Hypertension - Blood Pressure Regulation - Hypotension

Normal Systolic and Diastolic Blood Pressures
Systolic SBP and Diastolic Blood Pressure DBP; relationship with Cardiac Output CO and Total Peripheral Resistance TPR respectively.
0 SBP’s direct proportionality with CO.
Defining DBP.
DBP’s direct proportionality with TPR.
Effect of arterioloconstrictors and arteriolodilators on TPR and by extension DBP. Altering SBP by controlling CO.
Explanation and calculation of Mean Arterial Pressure MAP; Mean Systemic Blood Pressure
Cardiac Output CO = Stroke Volume and Heart Rate. Factors influencing Stroke Volume e.g. Preload, Contractility, Afterload.
Venous Return; Preload, factors influencing it i.e. Ventricular Filling Pressure, Filling Time.
Contractility and Afterload and how they affect Preload.
Total Peripheral Resistance TPR; contribution to Blood Pressure through changes in DBP; concepts of stressed and unstressed volumes and effect of vasodilation/arteriolodilation and Venoconstriction/Arterioloconstriction.
M.A.P = CO into TPR; Cardiac Output and Total Peripheral Resistance as interdependent variables and not independent ; i.e. if one increases the other decreases and vice versa.
Short term Rapid and Long term regulation of BP; i.e. Neurological and Renin-Angiotensin-Aldosterone system.
Detailed explanation of Neurological Regulation; how it counterbalances major fluctuations; Baroreceptors, Carotid Sinus and Aortic Arch Sinus; Role of Glossopharyngeal 9th Nerve and Vagus Nerve 10th Nerve, central regulation in Medulla through sympathetic and parasympathetic outflow tracts acting on SA node and Vasomotor center acting on veins and arteries.
Effect of Hypertension on sensitivity of nerve endings in Carotid Sinus Arch and S.A node and clinical implications of this phenomena.
Summary of neuronal blood pressure regulation and rapid control of blood pressure with emphasis on Parasympathetic and Sympathetic activity through afferent and efferent neurons.
Neuronal Blood Pressure Regulation NBPR; Clinical co-relates; Carotid Occlusion, Carotid Sinus Massage, its importance in managing Supraventricular Tachycardias SVT.
NBPR; Clinical co-relates; Postural changes in blood pressure, Orthostatic Hypotension, severe dehydration, use of sympatholytic or vasodilator drugs and compensatory rise in Sympathetic Nervous System SANS activity leading to rise in blood pressure.
NBPR; Clinical Co-relate; Volume load, compensatory rise in Parasympathetic Nervous System Activity PANS leading to fall in blood pressure.
Renin-Angiotensin-Aldosterone System RAA; Production/release of Renin; Effect of increased or decreased renal perfusion on JuxtaGlomerular Apparatus JG apparatus. Its role in increased reabsorption of Na+ in convoluted tubules and Loop of Henle. Decreased Na+ detection by JG apparatus leading to compensatory release of Renin.
RAA system: Increased Renin release in blood stream leading to release of Angiotensin-1 from the liver. Conversion of AT-1 to AT-2 by the enzyme Angiotensin-Conversion-Enzyme ACE present in cells of the lung.
RAA system: Role of AT-2 in increasing SBP and DBP through venoconstriction and arterioloconstriction respectively. AT-2’s role in activating thirst center in hypothalamus. AT-2’s role in activating sympathetic activity through receptors in post-ganglionic nerve fibers.
RAA system: AT-2’s effect on Adrenal Gland in producing Aldosterone. Detailed mechanism of Aldosterone’s action on DCT to increase reabsorption of Na+ and H2O salt-water retention and thus increased blood volume.
RAA system: AT-2’s effect in enhancing Na+ and H2O reabsorption through its action on Na+-H+ counter transporter and significance of Carbonic Anhydrase enzyme in this regard. AT’s role in maintaining GFR through constriction of efferent arterioles.
Drugs acting through RAA system: ACE inhibitors; Renal Artery Stenosis.
Drugs affecting RAA system: Angiotensin-Receptor Blockers ARBs.
Other Blood Pressure regulatory mechanisms; chemoreceptors; Central and peripheral types of chemoreceptors.
Cushing’s reaction, its clinical co-relates; Increased Intracerebral Pressure ICP in cases of Space Occupying Lesion SOL. Increased Cerebral Blood Flow, progressively increasing BP and progressively decreasing Pulse. Papilledema.
Other mechanisms: Anti-diuretic hormone ADH/Vasopressor hormone.