock 14
- 15. C/ Irreversible phase • If volume loss continues,or resuscitation is not sufficient vicious physiologic cycle will develop. • This progression to is often ininsidious and recognized only retrospect. shock 15
- 16. CLASSIFICAION • Classification of shock 1) Hypovolaemic 2) Cardiogenic 3) Obstructive 4)Distributive(septic,neurogenic,anaphylactic &traumatic) 5) Endocrine shock 16
- 17. 1)Hypovolaemic shock -Most common cause of shock in surgical or trauma patients. -Hypovolaemia may be due to a) Hemorrhagic or b) Non-hemorrhagic causes like poor oral intake, vomiting, diarrhea, urinary loss or “third spacing.” shock 17
- 18. CLASSIFICATION OF HEMORRHAGE class Parameter 1 2 3 4 Blood loss (ml) < 750 750-150 1500-2000 > 2000 Blood loss (%) < 15 15-30 30-40 >40 Heart rate (bpm) < 100 > 100 > 120 > 140 Blood pressure Normal Orthostatic Hypotension Severe hypotension CNS symptoms Normal Anxious Confused Obtunded shock 18
- 19. Clinical feature • Agitation • Cool extremities • Tachycardia • Weak or absent peripheral pulse • Hypotension with suggestive history shock 19
- 20. 2) Cardiogenic shock • Occurs due to primary failure of the heart to pump blood to the tissues in setting of adequate intravascular volume. • Hemodynamic criteria sustained hypotension(SBP<90mmHg for at least 30min ) decreased cardiac index(<2.2 L/min per square meter) elevated pulmonary artery wedge pressure (>15mmHg) shock 20
- 21. • MR ranges from 50-80%. • Causes include - myocardial infarction, - cardiac dysrhythmias, - valvular heart disease, - blunt myocardial injury and - cardiomyopathy. -myocarditis • Diagnosis needs ECG & ECHO. shock 21
- 22. 3) Obstructive shock • Reduction in preload because of mechanical obstruction of cardiac filling. • Causes -cardiac tamponade -tension pneumothorax -massive pulmonary embolus -air embolus -IVC obstruction shock 22
- 23. Diagnosis and treatment Tension pneumothorax is diagnosed clinically. Clinical findings respiratory distress Hypotension 3 of this Diminished breath sounds are enough Hyperresonance to percussion for Dx Shift of mediastinal structures Jugular vein distension • Rx-tube thoracotomy shock 23
- 24. • Cardiac tamponade Clinical feature Hypotension Muffled heart sound Beck’s triad Neck vein distension Dyspnea, orthopnea, cough Tachycardia Edema • ECHO becomes preferred test for the diagnosis. • Treatment-u/s guided pericardiocentesis. shock 24
- 25. 4) Distributive shock • Is a pattern of cardiovascular response characterizing a variety of conditions including septic shock, anaphylaxis and spinal cord injury. • There is vasodilatation with hypotension and low SVR. • Vasodilatation is caused by histamine in anaphylaxis, failure of sympathetic outflow in neurogenic shock & endotoxin in septic shock. shock 25
- 26. • Vasodilatory (septic) shock represents the final common pathway for prolonged and profound shock of any etiology. Has 30-50% MR in best setups. • Systemic Inflammatory Response Syndrome(SIRS)-a clinical syndrome that results from infectious or non infectious etiologies. shock 26
- 27. • Diagnostic criteria of SIRS( 2 of the following) 1)Temperature >38.3ºC or <36ºC 2) Heart rate >90 beats/min 3)Respiratory rate >20 breaths/min 4)WBC >12,000 cells/mm3, <4000 cells/mm3, or >10 percent immature (band) forms • Sepsis-SIRS with suspected or proven microbial etiology. • Sever sepsis-Sepsis with signs of organ dysfunction or hypo perfusion. shock 27
- 28. • Septic shock-severe sepsis with one or both of 1) Hypotension for > 1hr despite adequate fluid resuscitation or 2)Requiring vasopressors to keep SBP>90mmHg • Refractory septic shock-shock lasting for > 1 hour and doesn’t respond to fluid and vasopressors. NB:Adequate fluid resuscitation is defined as infusion of 40 to 60 ml/kg of saline solution. • MODS- >1 organ dysfunction which requires interventions to maintain homeostasis. shock 28
- 29. 5) Endocrine shock • Causes-hypo/hper thyrodism -adrenal insufficiency shock 29
- 30. Drawbacks of clinical examination • Capillary refill –may be brisk despite profound shock in septic shock. • Tachycardia-may be impaired in patients taking b-blocker, or pacemaker implantation. • Blood pressure-is last sign of shock. shock 30
- 31. Management • General principles • ABC of life Airway-maintain clear air way Breathing-ensure normal breathing Circulation-stop external bleeding - specific surgery to stop internal bleeding -restore blood volume -head down position -secure double IV line with large bore needle shock 31
- 32. -fluid resuscitation with crystalloid N/S or RL -Blood if Hgb is <10mg/dl -strict & close followup -supportive care-oxygen, inotrope -blood to crystalloid ratio is 1:3 shock 32
- 33. Hypovolaemic shock • Secure air way • Control hemorrhage in hemorrhagic • Blood transfusion if needed shock • Volume resuscitation(damage control resuscitation) NB.In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be addressed before other therapy is instituted. • Maintain normothermia - hypothermia is independent risk factor for death shock 33
- 34. • Based on response to fluid resuscitation patients can be; Responder-shows sustained cardiovascular improvement. Transient responders-shows improvement initially but returned back to previous state within 10-20min. Non-responders- severely volume depleted -ongoing loss of IV volume shock 34
- 35. Management of cardiogenic shock • ABC of life • Avoid fluid overload • Supplement oxygen • Inotropic support shock 35
- 36. Rx of septic shock Fluid resuscitation Emperic antibiotics which will be modified after culture and sensitivity. Maximum recommended dose, given IV. Oxygen supplementation Removal or drainage of focal source of infection Vasopressor-dopamin/dobutamin Steroid • Rx of neurogenic shock - secure airway & adequate ventilation -fluid resuscitation -vasoconstrictors shock 36
- 37. Monitoring patients in shock minimum • ECG • Pulse oxymetry • UOP • Blood pressure Additional modalities • CVP • Invasive BP • Cardiac out put • Base deficit • Serum lactate shock 37
- 38. COMPLICATIONS • The main complications of severe shock include: 1. Acute renal failure 2. Shock lung(ARDS) 3. MI 4. Gastrointestinal ulceration 5. Disseminated intravascular clotting 6. Multiorgan failure 7. Death shock 38
Editor's Notes
- #12: and local activation of inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypotension. The cellular and humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death. Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.
- #23: ffffffff
- #28: Severe sepsis — Severe sepsis refers to sepsis plus at least one of the following signs of hypoperfusion or organ dysfunction: Areas of mottled skin Capillary refilling requires three seconds or longer Urine output <0.5 mL/kg for at least one hour, or renal replacement therapy Lactate >2 mmol/L Abrupt change in mental status Abnormal electroencephalographic (EEG) findings Platelet count <100,000 platelets/mL Disseminated intravascular coagulation Acute lung injury or acute respiratory distress syndrome (ARDS) Cardiac dysfunction (ie, left ventricular systolic dysfunction), as defined by echocardiography or direct measurement of the cardiac index Septic shock — Septic shock exists if there is severe sepsis plus one or both of the following: Systemic mean blood pressure is <60 mmHg (or <80 mmHg if the patient has baseline hypertension) despite adequate fluid resuscitation Maintaining the systemic mean blood pressure >60 mmHg (or >80 mmHg if the patient has baseline hypertension) requires dopamine >5 mcg/kg per min, norepinephrine <0.25 mcg/kg per min, or epinephrine <0.25 mcg/kg per min despite adequate fluid resuscitation Adequate fluid resuscitation is defined as infusion of 20 to 30 mL/kg of starch, infusion of 40 to 60 mL/kg of saline solution, or a measured pulmonary capillary wedge pressure (PCWP, also known as the pulmonary artery occlusion pressure) of 12 to 20 mmHg. For patients who have a central venous catheter rather than a pulmonary arterial catheter, a central venous pressure (CVP) of 8 to 12 mmHg is a reasonable substitute.
- #33: bolus 0.5-2L over ½-2hr.For child-20ml/kg bolus.