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45 Cards in this Set
- Front
- Back
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THE ANATOMY OF BLOOD VESSELS
Three Layers: |
1. Tunica interna (intima)
1. Tunica media 2. Tunica externa (adventitia) |
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Blood flow to capillaries &
BP is controlled by..what? |
aperture
of arterioles |
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Capillary BP is decreased when...?
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When they are
downstream of high resistance arterioles |
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what is Blood pressure?
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The pressure exerted against the
arterial walls |
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What is Hydrostatic pressure
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The pressure exerted by fluid at
equilibrium due to the force of gravity |
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what is Venous pressure?
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The pressure exerted against the
venous walls |
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What are the factors of TPR (total peripheral resistance)?
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Vascular resistance
Viscosity turbulence |
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How is blood pressure controlled?
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BP is controlled mainly by Heart Rate,
Stroke Volume, & peripheral resistance |
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What does Sympathoadrenal activity do?
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It raises BP via
arteriolar vasoconstriction & by increased Cardiac Output |
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What role do the kidneys play in BP?
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The kidneys play a role in BP by regulating
blood volume & thus stroke volume |
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How does Sympathoadrenal activity raises BP?
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via
arteriolar vasoconstriction & by increased Cardiac Output |
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How does The kidneys play a role in BP?
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by regulating
blood volume & thus stroke volume |
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What is Cardiac output?
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The volume of blood pumped/min by
the left ventricle Heart Rate (HR) = 70 beats/min Stroke volume (SV) = blood pumped/beat by each ventricle Average is 70-80 ml/beat CO = SV x HR Total cardiac output is about 5.5L |
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Pulse pressure =
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(systolic pressure) – (diastolic pressure)
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MAP =
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CO x TPR where CO = HR x SV
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What influence HR?
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Normally Sympathetic & Parasympathetic
activity |
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What is the main
controller of HR |
Autonomic innervation of SA node
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What modify the rate of spontaneous
depolarization |
Sympathetic & Parasympathetic nerve
fibers |
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What does the Vagus nerve do?
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Decreased activity: increases heart rate
• Increased activity: slows heart rate |
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What does the Cardiac centre do?
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in medulla oblongata
coordinates activity of autonomic innervation |
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What does the Sympathetic endings in atria & ventricles do?
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they can
stimulate increased strength of contraction |
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What is Stroke Volume
Determined by? 3 variables |
End diastolic volume (EDV) = volume of blood in
ventricles at end of diastole (Reflected by PAWP) Total peripheral resistance (TPR) = impedance to blood flow in arteries Contractility = strength of ventricular contraction |
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What is Frank-Starling Law of the Heart?
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States that strength of
ventricular contraction varies directly with EDV Is an intrinsic property of myocardium As EDV increases, myocardium is stretched more, causing greater contraction & SV |
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At any given EDV,
contraction depends upon what? |
level
of sympathoadrenal activity |
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What happened with Capillary Exchange?
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Diffusion:
Filtration: Reabsorption: |
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What is Venous Return relying on?
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Blood volume & venous
pressure – Vasoconstriction caused by Sympathetic stimulation – Skeletal muscle pumps – Pressure drop during inhalation (thoracic pump mechanism) |
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What are veins called?
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capacitance
vessels – Have thin walls & stretch easily to accommodate more blood without increased pressure (higher compliance) |
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How is Atrial Stretch Receptors stimulated and activated?
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Are activated by increased venous return &
act to reduce BP • Stimulate reflex bradycardia (slow HR) |
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What inhibits Atrial Stretch Receptors ?
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Inhibit ADH (antidiuretic hormone) release
& promote secretion of ANP (atrial natriuretic peptide) 14 |
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What hormones Control of Cardiovascular Function
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ADH
• Angiotensin • Erythropoietin • ANP |
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Urine formation begins with...
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filtration of
plasma in glomerulus Filtrate passes through the nephron and is modified |
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When does ADH get released from the posterior pituitary?
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when
osmoreceptors detect high osmolality From excess salt intake or dehydration – Causes thirst – Stimulates H20 reabsorption from urine |
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When is ADH inhibited?
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ADH release inhibited
by low osmolality |
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What is Aldosterone hormone and what does it do?
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Steroidal hormone secreted by adrenal
cortex Helps maintain blood volume & pressure through reabsorption & retention of sodium & water Release stimulated by salt deprivation, low blood volume, & pressure |
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What does Renin-Angiotension System do?
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Decreased BP and blood flow (low blood
volume) • Kidney (Juxtaglomerular apparatus) secretes Renin (enzyme) Brings about the release of angiotensin converting enzyme (ACE) Angiotensin I converts to Angiotensin II Angiotensin II causes a number of effects all aimed at increasing blood pressure: • Vasoconstriction / aldosterone secretion / thirst |
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What does Atrial Natriuretic Peptide (ANP) do?
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Expanded blood volume is detected
by stretch receptors in left atrium & causes release of ANP Inhibits aldosterone production, promoting salt & water excretion to lower blood volume Promotes vasodilation |
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Secondary hypertension is caused by...
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known
disease processes |
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Classification of Blood Pressure for Adults
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BP Classification SBP (mmHg) DBP(mmHg)
Normal <120 And <80 Prehypertensive 120 – 139 Or 80 - 90 Stage I Hypertension 140 – 159 Or 90 – 99 Stage II Hypertension ≥ 160 Or ≥ 100 |
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What is Essential Hypertension?
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Constitutes most of hypertensives
Increase in peripheral resistance is universal CO & HR are elevated in many Secretion of renin, Angiotensin II, & aldosterone is variable Sustained high stress (which increases sympathetic activity) & high salt intake act synergistically in development of hypertension Prolonged high BP causes thickening of arterial walls, resulting in atherosclerosis Kidneys appear to be unable to properly excrete Na+ and H20 14 |
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How does BP Stimulates inflammatory response:
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Histamine and prostaglandins released
• Increase permeability of vascular endothelium • Allows Ca+, Na+. H2O to enter • Further thickening |
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What happened when there is Sustained high pressure in arterial
circuit: |
Damages blood vessel walls –arterioles in
particular Sustained vasoconstriction and pressure – thickening and strengthening of vessel • Hypertrophy of smooth muscle • Hyperplasia • Both lead to reduced lumen |
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What are the Dangers of Hypertension
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Patients are often asymptomatic until
substantial vascular damage occurs Contributes to atherosclerosis Increases workload of the heart leading to ventricular hypertrophy & congestive heart failure Often damages cerebral blood vessels leading to stroke These are why it is called the "silent killer" |
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What is the Treatment of Hypertension?
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Often includes lifestyle changes such as
cessation of smoking, moderation of alcohol intake, weight reduction, exercise, reduced Na+ intake, increased K+ intake. Drug treatments include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium channel blockers to decrease HR, ACE inhibitors to inhibit formation of Angiotensin II, & Angio II-receptor blockers. |
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What happends with Hypotension
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Consequence of myocardial injury or
acute/critical illness Postural (orthostatic) -Systolic and diastolic decrease on standing Poor arteriolar and venous constriction, lack of HR increase, decrease venous return |
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What can you expect while somebody is suffering Hypotension?
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If as a result of acute/ critical illness may
need INOTROPIC support Dobutamine/Dopamine - Calcium uptake and utilisation by cardiac cells Norepinephrine/Epinephrine- vasoconstriction |
