Unit 3 Pathophysiology - Chapter 32 structure and fuction of CV and lympathic system Flashcards
Circulatory system does what
Circulatory system
body’s transport system and communication system
Delivers:
* oxygen
* nutrients
* hormones
* blood cells
* immune cells
* metabolic wastes to kidneys and lungs for excretions
Circulatory system consists of
heart, blood vessels, lymphatic vessels via pulmonary circulation, systemic circulation, plus lymphatics
Low pressure pulmonary circulation
Driven by rt side of heart; to deliver blood to lungs for oxygenation
Higher pressure systemic circulation
Left side of heart; move oxygenated blood to body tissues and deliver waste products to lungs, kidneys, liver
Lymphatic vessels
collect fluids from interstitum and return fluids to circulatory system
important in movement of lymphocytes and leukocytes between different components of immune system
Heart consists
- 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
heart wall
- epicardium (outer), myocaridum (muscular layer), and endocardium (inner)
- heart contained within pericardium, a double walled sac
Myocardial layer of atria
receives blood, this layer is thinner than myocardial layer of ventricles (needed for pressure to pump to lungs or systemic circulation
Separate sides of heart
interatrial septum and interventricular septum
Blood flow?
- Unoxygenated blood (venous) enters rt atrium via superior and inferior venae cavae
- rt atrium => blood passes via right AV (tricuspid) into rt ventricle
- Now go thorugh pulmonic semilunar valve (pulmonary valve) into pulmonary artery for oxygenation from lungs
- oxygenated blood from lungs enter left atrium via four pulmonary veins (two from each lung side)
- left atrium => left AV valve (mitral) => left ventricle
- inflow => outflow to aortic semilunar valve (aortic valve) into aorta => body
Oxygenated blood to coronary arteries?
openings within semilunar valves at entrance of aorta
Deoxygenated blood from coronary veins?
Enter via coronary sinus at rt atrium
Pumping action of heart
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
Sinoatrial (SA) node
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
Collateral arteries
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
Extensive capillary network
Heart has one
normal ECG
sum of all cardiac action potentials
- P-wave: atrial depolarization
- QRS complex: sum of all ventricular depolarization
- ST interval: entire ventricular myocardium is depolarized
SA cardiac action potentials
rate 60-100 impulse per minutes
Conduction system possess?
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
How does cardiac potential travel?
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
Adrenergic receptor
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
Effects of sympathetic stimulation depend on whether
- a- or b-adrenergic receptors are most plentiful on cells of the effect tissue on cells of effector tissue
- NT is norepinephrine or epinephrine
- extent to which individual variations in receptor structure
Cardiovascular structures for adrenergic receptors
More B-receptors than a-receptors, so they predominate
B1, B2, B3 receptors
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
How does the sympathetic mechanism work on cardiac?
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
a-receptors (a1, a2)
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)
myocardial cells vs skeletal cells
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
Actin and myosin do what?
enable contraction via cross bridge;
- Acetylcholine relased from neural cell => enable sarcoplasmic reticulum to release Ca++ then calcium travels to troponin complex
- Ca++ binds to this complex and tropomyosin moves out of the way
- 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)
- l/t muscle movement
What is preload and afterload?
- 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)
Contractility
Potential for myocadrial fiber shortening during systole; depends on stretch during diastole (preload) and sympathetic stimulation of ventricles
Frank-starling law of the heart
myocardial stretch determines force of myocardial contraction (greater stretch means stronger contraction)
Laplaces’s law
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)
Blood flow entire system
- Left ventricle
- Aorta
- Arteries
- Branch of arterioles + capillaries
- O2, nutrients, other substances pass into interstitum for cell uptake
- Capillaries absorb products of cellular metabolism
- Venules (smallest veins) receive capilary blood
- Flow to larger veins until it reaches venae cavae
- Rt atrium
Vessel wall composition?
- tunic externica (outer layer)
- tunica media (middle layer)
- tunica intima (inner layer)
Tunica media (middle layer of vessels) of arteries close to heart?
Contain more elastic fiber d/t needing to be able to distent during systole and recoil during diastole
Precapillary sphincters
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
Distributing arteries further from heart?
Contain more smoother muscle fibers b/c they must be able to constrict an dialte within specific capillary beds
Blood flow through veins
Assisted by contraction of skeletal msucles (muscle pump) and backwards flow in lower body is prevented by one-way valves (deep veins in legs)
Resistance to blood flow
Depends on vessel length and radius + blood viscosity (greater length, narrower radius of lumen, and greater viscosity means greater resistance
Total peripheral resistance
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)
Can blood flow be influenced by neural stimulation?
Yes via vasoconstriction or vasodilation + other autonomic functions
Baroreceptors
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
Arterial chemoreceptors
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
Key vasoconstrictor hormones
- 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!
Adrenomedullin (ADM)
vasodilation peptide in CV, pulmonary, renal and other tissues
increased levels indicative of heart failure and myocardial infection, help categorize
Epinephrine + norepinephrine
Alpha (norepineprhine moreso than epinephrine)
BEta (eprinephrine > norepinephrine)
norepinephine and epinephrine released from adrenal medulla (more potent than E)
alpha => smooth muscle contraction
beta => smooth muscle relaxation
Vasodilator hormones
-
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)
Nitric oxide
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
Coronary circulation
not governed by same principles as flow through outher vascular beds
- Blood flows into coronary arteries during diastole rather than systole b/c cusps of aortic semilunar valves block the openings of cornary arteries
- Systolic contraction inhibits coronary artery flow by compressing the coronary arteries
Autoregulation and myoglobin
Autoregulation allows coronary vessels to maintain optimal perfusion despite systolic effects
Myoglobin in heart store O2 for use during systolic phase of cardiac cycle
Lymph
interstitial fluid plus immune system cells
Lympathic pathway
- Absorb lymph via Lympathic venules in capillary beds
- travels through larger lymphatic veins
- Empties into right lympathic duct and thoracic dut
- Drain into the rt and left subclavian veins
- BONUS - as lympth travels towards thoracic ducts - it passes through lymph nodes clustered around lymphatic vessels
Lymph nodes
sites of immune fx and ideally placed to sample fluid and cells moving from periphery into central circulation
ECG and Holter monitoring
detects disturbances of impulse generation or conduction
SPECT
stress testing; radiotracer imaging techniques
Echocardiography
detects structural and functional cardiac abnormailities over time
Cardiac catherization
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]
How to eval systemic vascular system?
waveform analysis, doppler ultrasonography, venography, arteriography
What is key driver of cardiovascular risk?
Age, the primary cause of death in persons older than age 65
Most common CV disease?
Hypertension followed by coronary artherosclerosis (buildup of plaque in an artery)
Most relevant age-associated physiologic changes in CV performance?
- 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
