Shock is a clinical syndrome in which there is an acute circulatory dysfunction leading to insufficient oxygen delivery to tissues and endorgan dysfunction.
Physiology of Shock :
Cardiac output is the most important determinant of tissue perfusion (volume of blood ejected by the heart per minute). It is the product of stroke-volume and the heart rate (CO= Stroke volume x Heart rate)
In young children and infants, the elevation of heart rate is the most important compensatory mechanism for increasing cardiac output.
Stroke-volume is determined by the pre-load, after-load and myocardial contractibility.
the volume of blood filling the ventricle at the onset of
diastole (ie. Venous return). So any reduction in the circulating
blood volume (hypovolemia) or an increase in the venous
capacitants as seen in distributive shock or an increase in
intrathoracic pressure which results in decreased venous return to
heart, decreases stroke volume and cardiac output.
- Myocardial Contractibility: can be affected by primary myocardial disease as well as other factors like acidosis, hypoxia, toxins, sepsis etc.
- Afterload : Is the force that the ventricles must overcome in order to eject blood and determined by the systemic vascular resistance. Increase in systemic vascular resistance causes an increase in the work of heart and decrease in cardiac output.
Causes of Shock
Hypovolemic Shock : arises primarily because of loss of preload as in diarrhea, vomiting or acute blood loss. Relative hypovolemia occurs secondary to peripheral pooling of blood volume and ‘third space’ losses as seen in septic shock.
Cardiogenic Shock: Is secondary to myocardial dysfunction: it can occur in all forms of prolonged shock regardless of aetiology. Among the commonest cause of cardiogenic shock encountered is severe sepsis. (this is contrary to the belief that cardiogenic shock occur on children with primary heart disease). Cardiogenic shock is best viewed as a pump failure resulting from decreased myocardial contractility leading to symptoms attributable to both a reduction in cardiac output and pulmonary congestion. This is often associated with a compensatory increase in systemic vascular resistance which has more deleterious effect on the failing heart. In addition to the usual features of hypoperfusion, these children will usually have chest retractions, grunting, gallop rhythm, raised JVP, hepatomegaly, basal crepitations and heart murmur.
Distributive Shock : Is characterized by vasodilation and capillary leak causing relative and absolute hypovolemia (more seen in septic shock and anapylaxis)
Septic shock : is a combination of distributive, cardiogenic and hypovolemic shock.
Early Septic Shock (warm shock): consist of a hyperdynamic state with increased cardiac output and low systemic vascular resistance. This is identified by the presence of
- Hyper or hypothermia (>38.50C or <360C)
- Tachypnoea / tachycardia
- Warm extremities, wide pulse pressure
- Flash CFT , Bounding pulses
- Normal / high BP
- Altered mental status
(Tachypnoea, disproportionate tachycardia and altered mental status in a febrile child should alert a physician to suspect warm shock)
Late Septic Shock: is easy to diagnose. Airway instability, bradycardia, cold extremities, absent peripheral pulses, delayed CFT, hypotension, progressive worsening of mental status and anuria are the features of decompensated shock.
Clinical progression and stages of shock
Shock is a progressive disorder. The progression may be fulminant as in massive hemorrhage or involving over a span of hours. This progression has been arbitrarily divided into 2 stages.
1) Early shock (compensated)
2) Progressive shock (decompenstated)
In early “compensated” shock vital organ function is maintained by intrinsic compensatory mechanisms, such as venoconstriction and peripheral vasoconstriction. Blood pressure is usually maintained, heart rate is increased, pulse pressure is narrow and signs of peripheral vasoconstriction (cold extremities and prolonged CFT) are present.
In decompensated shock, shock persists and despite intense arteriolar constriction and tachycardia, blood pressure and cardiac output declines. Patient may demonstrate impairment of major organ perfusion which may manifest as altered mentation, oliguria and myocardial ischemia.
Irreversible shock is a stage characterized by a progressive reduction in blood pressure and cardiac output leading to prolonged hypoperfuison of brain, heart and kidneys which leads to ischemic cell death in these organs with progressive worsening of coma, renal failure, pulmonary edema and ARDS (“shock not only stops the machine but also wrecks the machinery”).
Recognition and Assessment
Early recognition and management of shock is possible by doing a rapid cardiopulmonary assessment of a critically ill child using the ABC approach.
Assess if airway is i) patent ii) maintainable with positioning, suctioning etc. iii) or requires intervention such as intubation.
B. Breathing (assessed by)
Respiratory rate : often increased in shock to compensate for metabolic acidosis
Work of Breathing : Often normal in shock , which is referred as quiet or effortless tachypnoea. If associated with increased work of breathing suspect cardiogenic shock.
C. Circulation : (assessed by)
a) Heart Rate: Tachycardia is the earliest sign of shock to compensate for the decreased cardiac output
b) Pulse volume : weak distal pulses caused by peripheral vasoconstriction which occurs as a compensatory measure to preserve blood flow to vital organs such as brain, heart etc. In early septic shock with a high output state pulses are bounding.
c) Core- peripheral temperature difference > 20C is a sign of poor skin perfusion.
d) Capillary Refill Time : Prolonged CRT is seen in shock (more than 2 seconds)
e) Blood Pressure: Shock can occur in the presence of low / normal / high BP. Children’s cardiovascular system compensates well initially in shock- so hypotension is a late sign of shock
f) Skin colour : mottling, pallor etc indicate poor skin perfusion
g) Liver Span : Increased in cardiogenic shock ; also helps in assessing the fluid overload during the treatment of shock
h) Urine output : Normal urine output of 1-2 ml / kg/ hour is a reassuring sign of normal renal perfusion in shock
i) Cerebral Perfusion : assessed by AVPU Scale.
The first hour is considered as the ‘Golden hour’ and shock should be aggressively managed during this period, which involves securing a patent airway, administration of oxygen and establishment of intravenous access.
Oxygen : all children in shock should receive, high flow oxygen irrespective of oxygen saturation as they all have tissue hypoxia.
Breathing: Respiration should be supported by bag and mask or ventilatory assistance. Indications for intubation in shock are
a. rapidly progressive shock
b. GCS < 8
c. Severe pulmonary oedema
d. Cardiogenic shock
e. Severe metabolic acidosis
Vascular access must be rapidly established either by IV route or by intra-osseous route. Subsequently a central venous line may be required for CVP monitoring, vasoactive medications and to provide a more stable form of vascular access.
Fluid Therapy : Shock of all etiologies should be treated with isotonic fluids (Ringer lactate / N.Saline), which will augment the pre-load.
Here the fluid should be given rapidly as boluses of 20ml of N.Saline / R.Lactate. Child should be reassessed and if signs of shock persist multiple boluses are given often upto 40-60ml/ kg. Generally a child with hypovolemic shock responds to 2-3 boluses.
Patients with cardiogenic shock usually have normal or increased intravascular volume. An initial bolus of normal saline 10ml / kg over 20minutes should be given monitoring liver span and signs of fluid overload. If signs of fluid overload develops fluids should be stopped and inotrops to be started. CVP monitoring is very essential to protect against fluid overload. Dopamine is indicated when blood pressure is low and dobutamine is preferred when the blood pressure is normal or high. Both are started at 10 µgm/ kg/mt and titrated according to patient’s response. If resistant to dopamine/dobutamine afterload reducing agents (vasodialators) can be used. Correction of metabolic disturbances such as acidosis, hypoglycemia, hypocalcemia etc is also important to improve myocardial contractility
Septic Shock :
Septic Shock is characterized by severe vasodilatation and capillary leak with resultant hypovolemia requiring aggressive volume replacement. Some children might require fluids up to 200ml / kg in the first hour. Continuous monitoring of the heart rate, respiratory rate, peripheral perfusion, BP, GCS and urine output is essential. If liver span or work of breathing increases, fresh rales appear or gallop rhythm occurs more fluid is not advised even if the shock persists. Then dopamine infusion is started and the airway is rapidly secured and early ventilation is initiated.
Documented hypoglycemia and hypocalcemia should be corrected promptly.
Children with fluid refractory shock, require vasoactive support; dopamine is the first line drug started at 10- 15µgm/ kg/ minute at 15 minutes. If fluid refractory shock persists with high BP, dobutamine may be started. Dopamine and dobutamine resistant shock must be recognized quickly and at 45 minutes epinephrine is started for cold shock and noradrenaline for warm shock. Where shock persists with normal or high BP, after load reducing agents such as nitroglycerine or inodilators such as amrinone and milrinone are used.
In catecholamine resistant shock, considering the possibility of adrenal insufficiency, hydrocortisone 2mg/kg as a bolus followed by 2mg/kg infusion over 24 hours is given as per PALS guidelines.
VASO ACTIVE MEDICATIONS
All shock states, even hypovolemic have some form of impairment of myocardial function and use of vasoactive therapy to optimize cardiac output is therefore the cornerstone of shock therapy. In general, these drugs should be used once the volume resuscitation has been achieved.
Inotrops are the drugs, which improve myocardial contractility, very useful in cardiogenic and fluid refractory shock.
Dopamine: is the most commonly used vasoactive agent and is recommended as the first line agent in fluid refractory septic shock and for hypotension after resuscitation from cardiac arrest. It is usually started at 10 µg/kg/mt and then titrated to effect till 20 µg/kg/mt is reached. If there is no response adrenaline is started.
Dobutamine : is preferred in cardiogenic shock because it is a very selective stimulant of β1 receptors. It is used in normotensive/ hypertensive shock; often started at 10µg/kg/mt, it is titrated to response.
Adrenaline: is preferred in post arrest shock states, cardiogenic shock not responding to dobutamine and septic shock. It is started at 0.1 µg/kg/mt and titrated to effect.
Noradrenaline: is useful in warm septic shock because of its µ - adrenergic effect ; also used in spinal shock and anaphylaxis.
Vasodilators: reduce systemic and pulmonary vascular resistance, thus the ventricular after load, which improves stroke volume and cardiac output (eg: nitroglycerine, nitroprusside etc)
Preparation of vasoactive agents
Inodilators: combine inotropic stimulation of heart with vasodilatation of systemic and pulmonary vascular beds. These drugs increase cardiac output with little effect on myocardial oxygen demand and produce little change the heart rate; particularly useful in the treatment for cardiogenic shock and selected children with septic shock. Amrinone and milrinone come under this group. The dose of milrinone is 50-75 µg/kg/mt as loading dose followed by continuous infusion of 0.5 – 0.75 µg/kg/mt.
Vasopressin: is being considered in patents whose septic shock is refractory to fluid and high dose of vasopressor therapy. The effect of vasopressin include systemic vasoconstriction but with vasodilation of cerebral and pulmonary vessels ; it also enhances the sensitivity of vasculature to catecholamines and stimulates cortisol secretion (dose : 0.0003 – 0.008 µg/kg/mt)
Correction of metabolic abnormalities
a. Acidosis must be partially corrected, if the base defect is more than
6 meq/L with Sod. Bicarbonate
b. Hypocalcemia can impair the myocardial function and should be
corrected in case of documented hypocalcemia
c. Hypoglycemia is very common in shock states and should be
corrected with1-2 ml/kg of 25% dextrose
d. Electrocyle abnormalities : hyponatremia, hypernatremia, hyper and
hypo kalemia should be corrected.
Supportive therapy to prevent/ treat organ dysfunction
Antibiotics in septic shock:
Broad spectrum bactericidal antimicrobials should be administered when sepsis is suspected (cefotaxime/ceftriaxone or piperacillin tazobactum + aminogycoside/ vancomycin)
Shock is a medical emergency. Early identification and management is essential to prevent progression to multiorgan dysfunction syndrome. (MODS)The conventional goals of resuscitation with “ABC”- for airway, breathing and circulation, aggressive fluid therapy with vasoactive support, protection of various organ systems and correction of metabolic functions will improve the outcome of shock.