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HB 2 > CV Phy And Path 2 > Flashcards

CV Phy And Path 2 Flashcards

1
Q

Describe the electrical conduction and coordinated depolarization and repolarization of cardiac muscle. How can we measure this?

A

Proceeds like a wave across the heart

Can be measured as voltage changes on the skin (electrocardiogram ECG or EKG)

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2
Q

What is Einthoven’s triangle?

A

an imaginary formation of three limb leads in a triangle used in electrocardiography, formed by the two shoulders and the pubis

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3
Q

Describe the P wave on the EKG.

A

Starts as SA node fires

Atrial depolarization

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4
Q

What is the PR interval? What will cause a longer PR interval (segment)?

A

P to Q wave

Time between atrial depolarization and ventricular depolarization (AV delay)

0.16sec

Heart block will cause a longer PR interval

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5
Q

What is the PR segment? What will cause a longer PR interval (segment)?

A

AV nodal delay

Heart block

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6
Q

What is the QRS complex? How long is it?

A

Ventricular depolarization (atria repolarizing simultaneously)

Tall b/c ventricles are strong

0.08sec to 0.1sec

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7
Q

Describe the ST segment. What can cause elevation or depression in the segment?

A

Time during which ventricles are contracting and emptying

should be same level as isoelectric line (time doesn’t matter)

0.08 sec

Elevated in myocardial infarction (necrosis)
Depressed in angina (chest pain caused by reduced oxygen, hypoxia in myocardium)

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8
Q

Describe the QT interval.

A

Time taken from ventricles start to contract and finish relaxing

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9
Q

Describe the T wave.

A

Ventricular repolarization

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10
Q

What does each large and each small square represent on an EKG?

A

Large 0.20sec
Small 0.04 sec

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11
Q

What is hyperkalemia? How does it appear on an EKG?

A

Peaked T wave

Excessive K in blood (fatal)

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12
Q

Describe.a first degree block on an EKG.

A

Long PR interval

The electrical impulse still reaches the ventricles, but moves more slowly than normal through the AV node.

A PR interval of greater than 0.20sec without disruption of atrial to ventricular conduction

1:1 P wave to QRS ratio

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13
Q

Describe a second degree block: Mobitz type 1.

A

Each successive impulse from SA node is delayed slightly longer than the previous one

Progressive prolongation of the PR interval continues until an impulse fails to be conducted to the ventricles (P, no R)

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14
Q

Describe a second degree block, Mobitz type 2.

A

Each successive impulse from SA node is delayed slightly longer than the previous one

Progressive prolongation of the PR interval continues until an impulse fails to be conducted to the ventricles (no QRS complex)

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15
Q

Describe atrial fibrillation (A-fib) on an EKG.

A

Typically irregular QRS complexes
Absence or discrete P waves
Not fatal
Uncoordinated or rapid heart rhythm causing poor blood flow

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16
Q

Describe ventricular fibrillation (v-fib) on an EKG.

A

Irregular unformed QRS complexes without any clear P waves

Brain is vulnerable to hypoxia as a result of inculcation issue

Life threatening

Irregular heartbeat affecting the ventricles

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17
Q

Besides detesting heart beat how else can EKGs help in determining cardiac disorders?

A

EKG helps to localize cardiac disorders within the heart

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18
Q

How many times does the adult human heart beat per day? Per year? How much does it pump per day?

A

75 BPM x 60 m/hr x 24 hr/day = 108,000 beats/day

~ 40 million beats/year

5 L/min x 60 min/hr x 24 hr/day = 7,200 liters (~1,900 gallons) of blood pumped per day

19
Q

During what phases of the cardiac cycle are all valves closed?

A

Phases 3 and 5

20
Q

During what phases of the cardiac cycle are the semilunar valves open?

A

Phase 4

21
Q

During what phase of the cardiac cycle are the atrioventricular valve open?

A

1, 2, and 6

22
Q

What occurs during phase 1 of the cardiac cycle?

A

Ventricular filling
AV valve open, SL valve closed
Ends with the beginning of atrial contraction

Diastole

23
Q

What occurs during phase 2 of the cardiac cycle?

A

Atrial contraction
Ends with the closure of the AV valves (open in the beginning)
Ventricular End diastolic volume (EDV, blood volume after contraction)

Diastole

24
Q

What occurs during phase 3 of the cardiac cycle?

A

Isovolumetric ventricular contraction (pressure build up w/o ejection)
Begins with the closing of AV valves (S1)
Ventricular volume remains the same
Ends with opening of SL valves

Systole

25
Q

What occurs during phase 4 of the cardiac cycle?

A

Ventricular ejection to aorta
Begins with opening of SL valves
Ventricular volume decreases
Ends with closure of SL valves (S2)
Ventricular End systolic volume (ESV, blood left in ventricle after ejection)

Systole

26
Q

What happens during phase 5 of the cardiac cycle?

A

Isometric ventricular relaxation
Begins with closure of SL valves
Ends with opening of AV valves
Prevent back flow from aorta to ventricle

Diastole

27
Q

What occurs during phase 6 of the cardiac cycle?

A

Ventricular filling

Diastolic
AV valves open

28
Q

How do we calculate stroke volume (SV) and ejection fraction (EF)? What are the normal values?

A

Stroke Volume (SV) = EDV (phase 2 and 3) -ESV (phase 4 and 5), normal ~ 70 ml

Ejection Fraction (EF) = SV/EDV, normal > 60%

29
Q

What is the formula for Cardiac Output (CO)?

A

CO (L/min)= Heart Rate (bpm) x stroke volume (mL)

As we increase SV we must decrease HR to maintain stable CO and vice versa
L and R stroke volume arranged in series

30
Q

Describe intrinsic factors.

A

Affect stroke volume
Linked to EDV: Frank-starling Law
Preload

31
Q

What is the preload?

A

Degree of tension on the muscle when it begins to contract Volume of blood in ventricles at the end of diastole (EDV)
EDV at beginning of systole

32
Q

Describe extrinsic factors.

A

Independent of EDV
Affect ESV
After load

33
Q

What is the afterload?

A

Pressure after contraction
The load against which the muscle exerts its contractile force
Resistance left ventricle must overcome to circulate blood

34
Q

How does cardiac workload correlate to afterload?

A

As one increases the other increases

35
Q

What is increased in preload?

A

Hypervolemia
Regurgitation of cardiac valves
Heart failure

36
Q

What is increased in afterload?

A

Hypertension
vasoconstriction

37
Q

Why is the left ventricular wall thicker than the right?

A

Greater afterload in the systemic circulation than in the pulmonary circulation

38
Q

What is the Frank-Starling Law of the Heart?

A

Intrinsic
SV is proportional to EDV (maximal SV, optimal EDV; SV declines when EDV gets too high)
Force-length function of myocardium

39
Q

Describe the intrinsic relationship between heart rate and SV?

A

There is a trade off between HR and SV
Slower rate= more filling time and larger EDV
Faster rate= less filling time and smaller EDV
Atrial contribution to EDV is greater at higher rates

40
Q

Describe the contribution of atrial systole to CO during faster heart rates.

A

Contribution of atrial systole to CO (EDV) is greater during faster heart rates

41
Q

What is the effects of calcium on contractibility (extrinsic).

A

Increases contractibility
NE/EPI increase gCa+ in cardiac muscle fibers
NE/EPI also increases the rate of contraction and relaxation (reduces length of systole and ESV)

42
Q

What is the effects of potassium on contractibility (extrinsic).

A

Reduced contractility
Reduced rate of contraction

Hypercalemia- peaked T wave

43
Q

What determine contractility?

A

Intracellular Ca++

HB 2 (17 decks)

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