Therefore MAP=CO x TPR = HR x SV x TPR

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Transcription:

Regulation of MAP Flow = pressure gradient resistance CO = MAP TPR Therefore MAP=CO x TPR = HR x SV x TPR TPR is the total peripheral resistance: this is the combined resistance of all blood vessels (remember the importance of vasodilation and vasoconstriction) This means that MAP is completely determined by HR, SV and TPR

Regulation of MAP Short-term regulation seconds to minutes (baroreceptor( reflex) Involves heart and blood vessels Primarily neuronal control Long-term regulation minutes to days Regulation of blood volume Involves kidneys Primarily hormonal control

Renin-angiotensin-aldosterone system Most important hormonal system involved in regulating Na +

Circulatory Pressures Boron & Boulpaep,, fig 18.3

Arterial Pressure Systolic Pressure (120 mmhg) occurs with ventricular contraction Diastolic Pressure (80 mmhg) occurs with ventricular refilling BP thus reported as 120 / 80 (mmhg) Pulse Pressure difference between Sys. P. & Dias. P. 40 mmhg at rest MAP (Mean Arterial Pressure) an average pressure regulated pressure Diastolic MAP + = (Pulse P) 3 Sherwood 6 th Ed., fig 10.7

Blood Pressure Measurement: Auscultation Utilises sphygmomanometer Pressure cuff Mercury column Stethoscope Recorded at heart level via Brachial Artery Korotkoff sounds via Turbulent flow, upon Cuff pressure release Sherwood 6 th Ed., fig 10.8

Blood Pressure Auscultation Inflate cuff above Systolic pressure Slowly deflate cuff. Blood flows when BP > Cuff pressure Generates Korotkoff sounds. Clear tapping audible via stethoscope. Indicates Systolic Pressure Turbulent flow disappears as cuff deflates & artery diameter increases Diastolic pressure indicated via a constant muffled constant sound Sherwood 6 th Ed., fig 10.8

Baroreceptors Specialised nerve endings Respond to stretch of vessel wall; indirect response to changes in BP Location Carotid sinus Aortic Arch Type A fibres (myelinated) Low pressure (30-90 mmhg) Important at rest C fibres (unmyelinated) High pressure (70-140 mmhg) Increasingly active at higher pressures Sherwood 6 th Ed., fig 10.35

Central Control of CVS Involves integrated responses from: Medulla, hypothalamus, cerebral cortex, cerebellum Baroreceptor input to NTS in medulla (nucleus tractus solitarius) Output to: Parasympathetic NS (vagus) via nucleus ambiguus Cardiac control (limits HR) Sympathetic NS via rostral ventrolateral medulla Cardiac and blood vessel control ( ( ed contractile strength/tone) Hypothalamus & amygdala in cerebellum Overriding output during stress to raise BP

Summary Control of CVS Noble & Co.,, fig 3 3 10.3 & 10.4

Extra Inputs to CVS Control Atrial stretch receptors Myelinated vagal afferents sensitive to blood volume Located at junction of great veins and atria Influences endocrine regulation of blood volume via: Hypothalamic ADH renal water retention Renin-Angiotensin-aldosterone system (RAS) renal salt & water retention Atrial Natriuretic Peptide renal salt & water excretion Bainbridge reflex Vena cava stretch receptors neural mediated HR Avoids venous congestion

MAP = CO! TPR

Factors Affecting Blood Pressure Age & Sex Blood pressure increases with: High dietary intake of; salt, fat, cholesterol, and alcohol Smoking Obesity & diabetes Stress activity/exercise Hypertension Sys P > 160 mmhg Dias P > 100 mmhg White Coat Treatment Always address above factors Noble & Co.,, fig 10.7

Hypertension Primarily arises via ed peripheral flow resistance 5% of cases disturbance of normal physiological function e.g. renal diseases, adrenal diseases (associated with salt & water retention, & blood vol.) 95% of cases essential hypertension Mostly via aspects that affect arteriolar smooth muscle Cumulative effect of genetic, lifestyle & environmental factors

Hypertensive Drug Treatments Thiazide diuretics Inhibit Na + /K + /Cl - exchange in distal renal tubule β-blockers Reduce HR & contractility L-type Ca 2+ channel blockers Relaxation of vascular smooth muscle dilation & reduced resistance ACE inhibitors Diuretic actions Inhibit aldosterone formation α-blockers Reduce sympathetic tone Dilate arteriolar smooth muscle