Cardiogenic Shock : Where do we stand? Dr. Prasant Kr. Sahoo Consultant Cardiologist Kalinga...

Cardiogenic Shock : Where do we stand?

Dr. Prasant Kr. SahooConsultant CardiologistKalinga HospitalBhubaneswar

Structural mechanisms for cardiogenic shock

The key factor to cardiogenic shock is the amount of LV damaged

Ventricular damage and Heart Failure

25% LV affected : Heart failure manifested >40% ventricle affected:

Cardiogenic Shock

Aetiology of Cardiogenic Shock ( SHOCK registry)

Defining Cardiogenic Shock

Clinical CriteriaHaemodynamic Criteria

Diastolic Heart Failure

Impaired ventricular relaxation Decrease in passive ventricular distensibility Decrease in cardiac output is due to

inadequate ventricullar filling & not impaired systolic contraction

Ventricular hypertrophy, myocardial ischaemia with stunned myocardium, mechanical ventilation

Present in 40-50% of newly diagnosed cases of heart failure

Hemodynamic Alterations

The earliest sign of ventricular dysfunction is increase in cardiac filling pressures

The next stage is marked by a decrease in stroke volume & increase in heart rate

The final stage is characterized by decrease in cardiac output

Cardiogenic Shock:Clinical Criteria

Decreased peripheral perfusion # cold clammy skin # cyanosis # altered mental status # diminished urination ( <30ml/hr.)

Signs of Heart failure

Cardiogenic Shock :Haemodynamic criteria

SBP <80mmHg (less than 90mmHg if on inotropic agents / IABP)

Cardiac Index < 2.2L/min/m2

PCWP >18 mmHg

Killip Classification( Am. Jl. Card,1967;20,457)

Class Features Patients (%)

Death (%)

I No CHF 33 6

II S3,rales, CXR s/o CHF

38 17

III Pulmonary Oedema

10 38

IV Cardiogenic Shock

19 81

Diagnostic studies in Cardiogenic Shock

ECG Chest Xray Echocardiogram Haemodynamic monitoring Oxygen Saturation BNP

B-Natriuretic Peptide Released by ventricular myocardium in

response to ventricular volume & pressure overload

Plasma BNP >100pico/ml can be used as evidence of heart failure

Plasma BNP levels show direct correlation with severity of heart failure

Plasma BNP may be useful in monitoring clinical course of heart failure

ECG in Cardiogenic shock :How helpful ?

Infarct : type; location; old/fresh

Arrhythmias Aneurysm Pericardial Effusion

What to expect on CXR in pulmonary oedema ?

Acute Pulm. Oedema vs ARDS

Predicting Lt. atrial pressure from CXR

Pre oedema # upperlobe diversion / Kerley lines : 12-15 mmHg

Interstitial oedema # peribronchial cuffing : 15-20mmHg # hilar blurring : 19-24 mmHg

Alveolar blurring # bat’s wing shadowing : >25mmHg

Haemodynamic assesment

CVP line : unreliable, increase is only seen in later stages of right heart failure # poor reflection of LV function # limiting factors in lung disease # pulmonary embolism # RVMI

Swan Ganz catheter for PA pressures / PCWP : ideal

How useful is an Echo in Cardiogenic Shock ?

LV function (EF is normal in diastolic heart failure & reduced in systolic heart failure)

End diastolic volume will distinguish diastolic from systolic heart failure

Ventricular Septal rupture Degree of Mitral Regurgitation Tamponade Assesment of RV function Aortic Dissection

Echo in Right Heart Failure

Increase in right ventricular chamber size

Segmental wall motion abnormalities on the right

Paradoxical motion of IVS

Anterior wall MI

Mitral Regurgitation following MI

LV Aneurysm following MI

VSD following Acute MI

RVMI complicating IWMI

Management of Acute Pulmonary Oedema ( cardiac)

Posture & Oxygen Loop diuretics Nitrates Opiods ? Low dose Dopamine Dobutamine CPAP / Mechanical Ventilation

Management – Left-sided (systolic) Heart Failure

High PCWP/Low CO/High BP Nitroglycerine/Nitroprusside Vasodilation reduce afterload &

increase CO NTG – tolerance in 16-24 hrs Frusemide only if PCWP >20

Drugs in acute pulmonary oedema

Furosemide: 40-60mg initially, incremental doses 80-160mg. till diuresis

Nitroglycerine : 1-10mg/hr,titrate to achieve >30mmHg fall/ 30% fall / 105mmHg ( whichever is least)

Morphine: 3-5mg. Repeat at 15 mins. interval to total dose 15mg.

Management – Left-sided (systolic) Heart Failure

High PCWP/Low CO/Normal BP Ionodilators –Dobutamine/Milrinone Dobutamine increases O2

consumption Frusemide if PCWP >20 inspite of

NTG & Dobutamine

Role of Dobutamine as initial choice

May be deleterious as initial choice (furthur vasodilation in hypotensive patients)

Initial choice if SBP is approx. 90mmHg

Beneficial if excessive vasoconstriction present & elevated afterload

? Combination with Dopamine

Role of Phosphodiesterase inhibitors (Ionodilators )

Inotropic and vasodilator action Pts. Without adequate MAP may

not tolerate these drugs Little change in HR & BP Predispose to ventricular

arrhythmias

Milrinone : Tips for use

No evidence regarding efficacy beyond 48 hrs.

Dose: 50ug/kg bolus over 10 mins.followed by 0.375-0.750ug/kg/min

Contraindications: Acute MI;Tight AS;HOCM

Combination therapy: # with Dobutamine if BP is stable

# with high dose Dopamine if BP is low

Management – Left-sided (systolic) Heart Failure

High PCWP/Low CO/Low BP Dopamine/Noradrenaline to

increase MAP 60 mmHg Dopamine action is unpredictable &

can cause tachyarrhythmias Dobutamine IABP in post CABG/angioplasty

Inotropes in management of shock : Dosages

Inotrope Dose Clinical use

Dopamine 2.5-15 ug/kg/min renal vasodilator

Dobutamine 5-20ug/kg/min inotrope

Adrenaline Start 1-2ug/kg/min

Inotrope+ vasoconstrictor

Noradrenaline 1-10ug/kg/min Inotrope + vasoconstrictor

Use of Noradrenaline

If pt. is hypotensive even on large doses of Dopamine (>20ug/kg/min)

Caution # not for prolonged use # precipitation of tachycardia/ arrhythmias

Dopamine : dose related effects

Low doses (<4ug/kg/min): renal vasodilator

Intermediate doses ( 4-6 ug/kg/min) : enhances myocardial contractility

High doses ( >10ug/kg/min): vasoconstriction

Choice of Ionotrope in Cardiogenic Shock

SBP<70mmHg + clinical shock : Norepinephrine or Dopamine

SBP 70-100mmHg+clinical shock: Dopamine & then add Norepinephrine

SBP 70-100mmHg ;no clinical shock: Dobutamine

? Role of combination therapy

Management – Right (diastolic) Heart Failure

Incidence not known, may be associated with systolic heart failure

PCWP <15 – fluids till PCWP 20 If RVEDV <140ml/m2 – fluids PCWP>15, RVEDV 140–Dobutamine AV dissociation – sequential AV

pacing

Fluid challenge in MI

No pulmonary oedema on CXR # Ant. MI : 250ml # Inferior MI : 400ml Swan Ganz if no improvement

Based on PCWP # <18 mmHg : fluids # >18mmHg : Inotropes

Management of Cardiogenic shock

Establishment of diagnosis Intubation, Ventilation, oxygen

supplementation Swan Ganz catheterisation

# PCWP<18 : fluids # PCWP>18 : inotropes

Intra Aortic Balloon Pump (IABP) PTCA/CABG

Inotropes in HF : How they work?

Dopamine is beneficial as initial therapy of hypotensive patients in cardiogenic shock

How long to use Dopamine as initial agent?

Gradually uptitrate till SBP 90-100mmHg

If BP maintained with intermediate doses : think of adding Dobutamine

If high doses required: add Noradrenaline

Dobutamine: How it differs from Dopamine

No renal vasodilation Stronger beta2 effect

( arteriolar vasodilation)

Can dobutamine be the initial choice of therapy?

Device therapy for Cardiogenic Shock: A last resort ?

Use of IABP in Cardiogenic shock

Temporary haemodynamic stability

Bridge to revascularisation Hospital survival rates (IABP use,

without revascularisation):5-20

IABP : basic mechanism of action

Advantages of IABP in Cardiogenic shock

Increases CO by approx. 25% Reduces heart rate Enhances coronary perfusion Reduces LV filling pressure Prevents reocclusion of open

artery

Is there a role of early revascularisation in Cardiogenic shock ?

Cardiogenic Shock : Medical Trt. Vs Revascularisation ( SHOCK registry)

Septic Shock

Systolic BP <90mm Hg or MAP <60 mm

Drop in MAP >40 mm Hg in HTN

Organ hypoperfusion: signs? Unresponsive to IV fluids Dependant on pressors:

Dopamine/ Noradrenaline

Haemodynamic Profile in Shock

Hypovolemic Septic Cardiogenic

MAP

HR

CVP

PCWP

CO

SVR

Low Low Low

High High

Low Low / N / H High

Low High

LowLow

High High

High/l

Low / N / H

High / N / L

Low / N / H

Fluid Therapy

Fluid resuscitation may consist of natural or artificial colloids or crystalloids.

Grade C

Fluid Therapy

Fluid challenge over 30 min• 500–1000 ml crystalloid• 300–500 ml colloid

Repeat based on response and tolerance

Grade E

Vasopressors

Either norepinephrine or dopamine administered through a central catheter is the initial vasopressor or choice.• Failure of fluid resuscitation• During fluid resuscitation

Grade D

During Septic Shock

10 Days Post Shock

Diastole Systole

Diastole Systole

Images used with permission from Joseph E. Parrillo, MD

Inotropic Therapy

Consider dobutamine in patients with measured low cardiac output despite fluid resuscitation.

Continue to titrate vasopressor to mean arterial pressure of 65 mm Hg or greater.

Grade E

Steroids

Treat patients who still require vasopressors despite fluid replacement with hydrocortisone 200-300 mg/day, for 7 days in three or four divided doses or by continuous infusion.

Grade C