Physiology Exam 3

Pulmonary circulation

Blood flow from right side of the heart to alveoli back to the heart

Systemic circulation

Blood flow from left side of the heart to the whole bady back to the right side

Parallel flow

Systemic circulation routes which oxygenates one organ through one pathway, allowing for independent regulation of blood flow

Exceptions to parallel flow

Series, such as the hypophyseal portal system, where blood from the hypothalamic capillaries flows into the pituitary gland capillaries, also applies with hepatic portal system

Pericardium

Outer membrane of the heart that functions as a protective sac

Pericardial space purpose

Sits between the epicardium and parietal layer, allows lubricating fluid to support heart contractility

Epicardium

Comprised of epithelial and connective tissue

Myocardium

Muscular layer of the heart between the epi and endo cardium

Which side of the heart works harder and is under more pressure?

The left side is thicker and pushes harder due to arteriole resistance

Electrical flow

SA node → AV node → bundles of His → left and right bundles → purkinje fibers

Purpose of the chordae tendonae

Held by papillary muscles and prevent the valves from everting during contraction

How is blood regurgitation into the vena cava and pulmonary vein prevented if they have no valves?

Atrial muscle contraction collapses the venous entry points

Purpose of the fibrous heart skeleton

Prevents valves from overstretching and acts as a point of attachment for cardiac fibers

When do cardiac arteries perfuse cardiac cell muscles?

During relaxation

How do cardiac fibers compare to skeletal fibers?

Shorter, connected with intercalated disks, less T tubules and smaller SR

Intercalated disk composition and purpose

Desmosomes and gap junctions, allows for electrical conduction to make a functional syncytium

How are the ventricles and atria able to function as separate syncytium?

The fibrous skeleton functions as an electrical insulator, separating the two signals

Autorhythmicity

The ability for the heart to generate its own electrical impulses

Purpose of authrhythmic fibers

Act as a pacemaker for the heart, and form a conduction pathway for signals via functional syncytium

Generation of pacemaker potential

1st phase: Closure of voltage gated K+ channels while F-type channels open and let Na+ in

Pacemaker potential phase: F type channels close just before reaching threshold and T type voltage gated Ca2+ channels open until threshold is reached

Depolarizing phase: T type voltage gated Ca2+ channels close while L type voltage gated Ca2+ channels open and fully depolarize cell to make AP

Hyperpolarizing phase: After full depolarization and AP formation, Ca2+ L type channels close and K+ channels reopen, hyperpolarizing cell

Base rhythm of SA node fibers

100 BPM, or every 0.6 seconds

ANS effect of SA rhythm

Uses hormones through the PNS or SNS to alter strength and timing of rhythm but not change fundamental rate

Rate each node can generate signals at

SA: 100 BPM, 0.6 s

AV: 40-60 BPM, 1-1.33 s

Bundles, bundle branch, or purkinje: 20-35 BPM, 2-3 s

How do contractile cardiac fibers differ from autorhythmic fibers?

Lower resting membrane potentials at -90mV due to higher K+ permeability

AP generation in contractile fibers

Depolarizing phase: Fast voltage Na+ channels open

Initial repolarizing phase: Fast voltage Na+ channels close, and Fast voltage K+ channels open

Plateau: L-type voltage gated Ca channels open, fast voltage Na+ channels close, and slow voltage K+ channels open partially

Final repolarizing phase: L-type voltage gated Ca channels open and slow voltage K+ channels open fully

Excitation-contraction coupling

Calcium release into the EC space travels through L type Ca voltage channels into sarcoplasm, causes CICR channels to release more calcium from the SR

How is tetanus prevented in cardiac muscle?

Long refractory periods means the muscle cannot summate contractions

Atrial systole

Atrial contraction

Atrial diastole

Atrial relaxation

Q-T interval

Time between ventricular depolarization and repolarization

P-Q interval

Time between atrial and ventricular excitement

S-T interval

Period of ventricular depolarization before repolarization

Cardiac cycle phases

Passive ventricular filling → atrial contraction → isovolumetric ventricular contraction → ventricular ejection → isovolumetric ventricular relaxation

Passive ventricular filling

Higher atrial pressure than ventricular pressure, blood returns through veins to atria while semilunar valves are closed

Atrial contraction

Atrial depolarization causing systole, ventricles remain in diastole, atrial pressure increase forces blood through AV valves into ventricles

Isovolumetric ventricular contraction

Atrial diastole, ventricular depolarization causing systole and high pressure, closing both sets of valves and keeping muscle length isometric and volume isovolumetric

Ventricular ejection

AV valves open around 80 mmHg of pressure to overcome aortic and pulmonary trunk pressures, both ventricles eject equal amounts of blood

Stroke volume

End diastolic volume - end systolic volume

Ejection fraction

Stroke volume/end diastolic volume

Isovolumetric ventricular relaxation

Ventricular repolarization causing diastole, closing both valve sets briefly, when ventricular pressure drops AV valves open allowing ventricle to fill

Dicrotic wave

Pressure from blood slamming on SL valves during isovolumetric ventricular relaxation

Cardiac output

volume of blood ejected from each ventricle per minute, Stroke volume x HR

Preload

Degree of stretch in the heart before contraction, high force=high contractility, the more volume=greater contractility (Frank-Starling Law)

Factors which effect EDV

Venous return and filling time

Contractility and ionotropic effects

Positive ionotropic effects increase contractility, increase SV

Norepinephrine contractility pathway

Sympathetic nerves release NE and bind to beta receptors → G protein signals adenylyl cyclase to convert ATP to cAMP → Protein kinase A activated and phosphorylates L-type calcium channels → Ca channels in SR also phosphorylated, Ca allows for contraction → phospholamban phosphorylated so SERCA can corral Ca into SR, causing relaxation

Afterload

Pressure from the pulmonary trunk and aorta that must be overcome before ventricular ejection

What does increased afterload cause?

Decreased stroke volume, leaving more blood in the ventricles

Sympathetic heart regulation

Increased HR, increase action potential conduction between atria and ventricles, and increases contractility

Sympathetic HR increase pathway

NE binds to beta receptor → G protein activates and binds to adenylyl cyclase, turning ATP to cAMP → cAMP binds to F-type channels and causes Na to polarize cell for long periods of time → presence of Na allows for spontaneous depolarization, increasing AP frequency

Parasympathetic HR decrease pathway

Ach binds to muscarinic receptors → G protein activated and binds to K+ channels, hyperpolarizing cell → inhibition of adenylyl cyclase which limits F channel opening → decreased spontaneous depolarization

Factors which affect preload

Filling time and venous return

Factors which affect contractility

SNS, hormones, drugs, ions

Factors which affect HR

Age, hormones, ions, ANS divisions

Pressure reservoir

Contains pumping force from ventricular systole in elastic walls, pumps even when ventricles are in diastole

Why are arterioles resistance vessels?

Their small diameter causes blood flow to be resisted

Microcirculation

Blood flow between venules, arterioles, and capillaries

Capillary beds

A system of around 100 capillaries which perfuse an area of the body

Metarterioles

Bypasses through capillaries that directly exhcanges blood between an arteriole and venule

Precapillary sphincters

Smooth muscle rings that control blood flow through the capillaries by opening or closing metarterioles or arterioles

Vasomotion

Blood flow through capillaries resulting from precapillary

Continuous capillaries structure and permeability

Plasma membranes form a continuous tube where intercellular clefts cause brief pores, permeable to water and small solutes like sodium and glucose

Fenestrated capillaries structure and permeability

Larger pores and intercellular clefts with higher permeability to water and solutes

Sinusoids structure and permeability

Wider and more winding with large fenestrations and large intracellular clefts, permeable to blood cells and proteins

Why are postcapillary venules drippy?

Have loosely joined intracellular junctions

Skeletal muscle pump

Initially both valves are open, which allows the body to push blood when muscles contract

Respiratory pump

Inhalation causes thoracic pressure to decrease and increase abdominal pressure, bringing blood up the IVC

Where is the majority of blood located at rest?

In systemic venous circulation

Transcytosis

Blood substances use vesicles to move through cells, used for large, non-lipid soluble molecules

Bulk flow

Moves a lot of ions, molecules, or particles in one direction based on ion gradient

Reabsorption

Pressure driving movement from interstitial fluid into capillaries

Filtration

Pressure driving movement from capillaries into interstitial fluid

Capillary hydrostatic pressure

Water pressure exerted on the inner surface of the capillary walls, filtration

Interstitial fluid hydrostatic pressure

Water pressure exerted on the outer surface of the capillary walls, reabsorption

Plasma colloid hydrostatic pressure

Pressure due to colloid suspension in blood, reabsorption through osmosis of water into capillaries

Interstitial fluid colloid hydrostatic pressure

Pressure due to plasma proteins in interstitial fluid, filtration by causing fluid from blood to osmotise into interstitial spaces

Net filtration pressure

Overall shifts to filtration, which forces capillaries to pick up fluid

Lymph flow regulation

Smooth muscle contractions, skeletal and respiratory muscle pumps

Blood flow equation

F = Change in P/R

Resistance equation

R = (Blood viscosity)(vessel length)/vessel radius^4

Factors affecting viscosity

Anything that influences erythrocyte to volume balance, such as polycythemia, dehydration (increases) or anemia, hemorrhage (decreases)

Factors affect length

Obesity, does not lengthen vessels to increase pressure but rather makes more

Total peripheral resistance

All vascular resistances provided by the body

Laminar flow

How blood typically flows through vessels

Systolic pressure

Highest pressure attained in arteries during systole

Diastolic pressure

Lowest blood pressure attained in arteries during diastole

Pulse pressure

Difference between systolic and diastolic pressure

Mean arterial pressure

diastolic pressure + 1/3 PP

Cardiac output in terms of MAP

CO = MAP/TPR

MAP in terms of cardiac output

MAP = CO x TPR

Compliance

Ability of an object to stretch, c= change in volume/change in pressure

Difference between artery and vein compliance

Veins have higher compliance than arteries

Blood flow velocity and cross section relationship

Flow slowest when cross section is greatest, so capillary flow is slowest and elastic artery is greatest

Purpose of venoconstriction

Return blood back to the heart by reducing the amount in blood reservoirs

Venous pressure gradient

Pressure difference between the venules and right atrium, barely able to overcome gravity

Blood flow regulation at rest versus with exertion

Majority goes to digestive system and liver, then kidneys, with the majority of blood shifting to skeletal muscles during exertion, only exception is flow to the brain which remains constant no matter conditions

What regulates blood flow primarily?

Arterioles

Intrinsic control

Mechanisms within organs that control arteriole radii through physical changes or local mediators

Physical changes controlling blood flow

Warming or cooling, myogenic response where stretching of arterials causes a sustaining of blood pressure (If BP increases, arterioles stretched, causing contraction, keeping constriction and BP stable)

Myogenic response pathway

Stretch of smooth muscle causes mechanically gated channels to let Ca ions in → calmodulin and Ca binds together → Ca calmodulin complex activates MLCK, which phosphorylates myosin → Myosin binds to actin causing contraction and vasoconstriction