Circulatory shock Circulatory shock is a state of inadequate tissue perfusion with relatively or absolutely inadequate cardiac out put. Depending upon the cause of inability of the heart to pump sufficient blood volume for tissue perfusion circulatory shock can be divided into different types
Hypovolumic shock Hypovolemic shock is also called "cold shock." It is characterized by – Hypotension; – Rapid, thready Pulse; – Cold, Pale, Clammy Skin; – Intense Thirst; – Rapid Respiration; – Restlessness.
Hemorrhagic shock It illustrate the features of a major form of hypovolemic shock and the multiple compensatory reactions that come into play to defend ECF volume Hemorrhage Decrease arterial pressure Decrease cardiac out put Decrease blood volume Decrease venous return Decrease stroke volume
Compensatory reactions activated by hemorrhage. – Vasoconstriction – Tachycardia – Venoconstriction – Tachypnea→increased thoracic pumping – Restlessness→increased skeletal muscle pumping (in some cases) – Increased movement of interstitial fluid into capillaries – Increased secretion of norepinephrine and epinephrine – Increased secretion of vasopressin – Increased secretion of renin and aldosterone – Increased secretion of erythropoietin – Increased plasma protein synthesis
Anaphylactic Shock A good example is anaphylactic shock, a rapidly developing, severe allergic reaction that sometimes occurs when an individual who has previously been sensitized to an antigen is exposed to it. – The resultant antigen-antibody reaction releases large quantities of histamine, causing increased capillary permeability and widespread dilation of arterioles and capillaries.
Stages of Shock 1.Non progessive stage or Compensated stage Here circulatory compensatory mechnism cause Full recovery without help from outside therapy 2.Progressive stage-Decreased BP AND COP. Here without therapy,shock gets worse 3.Refractory shock or Irreversible stage (called before) Here patient does not respond to Treament. 12
Irreversible or refractory shock Factors contributing irreversible shock Cerebral ischemia – Depression of vasomotor and cardiac areas of the brain (vasodilatation, decreased BP, decreased HR) Myocardial depression due to Acidosis causes decreased COP Respiratory failure (ARDS) – triggered not only by shock but also by sepsis, lung contusion, other forms of trauma. – Damage to capillary endothelial cells and alveolar epithelial cells, with release of cytokines.
SEPTIC SHOCK Usually due to gram-negative bacteria Endotoxins released by gram-negative Bacteria—cause VASODILATATION(Skin is warmTherefore called WARM SHOCK). High fever Increased capillary permeability with loss of plasma in tissues Mortality is 30-50% 14
Cardiogenic shock Cause---Myocardial Infarction(pump failure) Causes symptoms of shock and congestion in the lungs ( Pulmonary oedema). Note—In Myocardial Infarction, shock occurs in 10% and has mortality of 60-90%. 15
Neurogenic shock In Neurogenic shock, there is decreased sympathetic activity, therefore, increased vascular capacity. Reason—Sudden loss of Vasomoter Tone resulting in massive dilation of veins therefore Venous pooling of blood and decreased venous return to heart. Causes of Neurogenic shock – -General Anesthesia, Spinal Anesthesia – -Brain damage 16
Fainting Type of distributive shock is neurogenic shock, in which there is sudden autonomic activity producing vasodilation, pooling of blood in the extremities, and fainting. These are called vasovagal attacks,. Other forms of syncope include – postural syncope, fainting due to pooling of blood in the dependent parts of the body on standing. – Micturition syncope, fainting during urination, It is due to the combination of the orthostasis and reflex bradycardia induced by voiding in these patients.
Fainting – Pressure on the carotid sinus, produced, for example, by a tight collar, can cause such marked bradycardia and vasodilation that fainting results (carotid sinus syncope). – Rarely, vasodilation and bradycardia may be precipitated by swallowing (deglutition syncope). – Cough syncope occurs when the increase in intrathoracic pressure during straining or coughing is sufficient to block venous return