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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
What may an S-T depression indicate?
- May indicate Myocardial Ischemia
26
Where does a pacemaker get inserted?
- Into the Subclavian vein and into the right atrium
27
Ablation Therapy (What is it?)
- Destroys a small amount of cardiac tissue to creates an electrical block along the pathway causing the arrhythmia
28
Implantable Cardioverter-Defibrillator (ICD) (What does it do?)
- 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
How much does heart and stroke cost the Canadian economy each year?
- Heart disease & stroke costs the Canadian economy more than $22.2billion every year.
30
Atherosclerosis (What is it?)
- “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
Atherosclerosis (1-3)
1. LDL cholesterol accumulates 2. Macrophages ingest collesterol 3. Smooth muscle cells uptake cholesterol
32
Atherosclerosis (Stable)
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
Atherosclerosis (Vulnerable)
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
Tonic control
Occurs via Catecholamines
35
Catecholamines:
They can be sympathetic or parasympathetic - only sympathetic catecholamines stimulate the circulatory system
36
Beta 2 receptors (Characteristics)
Beta 2 receptors have a greater affinity for epinephrine - They cause dilation in skeletal vessels
37
Alpha receptors (Characteristics)
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
Does blood pressure change normally durring the day?
Yes, that is why its important to measure at multiple times in the day and in different settings
39
Systolic Pressure
Systolic Pressure ▫ Highest pressure in the ventricles and arteries. ▫ Occurs during ventricular systole.
40
Diastolic pressure
Diastolic Pressure ▫ Lowest pressure in the ventricles and arteries. ▫ Occurs during ventricular diastole.
41
Pulse Pressure
Pulse Pressure ▫ Difference between the systolic & diastolic pressures.
42
Hypertension
Hypertension ▫ Blood pressure is chronically elevated. stage 1 (130-139 or 80-89) stage 2 (over 149 or over 90)
43
Hypotension
Hypotension ▫ Blood pressure is too low. ▫ Blood flow may become impaired.
44
High blood pressure (What can it cause?)
▫ 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
Edema
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
Congestive heart failure
Congestive heart failure arises when the right heart is a more effective pump than the left heart
47
Calcium channel blockers (What do they do?)
Calcium channel blockers. ▫ Targets: Cardiac & Vascular Smooth Muscle. ▫ Effect: Less Ca2+ entry. ▫ Result: Heart rate & contractility decrease (cardiac) and vasodilation (smooth).
48
MAP equation
MAP = DBP + 1/3 (SBP – DBP)
49
Baroreceptor reflex (What are they?)
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
Baroreceptors (What are they basically?)
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
Hemorrhage
Hemorrhage: the signals that occur right before reflexes kick in Hemorrhage causes ▫ Baroreceptor reflex ▫ Increase in sympathetic activity ▫ Decrease in parasympathetic activity
52
GI tract
GastroIntestinal tract
53
Resistance exercise results in?
Resistance exercise results in higher peak pressures
54
Upper body exercise results in?
Upper body exercise results in greater pressures relative to the amount of muscle used
55
Blood Pressure adaptations due to training?
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
What is the average resting CO?
Average resting CO (or Q) = 5 L/min.
57
What is the average exercise CO?
- Sedentary/Untrained: increase 20 L/min. - Trained: increase to 40 L/min.
58
What does afterload do durring exercise?
It decreases gradually as exercise intensity increases
59
Three mechanisms are responsible for the increase in SV observed during ACUTE exercise (What are they?)
1) Frank – Starling Mechanism. 2) Increased contractility due to sympathetic stimulation. 3) Reduced total peripheral resistance.
60
Adaptations to the cardiovascular system due to training?
▫ Stroke Volume, and Cardiac Output. ▫ Heart Size. ▫ Blood Pressure, Flow, and Volume. ▫ Resulting HR response
61
Contributing factors to increased stroke volume (with maximal exercise)
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
Static exercise causes what response on the body?
Fatiguing STATIC EXERCISE has a dramatic increase in MAP resulting in a strong “Pressor Load” on the heart
63
Aerobic exercise causes what response on the body?
Fatiguing AEROBIC EXERCISE has a proportional increase in HR, SV and SBP resulting in more venous return and “Volume Load” on the heart
64
Physiological hypertrophy (What happens when we exercise?)
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
Pathological hypertrophy (What is it?)
Changes in our heart due to conditions such as hypertension or hypotension where our body adapts to what condition we have
66
What will we not see in pathological changes
- An increase in myocyte length and width along with wall thickness

1st Year (37 decks)

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