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Flashcards in Physiology II Deck (45):

What are chronotropic effects? What are the mechanisms behind positive and negative chronotropic effects?

- chronotropic effects are changes on the heart rate; controlled by the autonomic nervous system
- positive effects (increased HR) via sympathetic activity: norepinephrine activates beta-1 receptors in the SA node, increasing the number of FUNNY F-type Na+ channels to increase the rate of phase 4 spontaneous depolarization (via Gs)
- negative effects (decreased HR) via parasympathetic activity: ACh activates M2 receptors in the SA node, decreasing the number of F-type Na+ channels AND opening K+-ACh channels (more K+ outflow = hyperpolarization) (via Gk, a type of Gi)


How do beta-blockers work?

- beta-blockers will block the beta-1 receptors of the SA node, preventing sympathetic stimulation of these cells
- this results in a negative chronotropic effect, and the heart rate will decrease
- lowered heart rate will result in lowered BP


What are dromotrophic effects? What are the mechanisms behind positive and negative dromotrophic effects?

- dromotrophic effects are changes on the conduction velocity; controlled by the autonomic nervous system
- positive effects (increased velocity) via sympathetic activity: stimulated beta-1 receptors raise conduction velocity in the AV node by increasing the number of TRANSIENT T-type Ca2+ channels in phase 0 (increased Ca2+ current = increased velocity)
- negative effects (decreased velocity) via parasympathetic activity: stimulated M2 receptors slow conduction velocity in the AV node by decreasing the number of T-type Ca2+ channels and opening K+-ACh channels (more K+ outflow = decreased inward current)


What is heart block and when does it occur?

- heart block occurs with excess negative dromotrophic effects (so when conduction velocity is very low)
- it occurs when the potentials fail to reach the ventricles via the AV node


What triggers the contraction of contractile cardiac cells? What determines the strength of the contraction?

- the calcium entering the cell during the plateau phase (phase 2) via the LONG-LASTING/SLOW L-type Ca2+ channels actually induces more calcium to enter the cell from the sarcoplasmic reticulum (this is called Ca2+ induced Ca2+ release)
- the calcium from the SR is the "trigger calcium" that will bind to the troponin C and initiate contraction
- *this means that the strength of the contraction is proportional to the intracellular calcium concentration*


What is contractility dependent on? How can we increase contractility?

- contractility depends on the rate of tension development and the peak tension
- we can increase contractility by increasing the amount of Ca2+ released by the sarcoplasmic reticulum via increasing the inward Ca2+ current during the plateau phase (phase 2, L-type Ca2+ channels) AND/OR via increasing the amount of Ca2+ stored in the SR (more storage = more release)


What are inotropic effects? What are the mechanisms behind positive and negative inotropic effects?

- inotropic effects are changes in contractility; controlled by the autonomic nervous system
- positive effects (increased contractility) via sympathetic activity: stimulation of beta-1 receptors results in the phosphorylation of sarcolemmal Ca2+ channels (this increases the Ca2+ inward current during the plateau phase) and phospholamban (this increases re-uptake of Ca2+ by the SR, increasing Ca2+ SR storage)
- negative effects (decreased contractility) via parasympathetic activity: stimulation of M2 receptors decreases the contractility of the ATRIA by decreasing inward Ca2+ current during the plateau phase and by opening K+-ACh channels to shorten the plateau phase


How is heart rate related to contractility?

- when heart rate increases, contractility increases
- this is because changes in the heart rate change the amount of Ca2+ inflow and storage, resulting in changes in the contractility


What is the positive staircase effect? What is it also known as?

- AKA the Bowditch staircase
- this is the effect on contractility that occurs with a changing heart rate
- if the heart rate is increased, subsequent beats result in an accumulation of Ca2+ in a step-wise fashion until the maximum contractility for that heart rate is reached


What is post extrasystolic potentiation?

- the tension developed after the beat of an extra-systole (an extra beat generated by a premature pacemaker) is greater than normal due to heart rate's effect on contractility
- note that the tension developed by the actual extra-systole is less than normal, but is greater than normal on the next beat because of the accumulation of Ca2+


What are cardiac glycosides? When are they used? How do they work?

- cardiac glycosides (digoxin, digitoxin, ovabain) are positive inotropic agents (they increase cardiac contractility) that are used in congestive heart failure (CHF: decreased contractility of the ventricles)
- they inhibit the Na+-K+-ATPase pump by binding to the extracellular K+ binding site, resulting in an increase in intracellular Na+ (because it can no longer be pumped out); this increase in Na+ stops the gradient that favors passive Na+ inflow, shutting down the Na+-Ca2+ exchanger and stopping Ca2+ outflow (increasing intracellular Ca2+ results in increased inotropism)
- (the exchanger usually brings Na+ in and Ca2+ out via secondary active transport)


What is preload? Afterload?

- preload: the (left) ventricular end-diastolic volume
- afterload: the aortic pressure that must be overcome in order for output to occur


What is stroke volume and its normal value? What about ejection fraction? Cardiac output?

- stroke volume: the volume of blood ejected by the (left) ventricle with each beat; normal value is about 70mL (stroke volume = end-diastolic volume - end-systolic volume)
- ejection fraction: the fraction of the end-diastolic volume that is ejected in each stroke volume; normal value is about 55% or greater (EF = stroke volume / end-diastolic volume x100)
- cardiac output: the total volume ejected by the (left) ventricle per unit time; normal value is about 5 L/min (cardiac output = stroke volume x heart rate)


What is the Frank-Starling relationship?

- this is the law that states the volume of blood ejected by the (left) ventricle depends on the volume present in the ventricle at the end of diastole
- in other words, the volume ejected by the heart in systole is equal to the volume received by the heart via venous return
- there is a limit, however: if the end-diastolic volume is too large, the ventricles won't be able to match the cardiac output to the venous return


What are the four points of the ventricular pressure-volume loop? What occurs between these four points?

- 1: diastole ends; pressure is low, volume is max (end-diastolic volume)
- 2: systole begins; pressure is high, volume is still max
- 3: systole ends; pressure is max, volume is lowest (end-systolic volume)
- 4: diastole begins; pressure is lowest, volume is still lowest
- from 1 to 2: isovolumetric contraction; diastole is over and the LV begins to contract, volume doesn't change
- from 2 to 3: ventricular ejection (systole); pressure in LV exceeds afterload and aortic valve opens, volume is expelled at high pressure
- from 3 to 4: isovolumetric relaxation; systole ends and the LV relaxes, pressure drops and aortic valve closes, volume doesn't change
- from 4 to 1: ventricular filling (diastole); LA pressure exceeds LV pressure and mitral valve opens to re-fill the ventricle at low pressure


Which two components make up the cardiac workload? Which is far more costly in terms of energy required? How do we know this to be true?

- cardiac work is equal to stroke volume x aortic pressure
- stroke volume is essentially volume work, aortic pressure is essentially pressure work
- pressure work is far more costly than volume work, meaning that most of the myocardial O2 consumption is used for pressure work, NOT for volume work
- we know this, because myocardial O2 consumption is greatly increased in HTN and aortic stenosis (these both increase pressure work), while only mildly increased during strenuous exercise (which increases volume work)


What is the normal oxygen consumption of the myocardium?

- about 250 ml/min
- *remember, most of the O2 consumption is used for pressure work rather than volume work*


Why is the left ventricle thicker than the right? Which Law does the explanation involve?

- the LV is thicker than the RV because of the Law of Laplace, which states that the thicker the wall of a sphere (the LV in this case), the greater the pressure that can be developed
- the LV is thicker because it needs to generate more pressure than the RV because aortic pressure is much greater than pulmonary pressure
- (remember, however, that cardiac output of the LV and RV are equal, so the volume work of the ventricles is the same, but the pressure work is different)


What are the seven phases of the cardiac cycle? At which phase does each heart sound occur?

- 1) atrial systole: passive filling of ventricles followed by an active burst due to atrial systole (this "burst" is S4, sometimes heard in patients with ventricular hypertrophy, where the atria contract against stiff, noncompliant ventricles)
- 2) isovolumetric ventricular contraction: ventricular pressure increases and the A-V valves close (this closing is S1, mitral valve closes slightly before the tricuspid valve)
- 3) rapid ventricular ejection: ventricular pressure continues to increase and the semi-lunar valves open, blood is rapidly ejected (atrial re-filling begins now as well)
- 4) reduced ventricular ejection: ventricles depolarize and relax while some blood still passes through the semi-lunar valves (atrial re-filling is continuing)
- 5) isovolumetric ventricular relaxation: ventricular pressure drops and semi-lunar valves close (this closing is S2, aortic valve closes slightly before pulmonary valve; splitting is exaggerated with inspiration)
- 6) rapid ventricular filling: ventricular pressure continues to drop and A-V valves open, ventricles rapidly re-fill (this rapid flow of blood is S3, sometimes heard in patients with volume overload, CHF, severe A-V regurg)
- 7) reduced ventricular filling: longest phase, AKA diastasis, diastole finishes during this phase


What are the heart sounds and when are they heard? Why does inspiration exaggerate the splitting of S2?

- S4: adventitious; heard during atrial contraction in patients with ventricular hypertrophy (the atria contract against stiff, non-compliant ventricles)
- S1: normal; A-V valves close during systole; mitral valve closes slightly before the tricuspid valve
- S2: normal; semi-lunar valves close during diastole; aortic valve closes slightly before the pulmonary valve*)
- S3: adventitious (normal in children); heard in patients with volume overload (due to congestive heart failure or severe A-V regurgitation) during diastole when the A-V valves open and the ventricles rapidly fill with blood
- *inspiration lowers intrathoracic pressure, increasing the venous return to the RA, which increases the RV stroke volume, thus prolonging the RV ejection and exaggerating the splitting of S2


What happens to cardiac output and venous return as right atrial pressure increases?

- as RA pressure increases, cardiac output increases (to a point*) and venous return decreases
- *CO will level off at its maximum of about 9 L/min (normal is about 5 L/min) once the RA pressure increases to about 4 mmHg
- (normal RA pressure is about 2 mmHg)


What mainly determines total peripheral resistance? How is total peripheral resistance related to cardiac output?

- TPR (total peripheral resistance) is mainly determined by the arterioles
- as TPR decreases, venous return increases (because low resistance means blood can more easily flow from the arterioles to the veins); increased venous return means increased cardiac output, so as TPR decreases, CO increases


What occurs in a steady state between cardiac output and venous return? When does the normal steady state occur? What happens when cardiac output and/or venous return changes?

- when in a steady state, cardiac output is equal to venous return
- the normal steady state (where CO and VR equal about 5 L/min each) occurs at a RA pressure of about 2 mmHg
- if cardiac output and/or venous return is changed, the steady state will change in order to make these two parameters equal once again


How is the steady state shifted in the presence of positive inotropes? Negative inotropes? What about by increasing blood volume? Decreasing blood volume? Increasing total peripheral resistance? Decreasing total peripheral resistance?

- positive inotropes: shift the steady state to the left (positive inotropes directly increase cardiac output, so RA pressure will decrease to also increase venous return)
- negative inotropes: shift the steady state to the right (CO decreases, RA pressure increases, VR decreases)
- increasing blood volume: shifts the steady state to the right (directly increases VR, so RA pressure will increase to also increase CO)
- decreasing blood volume: shifts it to the left (VR decreases, RA pressure decreases, VR decreases)
- increasing TPR: shifts the steady state down (increasing TPR means increasing the afterload, so CO and VR decrease; RA pressure can increase, decrease, or stay the same because it increases with decreased CO and decreases with decreased VR)
- decreasing TPR: shifts the steady state up (decreased afterload, increased CO, increased VR; RA pressure can increase, decrease, or stay the same)


At what level is mean arterial pressure usually constantly maintained at? How doe we calculate mean arterial pressure?

- normal MAP is maintained at about 100 mmHg
- a MAP greater than 60 mmHg is usually enough to sustain organs with adequate perfusion
- MAP = CO x TPR
- MAP = diastolic pressure + 1/3 pulse pressure
- MAP = 2/3 diastolic pressure + 1/3 systolic pressure


What are the two major systems that regulate mean arterial pressure?

- baroreceptor reflex: neurally mediated, fast, changes the autonomic input to the heart and blood vessels
- renin-angiotensin-aldosterone system: hormonally mediated, slow, changes the blood volume


How does the baroreceptor reflex regulate mean arterial pressure?

- baroreceptors located in the walls of the carotid sinus and the aortic arch send info to the cardiovascular centers located in the brain stem's reticular formation
- if the pressure is too high, parasympathetic activity will dominate; parasympathetic output works at the SA node to decrease pulse rate
- if the pressure is too low, sympathetic activity will dominate; sympathetic output works at the SA node to increase pule rate, cardiac muscle to increase contractility (and therefore stroke volume), arterioles to cause vasoconstriction (to increase TPR), and veins to cause venoconstriction (to decrease the unstressed volume)


Do baroreceptors respond more to increases or to decreases in blood pressure? Which nerves carry the info from the baroreceptors to the brain stem? Which nucleus in the brain stem collects the info before projecting to the cardiovascular centers?

- the carotid sinus baroreceptors respond well to both increases and decreases in blood pressure, but the aortic arch receptors respond mainly to increases only
- *both respond most strongly to the rate of the pressure change rather than the actual amplitude, so they respond most to rapid changes in MAP*
- the glossopharyngeal nerve (CN IX) carries the carotid sinus baroreceptors info
- the vagus nerve (CN X) carries the aortic arch baroreceptors info
- these nerves carry the info to the nucleus tractus solitarius in the brain stem, which then projects to the cardiovascular centers (vasoconstrictor center, cardiac accelerator center, and cardiac decelerator center)


What maneuver can be used to test a patient's baroreceptor reflex?

- the valsava maneuver
- this maneuver raises intrathoracic pressure, which decreases venous return, which decreases cardiac output, which will result in a lowered MAP
- an elevated heart rate is expected to develop as compensation for the lowered MAP (this is the baroreceptor reflex working)


How does the renin-angiotensin-aldosterone system regulate mean arterial pressure?

- kidney mechanoreceptors detect the renal perfusion pressure (which reflects the MAP)
- DECREASES in renal perfusion pressure (MAP) result in the conversion and release of prorenin to renin by the juxtaglomerular cells
- in the plasma, renin converts angiotensinogen to angiotensin I, which gets converted into angiotensin II by ACE (angiotensin converting enzyme) in the lungs
- angiotensin II stimulates the release of aldosterone, increases vasoconstriction (increases TPR), causes thirst, and increases ADH/vasopressin secretion; all of these work to increase blood volume and blood pressure


What is the main mechanism by which angiotensin II raises blood pressure?

- angiotensin II has many effects, but its main effect is to increase the secretion of aldosterone
- aldosterone is produced by the zona glomerulosa of the adrenal cortex
- it increases Na+ reabsorption by the principal cells of the distal tubules and collecting ducts of the kidneys
- this results in an increase in blood volume, which will cause an increase in blood pressure


In addition to the baroreceptor reflex and the renin-angiotensin-aldosterone system, what other four mechanisms also have effects on mean arterial pressure?

- chemoreceptors for O2 in carotid and aortic bodies: (primarily concerned with control of breathing) decreases in arterial pO2 results in vasoconstriction to increase perfusion
- chemoreceptors for CO2 and pH in the brain: (primarily concerned with control of breathing) increases in CO2 (decreases in pH) result in vasoconstriction to increase perfusion
- antidiuretic hormone/vasopressin: V1 receptors on vascular smooth muscle trigger vasoconstriction, V2 receptors on renal collecting ducts trigger H2O reabsorption
- atrial natriuretic peptide (ANP): secreted by the atria in response to INCREASED atrial pressure (thus, it senses the pressure of the venous system, not arterial) to cause VASODILATION and increased H2O renal EXCRETION to lower MAP


Which four forces make up the net pressure between capillaries and interstitial fluid? What do positive net pressures result in? Negative net pressures?

- (these are the Starling forces)
- capillary hydrostatic pressure (Pc): large force, favors filtration
- interstitial hydrostatic pressure (Pi): small force, favors absorption
- capillary oncotic pressure (PIc): large force, favors absorption
- interstitial oncotic pressure (PIi): small force, favors filtration
- positive net pressures result in filtration (fluid moves out of capillary into interstitial fluid)
- negative net pressures result in absorption (fluid moves out of interstitial fluid into capillary)


What is oncotic pressure? What is the main contributor to this pressure?

- oncotic pressure is the effective osmotic pressure of a fluid (AKA the colloid-osmotic pressure)
- it is mainly created by the protein concentration of the fluid
- fluids with large protein concentrations will have large oncotic pressures, which will OPPOSE filtration out of that fluid
- capillaries have large oncotic pressures, interstitial fluid has small oncotic pressures


What is edema? What causes it?

- edema is an increase in interstitial fluid volume; it forms when the volume of interstitial fluid exceeds the ability of the lymphatics to drain/return it to the vascular compartment
- can be caused by excess filtration (due to increased capillary hydrostatic pressure, decreased capillary oncotic pressure, or increased capillary permeability from burns/inflammation)
- can be caused by decreased lymphatic drainage (due to obstruction or surgical removal, etc.)


What can cause increased capillary hydrostatic pressure? Decreased capillary oncotic pressure? (note that these both result in edema.)

- increased capillary hydrostatic pressure (Pc): arteriolar dilation, venous constriction, increased venous pressure, heart failure
- decreased capillary oncotic pressure (PIc): decreased plasma protein via liver failure (loss of protein synthesis), protein malnutrition, nephrotic syndrome (protein loss in urine)


How are changes in blood flow to particular organs to match their metabolic needs achieved?

- by altering specific arteriolar resistances; this can be done by two broad mechanisms
- local (intrinsic) control: changes in local resistances are a direct response to local metabolites
- neural and hormonal (extrinsic) control: changes in local resistances are due to neural and/or hormonal input


Which two hypotheses explain the local (intrinsic) control of specific arteriolar resistance to match an organ's blood flow to it's metabolic needs?

- the myogenic hypothesis: when vascular smooth muscle is stretched, it is reflexively contracted (this explains the concept of autoregulation)
- the metabolic hypothesis: metabolic activity produces vasodilator metabolites (CO2, H+, K+, lactate, adenosine) (this explains the concepts of autoregulation, active and reactive hyperemia)


Which nerves, hormones, and compounds are involved in the neural/hormonal (extrinsic) control of specific arteriolar resistance to match an organ's blood flow to it's metabolic needs? What does each do?

- sympathetic innervation of vascular smooth muscle
- histamine (released by trauma) and bradykinin: dilates arterioles and constricts venules to increase capillary hydrostatic pressure (Pc)
- serotonin (released by blood vessel damage): local vasoconstriction to decrease blood loss
- prostaglandins: prostacyclin and PGEs vasodilate, thromboxane A2 and PGFs vasoconstrict
- angiotensin II and vasopressin/ADH: vasoconstriction
- ANP (released by raised atrial pressure): vasodilation


Which mechanisms mainly control coronary circulation? Cerebral circulation? Pulmonary? Renal? Skeletal muscle? Skin?

- coronary: local metabolites of O2 and adenosine (hypoxia causes vasodilation)
- cerebral: local metabolites of CO2 (pH) (hypoxia causes vasodilation)
- pulmonary: local metabolites of O2 (low ventilation causes VASOCONSTRICTION)
- renal: local metabolites via myogenic hypothesis
- skeletal muscle: sympathetic innervation at rest, and local metabolites of lactate, adenosine, K+ during exercise
- skin: sympathetic innervation (for heat retention or dissipation)


Which autonomic receptors are found on vascular smooth muscle? What does each result in when stimulated?

- sympathetic alpha-1 receptors: vasoconstriction
- parasympathetic M3 receptors: vasodilation (M3 receptor activation actually results in increased synthesis of NO to trigger the vasodilation; this does not occur in bronchial smooth muscle, so bronchiole constriction results instead)
- some vasculature also has sympathetic beta-2 receptors: vasodilation (these respond to adrenaline and trigger vasodilation during the fight-or-flight response)


How does the cardiovascular system respond to exercise?

- exercise results in an increased O2 demand in certain skeletal muscle
- the central nervous system will increase sympathetic and decrease parasympathetic output to cause a general increase in cardiac output and to cause vasoconstriction of the vessels supplying skin, splanchnic regions, kidneys, and inactive skeletal muscle to redirect blood flow from these "unused" areas
- active skeletal muscles generate local vasodilator metabolites (lactate, adenosine, K+) to trigger local responses of vasodilation to increase blood flow to these areas


How does the cardiovascular system respond to hemorrhage?

- hemorrhage is a rapid loss of blood volume and a resulting drop in MAP
- baroreceptor reflex will quickly elevate heart rate, contractility, vasoconstriction (to increase TPR), and venoconstriction (this increases venous return and stressed volume)
- RAAS will increase blood volume and also cause vasoconstriction (to increase TPR)
- capillaries will have a lower hydrostatic pressure (Pc) because of the vasoconstriction, thus favoring absorption into the capillaries
- (if these compensatory mechanisms fail, irreversible shock will develop)


How does the cardiovascular system respond to changes in posture (from supine to standing)?

- moving supine to standing causes blood to pool in the veins of the lower extremities, resulting in a drop in venous return, cardiac output, and MAP
- the baroreceptor reflex is the primary response and will increase sympathetic output to increase the blood pressure back to normal
- failure of a rapid reflex can result in orthostatic hypotension, light headedness, and syncope


How does heart failure affect the regulation of the cardiovascular system?

- heart failure results in raised venous pressure because of blood "backing up"
- this results in raised capillary filtration because of the increase in capillary hydrostatic pressure
- left heart failure will therefore cause edema in the lungs, and right heart failure will cause edema in the periphery
- to make matters worse, RAAS is activated because heart failure results in decreased MAP; the aldosterone secretion will increase Na+ retention and makes the edema even worse (by also increasing the capillary hydrostatic pressure by increasing blood volume)