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A+P 2 > chapter 18.5 > Flashcards

chapter 18.5 Flashcards

1
Q

Systole

A

period of heart contraction

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2
Q

Diastole:

A

period of heart relaxation

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3
Q

Cardiac cycle

A

blood flow through heart during one complete heartbeat

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4
Q

Atrial systole and diastole are followed by

cardiac Cycle represents series of

Mechanical events follow

A

ventricular systole and diastole

pressure and blood volume changes

electrical events seen on ECG

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5
Q

___ phases of the cardiac cycle

A

3
Ventricular filling: mid-to-late diastole

Ventricular systole

Isovolumetric relaxation (early diastole)

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6
Q

Ventricular filling: mid-to-late diastole
End diastolic volume (EDV)
(QRS wave)
-Atria finish contracting and return to diastole

A
  • Pressure is low; 80% of blood passively flows from atria through open AV valves into ventricles from atria (SL valves closed)
  • Atrial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle
  • —End diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole
  • Depolarization spreads to ventricles (QRS wave)
  • Atria finish contracting and return to diastole while ventricles begin systole
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7
Q 
Ventricular systole
End systolic volume (ESV):
Rising ventricular pressure causes closing of what valves
Pressure in aorta around
-End systolic volume (ESV):
A
  • Atria relax; ventricles begin to contract
  • Rising ventricular pressure causes closing of AV valves
  • Two phases
  • —-2a: Isovolumetric contraction phase: all valves are closed
  • —-2b: Ejection phase: ventricular pressure exceeds pressure in large arteries, forcing SL valves open
  • -Pressure in aorta around 120 mm Hg

-End systolic volume (ESV): volume of blood remaining in each ventricle after systole

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8
Q 
Isovolumetric relaxation: early diastole
Causes
Following 
Backflow of blood in aorta and pulmonary trunk 
Ventricles are totally
A
  • Following ventricular repolarization (T wave), ventricles are relaxed; atria are relaxed and filling
  • Backflow of blood in aorta and pulmonary trunk closes SL valves
  • -Causes dicrotic notch (brief rise in aortic pressure as blood rebounds off closed valve)
  • –Ventricles are totally closed chambers (isovolumetric)
  • When atrial pressure exceeds ventricular pressure, AV valves open; cycle begins again
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9
Q

Heart Sounds
two sounds
Pause between lub-dups indicates

A
  • Two sounds (lub-dup) associated with closing of heart valves
  • First sound is closing of AV valves at beginning of ventricular systole
  • Second sound is closing of SL valves at beginning of ventricular diastole
  • Pause between lub-dups indicates heart relaxation
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10
Q

Bicuspid valve closes

Differences allow

A

slightly before tricuspid, and aortic closes slightly before pulmonary valve

Differences allow auscultation of each valve when stethoscope is placed in four different regions

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11
Q

Heart murmurs:

A

abnormal heart sounds heard when blood hits obstructions

Usually indicate valve problems

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12
Q

Incompetent (or insufficient) valve:

A

fails to close completely, allowing backflow of blood

Causes swishing sound as blood regurgitates backward from ventricle into atria

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13
Q

Stenotic valve

A

fails to open completely, restricting blood flow through valve
Causes high-pitched sound or clicking as blood is forced through narrow valve

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14
Q 
Cardiac Output (CO)
normal=
A

Volume of blood pumped by each ventricle in 1 minute

CO = heart rate (HR) × stroke volume (SV)
HR = number of beats per minute
SV = volume of blood pumped out by one ventricle with each beat
Normal: 5.25 L/min

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15
Q

Regulation of Pumping

Maximal CO is

Maximal CO may reach

CO changes (increases/decreases) if either or both

A

4–5 times resting CO in nonathletic people (20–25 L/min)

35L/min in trained athletes

SV or HR is changed

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16
Q

Cardiac reserve

A

difference between resting and maximal CO

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17
Q

CO is affected by factors leading to:

A

Regulation of stroke volume

Regulation of heart rates

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18
Q

Mathematically: SV =

EDV is affected by length of
ESV is affected by
Normal SV =

A

EDV − ESV

ventricular diastole and venous pressure (~120 ml/beat)

arterial BP and force of ventricular contraction (~50 ml/beat)
120 ml − 50 ml = 70 ml/beat

19
Q

Three main factors that affect SV:

A

Preload
Contractility
Afterload

20
Q 
Preload
Changes in preload cause changes in 
Affects
Relationship between preload and SV called
Cardiac muscle exhibits a
A

degree of stretch of heart muscle

Preload: degree to which cardiac muscle cells are stretched just before they contract
-Changes in preload cause changes in SV
Affects EDV
Relationship between preload and SV called 
Frank-Starling law of the heart
Cardiac muscle exhibits a length-tension relationship
At rest, cardiac muscle cells are shorter than optimal length; leads to dramatic increase in contractile force

21
Q

Most important factor in preload stretching of cardiac muscle is

A

venous return—amount of blood returning to heart

  • Slow heartbeat and exercise increase venous return
  • Increased venous return distends (stretches) ventricles and increases contraction force
22
Q 
Contractility
Independent of 
Increased contractility \_\_\_\_ ESV
Positive inotropic agents
negative inotropic agents
A

-Contractile strength at given muscle length
-Independent of muscle stretch and EDV
-Increased contractility lowers ESV; caused by:
Sympathetic epinephrine release stimulates increased Ca 2+ influx, leading to more cross bridge formations

Positive inotropic agents
increase contractility
Thyroxine, glucagon, epinephrine, digitalis, high extracellular

negative inotropic agents
Acidosis

23
Q 
Afterload
-Aortic pressure is around
-Pulmonary trunk pressure is around 
-Hypertension\_\_\_\_\_\_afterload
 resulting in \_\_\_\_\_\_\_ESV and \_\_\_\_\_\_ SV
A

back pressure exerted by arterial blood
Afterload is pressure that ventricles must overcome to eject blood
-Back pressure from arterial blood pushing on SL valves is major pressure
-Aortic pressure is around 80 mm Hg
-Pulmonary trunk pressure is around 10 mm Hg

-Hypertension increases afterload, resulting in increased ESV and reduced SV

24
Q

Regulation of Heart Rate
If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by

-factors that increase and decrease heart rate

A

If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by increasing HR and contractility

Positive chronotropic factors increase heart rate
Negative chronotropic factors decrease heart rate

25
Q

Heart rate can be regulated by:

A

Autonomic nervous system
Chemicals
Other factors

26
Q

Autonomic nervous system regulation of heart rate
_______ nervous system can be activated by
is released and binds to

causing:

A
  • Sympathetic nervous system can be activated by emotional or physical stressors
  • Norepinephrine is released and binds to β1-adrenergic receptors on heart, causing:
  • -Pacemaker to fire more rapidly, increasing HR
  • –EDV decreased because of decreased fill time
  • -Increased contractility
  • –ESV decreased because of increased volume of ejected blood
27
Q

Autonomic nervous system

Because both EDV and ESV decrease,

A

SV can remain unchanged
Parasympathetic nervous system opposes sympathetic effects
Acetylcholine hyperpolarizes pacemaker cells by opening

28
Q

Autonomic nervous system regulation of heart rate

Heart at rest exhibits

A

vagal tone

  • Parasympathetic is dominant influence on heart rate
  • Decreases rate about 25 beats/min
  • Cutting vagal nerve leads to HR of ∼100
29
Q

When sympathetic is activated, parasympathetic is

A

inhibited, and vice-versa

30
Q

Atrial (Bainbridge) reflex

A
  • sympathetic reflex initiated by increased venous return, hence increased atrial filling
  • Atrial walls are stretched with increased volume
  • Stimulates SAnode, which increases HR
  • Also stimulates atrial stretch receptors that activate sympathetic reflexes
31
Q

Chemical regulation of heart rate

A

Hormones

  • Epinephrine from adrenal medulla increases heart rate and contractility
  • Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine

Ions
Intra- and extracellular ion concentrations must be maintained for normal heart function
Imbalances are very dangerous to heart

32
Q

Hypocalcemia

A

depresses heart

33
Q

Hypercalcemia:

A

increases HR and contractility

34
Q

Hyperkalemia:

A

alters electrical activity, which can lead to heart block and cardiac arrest, death

35
Q

Hypokalemia

A

results in feeble heartbeat; arrhythmias

36
Q

Other factors that influence heart rate

A

Age
Fetus has fastest HR; declines with age

Gender
Females have faster HR than males

Exercise
Increases HR
Trained atheles can have slow HR

Body temperature
HR increases with increased body temperature

37
Q

Tachycardia

A

abnormally fast heart rate (>100beats/min)

If persistent, may lead to fibrillation

38
Q

Bradycardia

A

heart rate slower than 60beats/min
May result in grossly inadequate blood circulation in nonathletes
May be desirable result of endurance training

39
Q

Congestive heart failure (CHF)

A

Progressive condition; CO is so low that blood circulation is inadequate to meet tissue needs
Reflects weakened myocardium caused by:

Coronary atherosclerosis: clogged arteries caused by fat buildup; impairs oxygen delivery to cardiac cells
–Heart becomes hypoxic, contracts inefficiently

40
Q

Congestive heart failure (CHF)
Persistent high blood pressure:

Multiple myocardial infarcts:
Dilated cardiomyopathy (DCM):
A

aortic pressure >90 mmHg causes myocardium to exert more force
Chronic increased ESV causes myocardium hypertrophy and weakness

Multiple myocardial infarcts: heart becomes weak as contractile cells are replaced with scar tissue
Dilated cardiomyopathy (DCM): ventricles stretch and become flabby, and myocardium deteriorates
Drug toxicity or chronic inflammation may play a role

41
Q

Congestive heart failure (CHF)
Either side of heart can be
Failure of either side ultimately

A

-Left-sided failure results in pulmonary congestion
Blood backs up in lungs
-Right-sided failure results in peripheral congestion
Blood pools in body organs, causing edema
-Failure of either side ultimately weakens other side
Leads to decompensated, seriously weakened heart
Treatment: removal of fluid, drugs to reduce afterload and increase contractility

42
Q

Frank starling

A

preload and SV

43
Q

chonotropic

A

heart rate

44
Q

inotropic

A

contractility

A+P 2 (13 decks)

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