Hello i am Brij Son Mishra Nursing profession today we will discuss about what is neonatal shock.? Type of shock, Clinical evalution and prevension and treatment.
DEFINITION AND PATHOPHYSIOLOGY: Shock is an acute state in which circulatory function is inadequate to supply sufficient amounts of O2 and other nutrients to tissues to meet metabolic demands. In most cases, cardiac output is low. In early shock, compensatory regional vasoconstriction (skin, skeletal muscle, splanchnic circulation) may temporarily maintain normal blood pressure and adequate blood flow to vital organs. As shock progresses, compensatory mechanisms fail and widespread cellular damage occurs. Insufficient O2 delivery to tissues causes anaerobic metabolism and lactic acidosis. If shock persists, irreversible injury to vital organs occurs; death ensues despite vigorous therapy that may temporarily return cardiovascular measurements to normal.
ETIOLOGY: A variety of factors, often in combination, may cause shock:
Hypovolemia (e.g., blood loss, inadequate placental transfusion, feto-maternal
transfusion, severe dehydration) Asphyxia (e.g., antepartum or intrapartum, respiratory failure, impaired oxygen
transport due to severe anemia or hemoglobinopathy) Cardiogenic causes (e.g., cardiomyopathy, dysrhythmia, congenital malformation,
hypocalcemia, severe hypoglycemia) Obstruction of venous return due to tension pneumothorax, excessive
ventilator pressures, cardiac tamponade Sepsis (especially early onset group B beta-hemolytic Streptococcal infection) Drugs (especially when hypovolemic infants, in whom blood pressure has been
Drug Dose Route Idication
DEFINITION AND PATHOPHYSIOLOGY: Shock is an acute state in which circulatory function is inadequate to supply sufficient amounts of O2 and other nutrients to tissues to meet metabolic demands. In most cases, cardiac output is low. In early shock, compensatory regional vasoconstriction (skin, skeletal muscle, splanchnic circulation) may temporarily maintain normal blood pressure and adequate blood flow to vital organs. As shock progresses, compensatory mechanisms fail and widespread cellular damage occurs. Insufficient O2 delivery to tissues causes anaerobic metabolism and lactic acidosis. If shock persists, irreversible injury to vital organs occurs; death ensues despite vigorous therapy that may temporarily return cardiovascular measurements to normal.
ETIOLOGY: A variety of factors, often in combination, may cause shock:
Hypovolemia (e.g., blood loss, inadequate placental transfusion, feto-maternal
transfusion, severe dehydration) Asphyxia (e.g., antepartum or intrapartum, respiratory failure, impaired oxygen
transport due to severe anemia or hemoglobinopathy) Cardiogenic causes (e.g., cardiomyopathy, dysrhythmia, congenital malformation,
hypocalcemia, severe hypoglycemia) Obstruction of venous return due to tension pneumothorax, excessive
ventilator pressures, cardiac tamponade Sepsis (especially early onset group B beta-hemolytic Streptococcal infection) Drugs (especially when hypovolemic infants, in whom blood pressure has been
maintained by vasoconstriction, are given vasodilators such as PGE1, isoproterenol or magnesium) Hypocarbia (severe)
CLINICAL EVALUATION: There are no clinical or laboratory findings specific to shock. The diagnosis is based on presence of several indicators of inadequate circulatory function. Various clinical and laboratory findings associated with shock include:
Cardiovascular findings:
Systemic arterial hypotension Narrow pulse pressure Central venous hypotension: with myocardial failure, central venous pressure is ↑ Tachycardia (In early asphyxia, bradycardia is present.) Respiratory findings:
Tachypnea Grunting respirations Retractions Apnea Other findings:
Prolonged capillary filling time Hypothermia Oliguria Metabolic Acidemia
TREATMENT: Specific therapy depends upon the cause of shock. Rapid recognition of shock and identification of underlying cause(s) are essential to prevent irreversible changes. With hypovolemia, intravascular volume must be increased, but cautiously
Volume replacement with blood or plasma expander should be in aliquots of 5 mL/kg every few minutes until circulatory function is adequate. Carefully assess the effects of volume replacement on heart rate, blood pressure, respiratory function, acid-base status and perfusion. After an adequate circulating blood volume has been achieved, replacement of other fluid deficits should be done more slowly, over several hours.
With asphyxial shock, treatment of respiratory failure with oxygen and assisted ventilation may be the only therapy needed. Do not give blood volume expanders during asphyxia as that will aggravate hypoxic myocardial failure. Alkali should be given only when there is significant metabolic acidemia (base deficit ≥ 10 mEq/L), the infant is receiving adequate assisted ventilation and PaCO2 is in the normal range. NaHCO3, given when ventilation is inadequate, leads to respiratory acidosis and may worsen the patient’s condition. THAMTM may cause apnea because of its effect of rapidly lowering PaCO2.
During resuscitation of an infant in shock, certain drugs are useful; these drugs, their indications, and their usual starting doses are listed in the table below. Dopamine is useful for treatment of infants in early shock as it is effective in raising systemic arterial blood pressure and often increases urinary output. Newborns in shock may require a dopamine dose of 30 mcg/kg/min or higher to obtain a pressor response. In contrast to older patients, such high doses of dopamine do not have adverse effects on urinary output in newborn infants. Dobutamine is less effective in newborns and often lowers blood pressure because of its vasodilating effects.Drug Dose Route Idication
Atropin 0.01ml/kg IV Sinus bradycardia
Calcium cloride10% 0.25mL/kg IV Hypocalcemia
Clcium gluconate 10% 1.0mL/kg IV Hypopocalcemia
Dopamine* 5.0 mcg/kg/min IV Hypotension low CO
Glucose 10% 1.3ml/kg over 2.5 min IV Hypoglycemia
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