Lecture 9 Cardiovascular Flashcards Preview

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Flashcards in Lecture 9 Cardiovascular Deck (60)
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1
Q

what causes blood to move throughout the circulatory system

A
  • pressure differences throughout the circulatory system

- pressure higher in aorta and decreases to almost 0 in vena cava

2
Q

2 parts of the heart

A
  • right = pulmonary, left = systemic
3
Q

4 chambers of the heat and general role

A

2 atria that receive blood
2 ventricle that pump blood out of heart
- left atria receives unoxygenated blood
- left ventricle pumps blood to lungs / pulmonary circulation
- right atria receives oxygenated blood from lungs
- right ventricle pumps oxygenated blood to the body

4
Q

2 types of valves, total of 4 valves

A
  • AV = atrioventricular - connects atria and ventricles
  • semilunar = goes from ventricles to arteries
  • AV = tricuspid in right heart and bicuspid aka mitral in left heart
  • semilunar = pulmonary valve in right heart and aortic valve in left heart
5
Q

part of heart that separates chambers

A

fibrous skeleton

- atria attached on top and ventricles attached to the bottom

6
Q

venous return meaning

A

unoxygenated blood that is returning to the heart through the superior and inferior vena cava

7
Q

describe flow of blood through the circulatory system (entire flow)

A

vena cava –> right atria –> tricuspid valve –> right ventricle –> pulmonary valve –> pulmonary arteries –> lungs and pulmonary capillaries and alveoli –> gas exchange and oxygenation –> pulmonary veins –> left atria –> mitral valve –> left ventricle –> aortic valve

8
Q

describe the relationship between resistance, pressure, and radius of the lumen

A
  • smaller radius –> increased resistance and pressure

- blood has to work harder if pressure and resistance are high

9
Q

which ventricle does more work and why

A
  • left ventricle works harder because blood pressure in systemic circulation is higher than that of pulmonary circulation
10
Q

describe how hypertension can lead to congestive heart failure

A

hypertension –> increased system blood pressure –> left ventricle has to work harder –> thickening of left ventricle heart muscle –> cavity of left ventricle becomes smaller –> not enough blood being pumped

11
Q

effect of exercise on cardiovascular system (blood pressure)

A
  • decreased systemic bp so heart doesnt have to work as hard
12
Q

eversion aka prolapsing of valves

A
  • valves flip out the opposite way
13
Q

what causes valves to open

A

changes in blood pressure

- when bp is higher downstream then upstream valves open

14
Q

papillary muscle

A

prevent valves from prolapsing

15
Q

chorda tendinea

A

tendons that connect valves and papillary muscle

16
Q

3 names for valves that can become prolapsed

A

regurgitative, incompetent, insufficient

17
Q

systole vs diastole

A
systole = contraction of ventricles 
diastole = relaxation of ventricles
18
Q

end diastolic volume

A

volume in ventricles after relaxation when it fills with blood

19
Q

end systolic volume

A

volume in ventricle after contraction when blood gets pushed out

20
Q

stroke volume and 2 representations

A

end diastolic volume - end systolic volume

  • how much blood as ejected
  • percent = amount ejected / end diastolic volume
21
Q

isovolumteric contraction

A
  • ventricles are contraction and AV valve is closed but semilunar valves have not yet opened
  • no change in volume
22
Q

isovolumetric relaxation

A
  • semilunar valves have closed and AV valves are still closed but are about to open
  • ventricles are relaxing
23
Q

describe flow / 5 parts of the heart beat

A
1 = isovolumetric contraction - ventricles being to contract and pressure rises but semilunar valves not yet open 
2 = ventricle contraction and semilunar valves open = blood is ejected 
3 = isovolumetric relaxation - AV and semilunar valves are closed, ventricles are relaxed 
4 = passive filling of ventricles due to pressure differences 
5 = atria contract to fill ventricles
24
Q

what causes sounds of the heart

A
lub = closing of AV valves 
dub = closing of semilunar valves
25
Q

heart murmur definition

A
  • abnormal heart sounds caused by abnormal flow of blood in heart
26
Q

2 causes of heart murmurs (just list them)

A
  • congenital = born with

- rheumatic fever

27
Q

rheumatic fever

A
  • antibodies made in response to strep end up binding to valves and causing autoimmune response
28
Q

systolic vs diastolic murmur and sound order

A
systolic = lub shhh dub 
diastolic  = lub dub shhh
29
Q

mitral valve prolapse - what type of murmur

A
  • mitral valves evert/prolapse when closed

- systolic because mitral/AV valves are closed during ventricle contraction

30
Q

mitral stenosis - meaning and what type of murmur

A
  • calcification of valves preventing them from opening fully
  • diastolic because AV / mitral valve open during ventricle relaxation when it is filling with blood
31
Q

septum description

A

separates right and left heart, thicker between ventricles

32
Q

congenital septal defect

A

hole in the septum, may close after birth but if not causes shunting of blood from one side of heart to the other

33
Q

gap junctions of myocardial cells

A

allow electricity to pass from one cell to another

34
Q

can electrical activity pass from chamber to chamber directly? why?

A

no! due to fibrous skeleton and septum

35
Q

pacemaker cells

A

cells that can generate their own AP

36
Q

HCN channels - what type, where found, when open, and meaning of HCN

A

Na+ VGIC channels

  • found in pacemaker cells only
  • H = hyperpolarization, CN = cAMP increases their frequency of AP
  • open during hyperpolarization causing pacemaker potential and pacemaker cell to reach threshold
37
Q

affect of sympathetic system on pacemaker cells (entire flow)

A

sympathetic –> epi/norepi from adrenal medulla –> bind to excitatory beta 1 adrenergic receptor –>

38
Q

describe all stages of AP for pacemaker cells

A

Na+ entering HCN causes pacemaker potential a spontaneous graded depoalrization –> Ca2+ enters VGIC channels causing steep depolarization –> K+ exits cause steep repolarization and hyperpolarization –> HCN channels open

39
Q

SA node - regular rate, location, and affect of parasympathetic

A
  • 100 bpm
  • right atria
  • parasympathetic Ach onto M2 muscarinic receptors, K+ exit causes hyperpolarization and decrease in heart rate
40
Q

atropine mechanism and effect on SA node

A
  • M2 antagonist, decreases affect of parasympathetic on heart
  • increases heart rate
41
Q

AV node - normal rate, location

A
  • 40-60 bpm
  • right atria
  • slower then SA node so never generates its own AP, always depolarized by the SA node
42
Q

AV bundle - alternate name, function

A
  • bundle of His
  • brings AP from SA node and right atria down septum and to bottom of the heart
  • splits off into left and right bundle branch and Purkinje fibers on the right
43
Q

Purkinje fibers

A
  • branch off from right bundle branch of AV bundle

- also has pacemaker cells 15-40 bpm

44
Q

sinus rhythm

A
  • heart rate is determined by SA node
45
Q

ectopic pacemaker

A

heart rate is determined by some node other than SA - AV node or Purkinje fibers, abnormal

46
Q

flow of electricity through heart

A

right atria –> left atria (both atria contract) –> travels down bundle of His to bottom of heart –> travels up heart and both ventricle contract while both atria relax (and repolarize)

47
Q

EKG function

A

measure electrical activity fo the heart

48
Q

P wave

A

atria depolarize

49
Q

QRS complex

A

ventricle depolarize

50
Q

T wave

A

ventricle repolarize

51
Q

myocardial cell RMP

A

-90 (instead of -70)

52
Q

plateau phase - what is it and what is the cause

A

Ca2+ entering cell makes absolute refractory period longer by keep cell depolarized for a longer period of time

53
Q

importance of plateau phase / long refractory period

A
  • gives heart contraction a chance to finish before next AP is generated
  • if plateau phase was not present back to back AP could be generated and heart would not relax and refill with blood = tetany
54
Q

excitation-contraction coupling meaning and flow

A
  • excitation of heart muscles causes their contraction
  • excitation / stimulus –> Ca2+ enters cells –> Ca2+ released from SR (storage inside cell) –> Ca2+ wave occurs –> Ca2+ binds to troponin and causes muscle contraction
55
Q

caffeine effect on heart and mechanism

A
  • inhibits the enzyme that breaks down cAMP

- mimics epi/norepi which increases cAMP and speed of HCN opening = increase in heart rate

56
Q

sympathetic/sympathoadrenal and parasympathetic effect on pacemaker cells (2 flows)

A
  • sympathoadrenal: epi/norepi from adrenal medulla –> beta 1 adrenergic receptors –> increase in cAMP –> HCN channels open faster –> increased heart rate
  • parasympathetic: Ach onto M2 muscarinic –> K+ channels open and K+ exits causing hyperpolarization –> heart rate decreased
57
Q

blood pressure in pulmonary circulation, aorta, and venous return

A
arterial = 100-120mmHg
pulmonar = 15 mmHg 
venous = 0-10 mmHg
58
Q

problem if pressure in pulmonary system was too high

A

if pressure too high blood would be squeezed out of capillaries and fill alveoli

59
Q

passive vs active filling and percentages

A
  • passive = AV valves open, pressure difference moves blood, 90% of filling
  • active = atria contract, 10% of ventricle filling
60
Q

pacemaker potential

A

spontaneous graded potential caused by HCN channels opening and Na+ entering