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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/m2, 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 25% in shock 75%

11% in shock 89%

SHOCK Registry, Circulation. 1995;91:873-81. GUSTO J Amer Coll Cardiol. 1995;26:668-74.

ICU

Schematic Diagram of Stunned Myocardium


Clamp

Wall motion abnormality Wall motion abnormality during occlusion

Coronary 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

Reperfusion

Significant residual stenosis Segments with both stunning and hibernation Segments with hibernating myocardium

Segments with myocardial stunning

Inotropic support

Relief of ischemia

No return of function
Return of myocardial function

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

ICU

Dopamine
Dopaminergic, Beta, Alpha: ranges ? Dopa: 1-5 ug/kg/min

? Renal flow Inoptropy/chronotropy Vasoconstriction

Beta: 5-10 ug/kg/min

Alpha: >10 ug/kg/min

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

ICU

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

Half life of approximately 2 hours (so its gonna last a while


Loading dose: 50 mcg/kg administered over 10 minutes followed by 0.375 mcg/kg/minute

Dose

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

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
1.0 0.8

Proportion Alive

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 25 30

Days after Randomization


Hochman JS, et al. N Engl J Med. 1999;341:625-34.

SHOCK Trial Mortality


ICU

100

80

P = 0.11

P = 0.027

P < 0.03
66.4 54.3

63.1

60

56

46.7
40

50.3

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.

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

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 (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 thrombus (platelet-dominated)

Plaque core

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


+ Troponin
or + CK-MB

&/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*

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.

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

Probability of Death or MI

0.15

0.10

Aspirin 75 mg
0.05

Risk ratio 0.52 95% CL 0.37 - 0.72


0 3 6 9 12

0.00

Months
Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93.

ICU

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)

.75 LMWH Better 1.0 UFH Better

(p= 0.029) 1.5

14

Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment ICU Elevation
%
14 12

Placebo + ASA

11.4% 9.3%

Death, MI, or Stroke

10

8
6 4 2 0

Clopidogrel + ASA

20% RRR P < 0.001 N = 12,562


0
3 6 9 12

Months of Follow-Up
N Engl J Med. 2001;345:494-502.

ICU

Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials
20

17.9 15.7 14.2 12.9

Placebo GP IIb/IIIa 12.8 11.8

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

ICU

ST-segment Depression Predicts Higher Risk of Mortality in ACS


% Cumulative Mortality at 6 Months
ST-segment depression 8.9%

10%
8% 6% 4% 2%

ST-segment elevation 6.8%

T-wave inversion 3.4%

30

60

90

120

150

180

Days from randomization


Savonitto S. J Am Med Assoc. 1999; 281: 707-711.

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. 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

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/unstable.pdf.

ICU

Ongoing Evaluation in an Early Conservative Strategy


Early medical management

Recurrent Symptoms/ischemia Heart failure Serious arrhythmia

Evaluate LV function

Patient stabilizes

EF < .40

EF .40
Stress Test

Not low risk

Low risk

Immediate angiography

Follow on Medical Rx

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 EF > .40 Stress Test

Not low risk Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/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, 3VD+LV Dys., or Diab. Mell.

1 or 2VD, Suitable for PCI


Clopidogrel, IIb/IIIa inhib. PCI

Normal

CABG

Consider Alternative Diagnosis

Discharge on ASA, Clopidogrel, Statin, ACEI


Braunwald E, et al. Circ. 2002;106:1893.

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/unstable.pdf

ICU

Tachydysrhythmias
Regular Irregular

Narrow complex

Wide complex

Narrow complex

Wide complex

Sinus Tachycardia Atrial 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

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

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