II The Heart Flashcards

1
Q

Circuit for each half of the heart

A
Left = pulmonary circuit
Right = systemic circuit
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2
Q

Two phases of the heart

A

Systole - contraction

Diastole - relaxation

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3
Q

Systole

A

contraction

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4
Q

Diastole

A

relaxation

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5
Q

Features of cardiac muscle

A
  1. Intercalated Discs
  2. Spontaneous Depolarization
  3. Prolonged Action Potential
  4. Prolonged Refractory Period
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6
Q

Sinoatrial Node (function, location, x/minute)

A

Pacemaker of heart
Right atrium
75x / minute

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7
Q

Atrioventricular (AV) Node (function)

A

Picks up pulse from atria - passes to interventricular septum

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8
Q

AV Bundle (Bundle of His)

A

forms left and right bundle branches

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9
Q

Steps in Conduction (5)

A
  1. SA node fires
  2. Stimulus passes over atria to AV node
  3. 100 msec delay at AV node, atria contract
  4. Impulse goes to AV bundle, bundle branches, purkinje fibers
  5. Ventricles contract
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10
Q

ECG - P Wave

A

Atrial depolariztion

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11
Q

ECG - P Wave

A

Atrial depolarization by end

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12
Q

ECG - T Wave

A

Ventricular Repolarization

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13
Q

ECG - PR Interval

A

Time from atrial to ventricular excitation

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14
Q

ECG - PR Interval

A

Time from atrial to ventricular excitation
PR interval is the period, measured in milliseconds, that extends from the beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the onset of ventricular depolarization); it is

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15
Q

ECG - QT interval

A

Normal QTc values. QTc is prolonged if > 440ms in men or > 460ms in women. QTc > 500 is associated with increased risk of torsades de pointes. QTc is abnormally short if < 350ms. A useful rule of thumb is that a normal QT is less than half the preceding PR interval

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16
Q

ECG - QRS interval

A

The normal duration (interval) of the QRS complex is between 0.08 and 0.10 seconds — that is, 80 and 100 milliseconds. When the duration is between 0.10 and 0.12 seconds, it is intermediate or slightly prolonged. A QRS duration of greater than 0.12 seconds is considered abnormal.

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17
Q

ECG - PQ segment

A

PR interval is the period, measured in milliseconds, that extends from the beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the onset of ventricular depolarization); it is normally between 120 and 200ms in duration.

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18
Q

ECG - ST segment

A

the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. It represents the interval between ventricular depolarization and repolarization

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19
Q

Two factors that impact END DIASTOLIC VOLUME

A

Venous pressure (high pressure = larger volume)

Filling time (longer filling time = higher volume)

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20
Q

Starling’s Law

A

More stretch = more contraction
Stretch = preload
The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant

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21
Q

Contractility

A

Amount of force at a given preload

22
Q

Factors that effect Contractility (Autonomic Nervous)

A
Autonomic nervous system
    Sympathetic Stimulation 
       Norepinephrine
       Epinephrine
       Both ++ contractility
    Parasympathetic Stimulation
       Acetylcholine  (ACh)
       - - Contractility
23
Q

Factors that influence STROKE VOLUME (3)

A
  1. End diastolic volume (amount of blood in ventricles at end of Diastole)
  2. Force of Ejection (push of ventricle on blood)
  3. Afterload
24
Q

Factors that effect Contractility (Ions)

A

Ions
High Ca++ . ++contractility
High K+ – contractility

25
Q

Factors that influence FORCE OF EJECTION

A

Arterial backpressure

Force of contraction

26
Q

Three general factors that impact CONTRACTILITY

A

Autonomic stimulation
Hormones
Ions

27
Q

Factors that effect Contractility (Autonomic Nervous)

A
Autonomic nervous system
    Sympathetic Stimulation 
       Norepinephrine
       Epinephrine
       Both ++ contractility
    Parasympathetic Stimulation
       Acetylcholine  (ACh)
       - - Contractility
28
Q

Ventricular Systole 4 steps

A
  1. QRS Wave ends - vents complete depolarizaiton
  2. Ventricles contract - pressure rises in ventricles (higher than atria)
  3. Blood forced into arteries (pressure rises in arteries, drops in ventricles)
  4. T Wave - ventricles repolarize
29
Q

Impact of Ventricular Systole (valves)

A

Force AV valves to close

Forces Aortic and Pulmonary Valves to open

30
Q

What causes Aortic and Pulmonary valves to open?

A

Ventricular Systole

31
Q

LUBB

A

AV valves closing

32
Q

Ventricular Diastole 5 steps

A
  1. Ventricles Relax (vent. pressure drops)
  2. High pressure in arteries (aortic/pulmonary valves close)
  3. Atria fill with blood (forces AV valves open)
  4. Atrial blood moves into ventricles (70% of filling)
  5. P Wave begins - start atrial depolarization
33
Q

Dubb

A

Aortic and Pulmonary valves closing

34
Q

Isovolumetric Contraction

A

Ventricles contract but no volume change.

all heart valves closed
in early systole

35
Q

Isovolumetric Relaxation

A

Ventricles release tension but volume doesn’t change

Beginning of Diastole

36
Q

Positive Inotropic Agents

A
Increase the strength of contraction
Noropenephrine
Epinephrine
Glucagon
Ca++
37
Q

Negative Inotropic Agents

A

Decrease the strength of contraction
Acetylcholine (ACh)
K+ (Potassium?)

38
Q

What is the length of an action potential for cardiac muscle?
How does this compare to skeletal muscle?

A

Cardiac 200-400ms
Skeletal 2-5 ms

Main difference is the intercollated discs and gap junctions?

39
Q

What is the length of the refractory period of cardiac muscle? What is the significance of this refractory period?

A

.4 seconds

repolarization is similar amount of time as contraction so that contractions cannot overlap . No tetanus.

40
Q

Afterload

A

is the resistance that the ventricle of the heart has to overcome to eject the blood from the ventricle chamber during systole. The resistance comes from the blood in the vessels and the constriction of the vessel walls.

41
Q

Why do the ventricles have a specialized conduction system?

A

Without this delay, the atria and ventricles would contract at the same time, and blood wouldn’t flow effectively from the atria to the ventricles. … The distal portion of the AV node is known as the bundle of His.

42
Q

What happens to the heart during the relaxation period of the cardiac cycle

A

he volume of blood in the ventricles at the end of diastole is referred to as the end-diastolic volume. The other phase of the cardiac cycle is called systole. This is the term used to describe the contraction of the heart.

43
Q

What happens during the ventricular filling period?

A

Ventricular muscle relaxes, intraventricular volume increases and pressure drops below atrial pressure. AV valves open as blood flows into the ventricles, atria contract to top off the ventricles.

44
Q

At what point during the ventricular filling period does atrial systole occur?

A

Most happens before the atrial systole

45
Q

cardioacceleratory center

A

Part of Sympathetic nervous system. Axon terminals release norepinephrine which stimulates SA node to depolarize with greater frequency or increase heart rate. Also decreases AV node delay to match increasing heart rate. Myocardium cells also stimulated to increase ventricular contraction.

46
Q

Cardioinhibitory center

A

Located in the medulla it is part of the parasympathetic nervous system. Depolarization travels through vagus nerve and axon terminals release acetylcholine. Inhibits SA node by decreasing the frequency of depolarization decreasing heart rate. It increases the length of AV delay. Does not innervate myocardium.

47
Q

Three cardiac receptor types

A

Proprioceptors

Baroreceptors

Chemoreceptors

48
Q

Proprioceptors

A
  • monitor position of joints and muscles

- send feedback during physical exercise

49
Q

Baroreceptors

A
  • Monitor pressure changes

- monitor stretch in walls of blood vessel

50
Q

Chemoreceptors

A

Monitor concentration of various chemicals in blood

51
Q

Where are baroreceptors located?

A

In the right and left internal carotid arteries and the aortic arch. Also in the right atrium, known as venus baroreceptor.

52
Q

How do baroreceptors react to blood pressure changes?

A

if the baroreceptors are detecting that blood pressure is too high, the cardio regulatory center of the medulla will also decrease sympathetic input to the blood vessels. This causes vasodilation, which decreases total peripheral resistance and decreases blood pressure.

The opposite happens when the baroreceptors of the aorta or carotid sinus detect a drop in blood pressure