Unit 3 Pathophysiology - Chapter 32 structure and fuction of CV and lympathic system

Question 1

Circulatory system does what

Circulatory system

Answer 1

body’s transport system and communication system

Delivers:
* oxygen
* nutrients
* hormones
* blood cells
* immune cells
* metabolic wastes to kidneys and lungs for excretions

Question 2

Circulatory system consists of

Answer 2

heart, blood vessels, lymphatic vessels via pulmonary circulation, systemic circulation, plus lymphatics

Question 3

Low pressure pulmonary circulation

Answer 3

Driven by rt side of heart; to deliver blood to lungs for oxygenation

Question 4

Higher pressure systemic circulation

Answer 4

Left side of heart; move oxygenated blood to body tissues and deliver waste products to lungs, kidneys, liver

Question 5

Lymphatic vessels

Answer 5

collect fluids from interstitum and return fluids to circulatory system

important in movement of lymphocytes and leukocytes between different components of immune system

Question 6

Heart consists

Answer 6

• Four chambers (two atriums => two atrium)
• four valves (two AV valves, tricuspid => mitral, two semilunar [pulmonic to aortic])
• muscular wall
• fibrous skeleton
• condunction system
• nerve fibers
• systemic vessels (coronary cirulations
• great vessels entering atria and ventricles

Question 7

heart wall

Answer 7

• epicardium (outer), myocaridum (muscular layer), and endocardium (inner)
• heart contained within pericardium, a double walled sac

Question 8

Myocardial layer of atria

Answer 8

receives blood, this layer is thinner than myocardial layer of ventricles (needed for pressure to pump to lungs or systemic circulation

Question 9

Separate sides of heart

Answer 9

interatrial septum and interventricular septum

Question 10

Blood flow?

Answer 10

1. Unoxygenated blood (venous) enters rt atrium via superior and inferior venae cavae
2. rt atrium => blood passes via right AV (tricuspid) into rt ventricle
3. Now go thorugh pulmonic semilunar valve (pulmonary valve) into pulmonary artery for oxygenation from lungs
4. oxygenated blood from lungs enter left atrium via four pulmonary veins (two from each lung side)
5. left atrium => left AV valve (mitral) => left ventricle
6. inflow => outflow to aortic semilunar valve (aortic valve) into aorta => body

Question 11

Oxygenated blood to coronary arteries?

Answer 11

openings within semilunar valves at entrance of aorta

Question 12

Deoxygenated blood from coronary veins?

Answer 12

Enter via coronary sinus at rt atrium

Question 13

Pumping action of heart

Answer 13

Two phases
* diastole - myocardium relaxes and chambers fill w/ blood
* systole - myocardium contracts, forcing blood out of the ventricles
* cardiac cycle: each one makes up for one heartbeat

Question 14

Sinoatrial (SA) node

Answer 14

generate electrical impulse and is the conduction system transmitting impulses (cardiac action potentials) that stimulate systolic contraction; autonomic nerves (sympathetic and parasympathetic fibers) adjust HR and systolic force, but do not stimulate heart to beat

Question 15

Collateral arteries

Answer 15

connections between same coronary artery or branches of rt and left

collateral growth is stimulated by shear stress (force that the blood flow exerts on the vessel wall), increased blood flow speed near an area of stenosis, and production of growth factors + cytokines

Question 16

Extensive capillary network

Answer 16

Heart has one

Question 17

normal ECG

Answer 17

sum of all cardiac action potentials

• P-wave: atrial depolarization
• QRS complex: sum of all ventricular depolarization
• ST interval: entire ventricular myocardium is depolarized

Question 18

SA cardiac action potentials

Answer 18

rate 60-100 impulse per minutes

Question 19

Conduction system possess?

Answer 19

Automaticity and rhythmicity

• automatic cells reutrn to threshold and depolarize rhythimcally w/o outside stimulus
• cell of SA node depolarize faster than other automatic cells (make it natural pacemaker of heart)
• IF SA node is disabled then AV node assumes control

Question 20

How does cardiac potential travel?

Answer 20

SA node => AV node => bund of His (AV bundle) => bundle branches => purkinje fibers => ventricular myocardium => impulse stopped there via refractory period of cells that have been polarized

refractory period ensures distaole (relaxation) will occur => complete cardiac cycle

Question 21

Adrenergic receptor

Answer 21

number, type, and fx govern autonomic (sympathetic) regulation of heart rate, contractile force, and dilation (constriction of coronary arteries); a1, a2, b1, b2, 3 in myocardium and coronary vessels determine effects of NT norepinephrine and epinephrine

Question 22

Effects of sympathetic stimulation depend on whether

Answer 22

1. a- or b-adrenergic receptors are most plentiful on cells of the effect tissue on cells of effector tissue
2. NT is norepinephrine or epinephrine
3. extent to which individual variations in receptor structure

Question 23

Cardiovascular structures for adrenergic receptors

Answer 23

More B-receptors than a-receptors, so they predominate

Question 24

B1, B2, B3 receptors

Answer 24

B1 - mostly in heart, mainly conduction system (AV and SA node, purkinje fibers) + atrial/ventricular myocardium + kidneys
B2 - heart and vascular smooth muscle
B3 - myocardium and coronary vessels

Stimulation of B1(more blood pumped) [one in the heart]
* increased heart rate (chronotropy)
* increased force of myocardial contraction (inotrophy)
* release renin => aldosterone + angiotensin II

Stimulation of B2 (increase coronary blood flow) [2 in the lungs]
* vasodilation b/c receptors on vascular smooth muscle (GI tract, bladder, uterus, liver, lungs)
* l/t urinary retention, decreased peristalsis, bronchodilation, inhibition of labor, vasodilation in heart via blood vessels (better bloodflow d/t being important organ), skeletal muscles better blood flow
* dilation of airways
* glucagon production (hormone); breakdown of glycogen to glucose in liver => pancreas
* do not mix up smooth muscle with cardiac muscle s:

Stimulation of B3 (opposes effects of B1, B2)
* decreases myocardial contractility (negative intropic effect)
* “safety” mechanism to prevent overstimulation

Question 25

How does the sympathetic mechanism work on cardiac?

Answer 25

Norepinephrine or circulating catecholamine interact w/ b-adrenergic receptor on cardiac cell membrane; final effect is increased influx of Ca++, which increases contractile strenght and speed of electrical impulses => increased sympathetic discharge dilates coronary vessels by causing release of vasodilating metabolies from increased myocardial contraction

Question 26

a-receptors (a1, a2)

Answer 26

Each a receptor has 3 subtypes, some sources say 9 of them (more of these receptors than beta receptors) a1-receptors: (presence of norepinephrine) * postsynaptic in systemic and coronary arteries * **smooth muscle** contraction and thus vasoconstriction **smooth muscle contraction** * iris => dilation * prostate => constrict * uretheral sphincter => urinary retention * pylorus and anal sphincter => limit food travel and stool a2(a)-receptor: * located on sympathetic ganglia and nerve terminals * norepinephrine on these receptors l/t inhibiting of more norepinephrine release providing a safety against high BP (this activation l/t vasodilation)

Question 27

myocardial cells vs skeletal cells

Answer 27

For myocardial cells: * transmit action potentials faster via intercalated disks * synthesizes more ATP d/t larger amount of mitochondria * more access to ions in interstitium d/t abdunance of tranverse tubules allowing myocardium to work constantly not needed in skeletal muscles

Question 28

Actin and myosin do what?

Answer 28

enable contraction via cross bridge; 1. Acetylcholine relased from neural cell => enable sarcoplasmic reticulum to release Ca++ then calcium travels to troponin complex 2. Ca++ binds to this complex and tropomyosin moves out of the way 3. Myosin can bind with the exposed exposed actin sites => actin pulled towards center of sarcomere causing shortening and contracting (myosin head has ATP => when attached to actin => head bends => ADP and phophate released => head resets / reattaches ATP for next contraction) 4. l/t muscle movement

Question 29

What is preload and afterload?

Answer 29

* Preload - pressure generated in ventricles at end of diastole, depending on amount of blood in ventricle * Afterload is resistance to ejection of blood from ventricle (afterload depends on pressure on aorta)

Question 30

Contractility

Answer 30

Potential for myocadrial fiber shortening during systole; depends on stretch during diastole (preload) and sympathetic stimulation of ventricles

Question 31

Frank-starling law of the heart

Answer 31

myocardial stretch determines force of myocardial contraction (greater stretch means stronger contraction)

Question 32

Laplaces's law

Answer 32

states amount of contractile force generated within a chamber depends on radius of chamber and thickness of its wall (small radis and thicker wall means GREATER force of contraction)

Question 33

Blood flow entire system

Answer 33

1. Left ventricle 2. Aorta 3. Arteries 4. Branch of arterioles + capillaries 5. **O2, nutrients, other substances** pass into interstitum for cell uptake 6. Capillaries absorb products of cellular metabolism 7. Venules (smallest veins) receive capilary blood 8. Flow to larger veins until it reaches venae cavae 9. Rt atrium

Question 34

Vessel wall composition?

Answer 34

1. tunic externica (outer layer) 2. tunica media (middle layer) 3. tunica intima (inner layer)

Question 35

Tunica media (middle layer of vessels) of arteries close to heart?

Answer 35

Contain more elastic fiber d/t needing to be able to distent during systole and recoil during diastole

Question 36

Precapillary sphincters

Answer 36

Controls blood flow into capillary beds (between arterioles and venules) via contraction and relaxation of these **smooth muscle bands** The endothelium (inner lining of cell cavities, organs) has prostagladins that can control this vasomotion

Question 37

Distributing arteries further from heart?

Answer 37

Contain more smoother muscle fibers b/c they must be able to constrict an dialte within specific capillary beds

Question 38

Blood flow through veins

Answer 38

Assisted by contraction of skeletal msucles (muscle pump) and backwards flow in lower body is **prevented** by one-way valves (deep veins in legs)

Question 39

Resistance to blood flow

Answer 39

Depends on vessel length and radius + blood viscosity (greater length, narrower radius of lumen, and greater viscosity means **greater resistance**

Question 40

Total peripheral resistance

Answer 40

Resistance to flow within entire circulatory sytem, depends on combined lengths and radii of all vessels + whether the vessels are arranged in series (circuit meaning greater resistance) or parallel (lesser resistance)

Question 41

Can blood flow be influenced by neural stimulation?

Answer 41

Yes via vasoconstriction or vasodilation + other autonomic functions

Question 42

Baroreceptors

Answer 42

stretch receptors mainly in aorta and carotid sinuses; when stretched or activated, these receptors reduce cardiac output by lowering HR and stroke volume and peripheral resistance, thus lowering blood pressure

Question 43

Arterial chemoreceptors

Answer 43

can be important for resp control; transmit impulses to medullary cardiovascular centers regulating BP * hypoxemia * increase in arterial PaCO2 * decrease in arterial blood PH **above conditions l/t reflexive increase in HR, stroke volume, and blood pressure**

Question 44

Key vasoconstrictor hormones

Answer 44

* **angiotensin II** (renin from kidneys => reacts w/ antiotensinogen from liver => angiotensin I (lungs make angiotensin converting enzyme) => makes angiotensin II => causes vasoconstriction + reacts w/ adrenal gland to stimulate release of **aldosterone** [acts on kidney to reabsorb NaCL + water]) * **vasopressin (antidiuretic hormone)** ==> decrease in blood volume or low blood pressure d/t dehydration or hemorrahge detected via baroreceptors in herat and large blood vessels => stimulate release of ADH from pituitary gland => reabsorbs water! increasing urine concentration /// **also cause vasoconstriction too** * **epinephrine and norepinephrine** refer to **alpha and beta receptor cards!**

Question 45

Adrenomedullin (ADM)

Answer 45

vasodilation peptide in CV, pulmonary, renal and other tissues increased levels indicative of heart failure and myocardial infection, help categorize

Question 46

Epinephrine + norepinephrine

Answer 46

Alpha (norepineprhine moreso than epinephrine) B**E**ta (eprinephrine > norepinephrine) norepinephine and epinephrine released from adrenal medulla (more potent than E) alpha => smooth muscle contraction beta => smooth muscle relaxation

Question 47

Vasodilator hormones

Answer 47

* **Atrial natriuretic peptide** or ANP - *** B-type natriuretic peptide** (BNP) * **C-type natriuretic peptide** (CNP) * **Urodilatin** -- natriuresis (excrete sodium) d/t icnreased renal blood flow Natriuresis (excretion of sodium in urine) and diuresis (inreased excretion of urine) d/t increased disastolic volume of heart => release these peptide hormones (increased ventricular blood volume?) * increased BNP means heart failure, pulmonary embolism, valvular HD, chronic CAD (correlates with overyhydration, malnutrition, and inflammation)

Question 48

Nitric oxide

Answer 48

formed by amino acid L-arginine in endothelial celss by ca++ dependent enzyme nitric oxide synthase * vascular homeostasis (dialtor tone, protect vessel from potential injury from platelets and cells circulating in blood) * decreased NO d/t impaired synthesis or excessive oxidative degradation => more risk factors d/t dysfunctional endothelial function

Question 49

Coronary circulation

Answer 49

not governed by same principles as flow through outher vascular beds 1. Blood flows into coronary arteries during **diastole** rather than systole b/c cusps of aortic semilunar valves block the openings of cornary arteries 2. Systolic contraction inhibits coronary artery flow by compressing the coronary arteries

Question 50

Autoregulation and myoglobin

Answer 50

Autoregulation allows coronary vessels to maintain optimal perfusion despite systolic effects Myoglobin in heart store O2 for use during systolic phase of cardiac cycle

Question 51

Lymph

Answer 51

interstitial fluid plus immune system cells

Question 52

Lympathic pathway

Answer 52

1. Absorb lymph via Lympathic venules in **capillary beds** 2. travels through larger lymphatic veins 3. Empties into right lympathic duct and thoracic dut 4. Drain into the rt and left subclavian veins 5. BONUS - as lympth travels towards thoracic ducts - it passes through lymph nodes clustered around lymphatic vessels

Question 53

Lymph nodes

Answer 53

sites of immune fx and ideally placed to sample fluid and cells moving from periphery into central circulation

Question 54

ECG and Holter monitoring

Answer 54

detects disturbances of impulse generation or conduction

Question 55

SPECT

Answer 55

stress testing; radiotracer imaging techniques

Question 56

Echocardiography

Answer 56

detects structural and functional cardiac abnormailities over time

Question 57

Cardiac catherization

Answer 57

measure o2 content and pressure of blood in the heart's chambers and to inject contrast media for x-ray examination of size and shape of chambers injection of contrast into coronary arteries (coronary angiography) [visualizes coronary circulation and tissue perfused by coronary arteries]

Question 58

How to eval systemic vascular system?

Answer 58

waveform analysis, doppler ultrasonography, venography, arteriography

Question 59

What is key driver of cardiovascular risk?

Answer 59

Age, the primary cause of death in persons older than age 65

Question 60

Most common CV disease?

Answer 60

Hypertension followed by coronary artherosclerosis (buildup of plaque in an artery)

Question 61

Most relevant age-associated physiologic changes in CV performance?

Answer 61

* myocardial and blood vessel stiffening * changes in neurogenic control for vascular tone * increased atrial fibrillation * loss of exercise capacity plus left ventricular hypertrophy and fibrosis