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Anatomy and Physiology > heart ii > Flashcards

heart ii Flashcards

1
Q

Sequence of excitiation

A

Cardiac pacemaker cells pass imipulses in order across heart in 220 ms

Sinoatrial node
atrioventricular node
atrioventricular bundle
right and left bundle branches
Subendocardial conducting network (Purkinje fibers)
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2
Q

Sinoatrial node

A
  • pacemaker of heart in right atrial wall
  • depolarizes fater than rest of myocardium
  • 75 impulses/minute = sinus rhythm
  • Inherent rate = 100/min, but PNS slows it down
  • Impulse spreads to atria and to AV node
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3
Q

Atrioventricular node

A
  • in inferior interatrial septum
  • Delays impulses by 0.1 s because fibers are small and have fewer gap junctions –> allows atrial contraction to finish b4 ventricular contraction
  • inherent rate of 40-50/min, but SA node speeds it up
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4
Q

Atrioventricular bundle

A
  • Bundle of His
  • in superior interventricular septum
  • only electrical connection between atria and ventricles
  • atria and ventricles not connected via gap junctions
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5
Q

Right and left bundle branches

A
  • two pathways in interventricular septum

- carry impulses toward apex of heart

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6
Q

Subendocardial conducting network

A
  • Purkinje fibers
  • complete pathway thru interventricular septum into apex and ventricular walls
  • more elaborate on left
  • AV bundle and Purkinje fibers depolarize at 30/min w/o AV node
  • Ventricular contraction immediately follows from apex toward atria
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7
Q

Arrhythmias

A

irregular heart rhythms

-uncoordinated atrial and ventricular contraction

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8
Q

Fibrillation

A
  • rapid, irregular contractions
  • if in ventricles, can’t pump blood and circulation ceases and brain dies
  • fixed with defibrillation
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9
Q

What can a defective SA node cause?

A

Ectopic foucs: abnormal pacemaker –> AV node takes over and sets junctional rhythm (40-60/min)

Extrasystole: premature contraction –> ectopic focus sets high rate –> can be from too much caffeine or nicotine

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10
Q

Results of defective AV node

A

Heart block: few (partial) or no (total) impulses reach ventricles –> ventricles beat at intrinsic rate which is too slow for life

Treated with artificial pacemaker

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11
Q

ECG/ EKC

A

electrocardiograms
P wave = atrial depolarization
QRS complex = ventricular depolarization and atrial repolarization
T wave = ventricular repolarization

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12
Q

Cardiac cycle

A

Bloodflow thru heart during one complete heartbeat: atrial systole/diastole followed by ventricular systole/diastole

Systole = contraction
Diastole = relaxation

caused by pressure and blood volume changes

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13
Q

Phases of the cardiac cycle

A
  1. Ventricular filling
  2. Ventricular systole
  3. Isovolumetric relaxation
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14
Q

Ventricular filling

A
  • happens during mid to late diastole
  • AV valves are open and pressure is low
  • Ventricle filling = 80% of blood passively flows to ventricles
  • atrial systole occurs, delivering the remaining 20%

-End diastolic volume = volume of blood in each ventricle at the end of ventricular diastole

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15
Q

Ventricular systole

A
  • atria relax and ventricles begin contraction
  • rising ventricular pressure and closing of AV valves
  • Isovolumetric contraction phase (all valves are closed)
  • Ventricular ejection phase= ventricular pressure exceeds pressure in large arteries forcing SL valves open

End systolic volume = volume of blood in ventricle after systole

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16
Q

Isovolumetric relaxation

A
  • early diastole
  • ventricles relax and atria are relaxed/filling
  • Backflow of blood in aorta and pulmonary trunk closes SL valves (dicrotic notch = brief ries in aortic pressure)
  • ventricles are totally closed off
  • When atrial pressure exceeds that of ventricles, AV valves open and cycle begins again
17
Q

Hear sounds

A

lub dup:

  1. Av valves close (start of systole)
  2. SL valves close (start of diastole)
    * pause = heart relaxation

Murmurs = abnormal heart sounds

  1. stenosis: valve doesn’t open right
  2. regurgitation: valve doesn’t close right
18
Q

Cardiac output

A

volume of blood pumped by each ventricle in a minute

CO= heart rate x stroke volume 
CO = (beats/min) x (volume of each beat)

Normal = 5.25 L/min at rest
Max CO is 4-5x resting CO
Athletes CO can be 35 L/min

19
Q

Cardiac reserve

A

dif between resting and max CO

20
Q

Regulation of stroke volume

A

SV = end diastolic volume - end systolic volume
EDV affected by length of ventricular diastole and venous pressure
ESV affected by arterial BP and force of ventricular contraction

21
Q

3 main factors affecting SV

A

Preload
Contractility
Afterload

22
Q

Preload

A
  • degree of stretch of cardiac muscle cells before they contract
  • “Frank-Starling law of heart”)
  • there’s a length-tension relationship
  • at rest, cardiac muscle cells are shorter than optimal length
  • VENOUS RETURN is most imp factor in stretching cardiac muscle (increased by slow heartbeat and exercise)
23
Q

Contractility

A
  • contractile strength at given muscle length independant of muscle stretch and EDV
  • Increased by sympathetic stimulation (more Ca influx –> more cross bridges) and positive ionotropic agents
  • Decreased by negative ionotropic agents
24
Q

positive vs negative ionotropic agents

A

Pos: thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca

Neg: acidosis, increased extracellular K, calcium channel blockers

25
Q

Afterload

A
  • pressure ventricles must overcome to eject blood

- hypertension increases afterload resulting in increased ESV and reduced SV

26
Q

What regulates heart rate

A

positive and negative chronotropic factors

SNS: releases NE which makes pacemaker fire more rapidly and increases contractility (binds to beta1-andrenergic receptors) (lowers EDV bc of decreased fill time)

PNS: Acetylcholine hyperpolarizes pacemaker cells by opening K channels–> slower HR, but little effect on contractility

27
Q

vagal tone

A

Heart at rest with PNS as dominant influence

28
Q

Extrinsic innervation of the heart

A

Heartbeat modified by ANS via cardiac centers in medulla oblongata

  • sympatheric increases rate and force
  • Parasympathetic decreases rate
  • Cardioacceleratory center = sympathetic –> affects SA, AV nodes, heart muscle, and coronary arteries
  • Cardioinhibitory center = parasympathetic and inhibits SA/AV nodes via vagus nerves
29
Q

Atrial (brainbridge) reflex

A
  • sympathetic reflex initiated by increased venous return –> increased atrial filliing
  • stretch of atrial walls stimulates SA node to increase HR
  • also stimulates atrial stretch receptors, activating sympathetic reflexes
30
Q

Chemical regulation of heart rate

A

Hormones

  • epinephrine from adrenal medulla increases heart rate and contractility
  • thyroxine increases heart rate and enhances NE and Epinephrine

Intra and extra- cellular ion concentrations (CA and K) must be maintained for normal heart function

31
Q

Hypocalcemia
Hypercalcemia
Hyperkalemia
Hypokalemia

A
  • depresses heart
  • increases heart rate and contractility
  • alters elec activity–> heart block and cardiac arrest
  • feeble heartbeat and arrhythmias
32
Q

Random factors that influence heart rate

A

Age: fetus has fast HR
Gender: females have faster HR
Exercise: increases HR
Body temp: increases HR with temp

33
Q

Tachycardia

A

abnormally fast heart rate (>100/min)

-if persistent, may lead to fibrillation

34
Q

Bradycardia

A

heart rate slower than 60/min

  • may result in inadequate blood circulation in nonathletes
  • desireable, though, in endurance athletes

Anatomy and Physiology (50 decks)

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