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KNES 260 > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

pericardium

A
  • tough inelastic sheath covering the heart
  • anchors the heart
  • acts as a constraint to enable ventricular interaction
  • pericardial fluid lubrication
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2
Q

heart valves

A
  • prevent backflow of blood
  • atrioventricular valves and semilunar valves
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3
Q

what do the pulmonary/aortic semilunar valves do?

A
  • prevent backflow from aorta (L) and pulmonary (R) artery back into ventricles
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4
Q

Tricuspid valve

A
  • the atrioventricular valve on the right side of the heart
  • prevents backflow from right ventricle to right atrium
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5
Q

Mitral Valve

A
  • atrioventricular valve on the left side
  • also called bicuspid valve
  • prevents backflow of blood from left ventricle to left atrium
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6
Q

Chordae tendonae

A
  • anchor atrioventricular valves to the papillary muscle (this is what makes sure there is no backflow)
  • as heart contracts, so do papillary muscles to control tension on chordae tendonae
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7
Q

Atrioventricular valves (open/closed)

A
  • open in filling (diastole)
  • close during contraction (systole)
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8
Q

Aortic and pulmonary valves (open/closed)

A
  • open during systole (contraction)
  • closed during relaxation (diastole)
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9
Q

Heart murmurs

A
  • stenosis leads to a whistling sound that is heart when valve should be open
  • insufficiency leads to a whirring sound that is heart when the vale should be closed
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9
Q

stenosis

A
  • a valve problem that occurs from the narrowing of a heart valve
  • causes faulty opening and therefore decreased ejection
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9
Q

valve insufficiency or regurgitation

A
  • faulty closure
  • backflow
  • decreased forward ejection
  • can be due to rheumatic heart disease (autoimmune)
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9
Q

ventricular tortion

A
  • allows for the most efficient ejection (with direction of heart fibers)
  • produces diastolic suction for more efficient filling
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10
Q

autorhythmic cells

A
  • type of myocardial cell
  • generates and spreads action potentials
  • pacemaker cells
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11
Q

contractile cells

A
  • type of myocardial cell
  • makes up 99% of all cardiac cells
  • mechanical work of contraction
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12
Q

how does electrical excitation in the heart differ from the remainder of the body?

A
  • rather than only influx of Na+ and efflux of K+, there is also Ca++ influx
  • pacemaker cells are utilized to excite other muscles
  • pacemaker potential refers to the SLOW rise in membrane potential (depolarization) prior to AP in the SA node
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13
Q

What are all of the steps in pacemaker potential

A
  • slow depolarization phase of SA node (first half):
  • K+ permeability decreases
  • Na+ permeability increases for slow influx of Na+
  • near midpoint of slow depolarization
  • Ca++ (T-type) channels open so voltage sensitive calcium moves in
  • threshold is reached
  • L-type Ca++ channels open so calcium moves in for rapid depolarization and AP
  • repolarization
  • L-type channels close
  • K+ (rectifier) channels open so K+ moves out of SA nodes
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14
Q

what does it mean that the SA node is autorhythmic

A
  • self generated
  • events repeat (around 70 times a minute)
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15
Q

other pacemaker regions

A
  • AV node (40 bmp)
  • Purkinje fibers (20 bmp) : have ectopic beats (extrasystoles)
  • both are depolarized by SA node before they depolarize themselves
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16
Q

Action potential of the myocardial contractile cells

A
  • Depolarization
  • Na+ moves in
  • Plateau
  • Ca++ moves in and stays depolarized
  • repolarization
  • K+ moves out
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17
Q

why does cardiac contractile cells have a long refractory period

A
  • long action potential (ensured by plateau) means long refractory period
  • this is important to prevent tetanus and allow for relaxation and diastolic filling each beat
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18
Q

Electrocardiogram (ECG)

A
  • external recording of electrical events
  • waves of the ECG can be correlated to specific electrical events
    *P-wave
  • QRS complex
  • T-wave
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19
Q

P-wave

A
  • atrial depolarization
  • initiates atrial contraction
  • initiated at SA node - spreads via gap junctions and internodal pathway throughout artia
  • there is a 100ms delay for this to reach AV node which allows for ventricles to contract after atrial contraction and ventricular filling
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20
Q

QRS complex

A
  • ventricular depolarization and atrial repolarization
  • initiates ventricular contraction
  • impulses move to bundle of HIS to bundle branches then to purkinje fibers
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21
Q

T- wave

A
  • ventricular repolarization
  • initiates ventricular relaxation
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22
Q

Sinus rhythm

A
  • normal
  • 60-120 bmp
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23
Q

tachycardia

A
  • rapid HR of more than 100 bmp
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24
Q

brachycardia

A
  • slow HR of less than 60 bmp
  • risk of fainting
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25
Q

arrhythmias

A
  • abnormal rhythms
  • can cause death, fainting, heart failure
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26
Q

atrial fibrulation

A
  • no organized pattern of atrial conduction
  • no P-waves
  • can affect ventricular filling
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27
Q

PVC’s

A
  • premature ventricular contraction
  • extra beat
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28
Q

atrial flutter

A
  • extra P waves
29
Q

heart block

A
  • impulses from SA node don’t reach AV node
30
Q

ventricular tachycardia

A
  • abnormal electrical cycling
31
Q

heart wall thickness

A
  • corresponds to peak pressures
  • Atria: 3-10 mm Hg
  • RV: 3-35 mm Hg
  • LV: 3-125 mm Hg
32
Q

what are the 4 phases of the cardiac cycle

A
  • diastolic filling
  • isovolumetric contraction
  • ejection
  • isovolumetric relaxation
33
Q

cardiac cycle overview

A
  • electrical events must always precede mechanical events
  • left and right side contract simultaneously
  • pressure changes are due to changes in volume of contractile state
34
Q

Diastolic filling

A
  • LAP>LVP
  • mitral valve is open
  • LVP<AP
  • aortic valve closed
35
Q

isovolumic contraction

A
  • QRS - LV contracts
  • LVP increases
  • once LVP>LAP mitral valve closes
36
Q

ejection

A
  • once LVP> AP aortic valve opens so blood is ejected into aorta
37
Q

isovolumetric relaxation

A
  • T-wave: relaxation and LVP decreases
  • once LVP<AP aortic valve closes
  • LVP still decreasing bc once LVP<LAP mitral valves open and blood moves into ventricle for filling
38
Q

stroke volume

A
  • amount of blood pumped in one beat
  • around 70 mL
  • affected by:
    1. Preload: myocardial stretching
    2. Contractility: force produced at given preload
    3. afterload: tension required for LV to open aortic semilunar valve
39
Q

Cardiac output

A
  • amount of blood pumped per minute
  • stroke volume multiplied by heart rate
40
Q

what impacts your HR

A
  • autonomic NS
  • sympathetic increases
  • parasympathetic decreases
  • age
  • gender
  • fitness
  • body temp2
41
Q

ischemia and infaract

A
  • blocked coronary artery
  • decreased blood flow and oxygen to heart muscle due to plaque or clot
  • poor muscle function, decreased stroke volume and cardiac output
  • treatment: CABG, vasodilators, angioplasty
42
Q

ischemia

A
  • transient
  • no permanent damage to heart muscle
  • symptoms occur when cardiac demand increases beyond what the heart can match
  • symptoms ease when demand decreases
43
Q

infarct

A
  • permanent blockage
  • muscle cells are permanently damaged
  • symptoms remain and worsen
  • “heart attack”
44
Q

atrial hypertension

A
  • causes include: smoking, stress, diet, age, genetics
  • increased atrial pressure - LVP must exceed this to open aortic valve and eject blood
  • shorter ejection time leads to lower stroke volume and cardiac output
45
Q

hypertension

A
  • higher risk of heart failure, haemorrhage, and stroke
  • treatments: exercise, diet, medications
46
Q

heart failure

A
  • compromised heart - valve stenosis, ischemia or infarct
  • decreased stroke volume is compensated with increased HR
  • eventually muscle becomes so fatigued in barely contracts
47
Q

pulmonary hypertension

A
  • RVP>LVP
  • septum inverts
  • myocardial compression
48
Q

cardiac aneurysm

A
  • bulge of ventricular wall
  • muscle weakness
  • congenital or from infarct
49
Q

blood flow

A
  • from higher to lower pressure
  • directly proportional to pressure gradient
  • inversely proportional to vascular resistance
50
Q

pressure change

A
  • driving pressure for systemic blood flow is created by LV
  • if blood vessels constrict, BP increases
51
Q

Resistance to blood flow

A
  • this is the measure of the opposition to blood flow
  • depends on:
  • blood viscosity
  • vessel length
  • vessel radius - has biggest effect
52
Q

vasculature layers

A
  • tunica intima: endothelium, areolar CT
  • tunica media: smooth muscle, elastin
  • tunica externa: connective tissue
53
Q

variance in blood vessel structure

A
  • arterioles: highest proportion of smooth muscle
  • capillaries: single layer of endothelium
  • arteries: reinforced with collagen and elastin
54
Q

arteries flow rate

A
  • they have high flow rate and high pressure
  • large radius for low resistance
  • collagen fibers with tensile strength
  • elastin fibers allow stretch and recoil of walls
  • systolic pressure of 120 and diastolic of 80
55
Q

arterioles blood flow

A
  • these are major resistance vessels
  • radius can be adjusted to distribute cardiac output among organs depending on needs
  • help regulate arterial BP
56
Q

arterioles - vasoconstriction

A
  • narrowing of vessel so increased resistance
  • contraction of smooth muscle
  • reduced flow
57
Q

arterioles - vasodialation

A
  • enlargement of vessel
  • relaxation of smooth muscle
  • reduced resistance and increased flow
  • occurs with:
  • decreased O2
  • increased CO2
  • increased acid
  • increased K+
  • increased osmolarity
  • adenosine release
58
Q

arterioles - extrinsic control

A
  • sympathetic input, hormones
  • Alpha 1 receptors: norepinephrine, vasoconstrict vessels
  • Beta 2 receptors: epinephrine, heart/skeletal muscle vasodilation
  • Angiotensin 2: vasoconstricts
59
Q

capillaries

A
  • thin walled for less diffusion distance
  • small radius to make the velocity of blood flow slower for more gas exchange time
  • extensively branched
60
Q

pre-capillary sphincters

A
  • constrict sphincter - close capillary bed (at rest it may be closed)
  • relax sphincter - opens capillary bed
  • metarteriole: runs between arteriole and a venule
61
Q

types of capillaries

A
  • continuous: most common, least permeable, in muscle, lungs, brain, CT
  • fenestrated: have pores, in kidneys and small intestine
  • sinusoids: large clefts for RBCs, proteins, found in liver, bone marrow, spleen
62
Q

what forces determine fluid flow between capillaries and tissue (4)

A
  • capillary BP: encourages fluid flow into tissue
  • interstitial fluid hydrostatic pressure
  • plasma colloid osmotic pressure: encourages fluid movement into capillary
  • interstitial fluid colloid osmotic pressure: opposed plasma colloid osmotic pressure
63
Q

what regulates capillary bulk flow

A
  • hydrostatic and osmotic pressure
64
Q

Lymphatic system

A
  • network of open ended vessels
  • drains fluid from tissues
  • lymph vessels have similar structure to veins, low pressure, contain valves
  • functions: return excess filtered fluid, defend against disease, transport absorbed fat, return filtered protein
65
Q

Venules

A
  • form when capillary beds unite
  • very porous - to allow WBC into tissues
66
Q

Veins

A
  • low pressure, low resistance
  • return blood to heart
  • slow flow
  • large radius
  • capillaries drain into venules that then merge into larger vessels
67
Q

Venous returns can be decreased by

A
  • venous compliance
68
Q

Venous return can be increased by

A
  • driving pressure from cardiac contraction
  • sympathetically induced venoconstriction
  • skeletal muscle activity
  • effect of venous valves
  • respiratory activity
  • effect of cardiac suction
69
Q

what are the determinants of blood pressure

A
  • cardiac output
  • total peripheral resistance
70
Q

short term blood pressure control

A
  • fast control (within seconds)
  • uses baroreceptors to send input to cardiovascular center
71
Q

short term respond to low BP

A
  • less firing of baroreceptors sends message to cardiovascular center
  • this triggers: increased vasoconstriction and venoconstriction, increase contractility so increased stroke volume, increased HR
  • these all increase cardiac output - so increased BP
72
Q

Long term BP control

A
  • altering blood volume
  • kidneys: direct renal mechanism and indirect renal (renin-angiotensin) mechanism
73
Q

direct renal mechanism

A
  • alters blood volume independent of hormones
  • increased BP or blood volume
  • increased filtration, so kidneys eliminate more urine
  • decreased BP of blood volume causes kidneys to conserve water
74
Q

renin-angiotensin mechanism

A
  • when there is low BP release of renin with triggers production of angiotensin II
  • angiotensin II causes aldosterone and ADH secretion for conservation of fluid

KNES 260 (5 decks)

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