Cardiogenic Shock And Arrhythmias
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Transcript of Cardiogenic Shock And Arrhythmias
Cardiogenic Shock, Acute Coronary Cardiogenic Shock, Acute Coronary Syndrome, Congestive Syndrome, Congestive
Heart Failure, and ArrhythmiasHeart Failure, and Arrhythmias
Dalhousie Critical Care Lecture SeriesDalhousie Critical Care Lecture Series
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/m2, PCWP > 15 mm Hg
Parrillo, J. 2005
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
Causes of Cardiogenic Shock
ICU
Evolution Of The Disease
Frequently, shock develops after presentation for myocardial infarction.
- SHOCK Registry • At presentation 25% in shock • Within 24 hours 75%
(median delay = 7 hours)
- GUSTO Trial • At presentation 11% in shock • After admission 89%
SHOCK Registry, Circulation. 1995;91:873-81.GUSTO J Amer Coll Cardiol. 1995;26:668-74.
Cardiogenic Shock
ICU
Wall motion abnormality
duringocclusion
Wall motionabnormality
From Kloner RA. Am J Med. 1986;86:14.
Gradual return offunction (hours to days)
Persistent wall motion abnormality(despite reperfusion
and viable myocytes)
Coronary occlusion
Coronary reperfusion
Return offunction
Clamp
Schematic Diagram of StunnedMyocardium
ICU
Cell deathCell death Significant Significant residual residual stenosisstenosis
ReperfusionReperfusion
Segments Segments withwith
myocardialmyocardialstunningstunning
Segments Segments withwithboth both
stunningstunningand and
hibernationhibernation
Segments Segments withwith
hibernatinghibernatingmyocardiummyocardium
Relief of Relief of ischemiaischemia
InotropicInotropicsupportsupport
No returnNo returnof functionof function
Return ofReturn ofmyocardial functionmyocardial function
Ischemic Myocardium
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
Initial Approach: Management
ICUDopamine
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
ICUDobutamine
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
ICUEpinepherine
Alpha and Beta 0.01 – 1.0 ug/kg/min Major Use: when you need A&B Like using dobutamine and levophed
mixed together
ICUMilrinone
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
ICUNorepinepherine
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
ICUUse of Inotropes
BP is not a reliable indicator of COCO = 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
ICUUse of Vasopressors
Often used in conjunction with inotropes counteract the vasodilation that occurs
Titrated to MAP
ICU
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
Intra-aortic Balloon Counterpulsation
ICU
Overall 30-Day Survival in the Overall 30-Day Survival in the StudyStudy
Hochman JS, et al. N Engl J Med. 1999;341:625-Hochman JS, et al. N Engl J Med. 1999;341:625-34.34.
Pro
po
rtio
n A
live
0
Days after Randomization
0.6
0.2
0.0
0.8Revascularization (n =152)
Medical therapy (n =150)
1.0
0.4
5 10 15 20 25 30
Survival = 53%
Survival = 44%
p = 0.11
Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock
ICU
46.7 50.354.356
63.166.4
0
20
40
60
80
100
%
P = 0.11 P = 0.027 P < 0.03
30 days 6 months 1 year
RevascMed Rx
SHOCK Trial Mortality
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)
ACC/AHA Class I Indication
ICU
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 Observations from the SHOCK Trial and Registry that
Challenge the Classic Paradigm
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 .
Pathophysiology of Cardiogenic Shock
Thus, excess nitric oxide and peroxy nitrites may be a major contributor to
cardiogenic shock complicating MI.
The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation.
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)
Acute Coronary Syndromes: Definitions
ICU
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.
Pathogenesis of Acute Coronary Syndromes
ICU
UA/NSTEMI:Partially-occlusive thrombus
(primarily platelets)
Intra-plaque thrombus (platelet-dominated)
Plaque core
STEMI:Occlusive thrombus (platelets,
red blood cells, and fibrin)
Intra-plaque thrombus
(platelet-dominated)
Plaque core
SUDDEN DEATH
UA = Unstable AnginaNSTEMI = Non-ST-segment Elevation Myocardial InfarctionSTEMI = ST-segment Elevation Myocardial Infarction
Structure of Thrombus Following Plaque Disruption
White HD. Am J Cardiol 1997;80 (4A):2B-10B.
ICU
Therapeutic goal: rapidly break apart fibrin mesh to quickly restore blood flow
ST-segment elevation MI Non-ST Elevation ACS* Non-ST Elevation MI
+ Troponinor + CK-MB
Consider fibrinolytic therapy, if indicated, or primary percutaneous coronary
intervention (PCI)
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
&/or
Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.
Diagnostic Algorithm for Acute Coronary Syndrome Management
ICU
0.00
0.05
0.10
0.15
0.20
0.25
0 3 6 9 12
Pro
bab
ilit
yo
f D
eath
or
MI
Placebo
Aspirin 75 mg
Risk ratio 0.5295% CL 0.37 - 0.72
Risk of MI and Death During Treatment Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin with Low-Dose Aspirin and IV Heparin
in Men with Unstable CADin Men with Unstable CAD
Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93.
Months
ICU
Trial:
FRIC(Dalteparin; n = 1,482)
FRAXIS(nadroparin; n = 2,357)
ESSENCE(enoxaparin; n = 3,171)
TIMI 11B(enoxaparin; n = 3,910)
Trial:
FRIC(Dalteparin; n = 1,482)
FRAXIS(nadroparin; n = 2,357)
ESSENCE(enoxaparin; n = 3,171)
TIMI 11B(enoxaparin; n = 3,910) .75 1.0 1.51.5.75 1.0 1.51.5
(p= 0.032)(p= 0.032)(p= 0.032)(p= 0.032)
(p= 0.029)(p= 0.029)(p= 0.029)(p= 0.029)
LMWHLMWHBetterBetter
LMWHLMWHBetterBetter
UFHUFHBetterBetterUFHUFH
BetterBetter
6
14
14
14
Day:
Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf
Low Molecular Weight Heparin (LMWH) vs. Unfractionated Haparin (UFH) in
Non-ST elevation ACS: Effect on Death, MI, Recurrent Ischemia
ICU
0
2
4
6
8
10
12
14
Dea
th,
MI,
or
Str
oke
Clopidogrel + ASA
3 6 9
Placebo + ASA
Months of Follow-Up
11.4%
9.3%
20% RRRP < 0.001
N = 12,562
0 12
%%
N Engl J Med. 2001;345:494-502.
Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-
Segment Elevation
ICU
15.7
5.6
17.9
11.712.8
14.2
3.8
12.9
10.311.8
0
5
10
15
20
Pri
mar
y E
nd
po
int
%
Placebo
GP IIb/IIIa
PURSUITPURSUIT30 days30 days
PURSUITPURSUIT30 days30 days
PRISM48 hrsPRISM48 hrs
PRISM PLUS7 days
PRISM PLUS7 days
P = 0.04P = 0.04P = 0.04P = 0.04 P = 0.01P = 0.01P = 0.01P = 0.01 P = 0.004P = 0.004P = 0.004P = 0.004
PARAGON A30 days
PARAGON A30 days
P = 0.48P = 0.48P = 0.48P = 0.48
PARAGON B30 days
PARAGON B30 days
P = 0.33P = 0.33
Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint
Results from the 5 Major Trials
ICU
30 60 90 120 150 180
10%
8%
6%
4%
2%
T-wave inversion3.4%
ST-segment elevation6.8%
ST-segment depression8.9%
Days from randomization
% Cumulative Mortality at 6 Months
Savonitto S. J Am Med Assoc. 1999; 281: 707-711.
ST-segment Depression PredictsHigher Risk of Mortality in ACS
ICU
ICU
Cannon. J Invas Cardiol. 2003;15:22B.
Troponin and ST-Segment Shift Predict
Benefit of Invasive Treatment Strategy
ICU
Class I
An early invasive strategy in patients with a high-risk indicator:
1. Recurrent angina/ischemia despite intensive anti-ischemic rx2. Elevated troponin-T or troponin-I3. New or presumably new ST-segment depression4. Recurrent angina/ischemia with CHF sx, S3, pulmonary edema, worsening
rales, or new or worsening MR5. High-risk findings on noninvasive stress testing6. Depressed LV systolic function (EF <40%)7. Hemodynamic instability8. Sustained ventricular tachycardia9. PCI within 6 months10.Prior CABG
Either early invasive or early conservative strategy if not high risk
ACC/AHA Guideline Update for the Management of Patients with
Unstable Angina and Non-ST-Segment Elevation MI
ICU
Start immediate Aspirin Heparin or low-molecular-weight heparin GP IIb-IIIa inhibitor
Adapted from Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.
At presentationST-segment depression &/or elevated cardiac troponin
Need to immediately arrest thrombus progression
Need to eliminate occlusive ruptured plaque
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
2002 ACC/AHA Guidelines for theManagement of High-risk NSTE
ACS
ICU
Recurrent Symptoms/ischemia
Heart failureSerious arrhythmia
Patient stabilizes
EF .40
Stress Test
Not low risk
Follow on Medical Rx
Evaluate LV function
EF < .40
Low risk
Early medical management
Immediate angiography
Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.
Ongoing Evaluation in an EarlyConservative Strategy
ICU
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 EF > .40 Stress Test
Not low risk Low risk
Follow on Medical RxBraunwald. Circulation. 2002;106:1893-2000.
www.acc.org/clinical/guidelines/unstable/unstable.pdf
ACC/AHA Guidelines for Unstable Angina and Non-ST-Segment Elevation MI Acute
Ischemia Pathway
ICU
UA/NSTEMIUA/NSTEMI
High Risk High Risk **
ASA, Heparin/ASA, Heparin/Enox.Enox., , block., Nitrates, Clopidogrelblock., Nitrates, Clopidogrel
RISK STRATIFY
Low RiskLow Risk
Braunwald E, et al.Circ. 2002;106:1893.
* Recurrent ischemia; Trop; ST; LV failure/dysf.; hemodynamic instability; VT; prior CABG
Enoxeparin. Preferred to UFH (IIa)
If coronary arteriography >24 hours
ACC/AHA REVISED GUIDELINES
ICU
Braunwald E, et al.Circ. 2002;106:1893.
LMCD, 3VD+LV Dys., LMCD, 3VD+LV Dys., or Diab. Mell.or Diab. Mell.
CABGCABG
High RiskHigh Risk
Cor. ArteriographyCor. Arteriography
1 or 2VD, Suitable 1 or 2VD, Suitable for PCIfor PCI NormalNormal
Clopidogrel, Clopidogrel, IIb/IIIa inhib.IIb/IIIa inhib.
Consider Alternative Consider Alternative DiagnosisDiagnosis
Discharge on ASA, Clopidogrel, Statin, ACEIDischarge on ASA, Clopidogrel, Statin, ACEI
PCIPCI
ACC/AHA REVISED GUIDELINES
ICU
II IIaIIa IIbIIb IIIIII
Braunwald. Circulation 2002;106:1893-2000.www.acc.org/clinical/guidelines/unstable/unstable.pdf
Discharge/Post-discharge Medications
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
ICU
Tachydysrhythmias
Regular Irregular
Narrow complex Wide complex Narrow complex Wide complex
Sinus TachycardiaAtrial Tachycardia
Atrial FlutterAVNRT/AVRT
Ventricular tachycardiaPacer-mediated
tachycardiaSVT with pre-existing BBB
SVT with rate-dependent BBB
MATAtrial Fibrillation
Atrial Flutter with variable block
Torsade des PointesVentricular fibrillation
ICUAfibAfib
ICUIncidence of Afib
ICURisk 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
ICUManagement
Stable vs. Unstable Unstable
Electrical, synchronized cardioversion 100J
Stable Rate vs rhythm control
Rate control Digoxin B blocker Verapamil
Rhythm control Diltiazam Amiodarone magnesium
ICURate 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
ICUChemical 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
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
Chemical Cardioversion
ICUAflutter
ICUSVT or Flutter?
flutter
ICU
ICU
ICUVtach
ICUVfib
ICUVtach
ICUHyperkalemia
ICUHyperkalemia
ICUSummary
Review ACLS guidelines