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Shock precedes Death and organ failure.

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  • Notes: The inadequate perfusion and oxygenation leads to first cellular dysfunction and then organ dysfunction.
    -Cellular effects include cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents into the
    extracellular space, and inadequate regulation of intracellular pH.
    -Systemic effects include alterations in the serum pH, endothelial dysfunction, as well as further stimulation of
    inflammatory and antiinflammatory cascades that lead to multiorgan dysfunction
  • Notes:
    Mortality due to shock is high. It is estimated that 35 to 60% of patients die within one month of the onset of septic shock. The mortality rate may be even higher among patients with cardiogenic shock; it is estimated to be 60 to 90%. Mortality due to hypovolemic shock is more variable.
    Early intervention can prevent the cascade of detrimental effects of O2 deprivation on the cells and organs
  • Notes:
    All forms of shock go through “stages “ of shock. How quickly the patient goes through the stages depends on the cause of shock, patient characteristics, and how quickly we intervene.
    For example, a healthy adult can be asymptomatic despite a 10% reduction in total effective blood volume. OR if a healthy patient is bleeding slowly from a bleeding ulcer, he will be able to compensate for the blood loss for a long time. If the blood loss is very rapid (e.g. from splenic rupture in Case 1), the patient may progress to death within minutes going through all stages within minutes to hours
    Preshock — Preshock is also referred to as warm shock or compensated shock. It is characterized by rapid
    compensation for diminished tissue perfusion by various homeostatic mechanisms. As an example,
    compensatory mechanisms during preshock may allow an otherwise healthy adult to be asymptomatic
    despite a 10 percent reduction in total effective blood volume. Tachycardia, peripheral vasoconstriction,
    and either a modest increase or decrease in systemic blood pressure may be the only clinical signs of shock.
    Shock — During shock, the compensatory mechanisms become overwhelmed and signs and symptoms of organ
    dysfunction appear. These include tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, oliguria,
    and cool clammy skin.
    End-organ dysfunction — Progressive end-organ dysfunction leads to irreversible organ damage and patient death.
    End organ dysfunction - typically correspond to a significant physiologic perturbation
    Examples include a 20 to 25% reduction in effective blood volume in hypovolemic shock, a fall in the cardiac
    index to less than 2.5 L/min/M2 in cardiogenic shock, or activation of innumerable mediators of the systemic
    inflammatory response syndrome (SIRS) in distributive shock.
    During this stage, urine output may decline further (culminating inanuria and acute renal failure), acidemia
    decreases the cardiac output and alters cellular metabolic processes, and restlessness evolves into agitation,
    obtundation, and coma.
    REFERENCES: Up to date - Shock to Adults: Types, presentation, diagnostic approach
  • Notes: This is a summary slide
  • Notes: The earlier table was oversimplified. Regardless of the type of SHOCK all components of the equation will compensate for
    the physiologic change induced by the insult, however some will be more effective than others
  • may be considered as the ventricular wall tension required to eject the stroke volume during systole.
    Afterload relates to the mechanical resistance to shortening of the cardiac muscle fibers.
  • Shock

    2. 2. Overview Definitions Initial Assessment – ABC Stages of Shock Physiologic Determinants of Shock Types of Shock Common Features of Shock Work-up Generic Approach to Management Case scenarios and Management Take Home Points
    3. 3. Definition of Shock Inadequate perfusion and oxygenation of cells Hypotension is not a requirement
    4. 4. Why should you care? High mortality - 20-90% Early on the effects of O2 deprivation on the cell are REVERSIBLE Early intervention reduces mortality
    5. 5. Remember! Assessment Intervention and Monitoring happens together in acute scenarios.
    6. 6. Initial Assesment - ABC Airway:  Does pt have mental status to protect airway?  GCS less than “eight” means “intubate”  Airway is compromised in anaphylaxis Breathing:  If pt is conversing with you, A & B are fine  Place patient on oxygen Circulation:  Vitals (HR, BP)  2 large bore (#16g) IV, start fluids (careful if cardiogenic shock), put on continuous monitor
    7. 7. ABC “DE” In a trauma, perform ABCDE, not just ABC Deficit or Disability  Assess for obvious neurologic deficit  Moving all four extremities? Pupils?  Glascow Coma Scale (M6, V5, E4) Exposure  Remove all clothing on trauma patients
    8. 8. TYPES OF SHOCK Type of Shock Insult Physiologic Effect Compensation Cardiogenic Heart fails to pump blood out •MI, arrhythmia, aortic stenosis, mitral regurg, ↓CO BaroRc ↑SVR Obstructive Heart pumps well, but the outflow is obstructed •Extracardiac obstructive causes such as PE, tension pneumothorax, tamponade ↓CO BaroRc ↑SVR Hypovolemic Heart pumps well, but not enough blood volume to pump •Hemorrhage •Fluid Loss (Vomiting, Diarrhea, Burns) ↓CO BaroRc ↑SVR Distributive Heart pumps well, but there is peripheral vasodilation •Septic, anaphylactic, and neurogenic shock •Pancreatitis, burns, multi-trauma via activation of the inflammatory response ↓SVR ↑CO
    9. 9. Stages of Shock Timeline and progression will depend on: -Cause -Patient Characteristics -Intervention Insult Preshock (Compensation) Shock (Compensation Overwhelmed) End organ Damage Death
    10. 10. Stages of Shock: Example Stage Pathophysiology Clinical Findings Insult Splenic Rupture -- Blood Loss Abdominal tenderness and girth Preshock Hemostatic compensation MAP =↓CO(HR x↓SV) x ↑ SVR Decreased CO is compensated by increase in HR and SVR MAP is maintained HR will be increased Extremities will be cool due to vasoconstriction Shock Compensatory mechanisms fail MAP is reduced Tachycardia, dyspnea, restlessness End organ dysfuncti on Cell death and organ failure Decreased renal function Liver failure Disseminated Intravascular Coagulopathy Death
    11. 11. Common Features of Shock Hypotension (not an absolute requirement)  SBP < 90mm Hg, not seen in “preshock” Cool, clammy skin  Vasoconstrictive mechanisms to redirect blood from periphery to vital organs  Exception is warm skin in early distrib. shock Oliguria (↓kidney perfusion) Altered mental status (↓brain perfusion) Metabolic acidosis
    12. 12. Hypovolemic Shock Distributive Shock Cardiogenic Shock Obstructive Shock HR Increased Increased (Normal in Neurogenic shock) May be increased or decreased Increased JVP Low Low High High BP Low Low Low Low SKIN Cold Warm (Cold in severe shock) Cold Cold CAP REFILL Slow Slow Slow Slow
    13. 13. Type of Shock Insult Physio logic Effect Compen sation Compensation Heart Rate Compensation Contractility Cardiogenic Heart fails to pump blood out ↓CO BaroRc ↑SVR ↑ ↑ Obstructive Heart pumps well, but the outflow is obstructed ↓CO BaroRc ↑SVR ↑ ↑ Hemorrhagic Heart pumps well, but not enough blood volume to pump ↓CO BaroRc ↑SVR ↑ ↑ Distributive Heart pumps well, but there is peripheral vasodilation ↓SVR ↑CO ↑ No Change - in neurogenic shock ↑ No Change - in neurogenic shock Compensatory Mechanisms
    14. 14. Additional Compensatory Mechanisms Renin-Angiotensin-Aldosterone Mechanism  AII components lead to vasoconstriction  Aldosterone leads to water conservation ADH leads to water retention and thirst Inflammatory cascade
    15. 15. Work-up History to determine etiology  Bleeding (recent surgery, trauma, GI bleed)  Allergies or prior anaphylaxis  Sx consistent with pancreatitis, EtOH history  Hx of CAD, MI, current chest pain/diaphoresis Examination  Mucous membranes, JVD, lung sounds, cardiac exam, abdomen, rectal (blood), neuro exam, skin (cold & clammy or warm) Investigations: Labs/Tests directed toward suspected dx’s
    17. 17. In Short  The oxygenated blood carried forward by the cardiac output has to reach the Vital organs,  this is only possible if there is a good pressure gradient  and the organ vascular resistance is low;  try to maintain the Blood pressure within the regional Auto regulation range,  I prefer to target the kidneys as they are a filter and require higher mean arterial pressures, essentially ensures all other organs are also perfused
    18. 18. OPTIMISE OXYGEN CONTENT Hb Check if appears pale or anaemic Check Hb and coagulation status Sao2 just a pulse oximeter tells you the SpO2 Check SaO2 on ABG
    19. 19. OPTIMISE CARDIAC OUTPUT CO = Stroke volume (SV) x Heart rate (HR) STROKE VOLUME depends on Preload Contractility Afterload
    20. 20. Check each component of Cardiac Output  Stroke Volume (depends on 3 factors)  Preload  Look at response to fluid bolus  If improves BP could be suggestive of decreased preload (volume) and a reasonable contractility.  If no improvement or worsening BP could be suggestive of a Contractility problem or excess preload (volume) situation  Look at CVP
    21. 21. Check each component of Cardiac Output  Contractility  Check any history suggestive of Ischaemic disease or CCF  Check ECHO and ECG results  A high systolic pressure could be suggestive of good contractility
    22. 22. Check each component of Cardiac Output  Afterload  Check Echo if suggestive of any obstructive features  If peripheries cold could indicate increased vascular resistance  If peripheries warm could indicate vasodilation and decreased vascular resistance  a low diastolic Blood pressure could indicate low vascular resistance  a high diastolic Blood pressure could indicate increased vascular resistance
    23. 23. Check each component of Cardiac Output  HR  If low, 2 possible interventions  electric  pacing  pharmacological intervention  if high, 2 possible interventions  electric  cardioversion  Defibrillation  pharmacological intervention
    24. 24. OPTIMISE BLOOD PRESSURE Product of Cardiac output and peripheral resitance. BP=CO X PR
    25. 25. OPTIMISE REGIONAL BLOOD FLOW Improve Blood pressure, which is a product of  Cardiac Output  peripheral resistance (squeeze) Improve, Regional Blood Flow = (p1-p2) / R, i.e. by increasing Mean Arterial pressure decreasing venous or the compartment pressure whichever is higher, and also decreasing the organ vascular resistance
    26. 26. Auto regulation range try to match Renal auto regulation range  Kidneys  MAP 80-180 mmHg  Brain  MAP 65-130 mmHg  Heart  MAP 50-150 mmHg  If hypertensive Autoregulation values could shift to right, essentially you will need Higher MAP (mean arterial pressure) to perfuse the vital organs.
    27. 27. Case 1 55yo male otherwise healthy who is fresh post-op from a colon resection for CA Called for tachycardia, hypotension, altered mental status, and abd distension On exam: pale, dry mucous membranes, disoriented, abdomen is tender and tense UOP is 15mL over past hour What else do you want to know? What is the most likely diagnosis?
    28. 28. Case 1 The one thing you want to know: Hct (Hgb) Dx: Hemorrhagic (hypovolemic) shock Management  ABC (need intubation? IV access?)  Wide open fluids and T&C 6 units PRBC  Send coags when sending for CBC  Make sure it’s not an MI (chest pain, EKG)  Give blood & prepare for re-exploration in OR
    29. 29. Case 2 75yo male PMH CAD, PVD, DM who is post-op from AAA repair complains of crushing substernal chest pain Stat 12-lead EKG shows ST elevation in 2 contiguous leads What do you do? What is the diagnosis?
    30. 30. Case 2 ABC, get good access, continuous monitor Dx: Acute ST elevation MI Treatment: “MONA”  Oxygen, Aspirin, Nitroglycerin, Morphine  Beta-blockade (no heparin or tPA due to surg)  Plavix & GP IIb/IIIa inhibitor (i.e. eptifibatide)  Stat cardiology consult for cardiac cath
    31. 31. Case 2, continued Cath reveals critical stenosis of left main s/p balloon angioplasty 24 hrs later, in ICU intubated Vitals: 80/50 On exam: cool, clammy extremities Echocardiogram: severe LV dysfunction What is the diagnosis & management?
    32. 32. Case 2, continued Dx: Cardiogenic shock 2ndary to STEMI Management  RESUSCITATIVE CARE (remember, ABC)  SUPPORTIVE CARE Ventilator support Inotropes and Vasopressors Cardiac output monitoring to optimize volume status and cardiac function  May need intra-aortic balloon pump  DEFINITIVE CARE  PCI Thrombolysis, Aspirin, Heparin (maintain coronary patency)
    33. 33. Case 3 60yo male heavy drinker brought in by EMS with nausea, vomiting, severe epigastric pain radiating to the back Tachycardic, hypotensive Altered mentation, dry mucous membranes, minimal UOP after Foley What is the most likely diagnosis?  Differential diagnosis? How do you manage this patient?
    34. 34. Case 3 Acute pancreatitis  DDx of acute abdomen: Perforated viscus, acute mesenteric ischemia, cholecystitis, SBO, Ruptured AAA, MI Hypovolemic shock from vomiting and Distributive shock from the inflammation: vasodilation, vasopermeability (3rd -space) Management  RESUSCITATIVE CARE (remember, ABC) These pts require heavy, heavy fluid resus SUPPORTIVE CARE NPO, NGT feed post-pyloric, consider CT scan DEFINITIVE CARE
    35. 35. Case 4 55yo male also post-op from colon resection for CA, epidural placed for post-operative pain control Called by nurse for hypotension and bradycardia Abdomen soft, no pallor, altered mentation Hct is 38 Most likely diagnosis?
    36. 36. Case 4 Neurogenic shock 2ndary to epidural Differentiated from hypovolemic due to bradycardia Management  RESUSCITATIVE CARE (remember, ABC) IVF  SUPPORTIVE CARE If BP does not respond, then alpha-agonist such as phenylephrine until above measures stabilize patient, then wean the vasopressor  DEFINITIVE CARE Turn down or turn off epidural,
    37. 37. Case 5 25yo male presents with diffuse abdominal pain of 1day duration, started initially as epigastric pain after a meal. Takes ibuprofen 3x a day. Vitals: hypotensive, tachycardic Tense abdomen, involuntary guarding, altered mental status, oliguric What is the diagnosis & management?
    38. 38. Case 5 Septic shock 2ndary to perf duodenal ulcer  This patient has diffuse peritonitis Management: Management  RESUSCITATIVE CARE (remember, ABC) IV & resuscitation (requires heavy fluids)  SUPPORTIVE CARE If pt, does not respond to fluids, may need vasopressors (norepinephrine)  Have beta-agonist effects to help pump function as well as alpha- agonist for periph vasoconstriction  DEFINITIVE CARE  Broad-spectrum IV antibiotics  Emergent OR for ex-lap, washout & repair
    39. 39. Take Home Points Shock = poor tissue perfusion/oxygenation Know difference btw compensated/uncomp shock 3 types are based on physiology of shock Hypovolemic due to decreased preload Cardiogenic due to decreased SV or CO Distributive due to decreased SVR Know the common signs a/w shock Oliguria, AMS, cool/clammy skin, acidosis Work-up & management starts with ABC Aggressive resuscitation except if cardiogenic Vasopressors if hypotensive despite fluids
    40. 40. Thanks
    41. 41. MAP Diastolic + 1/3 Pulse pressure