shock comprehensive
TRANSCRIPT
NEONATAL SHOCK and HYPOTENSION
Steven M. Donn, M.D.
Professor of PediatricsDirector, Neonatal-Perinatal Medicine
C.S. Mott Children’s HospitalUniversity of Michigan Health System
SHOCK
•A complex clinical syndrome caused by an acute failure of circulatory function and characterized by inadequate tissue and organ perfusion.
CONSEQUENCES OF SHOCK
• Inadequate oxygen and substrate delivery
• Inadequate metabolic waste removal
•Cellular dysfunction and death•May involve isolated organs or
entire organism
PATHOPHYSIOLOGY OF SHOCK
•Decreased cardiac output•Diminished vascular
integrity• Inability of blood to carry
out necessary functions
CARDIAC OUTPUT
•Product of: heart rate X stroke volume•Neonatal CO depends more
on HR than SV•Compromised at high or
low HR
CARDIAC OUTPUT
HEART RATE STROKE VOLUME
SYMPATHETIC END DIASTOLIC VOLUME
PARASYMPATHETIC END SYSTOLIC VOLUME
Stroke Volume
To increase cardiac output
Increase stroke volume
or
Increase heart rate
or
Increase both
STROKE VOLUME
•Preload•Afterload•Contractility
PRELOAD
•Corresponds to myocardial end-diastolic fiber length
•Determined by volume of blood filling ventricles during diastole
• Increases in preload increase SV up to a maximum, beyond which SV falls (Starling’s Law)
Preload
Equals
End Diastolic Volume
Stroke volume
AFTERLOAD
•Force that the myocardium generates during ejection against systemic and pulmonary vascular resistances
•Reduction in afterload increases SV
Stroke volume
Afterload
is
End-systolic Wall Stress
or
Resistance
Effects of changes in afterload on Frank-Starling curves. A shift from A to B occurs with increased afterload, and from A to C with decreased afterload.
100
Stroke volume
(mL)
LVEDP (mmHg)
50
0
0 10 20
CONTRACTILITY
•Semi-quantitative measure of ventricular function
• Increased contractility increases SV if both preload and afterload are unchanged
ALTERING CARDIAC OUTPUT
•Clinically significant alterations in preload, afterload, and contractility can be achieved by use of vasoactive drugs, inotropic agents, or changes in blood volume.
BLOOD FLOW TO TISSUES AND ORGANS
• Influenced by local vascular beds• Controlled by local and central
vasoregulation• Pressure-passive with loss of
autoregulation• Biochemical mediators different
for each bed and poorly understood
BLOOD FACTORS
• Fetal hemoglobin• Temperature
• pCO2
• pH• Oxygen
extraction
INADEQUATE TISSUE PERFUSION
•Pump problem• Inadequate volume•Abnormalities in vascular
beds•Flow restriction• Inadequate oxygen-release
HYPOTENSION
•Blood pressure lower than the expected reference range
•On first day of life: MAP ≈ GA (??)
SYSTOLIC BLOOD PRESSURE
TISSUE OXYGEN DELIVERY
• Influenced more by cardiac output and blood flow than by BP
•“Statistically abnormal” BP may not be pathologic.
•Hypotension is not synonymous with shock.
MORTALITY AND MORBIDITY
•Shock is a major cause of neonatal mortality and morbidity.
•Because shock accompanies other primary conditions, specific figures are not available.
CAUSES OF NEONATAL SHOCK
Hypovolemic acute blood, fluid/electrolyte loss
Distributive sepsis, vasodilators, myocardial depression, endothelial injury)
Cardiogenic cardiomyopathy, heart failure, arrhythmia, myocardial ischemia
Obstructive tension pneumothorax, cardiac tamponade
Dissociative severe anemia, methemoglobinemia
RISK FACTORS
•Umbilical cord accident•Placental abnormalities•Fetal/neonatal hemolysis•Fetal/neonatal hemorrhage
RISK FACTORS (2)
•Maternal infection•Maternal
anesthesia/hypotension• Intrauterine/intrapartum
asphyxia
RISK FACTORS (3)
•Neonatal sepsis•Air leak syndromes•Lung overdistention•Cardiac arrhythmia
CLINICAL MANIFESTATIONS
•Prolonged capillary refill•Tachycardia•Mottling of skin•Cool extremities•Decreased urine output
STAGES OF SHOCK
•Compensated•Uncompensated• Irreversible
COMPENSATED SHOCK
• Perfusion to vital organs preserved• Minimal or absent derangement of
vital signs (HR, RR, BP, Temp)• Increased angiotension,
vasopressin, catecholamine release• Decreased spontaneous activity• Pallor, tachycardia, cool skin,
prolonged capillary refill
UNCOMPENSATED SHOCK
• Delivery of oxygen and nutrients becomes marginal or inadequate
• Anaerobic metabolism → lactic acid• Decreased myocardial contractility• Release of chemical mediators,
enzymes, histamine, cytokines, xanthine oxidase (free radicals), PAF, bacterial toxins
UNCOMPENSATED SHOCK (2)
•Decreased oxidative phosphorylation
•Failure of Na+-K+ pump•Disrupted capillary
endothelium•Plasma protein leak•Decreased oncotic pressure
UNCOMPENSATED SHOCK (3)
•Sluggish blood flow, platelet adhesion, DIC
•Falling BP, very prolonged capillary refill, tachycardia, cold skin, tachypnea, oliguria/anuria
IRREVERSIBLE SHOCK
•Retrospective diagnosis•Major vital organs
extensively damaged•Death despite circulatory
restoration
WORK-UP
• Hct, electrolytes, glucose, cultures• Blood gases (preferably arterial)• Mixed venous blood gas (reflects
oxygen extraction and waste products at tissue level)
• Plasma lactate, pyruvate• Specific studies to rule out both
causes and sequelae
IMAGING STUDIES
•Chest radiograph•Echocardiogram/Doppler flow•Other, as clinically indicated
TREATMENT
• Initiate supportive measures immediately
•Secure airway, provide oxygen, PPV
•Achieve vascular access• Infuse volume
TREATMENT (2)
•Determine type of shock• Insert bladder catheter•Measure hourly urine
output
EVALUATION OF SHOCK
HYPOVOLEMIC SHOCK
•Most common cause of shock in the newborn
•Key to successful resuscitation is early recognition and controlled volume expansion
•Blood volume: 80-85 mL/kg
HYPOVOLEMIC SHOCK (2)
Volume Depletion:
Compensated 25%Uncompensated 25-40%Irreversible > 40%
HYPOVOLEMIC SHOCK (3)
• Initial fluid: 20 mL/kg•Replaces 25% of blood
volume•Repeat if circulatory
insufficiency persists.
HYPOVOLEMIC SHOCK (4)
• Once half of the blood volume is replaced, titrate further fluid against CVP or clinical parameters.
• Crystalloid v. colloid controversy: most recent reports favor crystalloid.
• Whole blood or reconstituted components for hemorrhage
CARDIOGENIC SHOCK
• Most commonly after asphyxia, structural heart problem, arrhythmia
• Myocardial ischemia reduces contractility and causes papillary muscle dysfunction and tricuspid valvular insufficiency.
CARDIOGENIC SHOCK (2)
• Clinical findings: peripheral edema, hepatomegaly, cardiomegaly, murmur
• Initiate treatment with inotrope (with or without peripheral vasodilators)
• Treat arrhythmia, structural disease• Avoid volume overload
DISTRIBUTIVE SHOCK
•Most common form is septic shock
•Cardiac output may be normal, even elevated, but unable to be adequately delivered to tissues because of microcirculatory abnormalities.
DISTRIBUTIVE SHOCK (2)• Early compensated phase
Increased cardiac output Decreased systemic vascular
resistance• Cardiovascular performance
deteriorates.• Normal relationship between CO
and SVR breaks down leading to intractable hypotension/shock.
DISTRIBUTIVE SHOCK (3)
•Little cardiac reserve•Survival depends on
maintenance of hyperdynamic circulatory state.
•Treat underlying condition(s).
DISTRIBUTIVE SHOCK (4)
•Early treatment: volume expansion
•Later treatment: inotropes, with or without peripheral vasodilators
•Look for evidence of organ damage and treat accordingly.
MECHANISMS OF INJURY: SEPTIC SHOCK
VOLUME EXPANDERS
• Saline• Albumin (5%)• Plasma• Lactated
Ringer’s• Whole blood• Blood products
VASOACTIVE DRUGS Constrictors
• Dopamine• Dobutamine• Epinephrine• Norepinephrine• Vasopressin
VASOACTIVE DRUGS Dilators
• Isoproterenol• Nitroprusside• Phentolamine• Amrinone• Milrinone
Agent Type Agent Dosage Comments
Volume expanders
Isotonic sodium 10-20 mL/kg IV Inexpensive, available
Albumin (5%) 10-20 mL/kg IV Expensive
Plasma 10-20 mL/kg IV Expensive
Lactated Ringer solution 10-20 mL/kg IV Inexpensive, available
Isotonic glucose 10-20 mL/kg/ IV Inexpensive, available
Whole blood products 10-20 mL/kg IV Limited availability
Reconstituted blood products
10-20 mL/kg IV Use O Neg
Vasocative drugs
Dopamine 5-20 mcg/kg/min IV Never administer intra-arterially
Dobutamine 5-20 mcg/kg/min IV Never administer intra-arterially
Epinephrine 0.05-1 mcg/kg/min IV Never administer intra-arterially
Hydralazine 0.1-0.5 mg/kg IV q3-6h Afterload reducer
Isoproterenol 0.05-0.5 mcg/kg/min IV Never administer intra-arterially
Nitroprusside 0.5-8 mcg/kg/min IV Afterload reducer
Norepinephrine 0.05-1 mcg/k/g/min IV Never administer intra-arterially
Phentolamine 1-20 mcg/kg/min IV Afterload reducer
AGENTS USED TO TREAT NEONATAL SHOCK
DOPAMINE
• Endogenous catecholamine• Precursor of norepinephrine• Affects all three determinants of
cardiovascular function• Major action from increased
contractility and peripheral vascular resistance
DOPAMINE
• Beneficial renal effects • Increased RPF and GFR• Increased hypoxic threshold of renal
tubular cells• Increased Na and free water clearance
• Endocrine effects• Decreased prolactin• Decreased TRH
DOPAMINE
• Prolonged clearance in renal or hepatic dysfunction
• Adverse effects• Excessive increased afterload• Ectopic beats• Tachycardia• Hyponatremia• Vasoconstriction (peripheral, pulmonary)• Extravasation/soft tissue injury
DOPAMINE DOSING
• Low 1-5 mcg/kg/min (renal)
• Medium 5-10 mcg/kg/min (cardiac)
• High 10-20 mcg/kg/min (SVR)
DOBUTAMINE
• Synthetic catecholamine• Greater inotropic activity• Increased C.O. through increased
SVR• Most effective dose: 5-
15 mcg/kg/min• May decrease pulmonary vascular
resistance
DOBUTAMINE
• Adverse effects:• Systemic hypo- or hypertension• Ectopic beats• Ventricular tachycardia and other
tachyarrhythmias
• Contraindications:• IHSS• Atrial Fibrillation
BIPYRIDINES
• Non-sympathomimetic agents• Newer class of inotropes• Function as phosphodiesterase
inhibitors•Amrinone•Milrinone
BIPYRIDINES
• Cardiac relaxation• Decreased PVR and SVR• Dilation of coronary arteries• Decreased afterload
• C.O. increased by improving contractility without increasing myocardial oxygen consumption
BIPYRIDINES
• Possess inotropic and vasodilating properties
• Milrinone 10-30 times more potent than amrinone
• Major complication is hypotension• Side effects:
• Thrombocytopenia (dose-related)• Supraventricular and ventricular
dysrhythmias
PRESSOR-RESISTANT HYPOTENSION
• Insufficiency of hypothalamic-pituitary axis or adrenal glands
• Prolonged activation of sympathetic nervous system and exogenous catecholamines:• Down-regulation of CV adrenergic
receptors• Desensitization of CVS to
catecholamines
PRESSOR-RESISTANT HYPOTENSION
• Genomic effects• Steroid-responsive element on genes of
adrenergic receptors• Increased sensitivity to catecholamines
• Non-Genomic effects• Inhibition of catecholamine metabolism• Increased cytosolic calcium availability in
myocardial and vascular smooth muscle cells
PRESSOR-RESISTANT HYPOTENSION
• Defined by the instability of the cardiovascular status and severity of capillary leak syndrome in the critically ill infant
• Not defined by establishing arbitrary dose limits for the pressor treatment
ASSESSING BLOOD PRESSURE• TREAT THE BABY• Numbers are guidelines• Assess key elements of tissue
oxygen delivery:• Heart rate• Central venous pressure• Capillary refill• Urine output• Acid-base status
INTRACTABLE SHOCK
• If volume expanders and vasoactive/inotropic drugs do not correct shock, glucocorticoids may be effective.
• Steroids rapidly up-regulate cardiovascular adrenergic receptor expression and serve as hormone replacement therapy if adrenal insufficiency exists.
FURTHER CARE
• Complications and prognosis are related to both underlying causes and injuries sustained during period of inadequate tissue perfusion.
• Neurodevelopmental screening and follow-up, including imaging, BAER, and others is indicated.