Special clinical situations and

management of cardiogenic shock

Paola Cogo
Ospedale Pediatrico Bambino Gesù
Rome
 Physiopathologic classification
• Contractile dysfunction
• Volume overload
• Left-right shunts

• Pressure overload
• Systemic outflow obstruction

• Decreased pulmonary blood flow

• CHD with Right-Left shunts

• Parallel circulation
• Transposition of the Great Arteries
Hypoxia

• Single ventricle
Cyanosis &/or LCOS
Myocardial dysfunction

• Hypoxia
• Sepsis
• Myocarditis
• Supraventricular Tachycardia (TPS)
• Anomalous origin of coronary arteries
• Metabolic cardiomyopathy

Maintain volume load, correct anemia, titrate inotrops

Correct metabolic acidosis
Excessive left to right shunts

• AV fistula
• Aorto-pulmonary window
• Truncus arteriosus
• AV-canal
• Ventricular septal defect
• Large PDA
• Unobstructive TAPVR
Maintain volume load, correct anemia, titrate inotrops
Correct metabolic acidosis
Right volume overload Management

 Diuretics
 Optimize cardiac output CO
 Inotrops
 Optimize hemoglobin
 Titrate pulmonary and systemic vascular resistance
 Systemic vasodilators
 Increase pCO2 by controlled hypoventilation
 Low FiO2
 Decreased pulmonary blood flow
Pulmonary atresia-intact VS
Pulmonary Atresia + VSD
Critical Pulmonary Valve Stenosis
Tetralogy of Fallot

Hypoxia
 Tetralogy di Fallot

EKG: right ventricular

hypertrophy
X-ray: shoe heart
Echocardiogram:
coronary pattern,
pulmonary arteries anatomy
Aortic Arch (left or right)
MAPCAS
Management of decreased pulmonary blood flow

Minimize right ventricle overload

 Prostaglandin
 Sedation (morfina, 0.15 mg/Kg)

 O2 therapy (hyperoxia test)

 Intubation if SaO2 <75%
 B blocker propanololo 0.05-0.1 mg/kg, esmololo 50 mcg/kg/min
 a-agonisti vasopressors(vasopressine 0.0005 U/kg/min, pheenilephrine 0.5-3 mcg/kg)
Acute obstruction of the systemic outflow

 Critical Aortic Stenosis

 Aortic Coartation
 Interrupted Aortic Arch
 HLHS

Arterial hypotension occurs late in the disease course

Left ventricle pressure overload: management

Early diagnosis and rapid management

Increase systemic blood flow
Prostaglandin
Inotrops
No vasodilators
Intubation and mechanical ventilation
Diuretics after hemodynamic stability
Don’t use high FiO2
Correct metabolic acidosis with Na HCO 3
Pathogenesis of heart failure
 LCOS diagnosis
Clinical signs Indagini strumentali:
Tachycardia
Oliguria
Delayed refill time Chest x-ray
Arterial hypotension Ecocardiography TT, TE
↑Δ central-peripheral temp
Acidosi
↑ base excess> 4
↑ lattate >2 mmol/L Monitoraggio:
in 2 consecutive samples

SaO2-SvO2 > 30%

SaO2-SvO2/SaO2 >0,5

SvO2 >50%
Proactive management

• Anticipate a particular clinical course

• Perceive an evolving clinical picture
• Change management early during the
perioperative period
“no drug specific treatment”

Oxygen
Oxygen transport
consumption
sedo-analgesia
Hemoglobin > 12 g/l
T° control
PaO2 ventilation
cooling
CO
(inotrops, mechanical Mechanical
assistance) ventilation sedation
and paralysis
 Guidelines
0 min
Recognize
Recognize decreased
decreased mental
mental status
status and
and perfusion.
perfusion.
Maintain
Maintain airway and establish access according to PALS
airway and establish access according to PALS guidelines.
guidelines.
5 min
Push
Push 20ml/kg
20ml/kg isotonic
isotonic saline
saline or
or colloid
colloid boluses
boluses up
up to
to and
and over
over 60
60 ml/kg
ml/kg
15 min Correct hypoglycemia and hypocalcemia. Give antibiotics after coltures
Correct hypoglycemia and hypocalcemia. Give antibiotics after coltures

Fluid refractory shock

Establish
Establish central
central venous
venous access,
access, begin
begin
dopamine
dopamine therapy
therapy and
and establish
establish arterial
arterial monitoring
monitoring ..

Fluid refractory-dopamine resistant shock

Titrate
Titrate epinephrine
epinephrine for
for cold
cold shock,
shock, norepinephrine
norepinephrine for
for warm
warm shock
shock to
to normal
normal
60 min MAP-CVP
MAP-CVP andand SvC
SvC O2
O2 saturation
saturation >> 70%70%

Briedly J CCM 2009

 Catecolamines resistent shock
Begin hydrocortisone
if at risk of
absolute adrenal
insufficiency

Normal BP cold shock Low BP cold shock Low BP warm shock

ScvO2 Sat <70% ScvO2 Sat <70% ScvO2>70%

Add vasodilator or
Type III Titrate volume Titrate volume
phosphodiesterase and epinephrine and norepinephrine
Inhibitor with volume load

Persistent cathecolamines resistant shock

Start cardiac output measurement and titrate therapy to obtain a CI > 3.3 and < 6 L/min/mq
Refractory shock Consider ECMO
 Cardiotonic agents
Catecholamines
• Endogenous
• Dopamine
• Epinephrine
• Norepinephrine
• Synthetic
• Dobutamine
• Isoproterenol
• Fenoldopam
Regulation of contractile function of the myocites

Hunter J NEJM 1999;341:1276

 Catecholamines & hemodynamic effects

Drug CO Contr HR SVR MAP PCWP

Dopamine ↥↥ ↥ ↥ ↥↔ ↥↔ ↥↔
↧
Dobutamine ↥↥ ↥↔ ↥ ↔ ↧↧ ↧↔ ↔
Isoproterenol ↥↥ ↔ ↥ ↥ ↧↧ ↧ ↧
Epinephrine ↥↥ ↥ ↔ ↥↔ ↥↔ ↥↔
↥↥ ↧
Norepinephrine ↥↔ ↥ ↥/↥ ↥↥ ↥↔ ↥↔
↧ ↥ ↥
Adverse effects of catecholamines

• Arrhythmogenesis
• Excessive chronotropy
• Increased O2 myocardial consumption
• Down-regulation of b adrenergic receptors
• Increased afterload which can raise impedance and decrease cardiac
output
• Increased intracellular calcium and induced apoptosis
Phosphodiesterase (PDE) inhibitors

• PDE is the enzyme responsible for the breakdown

of 3’5’ cyclic AMP. The fraction III is the
predominant form in cardiac and vascular smooth
muscle.
• PDE inhibitors ⇑ cAMP ⇒ ⇑ intracellular Ca2+ ⇒ ⇑
inotropism and ⇑ increased vasodilation
• Increased lusotropy or increased relaxation of the
ventricle during diastole
• Independent action from b-receptors
Regulation of contractile function of the myocites

Hunter J NEJM 1999;341:1276

Vasodilators
Indications

• Myocardial dysfunction secondary to dilated cardiomiopathy,

coronary insufficiency, cardiac surgery
• Systemic or pulmonary hypertension
• Valvular regurgitation leading to volume overload
 Vasodilators
• I.V. Vasodilators
• Nitroglycerin
• Sodium nitroprussiate
• Hydralazine
• Calcium antagonist
• Oral vasodilators
• Captopril
• Enalapril
Vasodilators hemodynamic effects

Drug CO PVR HR SVR MAP PCWP

ACE inhibitors ↥ ↥↔ ↔ ↧↧ ↥↔ ↥↔↧
Calcium ↥↔ ↧ ↥ ↧↧ ↧ ↧↔
Antagonist
Hydralazine ↥ ↧↔ ↥↥ ↧↧ ↧↧ ↧
↧
Nitroprussiate ↥ ↧↧ ↥↔ ↧↧ ↧ ↧
Nitroglycerin ↥ ↧ ↥↔ ↧ ↧ ↧↔
Neonatal myocardial dysfunction: inotropic drugs

 Dopamine (3-10 mg/kg/min)

 Dobutamine (5-20 mg/kg/min)
 Phosphodiesterase Inhibitors
(Milrinone, Enoximone) 0.75 -0.50 mg/kg/min
 Epinephrine (0.01-0.2 mg/kg/min)
 Calcium (5-10 mg/kg/h)
 Nitroprussiate 0.5-3 mg/kg/min
Conclusions
• CHD newborns are patients at high risk with increased morbidity and
mortality in the first few days of life
• The outcome is affected by flow and O2 delivery alterations during the
fetal life and in the immediate postnatal period.
• Early and accurate diagnosis of CHD and comorbidities is essencial for the
optimal neonatal care
• A multidisciplinary approach is the best way to improve mortality and
morbidity in CHD patients
Thank you!