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Anatomy & Physiology > heart ch 18- part A > Flashcards

heart ch 18- part A Flashcards

1
Q

cardiac muscle contraction

A
  • 1% of heart cells are autorhythmic (noncontractile)
  • cardiac muscle has a longer refractory period than skeletal muscle, less cramping
  • gap junctions ensure the heart contracts as a unit
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2
Q

function of autorhythmic cells

A
  • network of autorhythmic (noncontractile) cells that initiate and distribute impulses to coordinate depolarization and contraction of the heart
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3
Q

electrical conduction system

A
  1. starts with the SA node action potential (sinoatrial/pacemaker, upper right of right atrium)
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4
Q

SA node fires…

A

75 times per minute

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5
Q

autorythmic cells

A
  • have unstable resting potentials due to open slow Na+ channels
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6
Q

sequence of excitation/electrical conduction system

A
  1. SA node (sinoatrial node/pacemaker/fast Ca+t)
    • impulses 75 times per minute, auto depolarization
  2. AV node
    • smaller diameter fibers, fewer gap junctions: slower rate of diffusion of ions (delays 0.1 sec) depolarizes 50 times per minute w/o SA node so the atria can load ventricles
  3. AV bundle
    • only electrical connection between atria and ventricles
  4. right and left branches
    • go down interventricular septum and branch out. 2 pathways that carry impulses toward apex of heart.
  5. purkinje fibers
    • up apex and walls of L & R ventricles. AV bundle and purkinje fibers depolarize only 30 times w/o AV node input)
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7
Q

action potential graph explanation for contractile (99%) cells

A
  1. depolarization: Na+ influx through fast voltage gated channels. pos feedback loop opens other channels and reverses membrane potential. channels are then inactivated.
  2. plateau phase: due to Ca2+ influx through slow Ca2+ channels. (Ca dump moves tropomyosin out of the way) keeps cell depolarized because few K+ channels are open. **Need this phase so there’s no heart quiver
  3. repolarization: due to Ca2+ channels inactivating and K+ channels opening, allowing K+ efflux which brings membrane potential back to resting voltage.
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8
Q

why is the duration of action potential and contractile phase longer in cardiac muscle?

A

because unlike skeletal muscle, cardiac muscle has a plateau phase (long refractory period)

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9
Q

action potential of autorhythmic (noncontractile) cells graph explained

A
  • autorhythmic cells (depends on movement of Ca2+) and there is no plateau for this graph because sodium channels are always open!!!
  1. at threshold, Ca2+ channels open
  2. explosive Ca2+ influx produce rising phase of action potential
  3. repolarization results from inactivation of Ca2+ channels and opening of voltage gated K+ channels

in sum,
1. Leaky sodium channels (pacemaker potential)
2. rapid influx of calcium
3. top of graph, Ca closes K opens (change of charge)
4. potassium moves out (losing charge on inside, why there’s a negative slope)
5. all channels closed except sodium

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10
Q

homeostatic imbalances

A
  • defects in the intrinsic conduction system may result in:
  1. arrythmias: irregular heart rhythms
  2. uncoordinated atrial and ventricular contractions
  3. fibrillation: rapid irregular contractions; can’t pump blood
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11
Q

defective AV node may result in:

A
  • partial or total heart block
  • few or no impulses from SA node reach ventricles (result in ventricles reaching intrinsic rate, which is too slow)
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12
Q

vagus nerve

A

comes from brain stem and connects to heart

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13
Q

EKG steps

A

three parts (waves)
1. p wave: depolarization of atria caused by SA node
2. QRS complex/wave: ventricular depolarization
3. T wave: ventricular repolarization of SA node

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14
Q

AV node fires…

A

50 times per minutes

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15
Q

AV bundle fires…

A

30 times per minute

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16
Q

AV branches fire..

A

30 times per minute

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17
Q

purkinje fibers fire…

A

30 times per minute

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18
Q

EKG simplified steps

A
  1. depolarization of the atria, initiated by SA node, causes p wave
  2. repolarization of the atria (can’t see on EKG),
  3. septal depolarization (signal getting to bundle branches here)
  4. apical depolarization (at apex)
  5. ventricular wall depolarization
  6. repolarization of the ventricle
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19
Q

junctional rythym disorder

A

SA node non functional
no P waves

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20
Q

second degree heart block disorder

A

some P waves are absent, more QRS waves
AV node is weird

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21
Q

ventricular fibrilation disorder

A

can die because of improper build up of muscle tension in ventricles to pump out blood.

EKG is all over the place

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22
Q

atrial fibrillation

A

fluttering in atria, too many p waves

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23
Q

heart sounds

A
  • two sounds (lubDup) associated with closing heart valves
  • first sounds occurs as tricuspid and mitral valves close, signifying ventricular diastole and atrial systole
  • second sound occurs as aortic and pulmonary valves close, signifying ventricular systole and atrial diastole
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24
Q

heart murmurs

A

abnormal heart sounds indicates incompetent valves

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25
Q

phases of cardiac cycle: ventricular filling

A
  1. ventricular filling- mid to late diastole:
    • AV valves open
    • 80% of blood passively flows into ventricles
    • atrial systole delivers remaining 20%
    • end diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole
26
Q

phases of cardiac cycle: ventricular systole

A
  1. ventricular systole (AKA ventricular ejection)
    • atria relax and ventricles begin to contract
    • rising ventricular pressure results in closing of AV valves
    • isovolumetric contraction phase (all valves are closed)
    • in ejection phase, ventricular pressure exceeds pressure in large arteries (aorta, pulmonary trunk), forcing SL valves open.
    • end systolic volume (ESV): volume of blood remaining in each ventricle
27
Q

phases of cardiac cycle: isovolumetric relaxation

A
  1. isovolumetric relaxation (occurs in early diastole)
    • ventricles relax
    • backflow of blood in aorta and pulmonary trunk closes SL valves and causes brief rise in aortic pressure
28
Q

cardiac output (CO)

A
  • volume of blood pumped by each ventricle in one minute
  • CO= Heart rate * stroke volume
  • heart rate: # of BPM
  • stroke volume: volume of blood pumped out by a ventricle with each beat
29
Q

cardiac output in sedentary vs active people

A
  • sedentary: sedentary people have a higher CO at rest
  • active people have a higher CO when active
30
Q

cardiac output at rest

A
  • max CO is 4-5 times higher than resting CO in nonathletic people
  • max CO may reach 35 L/min in trained athletes
  • cardiac reserve: difference between resting and max CO
31
Q

regulation of stroke volume (SV)

A
  • SV= EDV-ESV
  • three main factors affect SV:
    • preload: atria contraction
  • contractility (starlings law: bit of stretch in muscle makes it contract better)
  • afterload: blood pressure/blood vessel flow
32
Q

afterload

A

pressure that must be overcome for ventricles to eject blood

  • hypertension (high blood pressure) increases afterload, resulting in increased ESV and reduced SV
33
Q

regulation of heart rate

A

-pos chronotropic factors increase herat rate
-neg decrease

caffeine is positive
vagus is negative, helps to slow heart rate

34
Q

autonomic nervous system regulation

A
  • parasympathetic: rest and digest
  • sympathetic: fight or flight
35
Q

sympathetic nervous system

A

sympathetic nervous system is activated by emotional or physical stressors

  • norepinephrine causes pacemaker to fire more rapidly (and increases preload and contractility)
36
Q

parasympathetic nervous system

A

… opposes sympathetic effects

  • acetylcholine hyperpolarizes pacemaker cells by opening K+ channels
37
Q

tachycardia

A

fast heart rate (greater than 100 BPM)
may lead to fibrillation if persistent

38
Q

bradycardia

A

slow heart rate (slower than 60 BPM)
may result in inadequate blood circulation

39
Q

congestive herat failure

A
  • umbrella term, sometimes not totally fatal
  • progressive condition where CO is so low that blood circulation is inadequate to meet tissue needs
40
Q

coronary bypass

A

method: restores blood flow by using blood vessels from other parts of your body to create a detour around blockages.

uses saphenous vein in leg and the mammary artery in chest

use cold blood to stop heart, ventilator to help breathe, and a heart lung bypass machine, allowing the heart to stop and pumps blood for the heart and adds O2 and other nutrients

41
Q

blood pressure

A

force exerted on vessel walls measured in mmHg.

42
Q

velocity of blood flow

A
  • is inversely related to the total cross sectional area
  • is fastest in the aorta, slowest in the capillaries, increasing again in veins
  • slow capillary flow allows adequate time for exchange between blood and tissues
43
Q

measuring blood pressure

A
  • measured using a sphygmomanometer
  • pressure is increased in the cuff until it exceeds systolic pressure in the brachial artery
  • pressure is released slowly and the examiner listens for first sound (systolic pressure), and last sound (diastolic pressure)
44
Q

hypotension

A

low blood pressure
- lack of perfusion
- often associated with long life

45
Q

hypertension

A

high blood pressure
- may be temporary changes during fever, exercise or emotional upset
- persistent in obese people
- prolonged hypertension causes problems during afterload and causes heart arrhythmias, failure, vascular disease, renal (kidney failure), and stroke

46
Q

blood flow through tissues

A
  • delivery of O2 and nutruents and removal of waste from tissues
  • changes in response to changing needs (increase in heart rate, for example)
47
Q

autoregulation of blood flow

A
  • automatic adjustment of blood flow to each tissue based on its requirements
  • controlled intrinsically by modifying diameter of local arterioles feeding the capillaries (opening/closing of capillaries, or sphincters opening and closing them, like when we blush)
48
Q

two types of autoregulation

A
  1. metabolic
  2. myogenic (stretch)
49
Q

metablic autoregulation

A
  • vasodilation of arterioles and relaxation of sphincters (only way to change diameter of capillaries)
  • this can occur in response to:
    declining O2 in tissues or histamine and cortisol
50
Q

myogenic autoregulation

A
  • uses vascular smooth muscle to keep tissue perfusion constant
  • uses stretching to increase tone and vasoconstriction
  • reduced stretch promotes vasodilation (relaxation) and increases blood flow to tissues
51
Q

long term autoregulation: angiogenesis

A
  • occurs when short term autoregulation can’t meet tissue nutrient regquirements
  • the number of vessels to a region increases and existing vessels enlarge

ex: we’re in high altitude for long periods

52
Q

circulatory shock

A

don’t have enough blood in blood vessels or perfusion to the brain and heart

treatment:
- elevate feet/legs
- keep body warm

53
Q

perfusion triangle

A
  1. heart (pump function): heart damage can’t move blood adequately to support perfusion
  2. blood vessels (container function): blood vessels dilate at once so the normal blood volume isn’t enough to fill system and provide adequate perfusion
  3. blood (content function): if blood or plasma is lost, the volume in the container isn’t enough to support perfusion in body
54
Q

blood vessels

as heart beats..

A

blood is propelled through arteries -> arterioles -> capillary beds

capillary beds are drained by the venules -> veins -> great veins (vena cavas)

55
Q

blood vessel walls

A
  1. tunica intima/endothelium (lines lumen or interior
  2. tunica media (innervated, controls blood flow from nerve stim) is smooth muscle that changes the diameter of the vessels and increases/decreases blood pressure
  3. tunica externa (adventitia) composed of fibrous connective tissue: supports and protects vessel
56
Q

elastic vs. muscular artery

A

elastic: largest diameter, lowest resistance, elasticity maintains blood pressure, not involved in vasoconstriction

muscular: “distributing arteries,” involved in vasoconstriction/dilation

57
Q

arteriole

A

most resistance due to friction, main agent of vasoconstriction/dilation to control blood flow to specific regions.

controlled by hormones (epinephrine), nerve, chemicals
**cold hands, nose, ears during thermoregulation

58
Q

vein valves only found…

A

in lower limbs to help oppose force of gravity

59
Q

arteriosclerosis

A

blood vessel gets thicker

60
Q

atherosclerosis

A

arteries clogged by fat or cholesterol

61
Q

aneurysm

A

bulging of blood vessel wall. can lead to atherosclerosis or rupture

Anatomy & Physiology (20 decks)

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