Cardiogenic Shock Acute Coronary Syndrome Congestive Heart Failure
- Slides: 59
Cardiogenic Shock, Acute Coronary Syndrome, Congestive Heart Failure, and Arrhythmias Dalhousie Critical Care Lecture Series
Cardiogenic Shock ICU Inadequate tissue perfusion resulting from cardiac dysfunction Clinical definition - decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume Hemodynamic definition - sustained systolic BP < 90 mm Hg, cardiac index < 2. 2 L/min/m 2, PCWP > 15 mm Hg Parrillo, J. 2005
Causes of Cardiogenic Shock ICU Acute MI • • • Pump failure Mechanical complications Right ventricular infarction Other conditions • • • End-stage cardiomyopathy Myocarditis (fulminant myocarditis) Myocardial contusion Prolonged cardiopulmonary bypass Septic shock with myocardial depression Valvular disease
Cardiogenic Shock ICU Evolution Of The Disease Frequently, shock develops after presentation for myocardial infarction. - - SHOCK Registry • At presentation • Within 24 hours (median delay = 7 hours) GUSTO Trial • At presentation • After admission SHOCK Registry, Circulation. 1995; 91: 873 -81. GUSTO J Amer Coll Cardiol. 1995; 26: 668 -74. 25% in shock 75% 11% in shock 89%
ICU Schematic Diagram of Stunned Myocardium Clamp Wall motion abnormality during occlusion Coronary reperfusion Persistent wall motion abnormality (despite reperfusion and viable myocytes) Return of function Gradual return of function (hours to days) From Kloner RA. Am J Med. 1986; 86: 14.
Ischemic Myocardium ICU Cell death Significant residual stenosis Reperfusion Segments with myocardial stunning Segments with both stunning and hibernation Inotropic support No return of function Return of myocardial function Segments with hibernating myocardium Relief of ischemia
Initial Approach: Management ICU Assure oxygenation • Intubation and ventilation if needed Venous access Pain relief Continuous EKG monitoring Hemodynamic support • • Fluid challenge if no pulmonary edema Vasopressors for hypotension - Dopamine Norepinephrine Dobutamine Milrinone
Dopamine ICU Dopaminergic, Beta, Alpha: ranges ? n Dopa: 1 -5 ug/kg/min n n? n Renal flow Beta: 5 -10 ug/kg/min n Inoptropy/chronotropy n Alpha: >10 ug/kg/min n Vasoconstriction n Major use: increasing HR, ? bp
Dobutamine ICU Beta (little alpha) n Inotropic/chronotropic n 2 -20 ug/kg/min n Major use: Systolic dysfunction n Caveat: can/will decrease MAP n Often used in conjunction with levophed n
Epinepherine ICU Alpha and Beta n 0. 01 – 1. 0 ug/kg/min n Major Use: when you need A&B n Like using dobutamine and levophed mixed together n
Milrinone ICU n n Used as an inotrope Mechanism of Action n n Side Effects n n 5 -15 minutes Duration n n can also cause vasodilatation but tends to have less chronotropy than dobutamine Onset of action n n Phosphodiesterase inhibitor decrease the rate of cyclic AMP degradation increase in cyclic AMP concentration leads to enhanced calcium influx into the cell, a rise in cell calcium concentration, and increased contractility Half life of approximately 2 hours (so its gonna last a while Dose n Loading dose: 50 mcg/kg administered over 10 minutes followed by 0. 375 mcg/kg/minute
Norepinepherine ICU Alpha and Beta n 0. 02 -3. 0 ug/kg/min n Major Use: when you need A&B n n? Drug of choice for septic shock n Good and bad for use in cardiogenic shock n May increase blood pressure n May decrease CO by increasing afterload n Will increase cardiac strain
Use of Inotropes ICU n BP is not a reliable indicator of CO CO = SV X HR MAP=SVR X CO if SVR is increased as CO drops then MAP will stay the same n Need to titrate to the CO n n Swan ganz CO measure U/O Lactate Sc. VO 2
Use of Vasopressors ICU n Often used in conjunction with inotropes n n counteract the vasodilation that occurs Titrated to MAP
ICU Intra-aortic Balloon Counterpulsation
Intra-aortic Balloon Counterpulsation ICU The only thing that reduces afterload and augments diastolic perfusion pressure Beneficial effects occur without increase in oxygen demand No improvement in blood flow distal to critical coronary stenosis No improvement in survival when used alone May be essential support mechanism as a bridge to definitive therapy
ICU Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock Overall 30 -Day Survival in the Study Proportion Alive 1. 0 0. 8 Revascularization (n =152) Survival = 53% 0. 6 0. 4 Medical therapy (n =150) Survival = 44% 0. 2 p = 0. 11 0. 0 0 5 10 15 20 Days after Randomization Hochman JS, et al. N Engl J Med. 1999; 341: 625 -34. 25 30
SHOCK Trial Mortality ICU 100 80 P = 0. 11 P = 0. 027 P < 0. 03 66. 4 63. 1 % 56 60 46. 7 50. 3 54. 3 40 Revasc Med Rx 20 0 30 days 6 months 1 year
ACC/AHA Class I Indication ICU Patients with ST segment elevation MI who have cardiogenic shock and are less than 75 years of age should be brought immediately or secondarily transferred to facilities capable of cardiac catheterization and rapid revascularization (PCI or CABG) if it can be performed within 18 hours of onset of shock. (Level of Evidence: A)
ICU Pathophysiology of Cardiogenic Shock Observations from the SHOCK Trial and Registry that Challenge the Classic Paradigm Average LVEF is only moderately severely depressed (30%), with a wide range of EFs and LV sizes noted. Systemic vascular resistance (SVR) on vasopressors is not elevated on average (~ 1350), with a very wide range of SVRs measured. A clinically evident systemic inflammatory response syndrome is often present in patients with CS. Most survivors (85%) have NYHA functional Class I-II CHF status. Hochman JS. Circ. 2003; 107: 2998 -3002.
Pathophysiology of Cardiogenic Shock ICU Cardiogenic shock IS NOT simply the result of severe depression of LV function due to extensive myocardial ischemia/injury. Depressed Myocardial Contractility combined with Inadequate Systemic Vasoconstriction resulting from a systemic inflammatory response to extensive myocardial ischemia/injury results in cardiogenic shock.
The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation. Thus, excess nitric oxide and peroxy nitrites may be a major contributor to cardiogenic shock complicating MI.
Acute Coronary Syndromes: Definitions ICU Acute coronary syndrome: Constellation of clinical symptoms compatible with acute myocardial ischemia © © © ST-segment elevation MI (STEMI) Non-ST-segment elevation MI (NSTEMI) Unstable angina: © © © Angina at rest (usually > 20 minutes) New-onset of class III or IV angina Increasing angina (from class I or II to III or IV)
ICU Pathogenesis of Acute Coronary Syndromes Plaque rupture Platelet adhesion Platelet activation Partially occlusive arterial thrombosis & unstable angina Microembolization & non-STsegment elevation MI Totally occlusive arterial thrombosis & ST-segment elevation MI White HD. Am J Cardiol 1997; 80 (4 A): 2 B-10 B.
ICU Structure of Thrombus Following Plaque Disruption UA/NSTEMI: Partially-occlusive thrombus (primarily platelets) Intra-plaque thrombus (platelet-dominated) STEMI: Occlusive thrombus (platelets, red blood cells, and fibrin) Intra-plaque thrombus (platelet-dominated) Plaque core UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction SUDDEN DEATH White HD. Am J Cardiol 1997; 80 (4 A): 2 B-10 B. Plaque core
ICU Diagnostic Algorithm for Acute Coronary Syndrome Management &/or ST-segment elevation MI Therapeutic goal: rapidly break apart fibrin mesh to quickly restore blood flow Consider fibrinolytic therapy, if indicated, or primary percutaneous coronary intervention (PCI) Non-ST Elevation ACS* + Troponin or + CK-MB Non-ST Elevation MI Therapeutic goal: prevent progression to complete occlusion of coronary artery and resultant MI or death Consider GP IIb-IIIa inhibitor + aspirin + heparin before early diagnostic catheterization Braunwald E, et al. 2002. http: //www. acc. org/clinical/guidelines/unstable. pdf.
0. 25 Placebo 0. 20 Probability of Death or MI ICU Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin in Men with Unstable CAD 0. 15 0. 10 Aspirin 75 mg 0. 05 Risk ratio 0. 52 95% CL 0. 37 - 0. 72 0. 00 0 3 6 Months Wallentin LC, et al. J Am Coll Cardiol, 1991; 18: 1587 -93. 9 12
ICU Low Molecular Weight Heparin (LMWH) vs. Unfractionated Haparin (UFH) in Non-ST elevation ACS: Effect on Death, MI, Recurrent Ischemia Trial: Day: FRIC 6 (Dalteparin; n = 1, 482) FRAXIS 14 (nadroparin; n = 2, 357) ESSENCE (enoxaparin; n = 3, 171) (p= 0. 032) 14 (p= 0. 029) 14 TIMI 11 B (enoxaparin; n = 3, 910) . 75 1. 0 LMWH Better 1. 5 UFH Better Braunwald. Circulation. 2002; 106: 1893 -2000. www. acc. org/clinical/guidelines/unstable. pdf
Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment ICU Elevation % 14 12 Death, MI, or Stroke 11. 4% Placebo + ASA 9. 3% 10 8 Clopidogrel + ASA 6 4 20% RRR P < 0. 001 N = 12, 562 2 0 0 3 6 9 Months of Follow-Up N Engl J Med. 2001; 345: 494 -502. 12
ICU Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials Primary Endpoint % 20 15 17. 9 Placebo GP IIb/IIIa 15. 7 14. 2 12. 9 11. 7 10. 3 12. 8 11. 8 10 5. 6 5 0 3. 8 P = 0. 04 PURSUIT 30 days P = 0. 01 PRISM 48 hrs P = 0. 004 P = 0. 48 P = 0. 33 PRISM PLUS 7 days PARAGON A 30 days PARAGON B 30 days
ICU ST-segment Depression Predicts Higher Risk of Mortality in ACS % Cumulative Mortality at 6 Months 10% ST-segment depression 8. 9% 8% ST-segment elevation 6. 8% 6% 4% T-wave inversion 3. 4% 2% 30 60 90 120 150 Days from randomization Savonitto S. J Am Med Assoc. 1999; 281: 707 -711. 180
ICU
ICU Troponin and ST-Segment Shift Predict Benefit of Invasive Treatment Strategy Cannon. J Invas Cardiol. 2003; 15: 22 B.
ICU ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI Class I An early invasive strategy in patients with a high-risk indicator: 1. Recurrent angina/ischemia despite intensive anti-ischemic rx 2. Elevated troponin-T or troponin-I 3. New or presumably new ST-segment depression 4. Recurrent angina/ischemia with CHF sx, S 3, pulmonary edema, worsening 5. rales, or new or worsening MR 6. 5. High-risk findings on noninvasive stress testing 7. 6. Depressed LV systolic function (EF <40%) 8. 7. Hemodynamic instability 9. 8. Sustained ventricular tachycardia 10. 9. PCI within 6 months 11. 10. Prior CABG Either early invasive or early conservative strategy if not high risk
ICU 2002 ACC/AHA Guidelines for the Management of High-risk NSTE ACS At presentation ST-segment depression &/or elevated cardiac troponin Need to immediately arrest thrombus progression Need to eliminate occlusive ruptured plaque Start immediate § Aspirin § Heparin or low-molecular-weight heparin § GP IIb-IIIa inhibitor Send for catheterization & revascularization within 24 -48 hours Cautionary information § No clopidogrel within 5 -7 days prior to CABG surgery § No enoxaparin within 24 hours prior to CABG surgery § No abciximab, if PCI is not planned Adapted from Braunwald E, et al. 2002. http: //www. acc. org/clinical/guidelines/unstable. pdf.
ICU Ongoing Evaluation in an Early Conservative Strategy Early medical management Recurrent Symptoms/ischemia Heart failure Serious arrhythmia Patient stabilizes Evaluate LV function EF <. 40 EF . 40 Stress Test Not low risk Immediate angiography Low risk Follow on Medical Rx Braunwald E, et al. 2002. http: //www. acc. org/clinical/guidelines/unstable. pdf.
ICU ACC/AHA Guidelines for Unstable Angina and Non-ST-Segment Elevation MI Acute Ischemia Pathway ST , positive cardiac markers, deep T-wave inversion, transient ST , or recurrent ischemia Aspirin, Beta Blockers, Nitrates, Antithrombin regimen, GP IIb-IIIa inhibitor, Monitoring (rhythm and ischemia) Early invasive strategy Immediate angiography 12 -24 hour angiography Early conservative strategy Patient stabilizes Recurrent symptoms/ischemia Heart failure Serious arrhythmia Evaluate LV Function EF <. 40 EF >. 40 Stress Test Not low risk Braunwald. Circulation. 2002; 106: 1893 -2000. www. acc. org/clinical/guidelines/unstable. pdf Low risk Follow on Medical Rx
ACC/AHA REVISED GUIDELINES ICU UA/NSTEMI ASA, Heparin/Enox. , block. , Nitrates, Clopidogrel RISK STRATIFY High Risk * Low Risk * Recurrent ischemia; Trop; ST; LV failure/dysf. ; hemodynamic instability; VT; prior CABG Enoxeparin. Preferred to UFH (IIa) If coronary arteriography >24 hours Braunwald E, et al. Circ. 2002; 106: 1893.
ACC/AHA REVISED GUIDELINES ICU High Risk Cor. Arteriography LMCD, 3 VD+LV Dys. , or Diab. Mell. CABG 1 or 2 VD, Suitable for PCI Clopidogrel, IIb/IIIa inhib. PCI Discharge on ASA, Clopidogrel, Statin, ACEI Braunwald E, et al. Circ. 2002; 106: 1893. Normal Consider Alternative Diagnosis
Discharge/Post-discharge Medications ICU I IIa IIb III ASA, if not contraindicated Clopidogrel, when ASA contraindicated Aspirin + Clopidogrel, for up to 9 months -blocker, if not contraindicated Lipid agents (statins) + diet ACE Inhibitor: CHF, EF < 40%, DM, or HTN Braunwald. Circulation 2002; 106: 1893 -2000. www. acc. org/clinical/guidelines/unstable. pdf
ICU Tachydysrhythmias Regular Irregular Narrow complex Wide complex Sinus Tachycardia Atrial Flutter AVNRT/AVRT Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB MAT Atrial Fibrillation Atrial Flutter with variable block Torsade des Pointes Ventricular fibrillation
ICU Afib
ICU Incidence of Afib
Risk Factors for Afib ICU n n n n MICU Electrolyte abnormalities High cardiac filling pressures Hypoxia Comorbid heart disease Sepsis MOF n n n SICU Post-op hypotension Post-op sepsis Post-op pulmonary edema PA catheters Blunt thoracic trauma
ICU Morbidity of Afib in the ICU
Management ICU n Stable vs. Unstable n Unstable Electrical, synchronized cardioversion n 100 J n n Stable n Rate vs rhythm control n n Rate control n Digoxin n B blocker n Verapamil Rhythm control n Diltiazam n Amiodarone n magnesium
Rate vs Rhythm control ICU In non ICU patients rate vs rhythm control seems to make no difference n In the ICU patients may not tolerate lose of the atrial kick (up to 25% reduction in CO) n Most patients with new onset afib in the ICU will require a trial of chemical cardioversion n
Chemical Cardioversion ICU n Amiodarone n 300 mg bolus, then 1 g over 24 hr infusion n 75% will convert in 24 hrs n 5% incidence of hypotension n Diltiazam n 25 mg bolus, 20 mg/h infusion n 70% conversion n 30% hypotension
Chemical Cardioversion ICU n Magnesium n 86% conversion rate n No side effects n 37 mg/kg bolus followed by 25 mg/kg/hr for 24 hrs (approx 3 gm bolus then 2 gm/hr for an 80 kg patient) n Benign neglect n 56% cardioversion
ICU Aflutter
ICU SVT or Flutter? flutter
ICU
ICU
ICU Vtach
ICU Vfib
ICU Vtach
ICU Hyperkalemia
ICU Hyperkalemia
Summary ICU n Review ACLS guidelines
- Right sided heart failure
- Congestive heart failure zones for management
- Congestive heart failure symtoms
- Edema assessment
- Acute coronary syndrome
- Anaphylactic shock pathophysiology flowchart
- Aortrix
- Negative chronotropic effect of digoxin
- "theodore spaulding"
- Theodore schreiber
- Cardiogenic shock algorithm
- Acute vs chronic heart failure
- Global registry of acute coronary events
- Coronary steal
- Classification of antianginal drugs
- Cardiovascular system crash course
- Coronary circulation of heart
- Coronary heart disease
- Cardiac plexus
- Spinal shock vs neurogenic shock
- Normovolemico
- Spinal shock vs neurogenic shock
- Spinal shock symptoms
- Cauda equina vs conus medullaris
- Cardiogenic vs noncardiogenic pulmonary edema
- Cardiogenic shocl
- Fhf
- Acute brain failure
- Cushings triad
- Acute liver failure
- Urinalysis
- Brittle fracture examples
- Capture beat
- Failure to capture vs failure to sense
- Dengue shock syndrome
- Double positive t cells
- Firas mussa
- Acute radiation syndrome
- Heart failure definition
- Dr nienkemper
- Donkey analogy heart failure
- Heart failure
- Diabetes and heart failure
- New york scale heart failure
- Acute pulmonary congestion histology
- Lvedp normal range
- Compensatory mechanisms of heart failure
- Heart failure complications
- Lmnop heart failure
- Pvkov
- Cardiomegay
- 5 cardiac landmarks
- Keith rn heart failure case study
- Chapter 24 heart failure drugs
- Chlorpromide
- Ligamentum venosum
- Mesa coronary calcium score
- Good morning blood
- Qfr coronary
- Coronary blood flow