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