Chapter 1 Shock
Clinically shock is defined as an entity showing signs of collapse following under-perfusion of cells and tissues.
Physiologically it is a state following upset of homeostasis between blood volume and vascular capacity. Disparity between blood volume and vascular capacity can be produced by:
- Reduction in blood volume
- Increase in the vascular bed
- By both the above mechanisms.
- Pinched face, shunken eyes, cold clammy skin
- Deadly pallor
- Rapid thready pulse
- Shallow sighing respiration
CLASSIFICATION OF SHOCK: (SEE TABLE 1.1)
STAGES OF SHOCK
- Early compensated shock
- Progressing “decompensated shock”
- Irreversible shock.
Shock, regardless of its cause, initiates a series of pathophysiological changes aimed at protecting the organism and preserving its vital functions as follows.
The fall in blood pressure due to inadequate cardiac output is sensed by the stretch receptors located in the aortic arch and carotid sinus with the consequent sympathoadrenal stimulation.
- The Vasomotor Center (VMC) activity is increased resulting in an enhanced peripheral resistance and the blood pressure is maintained. The heart rate increases (H.R. 1/BP Mary's Law) to restore the cardiac output.
- The reflex increase is sympathetic activity is further augmented by stimulation of peripheral (carotid and aortic bodies) and central (ventral surface of medulla) chemoreceptors. Hypoxia (O2 Lack) is the main stimulus to peripheral chemoreceptors whereas changes in pH have predominantly central effects.
The increased sympathetic cardiac activity increases the rate and strength of myocardial contraction. The arteriolar constriction is selective. The blood flow to skin, skeletal muscle, salivary glands, intestines, liver, and kidneys is reduced. The skin becomes cold, salivary secretion stops and mouth becomes dry, intestines manifest impaired digestion and water absorption.
However, blood flow to essential organs like brain, heart, diaphragm and intercostal muscles is maintained.
In case of true or apparent (e.g. sepsis, anaphylaxis, etc.) hypovolemia, there will be increased secretion of ACTH, growth hormone, glucagon, ADH, catecholamines and cortisol.
ADH helps in the reabsorption of H2O from the distal renal tubules. Glucagon stimulates gluconeogenesis and glycogenolysis thereby causing hyperglycemia and increased osmolarity which helps in the fluid shift from the interstitium to the intravascular compartment.
Activation of the Renin Angiotensin System
Due to decreased renal blood flow there is secretion of renin from the juxtaglomerular apparatus which leads to the formation of angiotensin, a potent vasoconstrictor which stimulates aldosterone secretion resulting in Na and H2O retention and increase of blood volume.
Due to intense sympathoadrenal and neuroendocrine response following hypovolemia there will be selective diversion of blood flow through meta-arteriolar shunt or thoroughfare channels as the closure of pre-and post- capillary sphincters occur (Fig. 1.1).
In the irreversible phase of shock, there is relaxation of the precapillary sphincters while postcapillary sphincters remain constricted and blood gets sequestrated in the microcirculatory unit.
The cellular changes are due to ischemia. Lack of oxygen and accumulation of waste products cause cell membrane dysfunction. Thus in muscle, the resting transmembrane potential can change from −90 to −60 mV.
Na and H2O enter the cell and K leaves it, which results in cellular swelling. Mitochondrial dysfunction occurs in prolonged shock, which will cause diminished ATP production. There is also lysosomal disruption with resultant release of lysosomal enzymes and intracellular autodigestion occurs. Widespread cellular damage may lead to multiorgan dysfunction syndrome (MODS).
Thus, the final pathway of shock is cell death. When large numbers of cells from vital organs have reached this stage shock becomes irreversible and death occurs.
This concept of irreversibility is important because it emphasizes the need to prevent the progression of shock.
Release of Prostaglandins
Tissue damage in shock stimulates the release of various inflammatory mediators including stimulation of phospholipase A2 and hence Arachidonic acid metabolism, producing eicosanoids viz. Prostaglandins and leucotrienes (Fig. 1.2).
ORGAN CHANGES IN SHOCK
If shock continues to the irreversible stage, end organ damage and multiorgan dysfunction syndrome occurs as follows.
- Lungs—Adult respiratory distress syndrome (ARDS) and shock lung.
- Kidney—Acute renal failure due to acute tubular necrosis.
- Liver—Centrilobular necrosis and fatty change.
- GI Tract—Hemorrhagic gastroenteropathy and ulceration.
- Brain—Hypoxic encephalopathy and confusion.
- Heart—Subendocardial hemorrhage, fatty changes.
- Disseminated intravascular coagulation or DIC.
INVESTIGATIONS AND ASSESSMENT
- Recording of urine output, pulse, BP, temperature and respiratory rate.
- Hb%, urea, electrolytes, creatinine and platelet count.
- Blood grouping and cross matching.
- Blood culture and estimation of arterial blood gases.
- ECG and cardiac enzymes.
+ = Stimulation.
- To ensure clear airway, adequate breathing and circulation.
- Provision of 100 percent oxygen by a face mask.
- Hypovolemic shock
- The patient is kept in head down position.
- Fluid replacement—Crystalloid solution like Ringer lactate is ideal in situations where Na and H2O loss is predominant and will also serve as initial treatment in hemorrhagic shock. Blood transfusion is advised in hemorrhagic shock and plasma transfusion in case of burns.
- Colloids, e.g. Gelatin (Hemaccele), Hydroxyethyl starch (HES) and Dextran remain longer in the circulation and draw extracellular fluid (ECF) into the circulation by osmotic pressure.
- The administration of crystalloids or colloids should be monitored by urine output and CVP measurements.
- Septic Shock
- Aim of treatment is to control infection and improve the hypovolemic state, caused by endotoxin induced peripheral vasodilatation. Blood culture should be done before antibiotic administration. A combination of 3rd generation cephalosporin, aminoglycoside and metronidazole should be effective against most organisms.
- onotrope use is indicated in severely ill patients to maintain cardiac output.
- Cardiogenic shock
- The patient should have complete bed rest and be monitored in a coronary care unit.
- Pain relief with Inj. Morphine or Pethidine HCl.
- Pharmacologic support
- Inotropes—Like Dopamine and Dobutamine for pump failure.
- Thrombolytic therapy with Aspirin and Streptokinase in case of myocardial infarction.
- Diuretics, cardiac glycosides and ACE inhibitors for patients with heart failure.
- Temporary cardiac pacing will increase cardiac output and heart rate in bradyarrhythmias.
- Anaphylactic shock
- Inj. Adrenaline − 0.5 ml 1 in. 10000 s.c.
- steroids and antihistaminic.