Cardiogenic Shock
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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/m2, PCWP > 15 mm Hg
Parrillo, J. 2005
Acute MI
Other conditions
End-stage cardiomyopathy Myocarditis (fulminant myocarditis) Myocardial contusion Prolonged cardiopulmonary bypass Septic shock with myocardial depression Valvular disease
Cardiogenic Shock
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Coronary occlusion
Coronary reperfusion Return of function Persistent wall motion abnormality (despite reperfusion and viable myocytes)
Ischemic Myocardium
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Cell death
Reperfusion
Significant residual stenosis Segments with both stunning and hibernation Segments with hibernating myocardium
Inotropic support
Relief of ischemia
No return of function
Return of myocardial function
Assure oxygenation
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Dopamine
Dopaminergic, Beta, Alpha: ranges ? Dopa: 1-5 ug/kg/min
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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
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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
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Milrinone
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
can also cause vasodilatation but tends to have less chronotropy than dobutamine 5-15 minutes
Side Effects
Onset of action
Duration
Dose
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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
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Use of Inotropes
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Use of Vasopressors
Titrated to MAP
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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
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Proportion Alive
Revascularization (n =152)
Survival = 53% 0.6 0.4
0.2
p = 0.11 0.0 0 5 10 15 20 25 30
100
80
P = 0.11
P = 0.027
P < 0.03
66.4 54.3
63.1
60
56
46.7
40
50.3
Revasc Med Rx
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)
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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.
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.
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)
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Plaque core
Plaque core
UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction
SUDDEN DEATH
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&/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 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
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Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin in Men with Unstable CAD
0.25
Placebo
0.20
Probability of Death or MI
0.15
0.10
Aspirin 75 mg
0.05
0.00
Months
Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93.
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Low Molecular Weight Heparin (LMWH) vs. Unfractionated Haparin (UFH) in Non-ST elevation ACS: Effect on Death, MI, Recurrent Ischemia
Trial:
FRIC
(Dalteparin; n = 1,482)
Day:
6 14 (p= 0.032) 14
FRAXIS
(nadroparin; n = 2,357)
ESSENCE
(enoxaparin; n = 3,171)
TIMI 11B
(enoxaparin; n = 3,910)
14
Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment ICU Elevation
%
14 12
Placebo + ASA
11.4% 9.3%
10
8
6 4 2 0
Clopidogrel + ASA
Months of Follow-Up
N Engl J Med. 2001;345:494-502.
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Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials
20
Primary Endpoint %
15
11.7 10.3
10
5.6
5
3.8 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
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10%
8% 6% 4% 2%
30
60
90
120
150
180
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ICU
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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. 2. 3. 4. Recurrent angina/ischemia despite intensive anti-ischemic rx Elevated troponin-T or troponin-I New or presumably new ST-segment depression 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
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Start immediate
Aspirin Heparin or low-molecular-weight heparin GP IIb-IIIa inhibitor
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
ICU
Evaluate LV function
Patient stabilizes
EF < .40
EF .40
Stress Test
Low risk
Immediate angiography
Follow on Medical Rx
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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)
Immediate angiography
Patient stabilizes
Evaluate LV Function
EF < .40 EF > .40 Stress Test
Low risk
Follow on Medical Rx
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
High Risk
Normal
CABG
Discharge/Post-discharge Medications
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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
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Tachydysrhythmias
Regular Irregular
Narrow complex
Wide complex
Narrow complex
Wide complex
Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB
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Afib
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Incidence of Afib
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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
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Management
Unstable
Stable
Rate control Digoxin B blocker Verapamil Rhythm control Diltiazam Amiodarone magnesium
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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
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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
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Aflutter
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SVT or Flutter?
flutter
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ICU
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Vtach
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Vfib
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Vtach
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Hyperkalemia
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Hyperkalemia
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Summary