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Systemic Physiology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Length of cardiac muscle action potential and why is it important

A

250ms, therefore the refractory period is long and therefore under normal conditions the muscles cannot undergo tetanic contractions

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2
Q

Resting membrane potential of cardiac muscle

A

-90mv

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3
Q

General shape of the action potential of cardiac muscle

A

there’s a sharp depolarization and then the bulk is a plateau which then repolarizes quickly (not as quick as the depolarization)

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4
Q

SA node, how many action potentials per minute, and how many potentials make its way through the conduction system, how do the action potentials spread

A

sinoatrial node, pacemaker, near the cardiac sinus in the right atrium, automaticity; will undergo around 100 action potentials per minute under normal conditions; not every change in membrane will make its way through the rest of the conduction system and this is why the number isn’t the same as heart rate; potentials will spread through the rest of the atria due to cells being connected by gap junctions

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5
Q

Will conduction pass from the atria to the ventricles

A

no, due to the connective tissue it prevents the conduction to pass through

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6
Q

AV node

A

atrial ventricular node, connected to interventricular septum, sends conduction to the bundle of His

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7
Q

Automaticity

A

undergo regular patterns of action potentials independent of the nervous system

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8
Q

Interventricular septum

A

tissue that runs down the middle of the heart

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9
Q

Bundle of His

A

divides into two branches, the right branch innervates to myocardial tissue of the right ventricle, left branch innervates to myocardial tissue of the left ventricle, sends conduction to Purkinje fibers

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10
Q

Purkinje fibers

A

extensions of specialized myocardial cells that make their way throughout the myocardium of the right and left ventricle

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11
Q

P wave

A

atrial depolarization, point just before contraction of atrial muscle

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12
Q

QRS waves, why is this larger than P wave

A

ventricular depolarization; due to the increased amount of myocardial tissue in the ventricles

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13
Q

T wave

A

ventricular repolarization

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14
Q

Missing EKG wave

A

atrial repolarization, is overshadowed by ventricular depolarization

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15
Q

Nodal cell resting membrane potential

A

-55 to -60

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16
Q

Where and why is there thin myocardium

A

the left ventricle has thicker myocardium than the right ventricle due to the left ventricle moving blood into the systemic circuit while the right ventricle moves blood into the pulmonary circuit; myocardium in the atrium is not as thick as in the ventricles because the atria don’t do much work moving blood into the ventricles, the pressure of blood entering the chambers is almost always enough to push blood down into the ventricles , the atria gives it the final push

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17
Q

Ventricular myocardial action potential length and corresponding EKG waves, regulated by what

A

is 250-300ms long; depolarizes from -90 to +20mv corresponds to depolarization of ventricles QRS, repolarization corresponds with the T wave; regulated by changes in permeability of sodium, calcium, and potassium

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18
Q

What causes the gradual repolarization of ventricular myocardial action potentials

A

decrease in potassium permeability meaning that the potassium efflux is decreased and positively charged potassium stays within the cell, the increase of permeability of calcium due to T type calcium channels opening, f type sodium channels will pen when the cell is in its most hyperpolarized state

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19
Q

What leads to repolarization of myocardial cells

A

decrease of calcium permeability and increase of potassium permeability

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20
Q

Central nervous system

A

brain and spinal cord

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21
Q

Peripheral nervous system

A

everything else connected to brain and spinal cord, somatic and autonomic, sympathetic and parasympathetic, acramine

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22
Q

Acramine parasympathetic nervous system

A

salivation, lacrimation, urination, digestion, defecation

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23
Q

Sympathetic and parasympathetic activity

A

are always active but one could overpower the other

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24
Q

Cardiac output

A

HR*SV, average cardiac output is 5L/min

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25
Q

Stroke volume

A

the amount of blood ejected from the ventricles at each contraction, around 70mL, this can increase through increasing the contractibility of the ventricles

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26
Q

End diastolic volume

A

how much blood does the ventricles fill with, could be caused by an increase of antria contractibility, can be increased due to an increase of bp which will increase the amount of blood returning to the heart

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27
Q

Sympathetic effects cardiac output

A

releases norepinephrine onto beta-1 adrenergic receptor along with epinephrine released by the adrenal medulla which has been acted on by the sympathetic nervous system increasing activity of the SA node and increasing conduction rate to the AV node, has input to the atrial and ventricular muscles effecting end diastolic volume

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28
Q

Adrenergic receptor

A

acts on norepinephrine, first discovered on the adrenal glands, there’s beta-1, beta-2, alpha-1, and alpha-2

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29
Q

Parasympathetic effects cardiac ouput

A

there’s no parasympathetic input to the ventricles therefore there’s no significant effect onto ventricular contraction therefore not effecting end diastolic volume, decreases heart rate and conduction rate of AV node and decreases activity of the SA node through releasing acetylcholine

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30
Q

Muscarinic receptor

A

binds acetylcholine on cardiac muscle

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31
Q

Beta-1 adrenergic receptors mechanism

A

g coupled receptor whose alpha subunit will activate adenylyl cyclase to create cAMP, cAMP will change an inactive cAMP dependent protein kinase to an active cAMP dependent protein kinase

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32
Q

What does an active cAMP dependent protein kinase do

A

lowers the sensitivity of L type calcium channels which will increase cytosolic calcium and lead to the nodal cells working faster and better and ventricular cells will contract with a greater force; makes it easier for ryanodine receptors to open within the sarcoplasmic reticulum and will be open longer when calcium is bound to it allowing for more calcium to come from the sarcoplasmic reticulum (calcium induced calcium released); the increased amount of calcium within the cytosol will allow for more binding to troponin and an increase of cross bridge cycling; makes troponin more sensitive to calcium; makes it difficult for some transporter protein calcium ATPase to operate and some will be induced, by blocking ATPase calcium will stay within the cytosol, by promoting activity the calcium gradient will increase as the concentration of calcium within the SR will increase leading to a larger current of calcium out the SR

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33
Q

Blood pressure

A

is due to cardiac output along with peripheral resistance

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34
Q

Peripheral resistance

A

how open the vessels are

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35
Q

Blocking beta-1 adrenergic receptors

A

most common treatments of high bp, ex/ atenolol which will bind to the receptor and lower cardiac output

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36
Q

Force of ventricular contraction

A

end diastolic volume can be the same while stroke volume increases leading to the ventricles needing to squeeze more, the force that develops during contraction during sympathetic stimulation is larger and occurs over a shorter period of time which will increase heart rate

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37
Q

Pericardium

A

outer layer with two layers separated by fluid

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38
Q

Epicardium

A

layer directly over the heart, also known as the visceral pericardium

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39
Q

Pericardium

A

outside layer, known as the parietal pericardium

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40
Q

Visceral membranes

A

membranes that directly cover organs

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41
Q

Parietal membranes

A

membranes that line cavities

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42
Q

Endocardium

A

layer of the heart that is in contact with the blood

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43
Q

Valves

A

separate chambers of the heart and vessels leading from the chambers, also found within veins, lymphatic system, prevent retrograde flow

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44
Q

Chordae Tendinae

A

tough fibrous strings that are attached to papillary muscles within the left and right ventricles

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45
Q

Papillary muscles

A

extensions of the myocardia within the left and right ventricles

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46
Q

How are the valves kept shut

A

papillary muscles remain rigid which leads to the chordae being taught

47
Q

Pathway of blood through the heart (beginning with left atrium)

A

left atrium, left bicuspid AV valve, left ventricle, aortic semilunar valve, aorta, arteries, arterioles, capillaries, venules, veins, vena cavae, right atrium, right tricuspid AV valve, right ventricle, pulmonary semilunar valve, pulmonary trunk, pulmonary arteries, capillaries of lungs, pulmonary veins

48
Q

How can you detect a valve defect

A

detected using a stethoscope not making the “lub” “dub” sound, the sounds refer to the shutting of valves and blood pushing against the valves, lub is arterial ventrial valves closing, dub is the semilunar valves closing

49
Q

Sphygomanometer

A

measures pulse pressure

50
Q

Systole

A

ventricles contract and move blood, compliance of vessels based on ventricular contraction that allows blood to apply pressure on the walls

51
Q

Diastole

A

ventricles relax and fill with blood, the pressure of the blood within the vessels during ventricular repolarization

52
Q

Mean arterial pressure

A

(systolic + 2diastolic) / 3

53
Q

Normal mean arterial pressure

A

93.3 given with an arterial pressure of 120/80

54
Q

How do we know what baroreceptors pick up on

A

120/80 and 130/70 yield similar mean arterial pressures but the firing rates of baroreceptors are not the same

55
Q

What do baroreceptors pick up on

A

changes in pulse pressure, the greater the difference the greater the firing rate

56
Q

Pulse pressure

A

difference between systolic and diastolic

57
Q

Smooth muscle in the arterials and in the veins

A

it’s more pronounced within the arteries and arterials but not as pronounced in veins

58
Q

Sympathetic constriction of veins leading to

A

increase venous pressure, increase venous return which will effect the amount of blood entering the atria and effecting the end diastolic volume

59
Q

Sympathetic increasing discharge to arterials

A

this is what we’re talking about when measuring blood pressure, arterials constrict and increase total peripheral resistance

60
Q

Total peripheral resistance

A

arterial pressure / cardiac output

61
Q

How much blood do the ventricles normally pump out

A

60% of the blood that fills it

62
Q

Systolic dysfunction

A

primarily caused by ischemia, occurs during a myocardial infarction, cardiac muscles can survive without oxygen for about 20 minutes, if there isn’t as much myocardia as before then the ventricles can’t pump out a much blood as normally, ventricles pump about 40-50% of blood

63
Q

Ischemia

A

loss of oxygenated blood to the myocardium

64
Q

Diastolic dysfunction

A

ventricles don’t have enough space to fill with blood normally, it’s one of the primary things associated with hypertension that hasn’t been treated for a long period of time (silent disease), if the heart can’t move blood into the systemic circuit and if there’s already hypertension in the arteries this can cause arteries to bulk up through hypertrophy of the ventricles losing space and compliancy of the myocardia,

65
Q

Cadiac failure

A

reduced cardiac output due to loss of myocardia or due to ventricular hypertrophy, the left ventricle can’t keep up with the right ventricle as it has the harder job of pushing blood throughout the systemic circuit

66
Q

Congested heart failure

A

happens before heart failure, blood can become congested and stay within the pulmonary circuit and lead to pulmonary edema leading to respiratory failure and cardiac arrest

67
Q

How to treat cardiac failure

A

reduce sympathetic nervous system function (atenolol), antagonists for alpha adrenergic receptors on the smooth muscle lining leading to reduction of cardiac output and peripheral resistance as blood vessels are vasodilated, promote parasympathetic activity, block ADH via antibiotics working as antagonists for it, give a diuretic

68
Q

What’s a side effect if cardiac failure goes untreated

A

people gain water weight very quickly, edema, one of the huge problems associated to heart failure

69
Q

Heart failure in the context of baroreceptor reflex

A

if there’s a drop in cardiac output (regardless of whether due to systolic or diastolic dysfunction), sympathetic activity will increase increasing water retention

70
Q

What happens with sustained hypertension and diastolic dysfunction

A

cardiac output will increase due and the diastolic dysfunction will help in keeping the heart in homeostasis

71
Q

Drugs to treat heart failure

A

diuretics, cardiac inotropic drugs, vasodilators, vasodilation promoters, beta adrenergic receptor blockers

72
Q

Diuretics

A

most important drug to treat heart failure, increase urinary excretion of sodium and water

73
Q

Digitalis

A

cardiac inotropic drugs, increase contractility of ventricles which doesn’t make sense because it stresses the heart that’s already overworked, increased contractibility of the remaining myocardial tissue, increases quality of life but not life span

74
Q

Alpha blocker

A

vasodilator, block norepinephrine and epinephrine at alpha-adrenergic receptors

75
Q

Renin-angiotensin-aldosterone system

A

There’s a drop in arterial pressure and ultimately a drop in oxygen delivery to the body or an increase in sympathetic discharge, the kidneys secrete renin which travels through the blood and takes angiotensinogen which is made by the liver and converts it to angiotensin I which will be converted to angiotensin II by angiotensin conversion enzyme (ACE), angiotensin II is a potent vasoconstrictor and promote the release of aldosterone from the adrenal cortex which will promote sodium reabsorption which will increase blood volume and blood pressure

76
Q

Angiotensin I

A

by itself it will not do anything, converted from angiotensinogen by renin

77
Q

Angiotensin conversion enzyme

A

found in the membranes of endothelial cells that line capillaries, especially those that are found in the lungs

78
Q

Angiotensin II

A

binds to vascular smooth muscle to vasoconstrict the vessel

79
Q

Sodium reabsorption

A

sodium will be lost via the urine in the lumen of kidney tubules, sodium within the kidney tubules will be moved back into the blood, by increasing sodium reabsorption water reabsorption has to increase

80
Q

ACE inhibitor

A

vasodilator, inhibits the conversion of angiotensin I to angiotensin II therefore dilation of vessels is promoted and aldosterone is not released

81
Q

Angiotensin blockers

A

blocking the receptor leads to vasodilation being promoted and aldosterone is not released

82
Q

Tunica intima

A

inner layer of the artery, synonymous with epithelium, blood makes contact with this layer, made of simple squamous epithelium and is found wherever the need for diffusion is high

83
Q

Endothelial cell functions

A

create a barrier, prevent blood loss, blood doesn’t normally adhere to it

84
Q

How does endothelial cells prevent blood loss

A

produce growth factors in response to damage, makes nitric oxide to vasodilate and endothelin to vasoconstrict, synthesizes active hormones such as angiotensin II from inactive precursors

85
Q

Atherosclerosis

A

hardening of the arteries through thickening and narrowing of the blood vessel due to build up of plaques typical cause of heart attacks, stroke, and peripheral vascular disease; injured endothelial cells release inflammatory cytokines (C-reactive protein), release less nitric oxide, secrete more vasoconstrictors (vascular endothelial growth factor, platelet-derived growth factor, endothelin-1); macrophages attach to the spot of injury via adhesion molecules (VCAM-1) and release enzymes and oxygen free radicals to create oxidative stress, oxidizing LDL and resulting in further injury to the vessel wall; oxidized LDL activates inflammatory and immune responses to promote superoxide production, decrease nitric oxide production, and smooth muscle cell proliferation; oxidized LDL will then move into the intima of the arterial wall and become engulfed by foam cells (macrophages); as these cells accumulate they form a lesion called a fatty streak; fatty streaks trigger further immunologic and inflammatory responses leading to vessel damage and vasoconstriction; macrophages stimulate smooth muscle proliferation causing collagen to form and move over the fatty streak forming a fibrous plaque; this plaque can become calcified and protrude into the lumen of the vessel and restrict blood flow (not all do this); plaques can rupture or ulcerate to cause sheer forces, microphage derived collagenases, elastases, matrix malloproteinases, cathepsins, and apoptosis of the cells at the edge of the plaque

86
Q

Atherosclerosis mechanism

A

injury to endothelial cell,

87
Q

How can endothelial cells be damaged

A

genetics, chemicals, failure of cholesterol regulation, autoimmune disorder, infection with bacteria (H. pylori), hypertension which is the main causer, age which can lower vessel wall compliance increased by sheer forces

88
Q

Resorption

A

absorbing a substance from a reservoir

89
Q

Reabsorption

A

substances that were eliminated and then absorbed

90
Q

Absorbed

A

substances taken from ingested material

91
Q

VCAM1

A

vascular cell adhesion molecule-1 will draw macrophages to a particular spot

92
Q

Oxidative stress

A

macrophages releasing oxygen free radical (superoxide) binding to LDL (phospholipids) causing damage, linked to increased levels of angiotensin II

93
Q

What happens to ruptured plaques

A

platelets will adhere to the surface of the ruptured or ulcerated area, coagulation cascade is initiated and a thrombus will begin to form which can create a blood clot (completely obstructing the lumen) ending with the arteries that are narrow and susceptible to vasoconstriction and thrombus formation

94
Q

Tunica media

A

middle layer of the artery, made of sooth muscle that’s interspersed with collagen

95
Q

Tunica externa/ adventitia

A

outer layer of the artery made of connective tissue

96
Q

Vein layers

A

has all the layers of the artery but the tunica media is not as pronounced leading to a larger diameter lumen

97
Q

How to increase venous pressure and what results

A

smooth muscle of the veins constrict, increasing venous return to increase end diastolic volume which increases stroke volume

98
Q

Varicose veins

A

breaking down of valves within the veins causing pooling of blood which can distort the veins and swell, occurs with age

99
Q

Arteriole

A

small diameter artery, has tunica intima and tunica media (which is only smooth muscle)

100
Q

Venule

A

small diameter vein with an endothelium

101
Q

Capillary

A

has simple squamous epithelium, contains psuedo-fenestrations allowing diffusion through the junctions and allow large molecules to move out

102
Q

Law of Laplace

A

talks about the thickness diameter of the vessel, there’s a certain pressure inside and pressure outside, the pressure is divided by the radius which gives an idea of how much pressure there is on the spot

103
Q

Aneurism

A

weakening of the vessel wall, could be balloon like dialation or the entire vessel, could be due to artherosclerotic plaques, when the wall burts it leads to hemorrhage

104
Q

Commonly accepted hypertension bp and AHA bp

A

140/90; 130/80

105
Q

Primary hypertension

A

is 95% of cases of high bp, due to unknown origins

106
Q

Secondary hypertension

A

associated with diabetes mellitus, glucose is high within the plasma and water has to balance this concluding with an increase blood volume

107
Q

Neurons releasing nitric oxide

A

neural control of blood pressure will lead to vasodilation of smooth muscles; nitric oxide activate guanylyl cyclase to create cGMP leading to decrease in calcium influx and increase in potassium deflux

108
Q

Vasopressin aka ADH

A

hormonal control of bp, made by supraoptic nucleus of the hypothalamus released a tthe posterior pituitary, resting of water increasing blood volume

109
Q

Hormonal vasoconstriction controls of bp

A

vasopressin, epinephrine, angiotensin II

110
Q

Arterial natriuretic peptide

A

hormonal controls of bp, made by the atria of the heart, promotes excretion of sodium, when you get rid of sodium you get rid of water lowering blood volume

111
Q

Myogenic response

A

local control of bp, when blood is damaged it will first constrict

112
Q

Endothelin

A

local control of bp, made by endothelial cells, very potent vasoconstrictor

113
Q

Eicosanoids

A

local control of bp, prostaglandin or a form of it is made by epithelial cells to vasodilate

114
Q

Treatments for hypertension

A

lifestyle changes, medications

Systemic Physiology (5 decks)

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