Transcript SCCM Online Critical Care Course: Cardiogenic Shock, Acute
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
ICU Causes of Cardiogenic Shock
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
ICU Cardiogenic Shock Evolution Of The Disease
Frequently, shock develops after presentation for myocardial infarction.
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• •
SHOCK Registry
At presentation Within 24 hours (median delay = 7 hours)
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• •
GUSTO Trial
At presentation After admission 25% in shock 75% 11% in shock 89%
SHOCK Registry, Circulation. 1995;91:873-81.
GUSTO J Amer Coll Cardiol. 1995;26:668-74
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ICU Schematic Diagram of Stunned Myocardium Clamp
Wall motion abnormality Coronary occlusion Wall motion abnormality during occlusion Coronary reperfusion Return of function Persistent wall motion abnormality (despite reperfusion and viable myocytes) Gradual return of function (hours to days)
From Kloner RA. Am J Med. 1986;86:14.
Ischemic Myocardium ICU Cell death No return of function Reperfusion Segments with myocardial stunning Significant residual stenosis Segments with both stunning and hibernation Segments with hibernating myocardium Inotropic support Relief of ischemia Return of myocardial function
ICU Initial Approach: Management
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
ICU
Dopamine
Dopaminergic, Beta, Alpha: ranges ?
Dopa: 1-5 ug/kg/min ? Renal flow Beta: 5-10 ug/kg/min Inoptropy/chronotropy Alpha: >10 ug/kg/min Vasoconstriction Major use: increasing HR, ?bp
ICU
Dobutamine
Beta (little alpha) Inotropic/chronotropic 2-20 ug/kg/min Major use: Systolic dysfunction Caveat: can/will decrease MAP Often used in conjunction with levophed
ICU
Epinepherine
Alpha and Beta 0.01 – 1.0 ug/kg/min Major Use: when you need A&B Like using dobutamine and levophed mixed together
Milrinone
ICU
Used as an inotrope Mechanism of Action 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 Side Effects can also cause vasodilatation but tends to have less chronotropy than dobutamine Onset of action 5-15 minutes Duration Half life of approximately 2 hours (so its gonna last a while Dose Loading dose: 50 mcg/kg administered over 10 minutes followed by 0.375 mcg/kg/minute
ICU
Norepinepherine
Alpha and Beta 0.02-3.0 ug/kg/min Major Use: when you need A&B ? Drug of choice for septic shock Good and bad for use in cardiogenic shock May increase blood pressure May decrease CO by increasing afterload Will increase cardiac strain
ICU
Use of Inotropes
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 Need to titrate to the CO Swan ganz CO measure U/O Lactate ScVO2
ICU
Use of Vasopressors
Often used in conjunction with inotropes counteract the vasodilation that occurs Titrated to MAP
ICU Intra-aortic Balloon Counterpulsation
ICU Intra-aortic Balloon Counterpulsation
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
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 P = 0.11
80
%
60 46.7
56 40 P = 0.027
50.3
63.1
P < 0.03
66.4
54.3
20 0 30 days 6 months 1 year Revasc Med Rx
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.
ICU Pathophysiology of Cardiogenic Shock
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
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-ST segment elevation MI Totally occlusive arterial thrombosis & ST-segment elevation MI
White HD. Am J Cardiol 1997;80 (4A):2B-10B.
ICU Structure of Thrombus Following Plaque Disruption UA/NSTEMI: Partially-occlusive thrombus (primarily platelets) STEMI: Occlusive thrombus (platelets, red blood cells, and fibrin) Intra-plaque Plaque core thrombus (platelet-dominated) 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 (4A):2B-10B.
ICU Diagnostic Algorithm for Acute Coronary Syndrome Management &/or + T roponin or + CK-MB 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* 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/unstable.pdf
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ICU Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin in Men with Unstable CAD 0.25
Placebo 0.20
0.15
0.10
0.05
0.00
0 3 6 Months
Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93.
Aspirin 75 mg Risk ratio 0.52
95% CL 0.37 - 0.72
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
(nadroparin; n = 2,357)
14 ESSENCE
(enoxaparin; n = 3,171)
(p= 0.032) 14 TIMI 11B
(enoxaparin; n = 3,910)
(p= 0.029) 14 .75
LMWH Better 1.0
UFH Better
Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf
1.5
ICU Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment Elevation % 14 Placebo 11.4% 12 + ASA 9.3% 10 8 Clopidogrel + ASA 6 4 2 0 0 3 6 9 Months of Follow-Up
N Engl J Med. 2001;345:494-502.
20% RRR P < 0.001
N = 12,562 12
ICU Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials 20 17.9
Placebo 15 15.7
14.2
GP IIb/IIIa 12.9
11.7
10.3
12.8
11.8
10 5 5.6
3.8
0 P = 0.04
PURSUIT 30 days P = 0.01
PRISM 48 hrs P = 0.004
PRISM PLUS 7 days P = 0.48
PARAGON A 30 days P = 0.33
PARAGON B 30 days
ICU 10% 8% 6% 4% 2% ST-segment Depression Predicts Higher Risk of Mortality in ACS % Cumulative Mortality at 6 Months ST-segment depression 8.9% ST-segment elevation 6.8% T-wave inversion 3.4% 30 60 90 120 Days from randomization 150
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;15:22B.
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, S3, pulmonary edema, worsening rales, or new or worsening MR 5. High-risk findings on noninvasive stress testing 6. Depressed LV systolic function (EF <40%) 7. Hemodynamic instability 8. Sustained ventricular tachycardia 9. PCI within 6 months 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
Aspirin
Heparin or low-molecular-weight heparin GP IIb-IIIa inhibitor Start immediate 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/unstable.pdf
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ICU Ongoing Evaluation in an Early Conservative Strategy Early medical management Recurrent Symptoms/ischemia Heart failure Serious arrhythmia Evaluate LV function EF < .40
EF
.40
Patient stabilizes Stress Test Not low risk Low risk Follow on Medical Rx Immediate angiography
Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/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 Early conservative strategy Immediate angiography 12-24 hour angiography Recurrent symptoms/ischemia Heart failure Serious arrhythmia Patient stabilizes Evaluate LV Function EF < .40
Braunwald. Circulation. 2002;106:1893-2000.
www.acc.org/clinical/guidelines/unstable/unstable.pdf
EF > .40
Stress Test Not low risk Low risk Follow on Medical Rx
ICU ACC/AHA REVISED GUIDELINES 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.
ICU ACC/AHA REVISED GUIDELINES High Risk Cor. Arteriography LMCD, 3VD+LV Dys., or Diab. Mell.
CABG 1 or 2VD, Suitable for PCI Clopidogrel, IIb/IIIa inhib.
PCI Normal Consider Alternative Diagnosis Discharge on ASA, Clopidogrel, Statin, ACEI
Braunwald E, et al.
Circ. 2002;106:1893.
ICU Discharge/Post-discharge Medications 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/unstable.pdf
ICU Tachydysrhythmias Narrow complex
Sinus Tachycardia Atrial Tachycardia Atrial Flutter AVNRT/AVRT
Regular Wide complex
Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB
Narrow complex
MAT Atrial Fibrillation Atrial Flutter with variable block
Irregular Wide complex
Torsade des Pointes Ventricular fibrillation
ICU
Afib
ICU
Incidence of Afib
ICU
Risk Factors for Afib
MICU Electrolyte abnormalities High cardiac filling pressures Hypoxia Comorbid heart disease Sepsis MOF SICU Post-op hypotension Post-op sepsis Post-op pulmonary edema PA catheters Blunt thoracic trauma
ICU
Morbidity of Afib in the ICU
ICU
Management
Stable vs. Unstable Unstable Electrical, synchronized cardioversion 100J Stable Rate vs rhythm control Rate control Digoxin B blocker Verapamil Rhythm control Diltiazam Amiodarone magnesium
ICU
Rate vs Rhythm control
In non ICU patients rate vs rhythm control seems to make no difference In the ICU patients may not tolerate lose of the atrial kick (up to 25% reduction in CO) Most patients with new onset afib in the ICU will require a trial of chemical cardioversion
ICU
Chemical Cardioversion
Amiodarone 300 mg bolus, then 1 g over 24 hr infusion 75% will convert in 24 hrs 5% incidence of hypotension Diltiazam 25 mg bolus, 20 mg/h infusion 70% conversion 30% hypotension
ICU
Chemical Cardioversion
Magnesium 86% conversion rate No side effects 37 mg/kg bolus followed by 25 mg/kg/hr for 24 hrs (approx 3 gm bolus then 2gm/hr for an 80kg patient) Benign neglect 56% cardioversion
ICU
Aflutter
ICU
SVT or Flutter?
flutter
ICU
ICU
ICU
Vtach
ICU
Vfib
ICU
Vtach
ICU
Hyperkalemia
ICU
Hyperkalemia
ICU
Summary
Review ACLS guidelines