BSCI202 Exam #2

Name the two subdivisions of the cardiovascular system and their respective functions.

-pulmonary circuit (right side of heart): receives oxygen-poor blood from body tissues and pumps it to lungs
-systemic circuit (left side): supplies oxygen and nutrients to the rest of the body

pulmonary circulation system: function and pathway

-function: carries deoxygenated blood to the lungs for gas exchange, then brings oxygenated blood back to the heart
-pathway: right atrium, tricuspid valve, right ventricle, pulmonary semilunar valve, pulmonary trunk, pulmonary arteries, capillaries within the lungs, pulmonary veins, left atrium

systemic circulation system: function and pathway

-function: carries blood to all tissues for nourishment, then transports deoxygenated blood back to heart
-pathway: left ventricle, aorta, other arteries, arterioles, capillaries (within tissues), venules, veins, venae cavae, right atrium

coronary circulation

supplies the cardiac muscle with O2/tnutrients, and collects CO2/waste

three layers of the heart wall (outer to inner)

epicardium (visceral layer of serous pericardium), myocardium, endocardium

histological differences of the layers of the heart wall

-epicardium: thin areolar CT + simple squamous epithelium facing pericardial cavity
-myocardium: cardiac muscular layer + pacemaker+contractile cells + cardiac skeleton
-endocardium: thin areolar CT + simple squamous epithelium facing cardiac cavity

the three layers of the heart wall are surrounded by

fibrous pericardium fused with parietal layer of serous pericardium (thick fibrous CT)

name the four valves

-two atrioventricular valves: tricuspid (right), bicuspid/mitral (left)
-two semilunar valves: pulmonary and aortic

do arteries/veins carry deoxygenated/oxygenated blood?

-arteries: carry oxygenated (except for pulmonary arteries)
-veins: carry deoxygenated (except for pulmonary veins)

chordae tendineae

collagenous cords that prevent atrioventricular valve inversion by anchoring the cusps to the papillary muscles (finger-like projections) on the floor of the ventricles, so that blood can’t backflow into the atria

fibrous skeleton

a layer of crisscrossing fibrous connective tissue that anchors muscle fibers, supports great vessels and valves

compare the myocardial walls of the 4 chambers

-atria have relatively thin walls because they only need to pump blood to the ventricles
-ventricle: left ventricle has thickest wall because it has to pump blood through the high-resistance systemic circuit

compare autorhythmic and contractile cells (abundance)

autorhythmic: 1%, contractile 99%

compare autorhythmic and contractile cells (function)

A: initiates electrical signal and sets the rhythm by spontaneously depolarizing to initiate the action potentials
C: contracts to generate the mechanical pumping force

compare autorhythmic and contractile cells (location)

A: the intrinsic conduction system (SA node, AV node, bundle of His, bundle branches, purkinje fibers)what’
C: bulk of myocardium in atria and ventricles

what’s unique about contractile cells’ action potential

distinct plateau phase in action potential caused by influx of calcium through slow channels - extends the refractory period so that the heart muscle can fully relax before it can be stimulated again

how are autorhythmic and contractile cells connected

by intercalated discs, which contain gap junctions for ions (the electrical signal) to flow freely so that the heart can contract as a functional syncytium (single, coordinated unit)

what is intrinsic conduction of the heart?

a network of noncontractile pacemaker cells that generate electrical impulses that induce myocardium to contract (makes the heart beat)

what’s the pathway of intrinsic conduction through the heart?

1) sinoatrial node in the superior part of the right atrium generates impulses
2) Bachmann’s Bundle carries signal from SA node through the atria to the AV node and left atrium

3) the impulses pause (0.1 sec) at the atrioventricular node in the inferior atrial septum in the right atrium
4) the atrioventricular bundle (bundle of His) in the interventricular septum conducts the impulses to the bundle branches
5) the bundle branches in the interventricular septum conduct the impulses through the interventricular septum to the apex
6) the subendocardial conducting network (Purkinje fibers) in the muscles of the ventricular walls depolarizes the contractile cells of both ventricles

describe the chronological order of any chamber of the heart

1) autorhythmic excitation by pacemaker cells
2) contractile cell excitation (depolarization)
3) contractile cell contraction (systole - physical shortening of the muscle fibers)

explain how sodium and potassium channels contribute to pacemaker potential

1) slow depolarization due to opening of Na channels and closing of K channels
2) action potential begins when pacemaker potential reaches threshold due to depolarization due to Ca influx through Ca channels
3) repolarization due to Ca channels inactivating and K channels opening, which allows potassium efflux to bring membrane potential back to its negative voltage

what is the plateau phase in contractile cells

occurs after the initial rapid depolarization when influx from slow-gated Ca channels open while there is also limited K efflux, so the membrane potential is in a plateau
-ensures the absolute refractory period lasts nearly as long as physical contraction itself

why is an extended refractory period important for contractile cells

-this is the time when the cell can’t be stimulated again
-long period means no tetanic contractions (sustained, fused contractions common in skeletal muscle), so heart has to fully relax (ventricles refill with blood) between beats/pump

how are contractions related to action potential

tension development (contraction) happens primarily in plateau phase and is consequently has enough time to develop maximum tension

why is the impulse delayed at the AV node?

to allow the atria to finish contracting and filling the ventricles before the ventricles depolarize - prevents premature closure of the atrioventricular valves

P wave

depolarization of the atria (immediately prior to atrial contraction)
-atria contract to squeeze remaining blood into ventricles, ventricles are filling with blood

QRS complex

depolarization of ventricles (electrical impulses traveling from AV node to Bundle of His and bundle branches to Purkinje fibers)
-triggers ventricular systole
-hidden event: atrial repolarization

T wave

repolarization of ventricles (ventricles relax - diastole)
-”dub”

PR segment

AV node delay - atria finish emptying

heart location

within mediastinum (medial cavity of thorax)

what causes heart attack

block/clot in coronary circulation or low BP

difference between interatrial and interventricular septum

interatrial is membranous, interventricular is mostly muscular

what causes the two sounds associated with closing of heart valves

-lub=AV valves close
-dup=SL valves close

heart murmurs

abnormal heart sounds - usually indicate incompetent or stenotic valves: mitral valve regurgitation

cardiac cycle

blood flows through heart during one complete heartbeat - diastole to diastole (P wave to P wave)

what happens in the PR interval?

signal travels from SA node to AV node

what happens in the ST segment?

this is when the ventricles are fully depolarized and contraction is occurring, but before they start to relax and repolarize

atrial fibrillation

atria can’t contract and relax in coordinated manner; cardiac rhythm isn’t regular but ventricles can still contract

ventricular fibrillation

emergency, life threatening: ventricles can’t fully contract nor relax so blood can’t be ejected properly - heart attack unless electrical shock

describe relationship of flow to pressure and resistance

flow=volume of blood moving through a vessel or heart chamber per unit of time
-directly proportional to pressure gradient
-inversely proportional to resistance

blood flow during heart expansion (diastole)

-pressure: as ventricles relax/expand, internal pressure drops significantly. once ventricular pressure falls below atrial pressure, the AV valves open
-flow/volume: blood flows from high-pressure atria into low-pressure ventricles (80% passive, 20% via atrial systole)

end diastolic volume (EDV)

the volume of blood in each ventricle at end of ventricular diastole

what does it mean that end diastolic volume is happening in both chambers simultaneously

both ventricles reach their maximum filling at the same time because the circulatory system works in a closed loop, so the right and left sides of the heart must pump the same amount of blood each beat so there is no back up

blood flow during heart contraction (systole)

-isovolumic contraction: the brief moment at the start of ventricular contraction where the squeeze begins but no blood has moved yet: as the ventricles begin to contract, pressure rises rapidly and closes the AV valves. SL valves are still closed so volume stays the same but pressure increases sharply
-ventricular ejection: once ventricular pressure exceeds the pressure in the great arteries (aorta/pulmonary trunk), SL valves open
-blood is ejected into circulation

describe ejection of blood during ventricular systole

rapid ejection followed by reduced ejection, lasts for plateau of myocardial AP at the level of contractile cells
-remaining volume = end systolic volume (ESV)

blood flow during isovolumic relaxation

-early ventricular diastole: ventricles relax and expand, pressure decreases rapidly
-SL valves close so now ALL valves are closed again and volume remains constant at ESV level while pressure continues to fall
-atria relaxed and filling
-when pressure of atria increases, AV valves open and cycle begins again

cardiac output

the total volume of blood pumped by each ventricle in one minute (the “flow rate” of the heart
-CO=HRxSV
-resting CO is 25 L/min

stroke volume

the actual volume of blood pumped out by one ventricle with each individual beat (average 70mL per beat at rest)
-SV=EDV-ESV

end diastolic vs end systolic volumes

-EDV: the maximum volume of blood in each ventricle at the very end of diastole: the blood available to be pumped
-ESV: the volume of blood remaining in the ventricle after it has finished contracting and ejecting blood (systole) (heart doesn’t empty completely with every beat)

ejection fraction

the percentage of blood pumped out of the ventricle relative to the total amount that was in it before the beat

(SV/EDV)% - measures heart’s pumping efficiency
-healthy and at rest EF >50%

cardiac reserve

difference between resting and maximal CO

what is the purpose of a cardiac reserve

the heart doesn’t eject 100% of its blood withe very beat. the ESV remains to provide this reserve for when you suddenly need to increase physical output (ex. running)

the three main factors affecting SV

-preload
-afterload
-contractility

preload & frank-starilng law

-preload: degree of stretch of cardiac muscle cells (sarcomere) before they contract
-frank-starling law: the more the heart muscle is stretched during filling (preload), the more forcefully it contracts during the next beat

afterload

pressure ventricles must overcome to eject blood; increased afterloa requires more force to achieve the same EV

increased contractility allows

greater SV at the same preload
-Ca is the most important (increased Ca = more crossbridges)

-contractility is independent of loading conditions (pre/after) - dependent on inotropic factors that make muscles more responsive to stimulation

regulation of CO through sympathetic nervous system

-norepinephrine acts on the SA node to increase the rate of spontaneous depolarization (positive chronotropic effect) - increases HR
-acts on contractile cells to increase Ca an Na influx, which increases contractility (positive inotropic effect) - increases SV
-end result: much increased CO

regulation of CO through parasympathetic nervous system

-acetylcholine via the vagus nerve that binds to receptors on SA node
-hyperpolarizes pacemaker cells (extends pacemaker potential) to slow the rate of firing (negative chronotropic effect) - slows HR
-has little effect on ventricular contractility
-decreases cardiac output

regulation of CO through hormones

-epinephrine/norepinephrine: released by the adrenal medulla to mimic the sympathetic nervous system to increase both HR and SV
-throxine: increases metabolic rate and sensitizes the heart to catecholamines, causing slower but more sustained increase in HR

chronotropic vs inotropics factors affect

-chronotropic: timing of APs (so heart rate)
-inotropic: muscle strength (so heart rate and stroke volume)

age effect on heart rate

fetus > infant/children > adult

sex effect on heart rate

females faster than males

exercise effect on heart rate

acute effect: increases HR
-chronic adaptation: lowers resting HR in trained individuals because exercise conditioning improves SV due to stronger, larger heart that allows for lower HR to maintain the same CO

body temperature effect on heart rate

temperature accelerates HR, hypothermia slows HR

high blood pressure effect

stable/high heart rate, decreased SV, decreased CO because high afterload resists ejection

dysfunctional ventricle effect

increased HR, decreased SV, decreased CO because the heart beats faster to compensate for weak squeeze (low contractility)

dysfunctional valve effect

stable HR, decreased SV, decreased CO because a narrow valve increases resistance (high afterload), making it harder to eject blood

importance of calcium and potassium

determine the strength of contraction and the ability of the heart to reset itself

effects of hypercalcemia/hypocalcemia

-hypercalcemia (too much in blood): increased HR and contractility because the heart gets excited
-hypocalcemia (too little in blood): depresses HR because not enough “keys” to unlock the muscle

effects of hyperkalemia/hypokalemia

-hyperkalemia (too much in blood): less negative resting membrane potential so increased depolarization/longer to reach repolarization because the cell can’t “reset” and stays closer to threshold “pre-charged” → can lead to cardiac arrest in systole
-hypokalemia (too little in blood): increased potassium gradient because inside becomes extra negative, harder to reach depolarization threshold, increased repolarization/hyperpolarization → ventricular fibrillation (because the electrical rest isn’t working so different parts of the heart muscle reset at different times)

arteries vs capillaries vs veins: function

-arteries: carry blood away from heart
-capillaries: contact tissue cells, thin walls for greater exchange
-veins: carry blood toward heart

arteries vs capillaries vs veins: physical characteristic

-arteries: thickest tunica media to allow them to constrict/dilate and regulate pressure, large arteries have high amounts of elastic tissue to allow expansion/recoil, smaller lumen than veins
-capillaries: only have tunica intima on basement membrane, so narrow RBCs travel in single file, some have tiny holes (fenestrations) to allow leakage into tissues
-veins: thin tunica media and thick tunica adventitia, large, irregular lumen, one-way valves made of tunica intima folds

explain tunics (deep to superficial) of arteries and veins

-tunica intima: endothelium lines lumen of all vessels
-tunica media: smooth muscle and elastin - vasoconstriction and vasodilation
-tunica adventitia: collagen fibers in fibrous tissue

importance of arterioles: pressure

arterioles are TINY resistance vessels that determine blood pressure because BP=COxTPR(total peripheral resistance). The steepest blood pressure drops occur here because they have a disproportionately thick tunica media that means even tiny contractions significantly narrow the lumen. by the time blood leaves to enter a capillary, the pressure is low enough that it won’t burst the fragile capillary walls.

perfusion

the amount of blood flow reaching a specific tissue/organ

importance of arterioles: controlling tissue perfusion

arterioles are like faucets that divert blood to exactly where needed. at rest, arterioles constrict because you don’t much blood in skeletal muscles. they are also very sensitive to local chemical changes (paracrine). they are also primary targets for sympathetic nervous system.

three types of capillaries

continuous, fenestrated, sinusoidal

continuous capillaries

-complete endothelium + basement membrane
-”leaky” tight junctions for small molecules + intercellular clefts
-locations: BBB, skeletal/smooth muscle, lungs

fenestrated capillaries

-“windows” + basement membrane
-allows for exchange of large molecules
-locations: small intestine, kidneys, choroid plexus, hypothalamus

sinusoid capillaries

-extensive intercellular gaps + incomplete basement membrane
-exchange of plasma proteins and even cells
-location: liver, red bone marrow, lymph nodes

how is venous return is possible for an individual standing given the characteristics of veins, gravity, etc.

-venous one-way valves: as blood is pushed upwards, the valves open. if gravity tries to pull blood back down, the “pockets” of the valves fill up and snap shut to prevent backflow and segment blood into smaller, manageable steps
-skeletal muscle pump physically squeezes the deep veins embedded within the muscle
-respiratory pump: as you breathe in, your diaphragm moves down and increases pressure in the abdominal cavity + decreases pressure in the thoracic (chest) cavity. this means blood is squeezed out of high-pressure abdominal veins and sucked into thoracic veins and right atrium
-when you stand up, sympathetic nervous system kicks in to send signals to tunica media to constrict and reduce volume of the “blood reservoir”, which increases vein pressure and pushes more blood back to the heart

vessel: relationship between cross-sectional area, velocity, and flow

v=Q/CA
-increasing CA decreases velocity of flow (Q) - decreased velocity in capillaries facilitates exchange of gas/ions/molecules

venule

formed when capillary beds converge

veins

formed when venules converge - more numerous than arteries/oles

blood pressure (mmHg)

force per unit area exerted on wall of blood vessel by blood

mean arterial pressure (MAP)

average pressure in a patient’s arteries during one full cardiac cycle (one heartbeat)
-MAP=diastolic BP+1/3(systolic BP-diastolic BP) because heart spends more time relaxing than contracting

importance of maintaining a constant MAP for organs

-MAP is the driving force that pushes blood through the resistance of the arterioles and into capillaries

-if MAP is too low, organs are “perfused” enough because they don’t get enough oxygen.
-if MAP is too high, it can damage fragile capillaries and overwork the heart

mechanisms to maintain constant MAP

MAP=(HRxSV)xTPR
-baroreceptor reflex: baroreceptors in neck and chest feel the drop in stretch when you stand up quickly, which triggers the sympathetic NS to raise CO and raise TPR (vasoconstriction).
-if MAP stays low, kidneys release renin, which creates Angiotensin II, which causes massive vasoconstriction and triggers the release of aldosterone, which makes the kidneys keep water to increase blood volume (which restores MAP)
-if MAP too high, the atria gets stretched an the heart releases ANP, which tells kidneys to dump sodium/water into urine - drops blood volume

heart rate as a parameter for MAP

-faster heart rate = more blood into the arteries per minute = raised pressure
-sympathetic nervous system releases norepinephrine for faster depolarization, parasympathetic uses vagus nerve to slow down

stroke volume as a parameter for MAP

-frank-starling law: more blood in = a bigger stretch = a harder pump: regulated by the kidneys (RAAS) because it controls how much water to keep
-contractility (how hard muscle contracts): regulated by calcium - more calcium = harder squeeze no matter how much blood is inside
-afterload: the reistance the heart must push against to open aortic valve

total peripheral resistance as a parameter for MAP

-vasoconstriction = pressure behind the narrowing skyrockets
-arterioles are primary site of resistance so small changes in diameter have massive effects on MAP
-angiotensin II from kidneys causes intense, body-wide vasoconstriction to save falling MAP
-vasodilators to open instantly drop high MAP

how do baroreceptors sense and regulate blood pressure

-definition: specialized mechanoreceptors in the aortic arch and carotid sinuses that stretch when blood pressure rises
-when BP high: receptors stretch more, firing rapid signals to the medulla oblongata in the brain
-when BP is low: stretching decreases, and the firing rate slows down, signaling the brain that it’s time to ramp things up

how does the sympathetic nervous system sense and regulate blood pressure

activated when BP is too low (“baroreflex”) - releases norepinephrine onto heart and blood vessels to increase heart rate and contractility + cause vasoconstriction

how does the parasympathetic nervous system sense and regulate blood pressure

activated when BP is too high - signals travel via vagus nerve to SA node in heart - releases acetylcholine to slow the heart rate (lower cardiac output and pressure)

renin-angiotensin-aldosterone system

manages BP over hours/days by adjusting blood volume and vascular tone

how does the renin-angiotensin-aldosterone system regulate blood pressure

1) when kidneys sense low BP/sodium, secrete enzyme renin
2) renin converts liver protein into angiotensin I
3)angiotensin-converting enzyme converts to angiotensin II
4) immediately narrows blood vessels, triggers release of aldosterone (tells kidneys to soak up sodium and water to increase blood volume), stimulates release of ADH to retain water

hypotension

-definition: blood pressure low enough to cause symptoms like dizziness, fainting, etc
-causes: dehydration, heart problems, standing up quickly
-treatments: increasing salt/fluid uptake, compression stocking, flurocortisone (retains sodium)

hypertension

-definition: force of the blood against the artery walls is high enough that it may eventually cause health problems
-high BP, high MAP, high pressure on vessel walls, vessel wall breaks, hemorrhage, hypovolemia/stroke
-causes: no single identifiable cause
-treatments: diuretics, calcium chanel blockers

function of respiratory system: gas exchange

supplying O2 and removing CO2 from body through external respiration (gas exchange between alveoli and pulmonary capillaries) and internal respiration (gas exchange between systemic blood vessels and tissues)

function of respiratory system: body pH regulation through ventilation

regulates levels of H+ ions and bicarbonate; achieved through ventilation because partial pressure of CO2 in the blood directly impacts pH