Systolic Blood Pressure peak pressure that blood exerts against vessel walls (specifically pressure in aorta), associated w/ ventricular contraction Diastolic Blood Pressure pressure blood exerts against vessel wall during diastole, normally lowest blood pressure in the aorta (pressure you have to exceed to open aortic valve) Never report blood pressure in odd numbers Graph specific to left side of heart Aorta Arteries Arterioles Capillaries Venules Veins Vena Cava (120 mmHg down to 2 mmHg) Blood flows down pressure gradient Falls rapidly from arteries to capillaries Believed that BP in brachial artery is almost the same as BP in aorta Pulse wave becomes harder to distinguish when you get down into smaller vessels Dont take pulse w/ your thumb b/c you have an artery in your thumb Mean Arterial Pressure (MAP) calculated number, tells you how hard the heart is working Arterioles nicknamed the resistance vessels, where steep pressure drop occurs Normally in constricted state, this is where most of peripheral resistance takes place If arterioles dilate you BP will fall so fast youll pass out When you walk some of you arterioles dilate to allow blood flow to the muscles that you are using
Arterial Blood Pressure
Pulse pressure difference between systolic and diastolic BPs = SBP DBP need to calculate this to find MAP MAP pressure that propels the blood into the tissues MAP = diastolic pressure + 1/3 of pulse pressure
Maintaining Blood Pressure
Ways to regulate blood pressure: Cardiac Output (Q) Peripheral Resistance (R) Blood Volume BP = Q x R BP varies directly w/ Q, R, and blood volume Q = MAP / R or MAP = Q x R Q = delta P/R or deltaP = Q x R
Controls of Blood Pressure
Short term controls: 1. Neural almost exclusively referring to sympathetic nervous system (exceptions concern sexual reproduction) Receptors are Alpha 1 and Beta 2 Alpha 1 in systemic blood vessels, cause vasoconstriction, resistance then goes up Beta 2 in coronary blood vessels, cause vasodilation Multiple ways to affect these receptors: 1. Baroreceptors located w/in carotid arteries, mechanical sensors so when you squeeze them you mimic and increase in BP BP in vessels increase and we stress/activate baroreceptors in carotid, there is a neuron that connects to the brain stem which causes the brain stem to secrete an inhibitory neurotransmitter to decrease sympathetic activity so HR, cardiac output, MAP, and BP decrease, we also decrease contractility Under negative feedback control Reaches the alpha 1 receptors in systemic vessels which decreases their activity and cause vasodilation which reduces resistance and also lowers BP If you decrease BP and stop activating baroreceptor then your sympathetic activity goes back up 2. Chemoreceptors 3. Brain centers (hypothalamus) increase stress increase BP 2. Humeral Normally secreted locally Nitric Oxide (NO/EDRF) Inflammatory chemicals (histamine, kinins) K+ increase induces vasodilation CO2 increase cause vasodilation H+ increase/decrease in pH - vasodilation 3. Hormonal Catecholamines Epinephrine, effect depends upon receptor Angiotensin II always a vasoconstrictor ADH retain water, increase blood volume Atrial Natriuretic Peptide makes you urinate, decrease blood volume Long Term Controls: Blood Volume decrease volume you decrease BP because there is less preload on the heart, there is a decrease in venous return so stroke volume decreases so Q decreases Aldosterone Angiotensin II ADH
Control of Arteriolar Smooth Muscle
Arterioles radius controls resistance In order to exercise and increase blood flow, resistance must decrease but not in all blood vessels Neuronal we can alter sympathetic tone but that affects all blood vessels, extrinsic effect Hormonal ANP, but that affects all blood vessels, extrinsic When leg muscles contracting when walking you release molecules into extracellular fluid such as H+, K+, CO2 and those molecules cause nearby blood vessels to dilate