Pt 2 Flashcards

1
Q

What are the 3 portions of an AP?

A
  1. Depolarization: opens fast sodium (Na+) channels, extracellular Na+ enters
    - rising phase of action po(-90mV to +30mV)
    - influx of Na+ will stop quickly
  2. Voltage change opens calcium (Ca+) channels, influx of extracellular Ca2+
    - Ca2+ influx prolongs depolarization- the plateau
    - Cells will contract as long as Ca2+ is entering
  3. Repolarization: results from inactivated Ca2+ channels; the opening of potassium (K+) channels - an efflux of K+
    - resting potential (-70mV) is restored
    - Ca2+ is either pumped out of the cell or into the SR
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2
Q

What does the plateau phase help ensure?

A

Sustained contraction ensures the efficient ejection of blood from ventricles, preventing tetany

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3
Q

List the 3 waves/deflections on a typical EKG.

A

o P wave
o QRS complex
o T wave

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4
Q

What electrical event causes P wave to appear?

A
  • Results from movement of depolarization wave from SA to AV node
  • Atria contract .1s after P wave begins
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5
Q

What electrical event causes QRS complex to appear?

A
  • 0.8s
  • Results from ventricular depolarization, precedes ventricular contraction
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6
Q

What electrical event causes T wave to appear?

A
  • 0.16s
  • Results from ventricular repolarization
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7
Q

Why is atrial repolarization not seen on a typical EKG?

A

EKG are composite of electrical activity, atrial repolarization happens same time as ventricular depolarization - hidden within QRS complex

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8
Q

What is the difference in an interval and a segment.

A

An interval is a duration of time that includes 1 segment and 1+ wave
A segment is a region between 2 waves

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9
Q

What is the possible clinical significance of an elevated or depressed ST segment?

A

Can indicate cardiac ischemia

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10
Q

List the 4 electrical events (depolarizations/repolarizations) and the 4 correlating mechanical events (systole/diastole) of each cardiac cycle. In each pairing, which occurs first - the electrical event or the mechanical event?

A

Atrial depolarization - Atrial systole
Atrial repolarization - Atrial diastole
Ventricular depolarization - Ventricular systole
Ventricular repolarization - Ventricular diastole
electrical events are all before mechanical

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11
Q

Regarding blood flow, what happens during systole?

A

Systole = contraction
Blood is forced out the heart’s chambers

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12
Q

Regarding blood flow, what happens during diastole?

A

Diastole = relaxation
Blood refills the heart’s chambers

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13
Q

List the 4 steps of the cardiac cycle.

A

Ventricular filling
Isovolumetric contraction
Ventricular ejection
Isovolumetric relaxation

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14
Q

What happens during ventricular filling?

A

 Pressure is low, blood flows from atria to ventricles
 AV valves are open, SL valves are closed
 Responsible for 80% of ventricular filling
 Following atrial depolarization; P wave, atrial systole occurs, and blood is compressed into the ventricles
 EDV ; the maximum volume of blood that the ventricles will contain in the cardiac cycle
 Atrial diastole and the start of ventricular depolarization

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15
Q

What happens during isovolumetric contraction?

A

 Atria relax, ventricles start contracting, pressure in ventricles rises
 AV valves close
 For a moment the ventricles are closed chambers with a constant blood volume
 Pressure cont. to rise until it exceeds the pressure in the great vessels
 SL valves open

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16
Q

What happens during ventricular ejection?

A

 Blood moves from the ventricles to the great vessels, pulmonary trunk vs aorta
 Pressure in the aorta is typically 120mmHg

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17
Q

What happens during isovolumetric relaxation?

A

 Following the T wave, the ventricles relax
 ESV; the un-ejected blood remaining in the ventricular chambers
 Ventricular pressure drops, blood slides from the great vessels vack towards the ventricles – SL valves close
 Ventricles are again closed chambers
 Dicrotic notch: a brief rise in aortic pressure caused by blood rebounding off the newly closed aortic valve

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18
Q

List whether AV and SL valves are open or closed during a particular step of the cardiac cycle

A

o Ventricular filling – AV valves open, SL valves closed
o Isovolumetric contraction – AV valves closed, SL valves open
o Ventricular ejection - SL valves open, AV valves closed
Isovolumetric relaxation - AV valves open

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19
Q

What is End Diastolic Volume (EDV)?

A

EDV – the max. volume of blood that the ventricles will contain in the cardiac cycle

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20
Q

What is End Systolic Volume (ESV)?

A

ESV – the un-ejected blood remaining in the ventricular chambers

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21
Q

What is the dicrotic notch? What causes it?

A

A brief rise in aortic pressure caused by blood rebounding off the newly closed aortic valve

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22
Q

Which is a higher-pressure circuit: the pulmonary or the systemic?

A

Systemic 120/80 mmHg vs pulmonary 24/10 mmHg

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23
Q

What is the average pressure in the pulmonary trunk?

A

Pulmonary trunk – 24/10 mmHg

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24
Q

What is the average pressure in the aorta?

A

Aorta – 120 mmHg

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25
Q

What causes the sounds heard during auscultation?

A

o Closure of the AV Valves is the 1st Sound (“lub”).
o Closure of the SL Valves is the 2nd Sound (“dup”).

26
Q

Define a heart murmur. How can a heart murmur eventually result in a weakened myocardium?

A

o An abnormal heart sound secondary to turbulent blood flow
o Can be indicative of a valve problem – insufficient/incompetent valves allowing regurgitation or backflow

27
Q

What is Cardiac Output (CO)?

A

Cardiac output = the amount of blood pumped by each ventricle per min
HR x SV
* 75bpm x 70 mL/min = 5250mL/min = 5.25L/min

28
Q

What is Stroke Volume (SV)?

A

Stroke volume = the amount of blood pumped by each ventricle per beat
- Correlates with the strength of ventricular contraction
- Typically about 70mL

29
Q

Define cardiac reserve. Why is it functionally important?

A

o The difference in resting CO and maximal CO
o 4-5x resting CO (20-25L/min)

30
Q

How do EDV and ESV relate to SV and therefore CO?

A

o EDV – typically 120mL
Depends on how long ventricular diastole lasts and what venous pressure is
o ESV – typically 50 mL
Depends on arterial pressure and the force of ventricular contraction
o SV = EDV-ESV
HR x SV = CO

31
Q

What is the typical ejection fraction for a healthy heart?

A

o 70mL/120mL x 100 = 60%
o Each ventricle pumps 60% of its blood with each contraction

32
Q

What 3 factors regulate stroke volume?

A

Preload
Frank-Starling Law
Contractility

33
Q

What is Preload?

A

o Preload – the degree to which muscle cells are stretched before contracting
Higher preload = higher SV

34
Q

what is Frank-Starling Law?

A

o Frank-Starling Law – a length-tension relationship – cardiac muscle cells are stretched to their optimal length for maximal contraction
Higher EDV will breed higher SV
Increased venous return – such as through exercise, with activity of SNS, or increased filling time – will increase preload
Low venous return might occur after blood loss or with tachycardia

35
Q

What is contractility?

A

o Contractility – the contractile strength achieved at a given muscle length
Will increase with rises in Ca2+ either from extracellular fluid or the sarcoplasmic reticulum
Increased contractility will increase SV and decrease ESV
Increased SNS activity will increases contractility
Epinephrine and norepinephrine increase Ca2+ entry and increase cross bridge cycling

36
Q

How do you calculate your maximal heart rate? How can you use that information to guide your exercise routines?

A

o 220 – your current age
o Moderate exercise, 40% of max hr
o High intensity exercise, 75-80% of max hr

37
Q

Be familiar with some positive ionotropic agents.

A

Epinephrine, norepinephrine, thyroxine, glucagon, high levels of extracellular Ca2+, and the drug digitalis

38
Q

Be familiar with some negative ionotropic agents.

A

Acidosis, rising extracellular K+ levels, and the Ca2+ channel blocker class of drugs – Amlodipine, Cardizem

39
Q

Sympathetic Nervous System (SNS) effect hr?

A

Emotional and physical stressors activate the SNS – epinephrine is released, the SA Node depolarizes more rapidly
SNS also increases heart contractility and speeds heart relaxation via enhanced Ca2+ movement
Enhanced contractility lowers ESV so SV doesn’t decline as it typically does with an increased HR

40
Q

Parasympathetic Nervous System (PNS) effect hr?

A

Reduces heart rate, mediated by Acetylcholine
Acetylcholine hyperpolarizes the membranes of its effector cells by opening K+ channels

41
Q

What is vagal tone?

A

Both the SNS and PNS are continuously sending signals to the heart – typically, the PNS predominates – “vagal tone”
An impairment of the vagus nerve will increase resting HR by ~25 bpm (75 bpm to 100 bpm)

42
Q

Define the atrial or Bainbridge reflex.

A

o An autonomic reflex initiated by increased venous return and increased atrial filling
o Stretching of the atrial walls increases heart rate by stimulating the SA Node and the atrial stretch receptors
o Stretch receptor activation triggers reflexive adjustments of autonomic output to the SA Node — increased HR

43
Q

List the hormones and ions that alter cardiac function – especially calcium and potassium.

A

o Hormones
Epinephrine: increases both heart rate and contractility
Thyroxine: increases heart rate, enhances the effects of epinephrine and norepinephrine
o Ions
Normal heart function depends on normal levels of intra and extracellular ions – electrolyte imbalances can be very dangerous
Hypocalcemia depresses heart function
Hypercalcemia stimulates heart function and can increase risk of arrythmia
Hypokalemia weakens heart contraction
Hyperkalemia alters the heart’s electrical activity, can increase risk of heart block and cardiac arrest

44
Q

what is epinephrine effect on heart?

A

Epinephrine: increases both heart rate and contractility

45
Q

what is Thyroxine effect on heart?

A

Thyroxine: increases heart rate, enhances the effects of epinephrine and norepinephrine

46
Q

what is ions effect on heart?

A

Normal heart function depends on normal levels of intra and extracellular ions – electrolyte imbalances can be very dangerous

47
Q

what is Hypocalcemia effect on heart?

A

Hypocalcemia depresses heart function

48
Q

what is Hypercalcemia effect on heart?

A

Hypercalcemia stimulates heart function and can increase risk of arrythmia

49
Q

what is Hypokalemia effect on heart?

A

Hypokalemia weakens heart contraction

50
Q

what is Hyperkalemia effect on heart?

A

Hyperkalemia alters the heart’s electrical activity, can increase risk of heart block and cardiac arrest

51
Q

How do biological sex, age, exercise, and temperature alter HR?

A

o Age: HR is 140-160 bpm in fetuses then declines
o Gender: HR is typically faster in females
o Exercise: HR increases secondary to activation of the SNS
BP also increases
BUT Resting HR will be lower in highly trained athletes – why? high SV, strong myocardium, low hr to maintain CO
o Temperature: heat increases HR, cold decreases HR

52
Q

Define heart failure. What are some ways that a myocardium can become weakened?

A

o Congestive Heart Failure: secondary to a weakened myocardium, the heart becomes an inefficient pump; circulation is not adequate to meet the tissues’ needs
o Myocardial infarction, tetany, angina pectoris

53
Q

What side of the heart is failing when peripheral congestion is seen? How about pulmonary congestion?

A

o Peripheral Congestion - Right side
o Pulmonary Congestion - Left side

54
Q

How does a diuretic work?

A

Diuretics: increase excretion of Na+,H2O by the kidneys

55
Q

What does the drug digitalis work?

A

Digitalis: increases heart contractilit

56
Q

What are the 4 primitive chambers of the heart? What do each of these chambers become as the heart matures?

A

o Sinus Venosus: receives all venous blood from the embryo – becomes the smooth-walled portions of the atria, the coronary sinus, and the SA node
o Atrium: becomes the pectinate muscle-ridged parts of the atria
o Ventricle: the strongest part of the embryonic heart – becomes the left ventricle
o Bulbus Cordis: has a cranial extension – the truncus arteriosus – becomes the pulmonary trunk, part of the aorta, and most of the right ventricle

57
Q

At what gestational age is the fetal heart contracting?

A

22 days

58
Q

Describe two ways nonfunctional fetal lungs are bypassed. What do these 2 bypass structures become after birth?

A

o Foramen Ovale: a hole in the interatrial septum, a bypass for the lungs – becomes the Fossa Ovalis in adults
o Ductus Arteriosus: a shunt between the pulmonary trunk and the aorta, another bypass for the lungs – becomes the Ligamentum Arteriosum in adults

59
Q

What are the two classes of congenital heart defects?

A

o Two Basic Types
Mixing of O2 rich and O2 poor blood – inadequately oxygenated blood reaches the body’s tissues
o Ex: septal defects, patent ductus arteriosus
Narrowed valves/vessels increase the heart’s workload
o Ex: Coarctation of the Aorta

60
Q

Define Tetralogy of Fallot. What are its 4 features?

A

o Tetralogy of Fallot (4): a serious condition in which cyanosis appears within minutes of birth - encompasses both types of defects
narrowed pulmonary trunk/pulmonary valve stenosed
hypertrophied right ventricle
ventricular septal defect
aorta receiving blood from both chambers

61
Q

Explain how a highly trained aerobic athlete could have a resting HR as low as 30-40 bpm.

A

o Regular, vigorous exercise enlarges the heart and makes it more efficient and powerful
o Aerobic exercise can clear fatty deposits from blood vessels and slow the development coronary heart disease
o The benefits of exercise persist into old age