AnatomyII-Test One part 3 Flashcards

1
Q

Heart Cells

A

Some cardiac muscle cells are self-excitable (autorhythmic) and initiate the depolarization of the whole heart
All cardiac muscle cells contracts as a unit
Have a long (250 ms) absolute refractory period
Have more mitochondria than skeletal muscles
Non autorhythmic contract similar to skeletal muscles

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2
Q

Intrinsic Conduction System

A

Initiate the action potentials which cause the muscles of the heart to contract and pump blood
Network of noncontractile (autorhythmic) cells

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3
Q

Autorhythmicity

A

Heart depolarizes and contracts without nervous system stimulation (Intrinsic)
Autorhythmic Cells (pacemaker cells)
Unstable resting membrane potentials
pacemaker potentials or prepotentials
Continuously depolarize, never rest
Due to opening of slow Na+ channels
Use calcium influx (rather than sodium) for rising phase of the action potential

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4
Q

Heart is stimulated by the

A

sympathetic cardioacceleratory center

 rate and force

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5
Q

Heart is inhibited by the

A

parasympathetic cardioinhibitory center

 rate

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6
Q

Electrocardiogram

A

Recorded by electrodes placed at specific points on the skin

Electrical activity resulting from the propagation of many action potentials

Composite of all action potentials generated by nodal and contractile cells at given time

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7
Q

PWave

A

depolarization SA node  atria

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8
Q

QRS Complex

A

ventricular depolarization and atrial repolarization

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9
Q

TWave

A

ventricular repolarization

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10
Q

Why EKG

A

Valuable in diagnosing diseases or ailments that damage the conductive abilities of the heart muscle
Damaged cardiac muscle cells no longer conduct electrical impulses
Electrical signals terminate at the damaged tissue
Alters the manner in which the heart contracts
A patient’s electrocardiogram can help determine the presence of damaged cardiac muscle based on the waveform as well as the time interval between electrical events

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11
Q

Heart Sounds

A

Heart sounds (lub-dup) are associated with closing of heart valves
First sound occurs as AV valves close and signifies beginning of systole (contraction)
Second sound occurs when SL valves close at the beginning of ventricular diastole (relaxation)

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12
Q

Diastole

Systole

A

relaxation of heart muscle

contraction of heart muscle

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13
Q

Ventricular filling

A

mid-to-late diastole
Heart blood pressure is low as blood enters atria (passively) and flows into ventricles
AV valves are open, then atrial systole occurs

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14
Q

Ventricular systole (contraction)

A

Atria relax
Rising ventricular pressure results in closing of AV valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves

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15
Q

Isovolumetric Relaxtion

A

early diastole
Ventricles relax
Backflow of blood in aorta and pulmonary trunk closes semilunar valves

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16
Q

Dicrotic Notch

A

brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves

17
Q

Cardiac Output

A

amount of blood pumped by each ventricle in one minute

18
Q

CO is the product of

A

heart rate (HR) and stroke volume (SV)

19
Q

HR

SV

A

the amount of blood pumped out by a ventricle with each beat

the number of heart beats per minute

20
Q

Cardiac Reserve

A

difference between resting and maximal CO

21
Q

EDV

ESV

A

amount of blood remaining in a ventricle after contraction

amount of blood collected in a ventricle during diastole

22
Q

Factors Affecting Stroke Volume

A

Preload
Contractility
Afterload

23
Q

Preload
Contractility
Afterload

A

amount ventricles are stretched by contained blood

cardiac cell contractile force due to factors other than EDV

back pressure exerted by blood in the large arteries leaving the heart

24
Q

Preload

A

or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Most important factor stretching cardiac muscle is venous return – amount of blood returning to heart
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV

25
Contractility
is the increase in contractile strength, independent of stretch and EDV ``` Increase in contractility comes from: Increased sympathetic stimulation  increased Ca2+ influx  more cross bridges Certain hormones Ca2+ and some drugs ```
26
Sympathetic stimulation
releases norepinephrine and initiates a cyclic AMP second-messenger system Results in elevated intracellular [Ca2+] of pacemaker cells
27
Agents/factors that decrease contractility include:
Acidosis Increased extracellular K+ Calcium channel blockers
28
Regulation of Heart Rate Positive chronotropic Negative chronotropic
factors decrease heart rate Sedatives factors increase heart rate Caffeine
29
Sympathetic nervous system activated by
emotional or physical stressors Norepinephrine causes pacemaker to fire more rapidly (and increases contractility) increase HR increase contractility
30
Parasympathetic nervous system opposes
sympathetic effects Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels  HR
31
Vagal Tone
Parasympathetic dominant influence | Heart at rest
32
Atrial (Bainbridge) reflex
sympathetic reflex initiated by increased venous return, hence increased atrial filling Stretch of atrial walls stimulates SA node  HR Also stimulates atrial stretch receptors, activating sympathetic reflexes
33
Hormones that increase heart rate
epinephrine and thyroxine | Intra- and extracellular ion concentrations must be maintained for normal heart function
34
Hypocalcemia | Hypercalcemia
depresses heart | increased HR and contractility
35
Hyperkalemia | Hypokalemia
alters electrical activity  heart block and cardiac arrest | feeble heartbeat; arrhythmias
36
Other Factors that Influence Heart Rate
Age Fetus has fastest HR Gender Females faster than males Exercise Increases HR Body temperature Increases with increased temperature
37
Tachycardia
abnormally fast heart rate (>100 beats/min)
38
Bradycardia
heart rate slower than 60 beats/min