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