Cardiogenic shock

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Cardiogenic Shock: Internal Medicine perspective 2011

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Cardiogenic shock

  1. 1. Cardiogenic Shock (CS): anInternal Medicine Perspective Michael G. Katz, M.D. Fellow in Cardiovascular Disease University of Rochester September 21, 2011
  2. 2. “What does it take to save a man who’s hearthas been COMPLETELY DESTROYED?” 2
  3. 3. GoalTo provide a clinical “toolbox”to diagnosis, differentiate, andmanage shock with anemphasis on cardiovascularetiologies. 3
  4. 4. Part I – Initial Evaluation of the Patient inShock•Pay close attentionPart II – Further Consideration WhenTreating Cardiogenic Shock•Feel free to drift off 4
  5. 5. Ventricle with ↓ systolic functionVentricular Pressure Ventricle with ↓ Stroke Compliance Volume End Diastolic Volume 5
  6. 6. CaseFriday night, 1:25am.Call from Joel Moore:“Hi, thanks for the call back. Is this the MICU Resident? This is Joel inthe trauma bay. Yeah, I have a 45 year old woman down here whowas found down. Don’t know how long. Anyway, she was unconsciousand intubated in the field. Looks like she’s hypotensive here. Westarted her on 5 of dopamine. Could you come down and take a look ather? No, noone is with her. No, the labs aren’t back yet. EKG? [rustleof papers] the machine says there’s ST changes and inferolateralischemia should be considered. ”20 mins later, you also find the CCU team evaluating the patient at thebedside. 6
  7. 7. Elevator thoughts:What is the cause of this patient’s hypotension?• Cardiogenic• Hypovolemic• Septic• Anaphylactic• NeurogenicIs this hypotensive patient in shock?What objective physical exam and laboratory data do I need to sort this out? 7
  8. 8. Hypotension becomes shock when there isinadequate tissue perfusion: • Systolic Blood pressure < 90mmHg, or • 40mmHg drop in blood pressure from baseline, or • MAP less than 60mmHgThe diagnosis of shock is easy to make.Your task as the Internist is to identify the cause of hypotension and correct it before death spiral of tissue necrosis, multiorgan system failure, and death ensues.(Maybe it’s too late… and the spiral has started.) 8
  9. 9. Primary survey - At the beside forhypotension:1. Determine if cardiac rhythm andrate are OK.2. Conduct “Foot of the bed” exam.3. Raise BP. Always remembering: CO = HR x SV 9
  10. 10. 1. Determine if cardiac rhythm and rate areOK.Of course, some rhythms cannot support life.Poor CO because: • HR low (profound bradycardia), or • SV low (rapid tachycardia and reduced diastolic filling time)Profound bradycardia: Atropine 0.5 mg IV x 2  Dobutamine drip (worldwill not end if given peripherally, fluids wide open)  TCP  call EPFellow for TVP (please ask ED staff or 7-16 for “Pacer Box”. It would behelpful to prep and drape the right neck.Unstable SVT/AF/Flutter/VT/VF – DCCV (consider IV midazolam if notsedated). 10
  11. 11. 2. Conduct “Foot of the bed” exam.This should take no more than 60 seconds: • VS • Mental status: “Hey, tell me you name. Do you know what hospital we’re in.” • Feel pulse (faster than finding a cuff) • Radial = SBP 80, Femoral = SBP 60, Carotid/Supraclavicular = SBP of 30. • JVP • Listen for rales • Place hand on toes/feet • Skin temp and color • Cap refill (normal less than 2 sec) – shout out to med-peds. • Foley output helpful (shock < 20 cc/hr) but don’t delay exam for this 11
  12. 12. (An important digression - Why are we doingthis stuff?)Historically, PAC is gold standard for hemodynamic monitoring anddifferentiating etiologies for shock.To differentiate types of shock and guide treatment most importantparameters are: CO and PCWPBy exam: • Rales, JVP, vascular fullness on CXR (if you have it) = “congestion” = elevated PCWP • Cool skin (not to be confused with clamminess) = low CO 12
  13. 13. Target StateConsider Sepsis vs. Consider “cardiogenic”Hypovolemia • inotropes • diuresis(bleeding or overdiuresis)• volume resuscitation• if resistant, consider pressors 13
  14. 14. Final part of beside exam – Does pt need to beintubated?obtundation (ensure airway protection)severe hypoxemia (cyanotic appearing)inappropriately high pCO2 (do they “have that look” / appear tired?)(Just do it. They were probably going to be intubated anyway.) 14
  15. 15. 3. Raise BPGIVE FLUID! – Regardless of suspected shock type.• Diagnostic AND therapeutic• 250 cc boluses • “wide open to gravity”  note that this is faster than “999.” Insist on this. • Noone ever drowned in a can of Coke • If they do, they probably needed intubation anyway. = 12 fl oz = 355 cc 15
  16. 16. Consider calcium chloride• Will increase contractility and raise BP no matter the cause of hypotension.• 1amp = 10 mg: can be given in ¼ amps, ½ amps, or full amps based on severity of hypotension.• First line tx for hyperkalemia = should be given empirically with wide complex bradycardia, especially if pt is unstable enough to merrit MICU/CCU consult.• Don’t be dissuaded by national shortage. 16
  17. 17. Secondary survey – Determine the etiology forShockMake sure you have ordered or reviewed the following: • EKG: evidence of MI or ischemia • HCT: rule out hypovolvemic shock from GIB (caution: could be normal) • ABG: hypoxia and acidosis will need to be corrected at some pointGood exam: • VS • JVP (CHF/volume depletion) • Stridor/wheeze (anaphylaxis/CHF), crackles/effusion (CHF) • Lateral PMI, gallop (CHF) New murmur (sepsis/CHF/endocarditis) • HSM (CHF) • Edema (CHF) • Melena or hematochezia (GIB) • Look for tampon if pt is obtunded (sepsis) • Urticaria (anaphylaxis) 17
  18. 18. PAC based approach… Type CO SVR CVP or Mixed PAOP VenousCardiogenicHypovolemicDistributive 18
  19. 19. Bedside approach 19
  20. 20. Conditions other than CHF p/w hypotensionand elevated JVP:TamponadeMassive PESVC syndromeTension PTX 20
  21. 21. Return to the caseHR 105, sinus tachBP 80/60 on 5 of dopaJVP 12 cm H2ONo rales2+ pitting edema to knees, cool skinWBC 10.2 HCT 40 Plts 250 SCr 2.1 AST 200 ALT 160 INR 1.3TropT 0.13 CK 260 CKMB 14pCXR demonstrates cardiomegally, right sided effusionEKG: sinus tach, RBBB, diffuse NSSTchanges Ben McClintic agrees toED sends pt for CTA, no evidence of PE bring pt to CCU for medicine of the highest order 21
  22. 22. What about echo?Not part of the algorithm for acute management.Would it change management? Does it clarify diagnosis?Clear evidence that septic shock results in profound (but reversible) depression in LVfunction. • Ann Intern Med 1984;100:483–490 • Crit Care Med 2009; 37:441–447One study found a 60% incidence of global LV hypokinesis in septic patients • Crit Care Med 2008; 36:1701–1706On the flip side, there are plenty of people with low LVEF that aren’t in cardiogenicshock.Of course, things are different if your working diagnosis is acute valvular dysfunction ormechanical complication of MI 22
  23. 23. 23
  24. 24. Decide etiologySelect appropriate pressor/inotrope 24
  25. 25. Receptors utilized by drugs β Adrenergic Dopaminergic α Adrenergic β1 α Ionotropy (strength) Neurologic Chronotropy (rate) 1 α2 β2 α1 Vasoconstriction α2 Inhibits vasocontriction Vasodilation Vasodilation
  26. 26. Blood PressurePhenylephrine TimePurely α1 adrenergic ∀↑ SVR and MAP Heart Rate • Can induce reflex bradycardia Time • Usually no change in CO • Most often used for septic Cardiac Output shock Time
  27. 27. Blood Pressure TimeNorepinephrineStimulates α1 and β1 receptors Heart Rate • Results in ↑ SVR • May ↑ HR (although ↑ afterload may abrogate effect on CO) Time • Most often used for septic shock Cardiac Output Time
  28. 28. Heart RateEpinephrineStimulates β1 mostly, but also α1 and Timeβ2 Cardiac Output ∀ ↑ Heart Rate ∀ ↑ CO ∀ ↑ SVR ∀ ↑SBP from α1 vasoconstriction in mesentary and skin Time ∀ ↓DBP from β2 mediated vasodilation in skeletal muscle Blood presssure • At high doses, α1 exceeds β2 effect, therefore MAP increases • Used for anaphylaxis, septic shock, cardiogenic shock (severe) Time
  29. 29. Heart RateDopamineLow doses: Dopaminergic receptor Timeagonist  Cardiac Output vasodilation of mesentery and renal arteriolesMedium doses: Direct stimulation ofβ1 receptors  Time ↑ HR, contractility and ultimately COHigh doses: Direct and indirect Blood Pressurestimulation of α1(NE release)  vasoconstriction Time
  30. 30. Heart RateDobutamineMostly β1, minimal α1 and B2 Time ∀↑ Heart rate and Contractility Cardiac Output increase CO ∀↓ MAP ∀ ↑ Cardiac output  vasodilation • At higher doses, β2 overcomes α1 Time additional vasodilation • Used in heart failure with an adequate Blood pressure or elevated MAP Time
  31. 31. Milrinone Heart RatePhosphodiesterase 3 inhibitor. Potentiates cAMP activity. In turnactivates cardiac calcium channels. TimePositive inotrope • increased calcium influx from sarcoplasmic reticulum (SR) during phase 2 of the cardiac action potential. Cardiac OutputLusitropic effect • Inreased reflux of calcium into the SR following the plateau phase increases relaxation speedVasodilatation Time • cAMP normally inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating smooth muscle myosin and causing contraction Blood pressureAgain, Ideal agent for heart failure with anadequate or elevated MAP. Time
  32. 32. Controversy Warning: Vasoactive agent ofchoice? 37
  33. 33. “When blood pressure is low, dopamine is the agent of firstchoice. If the patient is markedly hypotensive, intravenousnorepinephrine, which is a more potent vasoconstrictor with lesspotential for tachycardia, should be administered until systolicarterial pressure rises to at least 80 mm Hg, at which time achange to dopamine may be attempted, initiated at 2.5 to 5mcg/kg/min and titrated as needed to 5 to 15 mcg/kg/min. Oncearterial pressure is brought to at least 90 mm Hg, intravenousdobutamine may be given simultaneously in an attempt to reducethe rate of the dopamine infusion.” 38
  34. 34. However…Observational studies found that dopamine may be associated with rates ofdeath that are higher than those associated with the administration ofnorepinephrine.Sepsis Occurrence in Acutely Ill Patients (SOAP) study • Observational trial of 1058 patients who were in shock, showed that administration of dopamine was an independent risk factor for death in the intensive care unit (ICU). Crit Care Med 2006;34:589-97Overall, there was/is a dearth of RCT data regarding vasopressors for shock. • In a meta-analysis, only three randomized studies, with a totalof just 62 patients, were identified that compared the effects of dopamine and norepinephrine in patients with septic shock. Cochrane Database Syst Rev 2004;3:CD003709 39
  35. 35. • In this comparative-effectiveness trial, there was no significant difference in the overall survival rate between patients with shock who were treated with dopamine and those who were treated with norepinephrine• However, dopamine was associated with more cardiac arrhythmias and with a higher mortality rate among patients with cardiogenic shock 40
  36. 36. • RCT in 8 centers in Austria, Spain and Belgium.• trial included 1679 patients, of whom 858 were assigned to dopamine and 821 to norepinephrine for first line tx of shock.• Intervention was dopamine or noradrenaline to 20ug/kg/min or 0.19ug/kg/min respectively, at which point additional inotropic / vasopressor was allowed (cross over).• Of note, requirement for “adequacy” of fluid resuscitation was minimal • 500 -1000mls clear fluids in, no goal directed therapy) • thus patients may well have been under filled when the intervention began.• study was powered to have an 80% chance of detecting a 15 % mortality difference at 28 days – pretty good. 41
  37. 37. No significant difference 52 vs 48% OR 1.17 (0.97-1.42) Kaplan-Meier Curves for 28-Day Survival in the Intention-to-Treat Population
  38. 38. Dopamine Norepi 43
  39. 39. 44
  40. 40. The Cardiology/CCU perspective • LV pump failure is usually primary derangement • BUT other parts of circulatory system contribute because of inadequate compensation or defects • Many parts of the cascade are completely or partially reversible  which may explain good outcomes in CS survivors. 45
  41. 41. Peripheral Vasculature, Neurohormones,and Inflammation• Ongoing ischemia triggers release of catecholamines, which constrict peripheral arterioles to maintain perfusion of vital organs.• Vasopressin and angiotensin II levels increase in the setting of MI and shock• improvement in coronary and peripheral perfusion at the cost of increased afterload, which may further impair myocardial function• salt and water retention; this may improve perfusion but exacerbates pulmonary edema.So, SVR goes up? 48
  42. 42. Not necessarily…• In SHOCK trial: median SVR during CS in the normal range despite vasopressor therapy.• SVR may even be low! • sepsis was suspected in 18% of the SHOCK trial cohort. (Arch Intern Med 2005;165) • 74% of whom developed positive bacterial cultures • low SVR preceded the clinical diagnosis of infection and culture positivity by days 49
  43. 43. Were those people in SHOCKmisdiagnosed with CS which was reallysepsis?ORDoes CS beget SIRS, which facilitatesthe development of sepsis? 50
  44. 44. SIRS is more common with increasing duration of shock (Int J Cardiol.1999;72:3)• SIRS results in impaired perfusion of the intestinal tract, which enables transmigration of bacteria and sepsisCytokine levels (IL-6 and TNF-a) rise more dramatically over the 24 to 72hours after MI (Eur Heart J. 2005;26:1964)Other circulating factors (complement, procalcitonin, neopterin, C-reactive protein, and others) have been reported to contribute to SIRSin CS.Despite a promising randomized phase 2 study, a trial of complement(C5) inhibition in patients with MI found that pexelizumab did not reducethe development of shock or mortality (Circulation. 2003;108:1184,JAMA. 2007;297:43) 51
  45. 45. General Measures• Aithrombotic therapy with aspirin and heparin.• Clopidogrel • may be deferred until after emergency angiography, because on the basis of angiographic findings, coronary artery bypass grafting (CABG) may be performed immediately. • indicated in all patients who undergo PCI, and on the basis of extrapolation of data from MI patients who were not in shock• Negative inotropes and vasodilators (including nitroglycerin) should be avoided.• Arterial oxygenation and near-normal pH should be maintained to minimize ischemia.• Intensive insulin management with “tight” BG control. (Circulation. 2004;110:588–636) 52
  46. 46. Watch word = “optimization” CO = HR X SV CO = HR X (EDV – ESV) HR Preload Distensibility Afterload Contractility Lower transpulmomonary capillary pressuresGood filling pressures Afterload reduction Coronary Flow 53
  47. 47. Hemodynamic Monitoring and ManagementPA (Swan-Ganz) catheters can be helpful to• confirm the diagnosis of CS• ensure that filling pressures are adequate• and to guide changes in therapyThere has been a decline in PA catheter use relating to controversy sparked by a prospective observational study that suggested that PA catheters were associated with poor outcome (JAMA. 1996;276:889). No such association has been shown in CS. (Am J Med. 2005;118:482) 54
  48. 48. CVP does not necessarily reflect PCWP (or LApressure by extension) May be due to: • Compliance • Contractility • Afterload Sprung et al. Direct measurements and derived calculations using the pulmonary artery catheter. In: The pulmonary artery catheter: methodology and clinical applications. 1983:105-140. 55
  49. 49. Mechanical SupportRevascularization 56
  50. 50. Mechanical Support – IABP• Mainstay of mechanical therapy for CS. IABP• Improves coronary and peripheral perfusion via diastolic balloon inflation and augments LV performance via systolic balloon deflation with an acute decrease in afterload.• Not every patient has a hemodynamic response to IABP; response predicts better outcome. (Circulation. 2003;108(suppl I):I-672)• IABP support should be instituted as quickly as possible, even before any transfer for revascularization if a skilled operator is available and insertion can be performed quickly.• In the large National Registry of Myocardial Infarction, IABP use was independently associated with survival at centers with higher rates of IABP use, whether PCI, fibrinolytic therapy, or no reperfusion had been used. (Circulation. 2003;108:951–957). However, no RCT have been completed to date. 57
  51. 51. Revascularization 58
  52. 52. Aimed to test the superiority of a strategy of early committedrevascularization (ERV) over that of initial medical stabilization (IMS) 1492 screened shock pts 1190 pts placed in SHOCK registry To detect a 20% mortality difference between groups, study sought to enroll 328 pts Ultimately 302 pts enrolled • 152 ERV • 150 IMS The primary end point of the study, 30-day all-cause mortality. 59
  53. 53. Inclusion and ExclusionCardiogenic shock: clinical criteria• Systolic blood pressure <90 mm Hg for 30 minutes before inotropes/vasopressors, or vasopressors or IABP are required to maintain systolic blood pressure ≥90 mm Hg• Evidence of decreased organ perfusion• Heart rate ≥60 beats per minute (including paced rhythms)Cardiogenic shock: hemodynamic criteria• PCWP ≥15 mm Hg• Cardiac index ≤2.2 L/min/m2Only patients with CS arising from predominant left ventricular (LV) failure following MI with ST elevation or new left bundle branch block were included. PAC not necessary if AMI and congestion on CXR. 60
  54. 54. Exclusion criteria: • ventricular septal rupture • cardiac tamponade • severe valvular disease • isolated right ventricular CS • known dilated cardiomyopathy • shock from other causes (e.g., sepsis, hypovolemia) • prior severe systemic illness • refusal by the patients physician, and failure to provide informed consent 61
  55. 55. Findings of SHOCK and 1 year FUReperfusion• 13% absolute increase in 1-year survival in patients assigned to early Revascularization.• NNT < 8 to save 1 life 62
  56. 56. Timing and success of PCI• Increasing long-term mortality as time to revascularization increased from 0 to 8 hours• However, there is a survival benefit as long as 48 hours after MI and 18 hours after shock onset• 77% procedural success with percutaneous intervention in this setting is consistent with that of earlier reports and lower than that reported with primary angioplasty in the setting of all ST elevation MIs • This is presumably due to a combination of diffuse multivessel disease, large thrombus burden, and coronary hypoperfusion. • No reflow phenomenon may occur more often in CS• Successful percutaneous intervention in this setting is clearly associated with a superior outcome and procedural failure is associated with increased 30-day mortality (38% vs.79%; p=0.003) 63
  57. 57. PCI or CABG?• 37% of revascularization pts underwent CABG at a median of 2.7 hours after randomization.• Despite a higher prevalence of triple-vessel or left main disease and diabetes mellitus in patients who underwent CABG compared with PCI, survival and quality of life were similar.The rate of emergency CABG in CS is much lower in the community(10%) (JAMA. 2005;294:448–454)Only 15.2% of CABG got a LIMA. 64
  58. 58. Role of IABP• overall utilization of IABP in IMS was 86%, considerably higher than previous studies• (Some speculate that IABP improves thrombolytic efficacy see NRMI and TACTICS. TACTICS was terminated prematurely because of insufficient patient recruitment, but the results suggest a 9% absolute reduction of mortality at 6 months (p=0.23) with the combination of thrombolysis and IABP.) 65
  59. 59. Subgroup analysis, risk stratification, and takeaway points from SHOCKMortality from CS is high (~50%), but not as bad has historical figures of 80 to 90%Important considerations: • Age, • peripheral hypoperfusion, • anoxic brain damage, • LVEF, and • LV stroke workFemale sex does not appear to be an independent predictor of poor outcome.Revascularization provides benefit at every level of risk. The initial misperception thatelderly patients do not benefit from PCI arose from the interaction between treatmenteffect and age in the SHOCK trial. Lack of benefit for the elderly in the SHOCK trial waslikely due to imbalances in baseline ejection fraction between groups. 66
  60. 60. Health Care Policy and “Soft Rationing”Most models, especially those derived from SHOCK demonstrate thatbenefit is derived across the risk spectrum.It may not be feasible (or ethical) to perform PCI or CABG when theassociated mortality rate is 80%.ACC/AHA guidelines recommend (Circulation. 2004;110:588–636)• early revascularization in CS for those 75 years of age (class I), and• for suitable candidates 75 years of age (class IIa).Real-world revascularization rates range from 27% to 54% (JAMA.2005;294:448–454) 67
  61. 61. Why are real world numbers so low? Doesgetting “dinged” matter? – YES. In 2006, the New York Department of Health began to exclude cases of cardiogenic shock from public reports (367 cases 2004- 2006). 68
  62. 62. A group exists for whom additional treatment is futile: • irreversible multiple end-organ failure , or • anoxic brain damage has occurredRevascularization approach must be individualized.Most important consideration, especially for the elderly, is functionalstatus before the index event. 69
  63. 63. 70

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