PARAMETERS OF STROKE: Organ perfusion depends on arterial blood pressure (BP), which in turn depends on cardiac output (CO), peripheral vascular resistance (PVR). Cardiac output (CO) depends on the following equation (CO) = Stroke Volume x Heart rate. In turn, stroke volume depends on Preload (the amount of blood available to fill the ventricles), and after-load (amount of blood available for ejection from the heart). Any defect in any of these mentioned factors might result in shock. [PHYSIOLOGICAL FUNCTIONING OF THE HAERT]
CAUSES AND TYPES OF SHOCK: Shock can be classified into 3 types namely; hypovolemic shock, cardiogenic shock, and distributive shock.
HYPOVOLEMIC SHOCK: This type is caused by reduced blood volume, reduction in circulating blood volume results in a reduction of the preload which leads to inadequate left ventricular filling. The reduced preload culminates in decreased cardiac output which leads to widespread tissue hypoperfusion.
Causes of Hypovolemia: Hemorrhage, dehydration in cases of vomiting or diarrhoea.
CARDIOGENIC SHOCK: This is a shock that results from severe depression of cardiac performance, primarily resulting from pump failure of the right or left ventricle. The most common cause is left ventricular MI, shock occurs when more than 40% of ventricular mass is damaged.
Causes of cardiogenic shock include; 1)Acute MI occurs if ≥ 40% of ventricular mass are involved.
2) Ventricle outflow obstruction, e.g., aortic stenosis
3) Reduction in cardiac output, e.g. Aortic or mitral regurgitation
4) Arrhythmia - Cardiac tamponade (fluid accumulation in pericardial space)
5) Tension pneumothorax (gas accumulation in pleural space)
6) Massive pulmonary embolism - Severe pulmonary hypertension
DISTRIBUTIVE SHOCK: Refers to subtypes of shock caused by profound peripheral vasodilatation despite normal or high cardiac output and characterized by, inadequate perfusion of tissues due to mis-distribution of blood flow, and the blood is not reaching the tissues adequately.
Causes of Distributive Shock: Septic shock, anaphylactic shock, neurogenic shock. Septic Shock usually refers to serious bacterial infections caused by Gram-negative organisms.
Pathogenesis of distributive shock: Cell walls of microorganisms contain endotoxins which activate inflammatory mediators, that induce vasodilatation & increase capillary permeability resulting in reduced cardiac output and presenting with shock. [BACTERIAL TOXINS].
Anaphylactic shock: This is defined as a wide spread vasodilatation and vascular permeability, that results from the widespread allergic reaction to an antigen. This hypersensitivity reaction is life threatening. The pathophysiology is due to re-exposure to antigen, resulting in degradation of IgE bound mast cells and basophils. The released contents of granule lead to vasodilatation, increased vascular permeability, broncho-constriction and increased mucus production [IMMUNOGLOBULIN]
Neurogenic Shock: Shock that results from the loss of sympathetic tone causing massive vasodilatation in the venous vasculature, venous return to the heart, cardiac output, and the most common aetiology include: spinal cord injury, and severe pain.
Clinical Features of neurogenic shock: Low blood pressure, rapid, weak pulse, low urine output, confusion and CNS disturbance, cold extremities, cyanosis and loss of skin elasticity. [BLOOD PRESSURE]
Systemic Changes in Shock: All systems are affected, but the net results are: Lungs: Changes in the rate and depth of breathing, metabolic acidosis, which stimulates respiratory centers resulting in hyperventilation and adult respiratory distress syndrome (ARDS). Kidneys: The secretary function of the kidneys is always disturbed in shock. This is due to the circulatory collapse and hypotension but the secretion of renin may aggravate it by the kidney itself, aldosterone by the adrenal and antidiuretic hormone by the posterior pituitary gland. These hormones are secreted in an attempt to retain fluid and restore the blood volume as a compensatory mechanism.
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