1. Management of Shock Firas Obeidat, MD Firas Obeidat, MD

2. Introduction In normal conditions, the heart generates power and it does so in an extremely efficient manner. In normal conditions, the heart generates power and it does so in an extremely efficient manner. This power is used to deliver nutrients to and remove waste products from metabolizing tissues. This power is used to deliver nutrients to and remove waste products from metabolizing tissues. Failure of the heart to carry out these functions will lead to shock state. Failure of the heart to carry out these functions will lead to shock state.

3. Definition Shock is a state of inadequate tissue perfusion. Shock is a state of inadequate tissue perfusion. The reduction in oxygen delivery will lead to anaerobic metabolism and metabolic acidosis. The reduction in oxygen delivery will lead to anaerobic metabolism and metabolic acidosis. Compensatory mechanisms attempt to maintain perfusion to vital organs. Compensatory mechanisms attempt to maintain perfusion to vital organs. If adequate circulation is not rapidly restored MOF and death may occur. If adequate circulation is not rapidly restored MOF and death may occur.

4. Circulatory homeostasis Preload: Preload: - The majority of the blood during rest is in the venous system. - The majority of the blood during rest is in the venous system. - return of this venous blood to the heart will produce (VEDV) - return of this venous blood to the heart will produce (VEDV) a major determinant of CO a major determinant of CO Afterload: Afterload: - is the force acting to resist myocardial work during contraction - is the force acting to resist myocardial work during contraction - arterial pressure is the major component (vascular resistance) that influince the EF - arterial pressure is the major component (vascular resistance) that influince the EF

5. Stages / Spectrum of Shock “Preshock” /compensated/warm shock “Preshock” /compensated/warm shock - body is able to compensate for ↓ perfusion - body is able to compensate for ↓ perfusion - up to ~10% reduction in blood volume - up to ~10% reduction in blood volume - tachycardia to ↑ cardiac output & perfusion - tachycardia to ↑ cardiac output & perfusion “ Shock ” “ Shock ” - compensatory mechanisms overwhelmed - compensatory mechanisms overwhelmed - signs/symptoms of organ dysfunction - signs/symptoms of organ dysfunction - ~20-25% reduction in blood volume - ~20-25% reduction in blood volume “ End-organ dysfunction ” “ End-organ dysfunction ” - leading to irreversible organ damage/death - leading to irreversible organ damage/death

6. Physiologic Determinants Global tissue perfusion is determined by: Global tissue perfusion is determined by: Cardiac output (CO) Cardiac output (CO) Systemic vascular resistance (SVR) Systemic vascular resistance (SVR)

7. Types of shock Hypovolemia: ( ↓ preload)/ inadequate blood flow ) Hypovolemia: ( ↓ preload)/ inadequate blood flow ) - dehydration - dehydration - haemorrhage - haemorrhage - burns - burns - sepsis - sepsis Cardiogenic: (pump failure or ↓ SV) Cardiogenic: (pump failure or ↓ SV) - myocardial infarction/ischemia - myocardial infarction/ischemia - valvular disruption - valvular disruption - myocardial rupture - myocardial rupture

8. Types of shock Mechanical/obstruction: Mechanical/obstruction: Obstructed blood flow either into or out of the heart - pulmonary embolism - pulmonary embolism - cardiac tamponade - cardiac tamponade - tension pneumothorax - tension pneumothorax Distributive (vasodilatory) shock: ( ↓ SVR) / Distributive (vasodilatory) shock: ( ↓ SVR) / Inappropriately distributed blood flow and volume - neurogenic shock - neurogenic shock - septic shock - septic shock - anaphylaxis - anaphylaxis - addisonian crisis - addisonian crisis

9. Common Features of Shock Hypotension (not an absolute requirement) Hypotension (not an absolute requirement) - SBP < 90mm Hg, not seen in “preshock” - SBP < 90mm Hg, not seen in “preshock” Cool, clammy skin Cool, clammy skin - Vasoconstrictive mechanisms to redirect blood from periphery to vital organs - Vasoconstrictive mechanisms to redirect blood from periphery to vital organs - Exception is warm skin in early distrib. Shock - Exception is warm skin in early distrib. Shock Oliguria ( ↓ kidney perfusion) Oliguria ( ↓ kidney perfusion) Altered mental status ( ↓ brain perfusion)\ Altered mental status ( ↓ brain perfusion)\ Metabolic acidosis Metabolic acidosis

10. H&P / Work-up History to determine etiology History to determine etiology - Bleeding (recent surgery, trauma, GI bleed) - Bleeding (recent surgery, trauma, GI bleed) - Allergies or prior anaphylaxis - Allergies or prior anaphylaxis - Dx consistent with pancreatitis and others - Dx consistent with pancreatitis and others - Hx of CAD, MI, current chest pain - Hx of CAD, MI, current chest pain Physical examination Physical examination - Mucous membranes, lung sounds, cardiac exam, abdomen, rectal (blood), - Mucous membranes, lung sounds, cardiac exam, abdomen, rectal (blood), neuro exam, skin (cold & clammy or warm) neuro exam, skin (cold & clammy or warm) Labs/Tests directed toward suspected dx’s Labs/Tests directed toward suspected dx’s

11. Summary of management of shock state GOAL Restore tissue perfusion and oxygenation Ensure oxygenation optimize treat under- and ventilation haemodynamic status lying cause Adequate airway optimize ventricular filling control bleeding 100% oxygen optimize cardiac output control sepsis Intubate and ventilate support BP treat MI If necessary GOAL Prevent complications (metabolic acidosis, coagulopathy, renal failure, MOF and death

12. Continue Treat on basis of physiologic abnormality: Treat on basis of physiologic abnormality: Hypovolemic shock septic shock neurogenic shock cardiogenic shock * search for and * treat as in hypovolemia * treat as in hypovolemia * diuresis if EDV is high treat underlying cause * search for and treat * place in Trendelenberg‘s * control hypertension * gain vascular access underlying cause after position * initiate beta-blockade in most * give IVF initial resuscitation * use vasoconstrictors as cases * treat pain, hypothermia necessary * maintain Hb>10 g/dl and acidemia * search for and treat underlying and acidemia * search for and treat underlying cause cause

13. Hypovolemic shock Most common cause of shock in surgical patients Most common cause of shock in surgical patients Reduction in preload → VEDV & CO Reduction in preload → VEDV & CO this will be more severe in presence of decreased vascular tone like in sepsis this will be more severe in presence of decreased vascular tone like in sepsis Causes: Causes: - blood loss - blood loss - plasma loss ( burns, anaphylaxis, sepsis ) - plasma loss ( burns, anaphylaxis, sepsis ) - extracellular fluid loss ( GI loss, 3d space loss ) - extracellular fluid loss ( GI loss, 3d space loss )

14. Hypovolemic shock Pathophysiology: Pathophysiology: - ↓ intravascular volume → peripheral hypoperfusion - ↓ intravascular volume → peripheral hypoperfusion - compensatory responses: - compensatory responses: 1. PVR, redistribution of the blood to vital organs 1. PVR, redistribution of the blood to vital organs 2. adrenergic activity → HR & contractility → CO 2. adrenergic activity → HR & contractility → CO 3. 1 & 2 will maintain BP 3. 1 & 2 will maintain BP 4. decreased capillary hydrostatic pressure → influx of interstitial fluid 4. decreased capillary hydrostatic pressure → influx of interstitial fluid 5. acidosis, hypoxemia, high 2,3-DPG inhances tissue extraction of O2 5. acidosis, hypoxemia, high 2,3-DPG inhances tissue extraction of O2 with Rt shift of O2-Hb dissociation curve. with Rt shift of O2-Hb dissociation curve. 6. increased catecholamines and cortisol level, ADH → sodium and 6. increased catecholamines and cortisol level, ADH → sodium and water retention. water retention.

15. Hypovolemic shock The priority in the management is to restore CO and BP The priority in the management is to restore CO and BP Vascular access Vascular access Fluid challenge: Fluid challenge: - 500 ml RL or NS/5-10 min or 20 ml/kg (1-2 times) - 500 ml RL or NS/5-10 min or 20 ml/kg (1-2 times) - assess CVP and BP pre and post - assess CVP and BP pre and post - if CVP rises but BP doesn‘t →wrong position vs impaired cardiac contractility - if CVP rises but BP doesn‘t →wrong position vs impaired cardiac contractility - insertion of pulmonary cath. - insertion of pulmonary cath.

16. Hypovolemic shock Fluid therapy: Fluid therapy: - crystalloid solutions (NS, LR ) → - crystalloid solutions (NS, LR ) → * inexpensive and available * inexpensive and available * few side effects * few side effects * rapid redistribution throught the extracellular space ( 2-3 times of * rapid redistribution throught the extracellular space ( 2-3 times of estimated intravascular loss are required ) estimated intravascular loss are required ) - colloid solutions → natural vs synthetic ( blood, FFP, human albumin…) - colloid solutions → natural vs synthetic ( blood, FFP, human albumin…) * has large molecule, therefore more effective in expansion of intravascular * has large molecule, therefore more effective in expansion of intravascular volume. volume. * allergic reaction * allergic reaction * may interfere with coagulation * may interfere with coagulation * infection * infection * more expensive * more expensive

17. Hypovolemic shock - blood transfusion: - blood transfusion: * to maintain adequate oxygen carrying capacity * to maintain adequate oxygen carrying capacity * if possible fully coss-matched blood, if not grouped (non- cross-matched)(O-) * if possible fully coss-matched blood, if not grouped (non- cross-matched)(O-) * In general, packed RBCs, should be given to ensure that the patient's hemoglobin concentration is at least 7 g/dl. In pts with IHD 10 g/dl should be the goal. * In general, packed RBCs, should be given to ensure that the patient's hemoglobin concentration is at least 7 g/dl. In pts with IHD 10 g/dl should be the goal. * risk of infection, anaphylaxis and other life-threatening complications * risk of infection, anaphylaxis and other life-threatening complications

18. Adjuvant therapy Vasopressors / Inotropes: Essentially a few important principles to understand - Alpha/Peripheral squeeze on vessels - Beta/ Inotropic and/or chronotropic effect on heart ( ie increase cardiac contractility or increased HR.) It elevates BP at the expense of increased PVR and diminished tissue perfusion Use of such agents instead of adequate fluid resuscitation is inadvisable

19. Compressive shock cause: cause: compression of the following by external forces: compression of the following by external forces: - thin-walled champers of the heart (the atria and left ventricle) - thin-walled champers of the heart (the atria and left ventricle) - the great veins (systemic or pulmonary) - the great veins (systemic or pulmonary) - the great arteries (systemic or pulmonary) - the great arteries (systemic or pulmonary) - any combination of these. - any combination of these. Outcome: Outcome: decrease ventricular production of both pressure decrease ventricular production of both pressure and flow and flow

20. Compressive shock Clinical conditions: Clinical conditions: - pericardial tamponade - pericardial tamponade - tension pneumothoraces - tension pneumothoraces - positive pressure ventilation with large tidal volumes or high airway - positive pressure ventilation with large tidal volumes or high airway pressures pressures - elevated diaphragm (as in pregnancy) - elevated diaphragm (as in pregnancy) - displacement of abdominal viscera through a ruptured diaphragm - displacement of abdominal viscera through a ruptured diaphragm - abdominal compartment syndrome (e.g., from ascites, abdominal - abdominal compartment syndrome (e.g., from ascites, abdominal distention, bleeding) distention, bleeding)

21. Cardiogenic shock Due to muscle or rhythm problem Due to muscle or rhythm problem IHD is the most common cause IHD is the most common cause Other causes: Other causes: * cardiomyopathy * cardiomyopathy * tachy and bradyarrhythmias * tachy and bradyarrhythmias * acid-base or electrolyte imbalance * acid-base or electrolyte imbalance Outcome: decreased contractility and CO Outcome: decreased contractility and CO Management may require pulmonary artery catheter to achieve optimal filling as the heart is very sensitive to hypo and hypervolemia. Management may require pulmonary artery catheter to achieve optimal filling as the heart is very sensitive to hypo and hypervolemia.

22. Cardiogenic shock Goal of treatment: Goal of treatment: - is to achieve an acceptable LVESP - is to achieve an acceptable LVESP - an adequate MAP - an adequate MAP - adequate peripheral perfusion - adequate peripheral perfusion - acceptable heart rate, with no sign of myocardial ischemia - acceptable heart rate, with no sign of myocardial ischemia

23. Cardiogenic shock Diuretics and nitrates may help to reduce preload if the BP allows. Diuretics and nitrates may help to reduce preload if the BP allows. If low cardiac output state persists, inotropes will be required If low cardiac output state persists, inotropes will be required Adrenaline is the first choice: Adrenaline is the first choice: - increase cardiac output (B effects) - increase cardiac output (B effects) - maintain peripheral vasoconstricion ( ɚ effects) - maintain peripheral vasoconstricion ( ɚ effects)

24. NEUROGENIC SHOCK In spinal cord injury or regional anesthetic: In spinal cord injury or regional anesthetic: the denervation is localized ( only the vasculature in the denervated areas will be blocked) the denervation is localized ( only the vasculature in the denervated areas will be blocked) In general anesthesia: In general anesthesia: the vasculature throughout the body will be blocked. the vasculature throughout the body will be blocked. Outcome: Outcome: - small VEDV because of the pooling of blood in the denervated - small VEDV because of the pooling of blood in the denervated venules and small veins. venules and small veins. - low BP because of the arteriolar denervation and the depletion of the - low BP because of the arteriolar denervation and the depletion of the ventricular end-diastolic volumes. ventricular end-diastolic volumes.

25. NEUROGENIC SHOCK Cause: Cause: loss of autonomic innervation of the vasculature (denervation) loss of autonomic innervation of the vasculature (denervation) Commonly affected vessels: Commonly affected vessels: the arterioles, the venules, and the small veins the arterioles, the venules, and the small veins less common: the arteries but not to the same extent. less common: the arteries but not to the same extent. In some cases: the heart. In some cases: the heart. Clinical conditions: Clinical conditions: - spinal cord injury - spinal cord injury - regional anesthesia - regional anesthesia - administration of drugs that block the adrenergic nervous system - administration of drugs that block the adrenergic nervous system (including some systemically administered anesthetic agents), (including some systemically administered anesthetic agents), - certain neurologic disorders, and fainting. - certain neurologic disorders, and fainting.

26. NEUROGENIC SHOCK Treatment: Treatment: - Trendelenburg position - Trendelenburg position - administration of vasoconstrictors: for the initial management in - administration of vasoconstrictors: for the initial management in comparison with other forms of shock it is beneficial. comparison with other forms of shock it is beneficial.

27. Septic shock Infection Sepsis Severe Sepsis Septic Shock Bacteremia

28. Septic shock SIRS The systemic inflammatory response to a variety of severe clinical insults. Manifested by 2 or more of the following conditions: Temperature>38 deg C or <36 deg C HR>90 beats/min Respiratory Rate>20 breaths/min WBC>12,000 or <4,000 cells/mm3 SEPSIS The systemic response to infection. Manifested by the same criteria as SIRS. ( SIRS + documented infection)

29. Septic shock ) SEVERE SEPSIS Sepsis associated with organ dysfunction,hypoperfusion, or hypotension. Perfusion abnormalities include but are not limited to: lactic acidosis oliguria mental status SEPTIC SHOCK ( 40% of pts with gram –ve bacteremia and 20% gram +ve) Sepsis with hypotension (SBP<90), despite adequate fluid resuscitation and perfusion abnormalities as listed for severe sepsis. Patients on inotropic/ vasopressor agents may not be hypotensive.

30. Septic shock At early stage: At early stage: - the CO is increased and the PVR is reduced - the CO is increased and the PVR is reduced → mild hypotension and warm peripheries → mild hypotension and warm peripheries In advance stage: In advance stage: - CO decreases - CO decreases - more hypotension - more hypotension - peripheries are cold and clammy - peripheries are cold and clammy

31. Septic shock management: management: - IVF and inotropes to support BP and maintain optimal CO - IVF and inotropes to support BP and maintain optimal CO - blood, sputum, urine and body-cavity fluid cultures - blood, sputum, urine and body-cavity fluid cultures - removal of infection source (abscess, catheter….) - removal of infection source (abscess, catheter….) - empirical antibiotics after taking samples - empirical antibiotics after taking samples

32. Take Home Points Shock = poor tissue perfusion/oxygenation Shock = poor tissue perfusion/oxygenation - Know difference btw compensated/uncomp shock - Know difference btw compensated/uncomp shock 3 types are based on physiology of shock 3 types are based on physiology of shock - Hypovolemic due to decreased preload - Hypovolemic due to decreased preload - Cardiogenic due to decreased SV or CO - Cardiogenic due to decreased SV or CO - Distributive due to decreased SVR - Distributive due to decreased SVR Know the common signs a/w shock Know the common signs a/w shock - Oliguria, AMS, cool/clammy skin, acidosis - Oliguria, AMS, cool/clammy skin, acidosis Aggressive resuscitation except if cardiogenic Aggressive resuscitation except if cardiogenic Vasopressors if hypotensive despite fluids Vasopressors if hypotensive despite fluids

33. Thank you