MANAGEMENT OF CARDIOGENIC SHOCKPRESENTED BY:DR.HIRDESH CHAWLAJUNIOR RESIDENT DEPARTMENT OF MEDICINEKGMU,LUCKNOW

A Case A 72 yrs old male is brought to the ED

with sudden onset chest pain,diaphoresis, nausea and dyspnoea

No other medical history is known. Is agitated upon presentation and is

unable to give any history.

A Case Vitals upon arrival: HR 135, BP 80/60,

RR>40, SpO2 62% on room air. Obese male in respiratory distress using

accessory muscles for respiration. Moist cool skin,mottled extremities Orthopnoea present Tachycardic heart rate ( gallop rhythm). Bilateral Diffuse rales upon pulmonary exam. ABG shows- alkalosis with hypocapnia

A Case

CXR

DEFINITION Persistent and marked hypotension(>30 minutes)

with systolic arterial pressure <90mm Hg Reduction in cardiac index ie <2.2

litres/min/m2(with inotrope and mechanical support)

Presence of elevated left ventricle filling pressure(PCWP>18 mm Hg)

Signs and symptoms of end organ hypoperfusion(cold extremeties,increased lactate,mental obtundation,oliguria)

Differentiating Types of Shock

Causes of Cardiogenic Shock

Predominant LV Failure74.5%

Acute Severe MR

8.3%

VSD4.6%

Isolated RV Shock3.4%

Tamponade/rupture

1.7%Other7.5%

Shock RegistryJACC 2000 35:1063

RISK FACTORS Extensive damage to left myocardium(large anterior wall

MI)->40% LV mass loss Age > 70 years SBP < 120 mmHg Sinus tachycardia rate > 110/min. Bradycardia rate < 60/min. Increased time from onset of STEMI H/O Hypertension, diabetes mellitus Multi vessel coronary artery disease Prior MI or angina Prior diagnosis of heart failure, STEMI Left bundle branch block.

DIAGNOSIS

CLINICAL FINDINGS Physical signs- Elevated JVP, Third heard sound , ,Oliguria, signs

of Acute pulmonary edema(rales),diaphoretic,apprehensive and pale

AUSCULTATION- Parasternal thrill WITH Pansystolic murmur : ventricular septal

ruptured

Mitral regurgitation murmur may be limited to early systole HOCM : systolic murmur- louder upon valsalva and prompt standing

Tachycardia or bradycardia Systolic BP<90mm Hg with narrow pulse pressure Tachypnoea and Cheyne stokes respiration

Hemodynamics- decreased CO,increased SVR, decreased SvO2

Initial evaluation- PA catheterization, echocardiography,angiography

LABORATORY PARAMETERS KFT- progressively deranged LFT-markedly elevated transaminases Increased lactate levels Anion gap metabolic acidosis

compensated by respiratory alkalosis Arterial hypoxemia Elevated CKMB , trop t ,trop i

ELECTROCARDIOGRAM Acute coronary syndrome : STEMI,

NSTEMI, RV infarction Cardiomyopathy Arrhythmia

IMAGING MODALITIES Chest Roentgenogram- 1. Pulmonary vascular congestion and pulmonary edema2. Widened mediastinum3. Cardiomegaly(silhouette can be normal)4. Pericardial effusion5. Bilateral pleural effusion Echocardiogram with colour doppler- 1. VSD,2. severe MR, 3. Aortic dissection with AR,4. PE or tamponade 5. Ruptured free wall6. RV infarct:RV dilation and asynergy,abnormal interventricular and interatrial

septal motion, right To Left shunting through PFO7.  Both PA systolic pressure and wedge pressure can be accurately estimated

with Doppler echocardiography, and in particular, the finding of a short mitral deceleration time (≤140 ms) is highly predictive of pulmonary capillary wedge pressure ≥20 mm Hg in CS

Right Ventricular Infarction: Diagnosis Clinical findings:Shock with clear lungs,Elevated JVPKussmaul sign ECG:ST elevation in R sided leads Echo:Depressed RV function

Modified from Wellens. N Engl J Med 1999;340:381.

V4R

PULMONARY ARTERIAL CATHETERIZATION Exclude other causes of shock Diagnosis of cardiogenic shock

1-PCWP > 15, CI < 2.2

2-Large V wave on PCWP, very high PCWP = severe MR

3-Step up in oxygen sat.from RA to RV,large V wave on RA pressure- Ruptured Ventricular septum

4-High right sided filling pressure in the absense of elevated PCWP(RA > 10 and > 80% of PCWP) = RV infarct

5-Classic sign of cardiac tamponade (equalization of diastolic pressure among the cardiac chambers) = free wall ruptured.

6. Low mixed venous O2 saturations and elevated AV O2 difference-low CI and high fractional O2 extraction

TREATMENT

CAUSES OF SHOCK IN MI Massive Acute Myocardial Infarction Left ventricular dysfunction Acute mitral regurgitation Ventricular septal rupture Right ventricular infarction Cardiac Tamponade Cardiac Rupture

TREATMENT MODALITIES TEMPORARY SUPPORT 1. VASOPRESSORS 2. MECHANICAL SUPPORT

PERMANENT MEASURES 1. FIBRINOLYSIS 2. Revascularization- PCI/CABG 3. Cardiac transplantation

GENERAL MEASURES Management of reversible cause

Maintain SBP>90mm Hg and PCWP>20mm Hg

Correct hypoxia,acidosis-ventilatory support if reqd.

Control arrythmias-brady or tachyarrythmias

Control hyperglycemia by insulin.

Induction of hypothermia if possible(increase inotropy,decrease HR,vasoconstriction)

Maximize volume in case of RV infarction(maintain PCWP 18-20 mm Hg and Right atrial pressure 10-14 mm Hg)

Aspirin and low dose heparin in MI

Defer clopidogrel if CABG planned bt mandatory if PCI is planned.

VASOPRESSORS

DRUG INITIAL DOSE

MAINTENANCE DOSE

COMMENTS

DOPAMINE 1-2 mcg//kg/min

4-5mcg/kg/min

2-4 mcg/kg/min

5-20 mcg/kg/min

Inotropy,vasodilation,tachycardia,hypotension,arrythmia

Inotropy,vasoconstriction,tachycardia,hypotension, arrythmia

NORADRENALINE 0.2-1.5mcg/kg/min Vasoconstriction,inotropy,tachycardia, less arrythmia

DOBUTAMINE 1-2mcg/kg/min 2-20mcg/kg/min. Inotropy,vasodilation,tachycardia,hypotension, arrythmia

EPINEPHRINE 0.05-0.5mcg/kg/min Vasoconstriction,inotropy,tachycardia,hypotension

VASOPRESSIN 0.1-0.4 units/min

LEVOSIMENDAN 12mcg 0.2 Mcg/kg.min Vasodilation,inotropy,tachycardia,hypotension

MILRINONE 25-75mcg/kg bolus

0.1-0.75mcg/kg/min Vasodilation,inotropy,tachycardia,hypotension

Clinical Signs: Shock, Hypoperfusion, CHF, Acute Pulm EdemaMost likely major underlying disturbance?

Acute Pulmonary Edema

Hypovolemia Low-output cardiogenic shock

Arrhythmia

AdministerFurosemideMorphine

Oxygen intubationNitroglycerin

DopamineDobutamine

AdministerFluids

Blood transfusionsCause-specific interventions Check Blood Pressure

Bradycardia

Tachycardia

Check Blood Pressure

Systolic BP (>100 mm

Hg)

Systolic BP <90mm Hg

(NO signs/symptoms of shock)

Systolic BP <90 mm

Hg(signs/symptomsof shock)

Systolic BP (<70 mm Hg + signs/symptoms

of shock)

Manage accordingly

ACE Inhibitors

Nitroglycerin Dobutamine DopamineNorepinephrine

Systolic BP

(>100 mm Hg)

24

MECHANICAL SUPPORT INTRA AORTIC COUNTERPULSATION VENTRICULAR ASSIST DEVICES EXTRACORPOREAL MEMBRANE

OXYGENATION(ECMO)

INTRA AORTIC BALLOON COUNTERPULSATION

INDICATIONS OF IABP

28

29

Interpreting IABP waveforms

30

- The end of the balloon should be just distal (1-2 cm) to the takeoff of the left subclavian artery

- Position should be confirmed by fluoroscopy or chest x-ray

Positioning

Inflation occurs at aortic dicrotic notch and deflation occurs immediately before systole for maximum augmentation in diastole and maximum systolic unloading

Timing is usually adjusted as 1:2(one inflation in 2 beats)

CONTRAINDICATIONS TO IABP Significant aortic regurgitation or AV

shunting Abdominal aortic aneurysm or aortic

dissection Uncontrolled sepsis Uncontrolled bleeding disorder Severe bilateral PVD Bilateral femoral popliteal bypass grafts

COMPLICATIONS OF IABP Cholesterol Embolization CVA Sepsis Balloon rupture Thrombocytopenia Hemolysis Groin Infection Peripheral Neuropathy

PERCUTANEOUS LEFT VENTRICLE ASSIST DEVICES Percutaneous device placed by cannulation of

femoral vein-left atrium via septal puncture Blood returned by nonpulsatile motor to

femoral artery Another is motorised device placed across

aortic valve Percutaneous LVADs may rapidly reverse the

hemodynamic compromise seen in patients with CS that is refractory to IABP and vasopressor support.

HEARTMATE BLOOD PUMP

Tandem Heart LVAD-Extracorporeal devices Left atrial-to-femoral arterial

LVAD Low speed centrifugal

continuous flow pump Maximum flow 4L/minute

The TandemHeart removes blood from the left atrium using a cannula placed through the femoral vein and into the left atrium via transseptal puncture.

Blood is then returned to a systemic artery, usually the femoral, with retrograde perfusion of the abdominal and thoracic aorta.

Intracorporeal devices

IMPELLA LP 2.5 & LP 5.0 Helical propellar-axial flow Minimally –invasive,percutaneous

catheter LVADs. Insertion similar to IABP but

device rests across the aortic valve,with the tip in the LV cavity.

FDA approved for high risk PCI,post PCI,cardiogenic shock,myocarditis &bridge to decision.

Impella Axial flow pump Much simpler to use Increases cardiac output & unloads LV

Maximum 5L flow

Pressure Lumen

Motor Blood outlet

Blood Inlet

iVAC 3L device The PulseCath iVAC 3L is a minimal heart

circulatory left ventricular assist device is indicated in cases of left heart failure due to

acute myocardial infarction, as well as transitory heart dysfunction post-cardiac surgery.

Pulsatile blood flow (e.g. echocardiograph triggered) of up to 3 l/min should be obtained via an extracorporeal dual chamber membrane, with an unidirectional flow warranted by a two-way valve.

INDICATIONS FOR MECHANICAL CIRCULATORY SUPPORT BRIDGE TO RECOVERY-Cardiogenic

shock refractory to optimal medical management and reasonable expectation that myocardial injury is reversible and temporary(acute MI,acute myocarditis, postcardiotomy cardiogenic shock.

Contd. BRIDGE TO TRANSPLANTATION:-

Refractory to OMM in whom myocardial function is unlikely to recover(Long standing ischemic,valvular cardiomyopathy,severe acute MI or myocarditis)

Placed in patients with significant heart failure symptoms and on inotropes or with limiting symptoms at rest with preserved end organ perfusion

DESTINATION THERAPY:- ineligibility for heart transplantation, NYHA IIIB or IV for 45 of 60 days despite

OMM, LVEF <25%

COMPLICATIONS Damage to aortic wall Ischemia distal to site of insertion Thrombocytopenia Hemolysis Atheroemboli Infection Mechanical failure SIRS Use with caution in pts. Already had fibrinolytic

therapy

EXTRACORPOREAL MEMBRANE OXYGENATION

Introduction A procedure in which blood is taken

from a patient's circulation to have a process applied to it before it is returned to the circulation.

VENO ARTERIAL ECMO The drainage cannula is commonly

placed in IVC(via IJV or Femoral vein)

Blood is returned to patient through cannula in ascending aorta(central) or femoral artery(peripheral)

Bubble oxygenator

This type of oxygenator is used when CPB is needed for less than 2hours

In this, O2 is directly infused into a column of systemic venous blood through a diffusion plate

Membrane oxygenator

This type of oxygenator is used when CPB is needed for more than 2-3 hours

In this type of oxygenator, gas doesn’t come in direct contact with the blood

FIBRINOLYTIC AGENTSAGENT FIBRIN SPECIFICITY FIBRINOGEN

DEPLETIONANTIGENIC PATENCY RATE

Tenecteplase ++++ Minimal No 85%

Reteplase ++ Moderate No 84%

Alteplase ++ Mild No 73-84%

Streptokinase No Marked Yes 60-68%

DOSE OF FIBRINOLYTIC AGENTS Streptokinase- 1.5 million units IV given over 30-60 min.

Alteplase- bolus of 15 mg, infusion of 0.75mg/kg for 30 min. then 0.5 mg/kg for next 60 min.(total dose not to exceed 100 mg)

Reteplase- 10 units +10 units IV boluses 30 min, apart

Tenecteplase- single IV bolus1. Wt.<60kg-30 mg bolus2. 60-69 kg- 35 mg bolus3. 70-79 kg- 40 mg bolus4. 80-89 kg- 45 mg bolus5. >=90 kg- 50 mg bolus

Timing of PCI

As in MI without shock, earlier revascularization is better in CS(<75 years-class I,>=75 yrs-class IIa)

Presentation 0 to 6 hours after symptom onset was associated with the lowest mortality among CS patients undergoing primary PCI

In the SHOCK trial, there appeared to be increasing long-term mortality as time to revascularization increased from 0 to 8 hours.

However, there is a survival benefit as long as 48 hours after MI and 18 hours after shock onset

JAMA.2006;295:2511–2515.

Circulation. 2004;110:588–636

SHOCK TRIAL The SHOCK (Should We Emergently

Revascularize Occluded Coronaries for Cardiogenic Shock) trial gave 30-day and 6-month mortality rates after CABG of 47% and 50%, respectively, for patients

in cardiogenic shock. These rates were 56% and 63% with medical therapy alone.

CARDIAC TRANSPLANTATION (1) cardiogenic shock requiring mechanical support or

high-dose inotropic or vasopressor drugs (in which case the irreversibility of their course is usually clear);

(2) chronic progressive, refractory, or stage D heart failure symptoms despite optimal therapy;

(3) recurrent life-threatening arrhythmias despite maximal interventions, including implanted defibrillators;

(4) refractory angina without potential for

revascularization.

VENTRICULAR SEPTAL RUPTURE Incidence 1-2% Timing 2-5 days post MI Murmur +nt in 90% Thrill common Echo doppler - shunt PA cath O2 step up > 9% Treatment-IABP,Inotropic support Surgery usually within 48 hrs Mortality high in infero basal defects than in

antero apical defects.

FREE WALL RUPTURE Incidence: 1-6% Occurs during first week after MI Classic Patient: Elderly, Female,Hypertensive Early thrombolysis reduces incidence but

Late increases risk Echo: pericardial effusion, PA cath: equal diastolic pressure Treat with pericardiocentesis and early

surgical repair

J Am Coll Cardiol. 2000;36:1063–1070.

ACUTE MITRAL REGURGITATION Incidence: 1-2% Most often due to posterior Papillary rupture Echo for Differential Diagnosis:– Free-wall rupture– VSD– Infarct Extension PA Catheter: large v wave Afterload Reduction IABP Inotropic Therapy Early Surgical Intervention

J Am Coll Cardiol. 2000;36:1063–1070.

Management of Special Conditions The treatment of certain conditions that lead

to CS is marked by important differences from management of CS due to LV failure.

The recognition of LV outflow obstruction is critical in patients with hypotension, because diuretics and inotropic agents exacerbate obstruction.

Treatment of CS with hypertrophic obstructive cardiomyopathy includes volume resuscitation and beta-blockade.

THANK YOU