cardiogenic-shock-and-arrhythmias-1204661404371444-2.pdf

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Cardiogenic Shock, Acute Coronary

Syndrome, Congestive

Heart Failure, and Arrhythmias

Dalhousie Critical Care Lecture Series


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ICU

Inadequate tissue perfusion resulting from cardiac

dysfunction

Clinical definition - decreased cardiac output and tissue

hypoxia in the presence of adequate intravascularvolume

Hemodynamic definition - sustained systolic BP < 90 mm

Hg, cardiac index < 2.2 L/min/m2, PCWP > 15 mm Hg

Parrillo, J. 2005

Cardiogenic Shock


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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


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ICU

Evolution Of The DiseaseFrequently, 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


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ICU

Wall motionabnormality

duringocclusion

Wall motionabnormality

From Kloner RA. Am J Med.1986;86:14.

Gradual return offunction (hours to days)

Persistent wallmotion abnormality(despite reperfusionand viable myocytes)

Coronary occlusion

Coronary reperfusion

Return of

function

Clamp

Schematic Diagram of StunnedMyocardium


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ICU

Cell deathSignificant

residualstenosis

Reperfusion

Segments

withmyocardialstunning

Segmentswith

both stunningand

hibernation

Segments

withhibernatingmyocardium

Relief ofischemia

Inotropic

supportNo return

of function

Return ofmyocardial function

Ischemic Myocardium


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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


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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


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ICUDobutamine

Beta (little alpha)

Inotropic/chronotropic

2-20 ug/kg/min Major use: Systolic dysfunction

Caveat: can/will decrease MAP

Often used in conjunction withlevophed


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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


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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 influxinto the cell, a rise in cell calcium concentration, and increased

contractility Side Effects

can also cause vasodilatation but tends to have less chronotropy thandobutamine

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


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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


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ICUUse 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 willstay the same

Need to titrate to the CO

Swan ganz CO measure

U/O

Lactate

ScVO2


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ICUUse of Vasopressors

Often used in conjunction with

inotropes

counteract the vasodilation that occurs

Titrated to MAP


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ICU

Intra-aortic BalloonCounterpulsation


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ICU

The only thing that reduces afterload andaugments diastolic perfusion pressure

Beneficial effects occur without increase in oxygen

demandNo improvement in blood flow distal to criticalcoronary stenosis

No improvement in survival when used alone

May be essential support mechanism as a bridgeto definitive therapy

Intra-aortic Balloon Counterpulsation


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ICU

Overall 30-Day Survival in the Study

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

ProportionAlive

0

Days after Randomization

0.6

0.2

0.0

0.8Revascularization (n =152)

Medicaltherapy (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


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ICU

46.750.3

54.3

56

63.166.4

0

20

40

60

80

100

%

P = 0.11 P = 0.027 P < 0.03

30 days 6 months 1 year

Revasc

MedRx

SHOCK Trial Mortality


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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 rapidrevascularization (PCI or CABG) if it can be performed

within 18 hours of onset of shock. (Level of Evidence: A)

ACC/AHA Class I Indication


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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 notelevated 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 ShockObservations from the SHOCK Trial and

Registry that Challenge the ClassicParadigm


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ICU

Cardiogenic shock IS NOT simply the result of severedepression of LV function due to extensive myocardialischemia/injury.

Depressed Myo cardial Con tract i l i tycombined withInadequate System ic Vasocons tr ict ionresulting froma systemic inflammatory response to extensivemyocardial ischemia/injury results in cardiogenic shock .

Pathophysiology of Cardiogenic Shock


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Thus, excess nitric oxide and peroxy

nitrites may be a major contributor to

cardiogenic shock complicating MI.

The Overproduction of NitricOxide May Cause Both

Myocardial Depression andInappropriate Vasodilatation.


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ICU

Acu te 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 ang ina:

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


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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 CoronarySyndromes


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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 Angina

NSTEMI = Non-ST-segment Elevation Myocardial Infarction

STEMI = ST-segment Elevation Myocardial Infarction

Structure of Thrombus FollowingPlaque Disruption

White HD. Am J Cardiol 1997;80 (4A):2B-10B.


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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 AcuteCoronary Syndrome Management
http://www.acc.org/clinical/guidelines/unstable/unstable.pdfhttp://www.acc.org/clinical/guidelines/unstable/unstable.pdf


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ICU

0.00

0.05

0.10

0.15

0.20

0.25

0 3 6 9 12

Probabil

ity

ofDeatho

rMI

Placebo

Aspirin 75 mg

Risk ratio 0.5295% CL 0.37 - 0.72

Risk of MI and Death During Treatmentwith Low-Dose Aspirin and IV Heparin in

Men with Unstable CAD

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

Months

Low Molecular Weight Heparin (LMWH) vs


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ICU

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 1.5

(p= 0.032)

(p= 0.029)

LMWH

BetterUFH

Better

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


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ICU

0

2

4

6

8

10

12

14

Death,MI,orStroke

Clopidogrel

+ ASA

3 6 9

Placebo

+ ASA

Months of Follow-Up

11.4%

9.3%

20% RRR

P< 0.001

N = 12,562

0 12

%

N Engl J Med. 2001;345:494-502.

Effects of Clopidogrel in Addition to Aspirin inPatients with ACS without ST-Segment

Elevation


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ICU

15.7

5.6

17.9

11.712.8

14.2

3.8

12.9

10.3

11.8

0

5

10

15

20

P

rimaryEndpoint%

Placebo

GP IIb/IIIa

PURSUIT

30 days

PRISM

48 hrs

PRISM

PLUS

7 days

P = 0.04 P = 0.01 P = 0.004

PARAGON A

30 days

P = 0.48

PARAGON B

30 days

P = 0.33

Platelet Glycoprotein IIb/IIIa Inhibition forNon-ST elevation ACS Primary Endpoint

Results from the 5 Major Trials


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ICU

30 60 90 120 150 180

10%

8%

6%

4%

2%

T-wave inversion

3.4%

ST-segment elevation

6.8%

ST-segment depression

8.9%

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


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ICU


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ICU

Cannon. J Invas Cardiol. 2003;15:22B.

Troponin and ST-Segment Shift PredictBenefit of Invasive Treatment Strategy


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ICU

Class I

An ear ly in vasivestrategy in patients with a high-r iskindicator:

1. Recurrent angina/ischemia despite intensive anti-ischemic rx

2. 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


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ICU

Start immediate Aspirin

Heparin or low-molecular-weight heparin

GP IIb-IIIa inhibitor

Adapted from Braunwald E, et al. 2002.


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


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ICU

Recurrent

Symptoms/ischemia

Heart failureSerious arrhythmia

Patient

stabilizes

EF .40Stress 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.


Ongoing Evaluation in an EarlyConservative Strategy

ACC/AHA Guidelines for Unstable Angina and


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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

angiography12-24 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 Rx

Braunwald. Circulation. 2002;106:1893-2000.


ACC/AHA Guidelines for Unstable Angina andNon-ST-Segment Elevation MI Acute

Ischemia Pathway


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ICU

UA/NSTEMI

High Risk *

ASA, Heparin/Enox., block., Nitrates, Clopidogrel

RISK STRATIFY

Low Risk

Braunwald E, et al.

Circ. 2002;106:1893.

* Recurrent isch emia; Trop; ST; LV failure/dys f.;hemodynamic instabi l i ty ; VT; pr ior CABG

Enox eparin . Preferred to UFH (IIa) I f coronary arter iography >24 hours

ACC/AHA REVISED GUIDELINES


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ICU

Braunwald E, et al.

Circ. 2002;106:1893.

LMCD, 3VD+LV Dys.,

or Diab. Mell.

CABG

High Risk

Cor. Arteriography

1 or 2VD, Suitable

for PCI Normal

Clopidogrel,

IIb/IIIa inhib.Consider Alternative

Diagnosis

Discharge on ASA, Clopidogrel, Statin, ACEI

PCI

ACC/AHA REVISED GUIDELINES


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ICU

I IIa IIb III

Braunwald. Circulation 2002;106:1893-2000.


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


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ICU

Tachydysrhythmias

Regular Irregular

Narrowcomplex 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


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ICUAfib


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ICUIncidence of Afib


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ICURisk Factors for Afib

MICU

Electrolyteabnormalities

High cardiac fillingpressures

Hypoxia

Comorbid heart

disease Sepsis

MOF

SICU

Post-ophypotension

Post-op sepsis Post-op pulmonary

edema

PA catheters

Blunt thoracictrauma


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ICUMorbidity of Afib in the ICU


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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


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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


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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


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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


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ICUAflutter


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ICUSVT or Flutter?

flutter


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ICU


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ICU


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ICUVtach


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ICUVfib


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ICUVtach


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ICUHyperkalemia


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ICUHyperkalemia


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ICUSummary

Review ACLS guidelines

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