Physiology test 3

If the RR interval is 1 second in duration and the Q-T interval is 0.35 seconds, then what is the current heart rate?

60 beats per minute (only use RR interval)

alterations to capillary exchange

- acute standing increases hydrostatic pressure in legs and increases filtration -injury to capillaries causes fluid and proteins to leak into interstitial fluid which causes swelling. This increases osmotic pressure in interstitial fluid and increases absorption - kidney disease which increases volume of blood and hydrostatic pressure and increases solute elimination which decreases solutes and decreases osmotic pressure. these both increase filtration

Types of blood vessels

- arteries and arterioles --> away from the heart - veins/venules --> toward the heart, veins have the largest diameter - smooth muscle - connective tissue: collagen which provides extra strength and prevents rupture, and elastin which provides additional stretch - microcirculation: capillaries: endothelial cells and basement membrane

regulating arteriole resistance: extrinsic control

- autonomic nervous system and/or hormones - systemic - signals here influence the entire system

estimating blood pressure

- brachial artery proxy for the aorta, pressure is measured here because it is easy to access - sphygmomanometer with a stethoscope where you are listening for korotkoff sounds (turbulent flow)

Systemic circulation

- flow = cardiac output - change in pressure = mean arterial pressure - resistance = total peripheral resistance -CO = MAP/TPR - MAP drives blood flow through systemic circuit - TPR resists/impedes blood flow

Factors influencing cardiac output

- increased activity of sympathetic nerves to heart, which increases stroke volume in ventricular myocardium and the heart rate in SA node, which increases cardiac output -decreases activity of parasympathetic nerves to heart which increases heart rate, which increases cardiac output CO = SV x HR

regulating arteriole resistance: intrinsic control

- individual organ or tissue are receiving the bloodflow to its own region, wants to influence independent control -

Fenestrated capillaries

- large pores with variable size - in kidneys, intestines, and endocrine glands -pores are all working to increase the leakiness and allow for more exchange

Osmotic vs hydrostatic pressure

- near arteriole side hydrostatic pressure is greater than osmotic and bulk flow is filtration - near venules the osmotic pressure is greater than hydrostatic pressure and bulk flow is absorption

Factors that influence blood Volume

-EDV size: end-diastolic pressure (preload), primary determinant of end-diastolic volume. preload determinants: filling time(heart rate), atrial contractile force, central venous pressure (venous return, how much blood is coming back -Stroke volume factors: EDV, contractile force, counter-pressure

Fluid Flow of any liquid or gas

-Flow = change in pressure gradient/resistance -resistance = force that impedes flow

Capillaries

-Site of exchange between blood and tissue - smallest vessels with the thinnest walls, short, and most abundant (10-40 billion in humans), lots of surface area - capillary beds which are a cluster of vessels - slowest blood flow - leaky - BBB has leaky capillaries, other capillaries contain pores between these endothelial cells that help further facilitate solute exchange

Ventricular vs aortic pressure (start and end of phase 3)

-aortic pressure is just below ventricular -MAP = mean arterial pressure (average aortic pressure - SP = peak during systole (systolic pressure) - DP = lowest pressure in aorta (diastolic pressure)

Sympathetic nervous system regulation (extrinsic arteriole regulation)

-at the system level, not organ/tissue specific. - alpha receptors cause vasoconstriction in arterioles - beta receptors cause vasodilation in arterioles

pressure gradient

-blood flow driving force. -arterial pressure (MAP) vs average venous pressure (CVP) - pressure right next to the heart: vena cava pressure = 0 mmhg, aortic pressure = 85mmHg, Change in pressure = 85-0=85

Arterioles

-greatest resistance to blood flow - small radius - little elastin - smooth muscle - the largest drop in pressure occurs in the arterioles - arterioles are regulated and we can monitor resistance with its vessel radius - vasoconstriction: a contraction in smooth muscle decreases the radius, increasing tension, and as a result, increasing the resistance - vasodilation: where we relax smooth muscle to increase the radius, decreasing tension, decreasing resistance.

Factors increasing stroke volume

-increase in venous return which increases end-diastolic volume (ventricle), which increases stroke volume -increase in sympathetic activity or epinephrine which increases contractility (ventricle) which increases stroke volume - decrease in arterial pressure (afterload)

Blood volume

-increased blood volume increases venous pressure - decreased blood volume decreases venous pressure - long-term regulation of blood pressure done through regulating blood volume by the kidneys

Sinusoids (capillary)

-large blood filled spaces in the liver, spleen, and bone marrow - linked by fenestrated endothelial cells - no basement membrane to help further facilitate exchange

veins

-less smooth muscle than arteries -stretch more than arteries but there is a smaller pressure change when you stretch them - venous stretch acts as a volume reservoir - one way valves

Capillary exchange (lipids, water soluble, proteins)

-lipid soluble substance diffuse through direct diffusion (fatty acids, steroids and gases CO2 O2) lipophilic - water soluble substance which are smaller diffuse through pores (glucose and ions) - electrochemical gradient dictates direction - waste is higher in tissue - nutrients are lower in tissue - proteins diffuse via transcytosis (endocytosis on capillary side and exocytosis on interstitial fluid side) - pores are closed in BBB so their is transport compensation

Continuous capillaries

-most common - tight junctions link endothelial cells (intercellular clefts)

Frank-starling law optimal length

-optimal length is not at rest - stretch: closer to the optimal length - increased EDV is also closer to the optimal length

skeletal muscle pump

-skeletal muscle contraction compresses the veins between them which increases venous pressure. - one way valves

venules

-smaller than arterioles -little smooth muscle - venules closest to capillaries have no smooth muscles

Steps of Cardiac Excitation Contraction Coupling (ECC)

1. Action potential causes a depolarization spread through gap junction. This is how the contraction actually occurs (dif from skeletal) 2. Depolarization travels down T tubules and plasma membrane 3. Depolarization opens voltage-gated calcium channels. Stimulates of calcium through voltage gated calcium channels and is on sarcoplasmic reticulum and plasma membrane. Inside cell and extracellular (dif from skeletal) 4. Calcium levels increase in the sarcoplasm. This triggers calcium mediated calcium release. Positive feedback loop to dump as much calcium as possible into the cytosol 5. Calcium binds to troponin which moves tropomyosin out of the way 6. Crossbridge cycling occurs (contraction). The power stroke is generating force 7. Calcium is removed to stop crossbridge cycle. We still have ATP driven calcium pumps in SRR where we are actively pumping calcium back into SR, also in plasma membrane. Sodium channel exchanger in plasma membrane (secondary active transport). (some new)

Describe the effect of end-diastolic volume on stroke volume (be sure to include the cellular/molecular mechanism at play here)

An increase in end-diastolic volume stretches muscle cells in the ventricle to lengths closer to optimum which increases the strength of contraction (increased stroke volume)

The Frank-Starling Law (or the Maestrini Law) is due to what value changing and what general muscle fiber property?

As the end diastolic volume (EDV) increases, this stretches the ventricles which brings the muscle fibers closer to their optimal length. This means that the cardiac muscle fibers will be able to have more myosin heads participating in this process and thus generate more force. The opposite will also be true, that as EDV decreases that the muscle fibers get further from their optimal length and will have fewer myosin heads able to participate in moving actin fibers and thus less force generated.

What does the atria and ventricles contract according to?

Atria: sinus rhythm generated by SA Ventricles: bundle of his discharge (bundle of his discharges slowly)

Intrinsic arteriole regulation

Changes in arteriole resistance can be caused by changes in the composition of the extracellular fluid, cues included O2, CO2, K+, or H+ concentration. -Increasing metabolic activity causes vasodilation (decreases arteriole resistance) - decreasing metabolic activity causes vasoconstriction (increase in arterial resistance.

Which of the following statements is FALSE? A) Sympathetic activation increases the rate of action potential firing in the SA node B) Parasympathetic activation decreases the rate of action potential firing in the SA node C) Sympathetic activation can decrease the delay between atrial and ventricular contraction D) Parasympathetic activation reduces cardiac action potential duration E) Sympathetic activation can open T-type Ca++channels

D) Parasympathetic activation reduces cardiac action potential duration

Two different measures are collected when examining your blood pressure. Which statement is most accurate with respect to those measures? A) Diastolic pressure is due to the contraction of the aorta following its stretch B)Diastolic pressure is a measure of the highest arterial pressure that is just below peak ventricular pressure C)Systolic pressure is a measure of the lowest arterial pressure that is just above the lowest ventricular pressure D.)Systolic pressure is a measure of the highest arterial pressure that is just below peak ventricular pressure E) Systolic pressure is a measure of the highest arterial pressure that occurs during the dicrotic notch

D)Systolic pressure is a measure of the highest arterial pressure that is just below peak ventricular pressure

Cardiac output is determined by what two variables?

Heart rate and stroke volume

Respiratory pump

Inhalation - diaphragm causes a decrease in thoracic cavity pressure and an increase in abdominal cavity pressure. The pressure gradient pushes blood from abdominal veins towards thoracic veins Exhalation - increase in thoracic cavity pressure and a decrease in abdominal cavity pressure. the pressure gradient is from the thoracic cavity to the heart

abnormal SA node rates

Sinus rhythm: Pace generated by the SA node Sinus tachycardia is a fast rate Sinus bradycardia is a slow rate

Please describe what the Frank-Starling law means..

The Frank-Starling law means that when more blood comes into the ventricle, more blood will be pumped out of the ventricle. The opposite is also true, meaning that as less blood comes into the ventricle less blood is pumped out of the ventricle. This is all predicated upon the existence of the optimal length principle (which applies to all striated muscle, thus skeletal and cardiac) and that at rest the cardiac muscle is not at its optimal length. So as the ventricular myocardium (i.e. cardiac fibers that drive ventricular contraction) is stretched, these cardiac muscle fibers get closer to their optimal length. As they are closer to their optimal length more myosin heads are able to bind to actin and participate in the crossbridge cycle (i.e. generate force)

myogenic response (Intrinsic arteriole regulation)

There are stretch receptors in some smooth muscle that contract when stretched and relax when not stretched - this response helps maintain rate of blood flow and increased flow/increased pressure gradient to an individual organ (opposite is also true)

Cardiac Cycle phase 3

Ventricular ejection - remainder of systole - pressure is eventually greater in ventricles than arteries which forces the semilunar valves open (aortic and pulmonary), atrioventricular valves are closed - blood moves from ventricle to aorta - blood is finally being ejected

Arrhythmia

abnormal recorded electrical activity

blood viscosity 3

affects blood flow. - concentration of cells and extracellular proteins

Frank-starling law autonomic nervous system

alters the position of the curve - increased sympathetic (increase stroke volume) - decreased sympathetic (decrease stroke volume) - parasympathetic activity is not working here because it does not innervate the ventricular myocardium

arterial blood pressure

aorta stretches during systole, the left ventricle is ejecting blood faster than it can be emptied from the aorta, this ensures continuous blood flow - arteries = pressure reservoir because they store energy as they stretch

Continuous blood flow

aorta stretches during ventricular ejection too fast, this stretch acts as energy storage - this stored energy is released during diastole as the aortic valve is shut. This helps maintain blood flow throughout the cardiac cycle. The excess blood is expelled into the vasculature even when the ventricle is not contracting, blood can keep flowing because we stored the excess energy as stretch.

During phase 1 (mid diastole; ventricular filling), describe the state of Aortic valve, the AV valves, and the ventricular muscles.

aortic valve is closed, AV valves are open, ventricular muscles are relaxed

Systemic and pulmonary circuits

blood flows from highest to lowest pressure -systemic: left ventricle through body to right atrium - pulmonary: right ventricle through the lung and to the left atrium. pressure in systemic circuit is much higher than pulmonary in the arteries all the way to the veins where the pressure in both is close to zero

EDV

blood in the ventricle at the end of diastole

ESV

blood in the ventricle at the end of systole

Net filtration pressure

determines the direction of bulk flow - filtration (hydrostatic) - absorption (osmotic) - more net filtration than absorption - excess fluid goes to the lymphatic system where it is filtered and returned to circulation

Aortic pressure

blood pressure readings. - the dicrotic notch is the end of systole when the aortic valves are going to close. A change in turbulent blood flow is what gives the dicrotic notch - end of systole means diastole is starting and the blood pooled in aorta is slowly ejected, this allows for circulation to be continuous.

P wave (EKG)

caused by atrial depolarization

QRS (EKG)

caused by initial ventricular depolarization, Na driven portion of contractile cells in the ventricles

Other drivers of Intrinsic arteriole regulation

change in blood flow also changes the composition of extracellular fluid - ex: blocked blood vessel which decreases oxygen in target tissue and increases CO2. - this causes vasodilation to occur to increase blood flow and radius of arteriole to remove blockage -active hyperemia

Total peripheral resistance

combined resistance of all the blood vessels within a circuit - change in part of the network changes the speed of flow in the entire circuit ex: vasoconstriction anywhere in the network increases resistance in that part of the network and decreases flow in that part of the network. This also changes the speed of flow in the entire circuit.

vasodilation

correcting problem that is causing the change, reduces arteriole resistance - increases blood flow - more oxygen - more CO2 clearance - active hyperemia: higher than steady state blood flow increasing size of arterioles so it is easier for blood to flow through

Independent regulation of blood flow

different proportional flow, depends on what share of the pie it is getting - bidirectional changes - large proportional changes

varicose veins

due to faulty/leaky valves

Q-T interval

duration of ventricular contraction (also ventricular systole)

T-Q segment

duration of ventricular relaxation (ventricular diastole)

skeletal muscle pump - contraction

during contraction the distal valve prevents backflow and is closed and the proximal valve is closer

skeletal muscle pump - relaxation

during relaxation the proximal valve prevents backflow and is closed and the distal valve is open and it flows down pressure gradient

vessel length 2

factor affecting blood flow, changes as you grow

hydrostatic pressure

fluid pressure in capillaries - highest at the arteriole end - decreases across its length lowest at the venule end - capillary hydrostatic pressure is always higher than interstitial fluid hydrostatic pressure - interstitial pressure does not change and the - pressure gradient is always pushing fluid out of capillaries into interstitial fluid, always in direction of filtration - decreases across length of capillary

ejection fraction

fraction of EDV that ends up being ejected during a heartbeat ejection fraction = SV/EDV

filtration

from blood into interstitial fluid

absorption

from interstitial fluid into blood

parasympathetic cardiac regulation (AV node)

parasympathetic neurons hyperpolarize the AV node and conduction fibers - increases the delay between SA and AV nodes - decreases heart rate

lymphatic system

has very large openings (lymphatic capillaries) that facilitate exchange and allow protein and large particles to enter freely - nodes filter foreign material - macrophages which specialize in phagocytosis and the immune system which filters bacteria - blood is returned to circulation

Overview of cardiac cycle

includes contraction/relaxation, valve action, pressure changes, changes in blood volume Left side and ventricle dominant because it is responsible for pumping blood to the entire body

example of Intrinsic arteriole regulation

increased metabolic rate - O2 consumed increases so there is less available - CO2 production increases (more waste) - these both induce vasodilation and indicates a need for more blood there.

Pressure gradients and capillary exchange

influences all solutes - bulk flow - filtration and absorption to maintain fluid balance between blood plasma and interstitial fluid of tissue - when this isnt balanced an edema can form which is when more fluid enters the interstitial fluid which leads to swelling

Cardiac cycle phase 2

isovolumetric ventricular contraction - early systole - ventricle contracts which increases pressure - both AV and semilunar valves are closed, pressure is lower in ventricles than arteries, but the pressure in ventricles is higher than in atria - isovolumetric = volume of blood does not change, all valves are closed and pressure keeps building

Cardiac cycle phase 4

isovolumetric ventricular relaxation - early diastole - ventricle relaxes which decreases pressure. The pressure in ventricles is lower than arteries (aortic pressure) but higher than atria. All valves are shut so no blood is exiting or entering. - last phase, process then restarts and continues cycling - ventricular pressure decreases until it is below atrial pressure

Fibrillation

loss of coordinated electrical activity atrial fibrillation: not deadly and is where the heart feels weird short term ventricular fibrillation: deadly and is corrected by defibrillation which provides a large current to depolarize all the muscles simultaneously in hopes of returning them to normal activity.

2 distinct sounds of the heart

lubb - DUBB -1st sound: softer lubb during phase 2 when AV valves are closing -2nd sound: louder DUBB during phase 4 when the semilunar valves are closing - it is turbulent flow the causes the sound not the valves slapping shut

vessel radius 1

most important factor determining resistance and blood flow, smaller opening = more resistance vasoconstriction = contraction (increased resistance), decreased radius vasodilation = relaxation (decreased resistance), increase radius

Autonomic regulation of heart rate

parasympathetic and sympathetic send projections to the SA and AV node, sympathetic sends to conduction fibers and ventricles

Parasympathetic cardiac regulation (SA node)

parasympathetic neurons decrease the rate of SA node action potentials which release acetylcholine, activate muscarinic receptors. - slows heart rate - close t-type and funny channels (causes less Ca and Na to flow into the cell, causes more K+ channels to open, which slightly hyperpolarizes the cell. - this is an inhibitory signal making the pacemaker cells have to produce more depolarization current and it is going to take longer to get to threshold.

When comparing the cardiac and skeletal muscle ECC, are there any differences in what depolarization opens? If so, what are those differences. If not, please highlight another difference between the two processes

polarization causes channels specific for calcium to open in both processes, but in skeletal muscle calcium passes through ryanodine receptors embedded in the sarcoplasmic reticulum. These receptors are opened by a DHP receptors embedded in T-tubules. However in cardiac muscle, depolarization stimulates voltage-gated calcium channels embedded in both the sarcoplasmic reticulum and plasma membrane to open.

What single factor ultimately determines whether or not blood is moved as well as the direction of movement?

pressure

Osmotic pressure

pressure from non-permeable solutes (proteins) - capillary osmotic pressure is greater than interstitial fluid osmotic pressure - osmotic pressure gradient is pulling fluid from the interstitial fluid into capillaries (absorption) - higher concentration of nonpermeable solutes will pull fluid towards it. - remains constant

factors that influence venous pressure

pressure gradient drives venous return and it is a domino effect - skeletal muscle pump - respiratory pump - blood volume - venomotor tone

Electrocardiogram (ECG/EKG)

record of the spread of electrical current through the heart as a function of time. Measures differences in electrical potential between points (leads) (Einthoven's triangle). Need 3 leads to record an EKG.

hormonal regulation (extrinsic arteriole regulation)

regulate radius of arterioles - vasopressin (ADH) promotes vasoconstriction (this is an antidiruetic secreted by neurons in hypothalamus where it is released into the blood stream in the posterior pituitary. - angiotensin II promotes vasoconstriction. This is derived from an inactive protein pre-cursor that is always present in blood plasma, just waiting on two enzymes to generate angiotensin II.

pre-capillary sphincters

smooth muscle rings that respond to intrinsic factors (CO2, O2) - contraction of muscles decreases blood flow - relaxation increases blood flow -metabolites drive contraction and relaxation - capillaries do not have smooth muscle, but they utilize it to alter their flow

Ventricular vs atrial pressure (2 and 4)

start of phase 2 (end of diastole), end of phase 4 -start of ventricular contraction, ventricular pressure is higher than atrial. (look in notes for image) Before phase 2 and after phase 4 atrial pressure is slightly higher than ventricular (during atrial contraction)

Frank-starling law

stroke volume (output) matches the venous return (input) - increase EDV increases ventricular contractile force, which increases stroke volume (opposite is also true) More blood into the ventricle then more blood is pushed out

sympathetic cardiac regulation (AV node)

sympathetic neurons depolarize the AV node and conduction fibers - this decreases the ventricular delay necessary for faster heart rate - heart rate increases -This shortens systole more than diastole so we can squeeze the blood out faster, leave diastole alone so we can give the ventricles enough time to properly fill

sympathetic cardiac regulation (SA node)

sympathetic neurons increase the rate of SA action potentials by releasing norepinephrine to activate beta-1 receptors in SA node (pacemaker cells) - increases heart rate - opens funny and T-type channels which allows for more sodium and calcium influx into the cell which gets us to threshold faster, which increases rate of spontaneous depolarization, which increases rate of SA node action potentials, which increases heart rate

Sympathetic ventricular contraction

sympathetic neurons signal ventricular contractile cells which increase the contractile force generated, and increase the rate of contraction and an increased rate of relaxation. as contractile force is increased, the duration fo the contraction is decreased. This allows us to increase heart rate (all of this is impacting systole)

During isovolumetric ventricular relaxation (phase 4), describe the state of Aortic valve, the AV valves, and the ventricular muscles.

the AV and semilunar valves are closed and ventricular pressure is decreasing

Active vs reactive hyperemia

the cues and the response is the same but the cause is different (metabolism vs blood flow) - active is caused by an increase in metabolic rate and reactive is caused by a decrease in blood flow

R-R interval

time between heartbeats (how long your heartbeat is)

systole

ventricular contraction (systole squeeze)

Cardiac cycle phase 1

ventricular filling -mid to late diastole -pressure is greater in atria than ventricles so the Atrioventricular valves are pushed open, blood moves from atrium to ventricles - passive phase and active phase. - passive phase there is no contraction and is ventricular filling - active phaseL have atrial contraction (end of phase), forces as much blood into ventricles before they begin to contract, once ventricles contract it overpowers the pressure and forces AV valves shut

diastole

ventricular relaxation

T wave (EKG)

ventricular repolarization

Stoke Volume (SV)

volume of blood ejected by the ventricle each beat SV = end-diastolic volume(EDV) - end systolic volume (ESV)

Cardiac Output (CO)

volume of blood pumped by the ventricle each minute -CO = SV x heart rate -average CO is 5 liters/min at rest (0.07 L(per beat) x 72 beats/min) - average total blood volume is 5.5 liters

degree blockages

when ventricular contraction is not normal. Altered AV node conduction. For example: third degree is when there is no conduction and can lead to cardiac arrest The atria and ventricle are contracting independent of each other which is bad