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1st Year > KIN 103 Midterm (Lecture 1-3) > Flashcards

KIN 103 Midterm (Lecture 1-3) Flashcards

1
Q

ECG interpretation (What is block counting?)

A

5mm = 0.20 sec
1mm = 0.04 sec
1500 mm = 1 min

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2
Q

Autorhythmic Cells (What do they do?)

A
  • Generate action potentials spontaneously.
  • Make up about 1% of myocardial cells.
  • Do not contribute to the contractile force of the heart.
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3
Q

How is Parasympathetic Heart activity stimulated

A

By the medulla oblongata

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4
Q

How is Sympathetic Heart activity stimulated?

A

By T1 - T4 of the thoracic plexus

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5
Q

How does the conducting system of the heart flow?

A
  1. SA node
  2. Internodal pathways
  3. AV node
  4. AV bundles
  5. Bundle branches
  6. Purkinje Fibers
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6
Q

Einthoven’s Triangle (What is it?)

A

Right arm (+) - Left arm (- & +)
Left leg (-)

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7
Q

How to read ECG’s (What does an up mean?)

A
  • It means the net current flow is to the positive electrode
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8
Q

How to read ECG’s (What does a down mean?)

A
  • It means the net current flow is to the negative electrode
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9
Q

How is the P- wave generated?

A

The P-wave is generated by activation of the muscle of both atria.

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10
Q

How is the Q- wave generated?

A

The interventricular septum activates from left to right.This generates the Q-wave

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11
Q

How is the R- wave generated?

A

The left and right ventricular free walls, which form the bulk of the muscle of both ventricles, gets activated. This generates the R-wave.

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12
Q

How is the S- wave generated?

A

A few small areas of the ventricles are activated at a rather late stage. This generates the S-wave

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13
Q

How is the T- wave generated?

A

Finally, the ventricular muscle repolarizes. This generates the T-wave.

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14
Q

Tachycardia

A

HR > 100 bpm
Greater than 100mpm

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15
Q

Bradycardia

A

Bradycardia: HR < 60 bpm
Less than 60 bpm

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16
Q

Arrhythmias (What is it?)

A
  • Electrical problems in the generation or conductance of action potentials.
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17
Q

Arrhythmias (How is it seen on an ECG?)

A
  • These can be seen on an ECG and may include:
  • Missed or extra beats.
  • Atrial Fibrillation.
  • Premature Ventricular Contractions (PVCs).
  • Altered waves or segments
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18
Q

First-Degree Atrioventricular (AV) Block (How is it shown on an ECG)

A

It is displayed as:
- Increases duration of PR interval.
- Increases delay between atrial and ventricular contraction (greater than 0.20s or one big block).

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19
Q

Second-Degree AV Block (How is it shown on an ECG?)

A

It is displayed as:
- Slowed, sometimes stopped conduction through AV node.
- Lose 1-to-1 relationship between P wave and QRS complex. Dropped QRS every 2-5 beats.
- How does this effect the relationship between atrial and ventricular contraction?

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20
Q

Third-Degree (Complete) AV Block (How is it shown on an ECG?)

A

It is displayed as:
- Loss of conduction through the AV node.
- P wave becomes independent of QRS.
- Atrial and ventricular contractions are independent (2 different rates).

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21
Q

Atrial Fibrillation (How is it shown on an ECG?)

A

It is displayed as:
- SA node is not acting as pacemaker.
- Absence of P waves and irregular rate.
- There may be no symptoms, but it is often associated with palpitations, fainting, chest pain, or heart failure.

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22
Q

Premature Ventricular Contractions (PVCs)
(How is it shown on an ECG?)

A

it is displayed as:
- Extra beats occur under influence of autorhythmic cells other than the SA node.
- The QRS complex and T waves will look abnormal compared to a normal ECG

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23
Q

When do PVCs need to be treated?

A

PVCs need to be treated when they occur at the rate of > 6 per minute.

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24
Q

Ventricular Fibrillation (VF)

A
  • Basically causes nonsense waves with no form to them at all
  • It is a cause of cardiac arrest and can result in death without immediate medical intervention.
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25
Q

What may an S-T depression indicate?

A
  • May indicate Myocardial Ischemia
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26
Q

Where does a pacemaker get inserted?

A
  • Into the Subclavian vein and into the right atrium
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27
Q

Ablation Therapy (What is it?)

A
  • Destroys a small amount of cardiac tissue to creates an electrical block along the pathway causing the arrhythmia
28
Q

Implantable Cardioverter-Defibrillator (ICD) (What does it do?)

A
  • The ICD continuously monitors heart rhythm.
    - If rhythm is too slow, it paces the heart as a pacemaker would.
    - If it detects VT or VF, it sends out an electrical shock(s) to reset the heart to a normal rhythm.
29
Q

How much does heart and stroke cost the Canadian economy each year?

A
  • Heart disease & stroke costs the
    Canadian economy more than
    $22.2billion every year.
30
Q

Atherosclerosis (What is it?)

A
  • “hardening of the arteries
    ▫ Fat deposits on walls of arterial blood vessels.
    ▫ Results in plaque formation:
     Stable – separate from blood and do not form clots.
     Vulnerable – can rupture and initiate clot formation.
31
Q

Atherosclerosis (1-3)

A
  1. LDL cholesterol accumulates
  2. Macrophages ingest collesterol
  3. Smooth muscle cells uptake cholesterol
32
Q

Atherosclerosis (Stable)

A
  1. A lipid core forms in epithelium
  2. Fibrous tissue isolates the build up
  3. Smooth muscle divides to isolate further
  4. Calcifications are deposited in plaque
33
Q

Atherosclerosis (Vulnerable)

A
  1. Macrophages release enzymes to dissolve collagen and convert stable plaques into unstable ones
  2. Platelets that are exposed to collagen activate and initiate a blood clot
34
Q

Tonic control

A

Occurs via Catecholamines

35
Q

Catecholamines:

A

They can be sympathetic or parasympathetic
- only sympathetic catecholamines stimulate the circulatory system

36
Q

Beta 2 receptors (Characteristics)

A

Beta 2 receptors have a greater affinity for epinephrine
- They cause dilation in skeletal vessels

37
Q

Alpha receptors (Characteristics)

A

Alpha receptors have a greater sensitivity to Norepinephrine because these vessels are generally innervated tonically by sympathetic nerves
- They cause constriction in intestinal vessels

38
Q

Does blood pressure change normally durring the day?

A

Yes, that is why its important to measure at multiple times in the day and in different settings

39
Q

Systolic Pressure

A

Systolic Pressure
▫ Highest pressure in the ventricles and arteries.
▫ Occurs during ventricular systole.

40
Q

Diastolic pressure

A

Diastolic Pressure
▫ Lowest pressure in the ventricles and arteries.
▫ Occurs during ventricular diastole.

41
Q

Pulse Pressure

A

Pulse Pressure
▫ Difference between the systolic & diastolic
pressures.

42
Q

Hypertension

A

Hypertension
▫ Blood pressure is chronically elevated.
stage 1 (130-139 or 80-89)
stage 2 (over 149 or over 90)

43
Q

Hypotension

A

Hypotension
▫ Blood pressure is too low.
▫ Blood flow may become impaired.

44
Q

High blood pressure (What can it cause?)

A

▫ Increased afterload, but stroke volume
remains unchanged.
▫ This chronically high resistance leads to
cardiac hypertrophy.
▫ Pressure feedback to the lungs (edema) and right heart can lead to congestive heart
failure

45
Q

Edema

A

Edema is a sign that normal exchange between the circulatory system and the lymphatics has been disrupted.
- Causes:
(1) inadequate drainage of lymph or
(2) blood capillary filtration that greatly exceeds capillary absorption.

46
Q

Congestive heart failure

A

Congestive heart failure arises when the right heart is a more
effective pump than the left heart

47
Q

Calcium channel blockers (What do they do?)

A

Calcium channel blockers.
▫ Targets: Cardiac & Vascular Smooth Muscle.
▫ Effect: Less Ca2+ entry.
▫ Result: Heart rate & contractility decrease (cardiac)
and vasodilation (smooth).

48
Q

MAP equation

A

MAP = DBP + 1/3 (SBP – DBP)

49
Q

Baroreceptor reflex (What are they?)

A

The baroreceptor reflex is the primary reflex pathway for control of Mean Arterial Pressure
* Baroreceptors are stretch sensitive
mechanoreceptors.
* They are located in the walls of the aorta
and carotid arteries.
* When blood pressure increases, stretch
increases.
* When stretch increases, there is an
increase in afferent firing of the carotid
sinus nerve.

50
Q

Baroreceptors (What are they basically?)

A

They are receptors in the aorta and carotid arteries that send signals to the carotid sinus nerve when stretching occurs due to increased MAP
- The speed at which they send signals is indicative of pressure
- As signal speed stops CVCC increases, as it increases CVCC decreases

51
Q

Hemorrhage

A

Hemorrhage: the signals that occur right before reflexes kick in
Hemorrhage causes
▫ Baroreceptor reflex
▫ Increase in
sympathetic activity
▫ Decrease in
parasympathetic
activity

52
Q

GI tract

A

GastroIntestinal tract

53
Q

Resistance exercise results in?

A

Resistance exercise results in higher peak pressures

54
Q

Upper body exercise results in?

A

Upper body exercise results in greater pressures relative to the amount of muscle used

55
Q

Blood Pressure adaptations due to training?

A

Blood Pressure
* Both systolic and diastolic blood pressure are
reduced at rest with training.
* This is the most pronounced in hypertensive
individuals (both Stage 1 and 2).
▫ Training-induced reduction in sympathetic
hormones (catecholamines) contributes to the
lowering effect of regular exercise on blood
pressure.
* May also be reduced during submaximal exercise.

56
Q

What is the average resting CO?

A

Average resting CO (or Q) = 5 L/min.

57
Q

What is the average exercise CO?

A
  • Sedentary/Untrained: increase 20 L/min.
  • Trained: increase to 40 L/min.
58
Q

What does afterload do durring exercise?

A

It decreases gradually as exercise intensity increases

59
Q

Three mechanisms are responsible for the
increase in SV observed during ACUTE
exercise (What are they?)

A

1) Frank – Starling Mechanism.
2) Increased contractility due to
sympathetic stimulation.
3) Reduced total peripheral resistance.

60
Q

Adaptations to the cardiovascular
system due to training?

A

▫ Stroke Volume, and Cardiac Output.
▫ Heart Size.
▫ Blood Pressure, Flow, and Volume.
▫ Resulting HR response

61
Q

Contributing factors to increased stroke
volume (with maximal exercise)

A

Contributing factors to increased stroke
volume include:
▫ Greater End Diastolic Volume.
 Increased plasma volume and filling time.
▫ Increased ventricle size.
 Greater stretch and volume

62
Q

Static exercise causes what response on the body?

A

Fatiguing STATIC EXERCISE has a dramatic increase in MAP resulting in a strong “Pressor Load” on the heart

63
Q

Aerobic exercise causes what response on the body?

A

Fatiguing AEROBIC EXERCISE has a proportional increase in HR, SV and SBP resulting in more venous return and “Volume Load” on the heart

64
Q

Physiological hypertrophy (What happens when we exercise?)

A

Physiological Hypertrophy
* The left ventricle largens due to increased filling (↑EDV).
* Some increase in left ventricular wall size also occurs resulting in more forceful contraction.

65
Q

Pathological hypertrophy (What is it?)

A

Changes in our heart due to conditions such as hypertension or hypotension where our body adapts to what condition we have

66
Q

What will we not see in pathological changes

A
  • An increase in myocyte length and width along with wall thickness

1st Year (37 decks)

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