Newman Flashcards

1
Q

What do the leads of an ECG do?

A

look at the electrical activity of the heart from many different angles

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2
Q

What leads look at the bottom of the heart (inferior)?

A

II, III, aVF

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3
Q

What leads are precordial (anterior) or located over the sternum?

A

V leads

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4
Q

Can the heart work without atrial depolarization (P wave)?

A

yes

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5
Q

What is the PR segment?

A

conduction from atrium to the ventricle

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6
Q

What are Q waves?

A

depolarization of intraventricular septum

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7
Q

What part of the ECG will tell you a lot about ischemic heart disease?

A

ST segment

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8
Q

What are the 2 major reasons for ischemia?

A

1) coronary arteries are not supplying enough oxygen
2) heart is demanding too much oxygen
* supply demand mismatch

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9
Q

What would you see on an ECG of myocardial ischemia?

A

ST segment depression

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10
Q

What are the two major determinants of myocardial oxygen demand? *on test

A

1) heart rate

2) systolic blood pressure

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11
Q

What is a STEMI?

A

myocardial infarction that is shown by ST elevation in either II, III, AVF (inferior) or V leads (anterior)

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12
Q

How do you calculate HR from the ECG?

A

300/ # of large boxes between QRS

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13
Q

What is the most common cause of stroke?

A

atrial fibrillation

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14
Q

What causes atrial fibrillaiton?

A

multiple “whimpy” depolarizations in the artrium that are not coming from SA node

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15
Q

What causes QT prolongation?

A

medications and metabolite abnormalities: alteration of potassium channel

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16
Q

What does an ECG of 3rd degree heart block look like?

A

P waves are independent of QRS

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17
Q

How do you treat someone at risk of ventricular fibrillation?

A

implanted cardioverter defibrillator (shock goes off when HR gets around 180-200 beats/min)

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18
Q

What does a “pacemaker” treat? What triggers it?

A

complete heart block

low heart rate (below set point) triggers this

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19
Q

What is the definition of CHF? What causes it?

A

Symptoms and signs resulting from cardiac dysfunction. Dysfunction may be caused by damage to the heart or external forces preventing the adequate forward flow of blood from the heart to the peripheral organs.

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20
Q

What does increased proload do to SV?

A

increases

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21
Q

What does increased afterload do to SV?

A

decreases (it is a form of resistance)

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22
Q

What are the 2 determinants of afterload?

A

1) size of ventricle

2) systolic BP

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23
Q

What is contractility?

A

ability of heart to contract (how well are myocytes working) that is independent of preload or afterload

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24
Q

What is the ejection fraction?

A

EF= SV/EDV

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25
Q

What is the major determinant of heart failure?

A

ejection fraction being low

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26
Q

How might you get the external JV to stick out?

A

Valsalva manuever (straining)

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27
Q

What are you measuring when you measure JVP?

A

right atrial pressure

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28
Q

What pathologic processes directly damage the myocardium and result in CHF?

A
MI
infection (viruses)
amyloidosis
drugs (doxorubicin)
cocaine, alcohol
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29
Q

What is the first thing you look for when you suspect heart failure?

A

JVP

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30
Q

What can cause heart failure without directly damaging myocardial cells?

A

valve problems
pericardial disease
High output states: anemia; hyperthyroidism

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31
Q

What is a normal finding when you palpate the patients chest for the PMI?

A

feel sustained, apical impulse right below right nipple (size of the dime) with interphalangial joints

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32
Q

What is a major sign of heart failure associated with palpitation?

A

apical impulse pushed to the left (larger)

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33
Q

What heart sound is diagnostic of heart failure?

A

S3

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34
Q

How do you listen for S3?

A

Listen at apical impulse with bell, put just enough pressure on the stethoscope to keep the air out. Press hard and ease up.

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35
Q

When does the a wave occur?

A

right before carotid pulse

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36
Q

What does the a wave in venous pulsation signify?

A

atrial contraction

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37
Q

What does the c wave in venous pulsation signify?

A

beginning of systole (he said you never see this)

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38
Q

What is the x descent in venous pulsation?

A

relaxation of atria

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39
Q

What is the v wave in venous pulsation?

A

ventricular contraction

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40
Q

What is the y descent in venous pulsation?

A

relaxation of ventricle

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41
Q

What are the two major humoral manifestation of the renin-angiotensin-aldosterone curve?* on test

A

Kidney thinks your body is dehydrated if it is getting poor perfusion, so it releases lots of rein. Which will lead to:
1) vasoconstriction of the vessels (increase afterload)
2) retention of salt and fluid, release of potassium (via aldosterone)
(can reduce CO and GFR)

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42
Q

What was the first drug shown to save lives in CHF? What is the second?

A

ACE inhibitors

Spirinolactone

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43
Q

What is the most potent vasoconstrictor in the body?

A

angiotensin II

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44
Q

What, other than drugs, can be used to treat CHF?

A

heart transplant

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45
Q

What is the cause of chronic, stable angina? *on exam

A

mismatch between myocardial oxygen supply and myocardial oxygen demand

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46
Q

What is characteristic of the chest pain in chronic, stable angina?

A
  • caused by exertion (increase in systolic BP)
  • always more than 5 minutes
  • tightness or pressing pain that can radiate down arm
  • SNS in overdrive- turn white as a ghost and get sweaty
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47
Q

What do you see on a treadmill test of someone with ischemia from chronic stable angina?

A

ST segment depression

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48
Q

What is the characteristic description of a patient with unstable angina?

A

patient waking up in the middle of the night with severe chest pain, sweaty, and pale

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49
Q

What does the ECG of someone with unstable angina look like?

A

Normal
inverted T waves
NO STEMI!

50
Q

Why does unstable angina occur?

A

plaque ruptures at edges and releases cytokines like endothelin, prostaglandins, etc. that cause platelet recruitment and vasospasm (thrombosis)

51
Q

What are the 3 main treatments for ischemic heart disease?

A

1) angioplasty (balloon shoves plaque against wall)
2) Stent (only better for survival of STEMI)
3) bypass (with internal mammory artery—from subclavian artery to LAD)

52
Q

If patient has chest pain, what type of tests could you order?

A

1) stress test (test for IHD)

2) coronary angiogram (test for CAD)

53
Q

When can a stress test tell a patient?

A

Can give you an idea of how likely the person is to have a recurrent MI at a certain HR.

54
Q

What is the #1 thing you want to know in a patient who has had an MI? How can you tell this?

A

How much damage is done. Look at EF!

55
Q

If you have 3 blocked coronary arteries, what is the best treatment?

A

bypass

56
Q

If you have 1 blocked coronary artery, what is the best treatment?

A

stent

57
Q

What can lead to an MI in a very young patient with no atherosclerosis?

A

severe anemia
emboli from diseased valve
drugs (cocaine)

58
Q

What are the 3 major symptoms of aortic stenosis?

A

Syncope, angina, CHF

59
Q

What are the two basic mechanisms for bradyarrhythmias.?

A

1) Decreased automaticity of the sinus node

2) Blocked conduction (atria cannot conduct to ventricle)

60
Q

What can cause reduced automaticity?

A

This can occur during periods of increased vagal tone (sleep), with increasing age, hypothyroidism or secondary to drugs.

61
Q

What happens if the SA node stops firing?

A

the heart will be activated at a slower rate (prolong phase 4) by other cardiac tissues with pacemaker activity.

62
Q

What is heart block? What is its effect?

A

The AV node and the bundle of His are the only sites of conduction between the atria and ventricles, if these become “blocked” it may lead to bradycardia.

63
Q

Would you describe 3rd degree AV block?

A

no association between atrial and ventricular activity

64
Q

What portions of the action potential are most important for arrhythmias?

A

3 and 4

65
Q

What is the refractory period?

A

part of cardiac cycle where you cannot stimulate another action potential (must recover)

66
Q

What does a tall QRS tell you?

A

ventricular hypertrophy- caused by HTN and aortic stenosis

-Risk factor for CAD

67
Q

What is the normal width of the QRS?

A

3 little boxes

68
Q

What are the three basic mechanisms for tachyarrhythmias?

A

1) Increased automaticity (things firing that should not!1)
2) “Triggered automaticity” (delayed afterpotentials)
3) Re-entry

69
Q

What factors can increase automaticity?

A

symptathetic tone
catecholamines
carbon dioxide increase/ low oxygen (emphysema)
High calcium

70
Q

What factors can decrease automaticity?

A

parasympathetic tone
high oxygen
high potassium

71
Q

What is a “late afterpotential”?

A

alteration of potassium current leads to small depolarizations that occur after phase 3 and some occur during phase 4.

72
Q

How can a late afterpotential lead to an arrhythmia?

A

if sodium and calcium channels “kick in” during a late afterpotential

73
Q

What is required for reentry?

A

2 parallel pathways with different conduction properties (1 fast and 1 slow)

74
Q

How does reentry work?

A

Goes down fast pathway and depolarizes very quickly. If extra beat is sent down, it can go through slow pathway and come back up the depolarized fast side, creating a loop.

75
Q

What is missing from a junctional rhythm? Who gets these?

A
P waves (stimulus from AV node)
people with kidney disease
76
Q

Who commonly gets atrial tachycardia?

A

people with lung disease

77
Q

Patient has tachycardia and stroke, what is the most common reason?

A

reentry (atrial fibrillation)

78
Q

What can predispose to late after potentials and arrhythmia?

A

prolonged QT interval (prolongs AP)

79
Q

What is your major concern in a patient with heart failure who has syncope?

A

ventricular fibrillation

80
Q

True or false: you can determine the cause of an arrhythmia just by looking at the ECG.

A

No, all dysrhythmias could be cause by any of the 3 mechanisms and this cannot be determined by the ECG alone

81
Q

What must you look for to determine if an arrhythmia is due to re-entry?

A

you have to look at the ECG to see if it is re-entry (narrow QRS)

82
Q

What is a cause of a long QT interval?

A

drugs (quinidine)
congenital syndrome
problems with Calcium and magnesium

83
Q

What is characteristic of v fib ECG?

A

o Wide QRS

o Irregular rhythm

84
Q

What is characteristic of a fib ECG?

A

o Narrow QRS
o No P wave
o Irregular distances between QRS

85
Q

You can determine the severity of mitral valve stenosis by knowing what?

A

the pressure gradient across the valve

*greater pressure gradient indicates greater severity

86
Q

What is the key determinants to what opens and closes valves?

A

pressure gradients on either side of the heart valve

87
Q

What occurs due to pressure overload in stenosis?

A

concentric hypertrophy (myocytes replicate in PARALLEL)–heart muscle becomes much thicker

88
Q

What occurs due to volume overload in regurgitation?

A

eccentric hypertrophy (cardiac factors replicate in series)–leading to dilation

89
Q

What are the causes of acute regurgitation?

A

ischemia, infection, dissection

90
Q

How does acute regurgitation pathophysiology differ from chronic?

A

heart does not have time to dilate, smaller atrium will generate LOTS of pressure (prominent v wave) and you will hear a LOUD murmur

91
Q

Mitral valve murmurs are heard where?

A

apical impulse

92
Q

Aortic valve murmurs are heard where?

A

underneath the right clavicle

93
Q

How do you tell if a murmur is systolic?

A

carotid pulse is consistent with systole

94
Q

Where do you hear the tricuspid valve?

A

just left of the sternum

95
Q

Where do you hear the pulmonic valve?

A

just below the left clavicle

96
Q

What is specific of the heart sound heard with mitral stenosis?

A

LOUD FIRST HEART SOUND

97
Q

What is the key to hypertrophic obstructive cardiac myopathy?

A

decreasing the intraventricular volume (Valsalva maneuver) will increase the murmur

98
Q

What are the causes of mitral regurgitation?

A
  • Diseases that affect supporting structures
  • Diseases affecting leaflets
  • mitral valve prolapse!!***
  • Dilation of the annulus (LV dilates due to old MI, etc.)
99
Q

What is characteristic of aortic stenosis? **on test!

A
  • Concentric hypertrophy

- Delayed arterial pulse, weakened arterial pulse**

100
Q

What causes the wide pulse pressure of aortic regurgitation?

A

Diastolic decreases due to backflow from aorta into ventricle, systolic increases due to increased compensatory SV (because you have increased proload)

101
Q

What type of pulse do you get with aortic regurgitation?

A

brisk pulse

102
Q

What are the 2 conditions required for infective endocarditis?

A

1) bugs in the blood

2) abnormal heart valve

103
Q

What are the 2 adverse effects with endocarditis?

A

1) Valve destruction (cause of acute regurgitation)
2) Embolization (sepsis)
- if mitral- stroke, MI, kidney problem, etc.
- if tricuspid- PE

104
Q

What are the indications for surgery in infectious endocarditis?

A

1) Heart failure unresponsive to medical management
2) Uncontrolled infection
3) recurrent major embolization

105
Q

What is the difference in adaptations in aortic stenosis and aortic regurgitation?

A

Aortic stenosis- concentric hypertrophy of LV, also seen with HTN
Aortic regurgitation- eccentric hypertrophy due to dilation of the LV

106
Q

What do you look at when you are trying to diagnose bacterial endocarditis?

A

1) Echo

2) Blood culture

107
Q

What are 5 causes of acute pericarditis?

A

1) Infection
2) collagen-vascular disease
3) Neoplasm
4) metabolic (renal failure)
5) Injury

108
Q

What is pericarditis?

A

inflammaiton of the pericardium

109
Q

Describe the chest pain of pericarditis.**

A

Positional Nature: Worse when lie on back, better when they lean forward.

110
Q

Where do you place the stethoscope when you listen for pericarditis? What do you hear?***

A

does not matter

you hear a rub!!

111
Q

What does pericarditis do to the ECG?

A

ST elevation in ALL leads

112
Q

What is pericardial effusion?

A

greater than normal quantity of blood in the pericardial sac

113
Q

What are causes of pericardial effusion?

A
  • infection (Tb)
  • chest malignancy (irritates the pericardium)
  • chronic thyroid disease
  • kidney failure patients
  • NOT with CHF
114
Q

What do you worry about with pericardial effusion? Why?

A
  • rapid filling
  • too much over a long period of time (heart can accept less and less blood, so LVEDV decreases and CO decreases via Frank-Starling mechanisms)
115
Q

What is pericardial tamponade?

A

pericardial tamponade is an example of diastolic dysfunction of the heart–heart is completely normal, it just does not get enough blood.

116
Q

What is pulsus paradoxus?

A

inhale pulse goes away, exhale the pulse comes back

*Pericardial tamponade!

117
Q

What normally happens to systolic BP when you inhale?

A

when you inhale, normally blood comes to RA, expands into pericardial sac, and Septum expands to accomodate blood which decreases LV (and systolic pressure will drop due to decreased CO).

118
Q

What happens to systolic BP when you inhale if you have cardiac tamponade?

A

RA cannot expand out into the pericardium, so the IV will encroach a lot on the LV cavity, you get large decrease in cardiac output so huge drop systolic pressure when you inhale.

119
Q

When you see someone presenting with marked systemic congestion (ascites, hepatoegaly, increased JVP with inspiration) what should you consider?

A

consider constrictive pericarditis

120
Q

What is “Beck’s Triad” for pericardial tamponade?

A

1) Hypotension
2) Elevated JVP
3) Muffled heart sounds