shock comprehensive

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.