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* DIT each session > Day 6.1 Cardio > Flashcards

Day 6.1 Cardio Flashcards

1
Q

Causes of increased ESR

A 
Infection (osteomyelitis)
Inflammation (e.g. temporal arthritis, polymyalgia rheumatica)
Cancer
Pregnancy
SLE
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2
Q

Causes of decreased ESR

A

Sickle cell (altered shape)
Polycythemia (too many)
CHF (unknown why)

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3
Q

Toxic side effects of TCA use

A

Convulsion
Coma
Cardiotoxicity (Tri C’s)

Repsi depression and hyperpyrexia

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4
Q

What anti-seizure drugs are used to treat bipolar disorder?

A

Lamotrigine
Carbamazepine
Valproate (Valproic acid)

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5
Q

Coronary arteries

A

RCA and LCA come off of aorta.

LCA gives LAD and CFX

RCA gives PDA (80%) and Acute marginal artery

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6
Q

What does the LAD supply?

A

Apex and anterior interventricular septum

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7
Q

What does CFX supply?

A

Posterior LV

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8
Q

What does PDA supply?

A

aka posterior interventricular artery
Posterior septum
Inferior part of LV

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9
Q

What does the AMA (acute marginal artery) supply?

A

RV

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10
Q

What supplies the SA and AV nodes?

A

RCA

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11
Q

Where does PDA arise from?

A

80% arise from RCA

20% arise from CFX (from LCA)

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12
Q

Most common site of coronary artery occlusion

A

LAD (anterior interventricular septum)

This is called an anterior wall MI

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13
Q

When do coronary arteries fill?

A

Diastole

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14
Q

Effects of LA enlargement

A

LA is most posterior part of heart.
Enlgmt causes dysphagia d/t compression of esophageal nerve
hoarseness d/t compression of recurrent laryngeal nerve (vagus)

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15
Q

CO eqn

A

CO = SV x HR

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16
Q

Fick principle eqn

A

CO = rate of O2 consumption / [arterial O2 content - venous O2 content]

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17
Q

MAP eqn

A 
MAP = CO x TPR
(P = Q x R)

MAP = 1/3 systolic + 2/3 diastolic

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18
Q

Pulse pressure

A

PP = systolic - diastolic

proportional to SV: if SV increases, PP increases.

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19
Q

SV eqn

A

SV = EDV- ESV

SV = CO / HR

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20
Q

What variables affect SV?

A

Contractility
Afterload
Preload

Increased contractility = increased SV
Increased afterload = decreased SV
Increased preload = increased SV

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21
Q

4 things that make contractility increase

and therefore SV increases too

A
  1. Catecholamines (B1 receptor)- increased activity of Ca2+ pump in SR
  2. Increased intracellular Ca2+
  3. Decreased extracellular sodium (so Na+/Ca2+ exchger works less, more Ca2+ stays inside cell)
  4. Digitalis (Increased intracellular Na+, so Na+/Ca2+ exchgr works less, more Ca2+ stays inside). aka digoxin.
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22
Q

5 things that make contractility decrease

and therefore SV decreases too

A
  1. B1 blockade
  2. Heart failure
  3. Acidosis
  4. Hypoxia/hypercapnia
  5. Non-dihydropyridine Ca2+ chnl blockers: Verapamil
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23
Q

What happens to CO during exercise?

A

Initially it goes up, bc of increased SV.

After prolonged exercise, CO increases as a result of increased HR.

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24
Q

What happens to CO if heart rate is too high?

A

Diastolic filling is incomplete (not enough time to fill) so CO decreases
eg in ventricular tachycardia

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25
Q

What is preload?

A

Preload = ventricular EDV

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26
Q

What is afterload?

A

Afterload = mean arterial prs (MAP)

proportional to TPR

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27
Q

Do venodilators affect preload or afterload?

A

They decrease preload (blood pools in veins, so less goes back to heart)
e.g. Nitroglycerin

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28
Q

Do vasodilators affect preload or afterload?

A

They decrease afterload bc they dilate arteries
Eg hydralazine
Afterload = Arterial!

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29
Q

In what conditions does SV increase?

A

Anx (bc catecholamine surge)
Exercise (bc increased preload, also increased catecholamines)
Pregnancy (higher blood vol, so higher preload)

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30
Q

What happens to SV in heart failure

A

decreases

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31
Q

What increases myocardial O2 demand?

A

Increased afterload (increased arterial prs)
Increased contractility
Increased HR
Increased heart size (increased wall tension)

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32
Q

Diff bt non-dyhydropyridine Ca2+ chnl blockers and dihydropyridine

A

Non-dyhydropyridine Ca2+ chnl blockers = verapamil. Works at heart.

Dyhydropyridine work at blood vessels.

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33
Q

Drugs that decrease O2 demand in heart attack

A

ACE inhibitors and ARBs decrease afterload

Beta-blockers (metoprolol) decrease HR and contractility

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34
Q

In what condition is there increased heart size?

A

Hypertrophic cardiomyopathy.

Higher risk for heart attack and sudden cardiac death since this increases O2 demand on the heart.

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35
Q

What does the starling curve show?

A

That the force of contraction is proportional to the initial length of cardiac muscle fiber (preload).

Plots CO or SV against Ventricular EDV or preload

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36
Q

EF eqn

A

EF = SV / EDV

EF = [EDV -ESV] / EDV

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37
Q

What is EF normally?

A

> = 55%

It’s an index of ventricular contractility

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38
Q

Eqn for resistance, prs, flow

A 
P = Q x R
(MAP = CO x TPR)
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39
Q

Eqn for resistance

A

R = 8nl / [pi x r^4]

8.viscosity.length / pi.radius to the 4th

directly prop to visc, inversely prop to radius^4

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40
Q

What determines velocity, physiologically?

A 
Mostly the hematocrit. As you increase velocity, you increase resistance.
Viscosity is increased in:
polycythemia (too many RBCs)
hyperproteinemic states (mult myeloma)
hereditary spherocytosis
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41
Q

Which vessels account for most of the TPR?

A

Arterioles

they regulate capillary flow

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42
Q

Resistance of vessels in a series

A

Rseries = R1 + R2 + R3…

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43
Q

Resistance of vessels in parallel

A

Rparallel = 1/R1 + 1/R2 + 1/R3…

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44
Q

Cardiac cycle Phase 1

A

Isovolumetric contraction

  • period bt mitral valve closing and aortic valve opening
  • highest O2 consumption
  • this is systole
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45
Q

Cardiac cycle Phase 2

A

Systolic ejection

  • period bt aortic valve opening and closing
  • lose SV
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46
Q

Cardiac cycle Phase 3

A

Isovolumetric relaxaing

-period bt aortic valve closing and mitral valve opening

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47
Q

Cardiac cycle Phase 4 & 5

A

4: Rapid filling (just after mitral opens)
5: Reduced filling (just before mitral valve closing)
- gain the SV

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48
Q

S1

A

Mitral and tricuspid closure
Loudest at mitral area
point bt phase 5 and phase 1

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49
Q

S2

A

Aortic and pulmonary valve closure
loudest at left sternal border
point bt phase 2 and 3

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50
Q

S3

A

In early diastole during rapid ventricular filling phase (phase 4)
assoc w increased filling prs
more common in dilated ventricles
normal in kids and prego

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51
Q

S4

A

“atrial kick” in late diastole (phase 5)
high atrial prs
assoc w ventricular hypertrophy
LA has to push against a stiff LV wall

52
Q

Waves of the jugular venous pulse

A

JVP: a, c, x, v, y (at carter’s x-ing, vehicles yield
a wave: atrial contraction
c wave: RV contraction (tricuspid valve bulges into atrium)
x descent: ventricles empty
v wave: increased atrial prs d/t filling against closed tricuspid valve.
y descent: diastole. atria empty into ventricles.

53
Q

S2 splitting (normal)

A

aortic valve closes slightly before pulmonic.
inspiration increases this difference.

inspiration means a drop in intrathoracic prs, which increases the capacity of pulmonary circulation.
pulmonic valve closes later to accommodate more blood entering the lungs
aortic valve closes earlier bc of decreased return to left heart.
normal in athletes and young ppl

54
Q

Wide S2 split

A

a/w pulmonic stenosis or RBBB
(slightly) more with inspiration

seen in conditions that delay RV emptying. delay in emptying causes delayed pulmonic sound (on both insp and expiration). an exaggeration of normal splitting.

55
Q

Fixed splitting in S2

A

a/w ASD
doesn’t chg w inspiration

ASD leads to L–>R shunt and therefore flow thru pulmonic valve is increased- so regardless of breath, pulmonic closure is very delayed.

56
Q

Paradoxial splitting S2

A

A/w aortic stenosis or LBBB
pulmonary shuts before aortic!
thus it’s decreased(!) on inspiration

seen in conditions that delay LV emptying.
normal order of valve closure is reversed.
on inspiration, the later P and the earlier aortic sounds move closer to each other, “paradoxically” eliminating the split.

57
Q

Starling curve: what happens to the curve with exercise?

A

Shifts up (kinda left)
for a given preload, you are pushing out more blood during exercise
d/t the increased contractility w exercise.
anything that causes increased contractility will do this (catecholamines, digitalis, sympathetic stimulation)

58
Q

Starling curve: what happens to the curve with CHF or digitalis?

A

It moves down (to the right)
For a given preload, you are pumping out less blood.
D/t less contractility
anything that decreases contractility will decrease CO or SV. (drugs, loss of myocardium in MI)
In very bad CHF, curve will be a lot lower and more toward the right.

59
Q

What causes the aortic valve to open?

A

Prs in ventricle exceeds prs in aorta

60
Q

What causes mitral valve to open?

A

Prs in LA exceeds prs in LV

61
Q

In what dz’s do you lose elasticity of the aorta?

A

Marfan’s

Syphilis (tree-barking)

62
Q

What can cause rapid ventricular filling (S3)?

A

CHF
Mitral regurg
L–>R shunt (ASD, VSD, PDA)
Dilated cardiomyopathy

63
Q

What does QRS represent?

A

Ventricular contraction

64
Q

Heart sound are not actually d/t valves closing. What causes them?

A

The turbulent flow right AFTER the valves close.

So on graph will see mitral closing, then S1; Aortic closing, then S2

65
Q

What can cause atrial kick S4?

A

Hypertrophic cardiomyopathy
Aortic stenosis
Chronic HTN w LVH
After an MI

66
Q

Windkessel effect

A

Dicrotic notch in aortic prs curve.
After systole, the aortic prs drops, but goes up again slightly right after the ejection. Prs increases d/t elasticity of the aorta (like rubber band).
This is when the coronary arteries fill!

67
Q

What happens to the cardiac cycle graph when preload is increased?

A

It gets wider (to the right) bc increased preload increases SV
The width of the graph is the SV.

68
Q

What happens to the cardiac cycle graph when you increase afterload?

A

It gets taller and skinnier in width.
Increased afterload means increased aortic prs (so taller) and decreased SV (so skinnier)
Increasing the afterload also increases ESV.

69
Q

What happens to the cardiac cycle graph when contractility is increased?

A

It gets wider (on both sides) and taller.
Increasing contractility increases SV (so wider) and increases EF and decreases ESV.
These mean that the pressure is increased (so taller).

70
Q

What is TPR a measurement of?

A

Afterload

71
Q

Cardiac and vascular fn curve: what 2 things are plotted?

A

CO and Venous return (wrt RA pressure or EDV)

72
Q

If the cardiac and vasc fn curve of CO shifts right, what happened?

A

Either decreased contractility (inotropy)

Or increased afterload (increased TPR)

73
Q

If the cardiac and vasc fn curve of CO shifts left, what happened?

A

Either increased contractility

Or decreased afterload

74
Q

What happens to pressure and blood flow on inspiration?

A

Inspire - diaphragm goes down.
ITP increases
More space for blood to fill heart- so RV vol increases. This is why you get splitting on inspiration.

75
Q

Ventricular AP: Phase 0

A

Rapid upstroke

Volt-gated Na+ chnls open (Na+ comes in)

76
Q

Ventricular AP: Phase 1

A

Initial repolarization
Volt-gated Na+ chnls are inactived
Volt-gated K+ chnls start to open (K+ goes out)

77
Q

Ventricular AP: Phase 2

A

Plateau
Ca2+ influx thru volt-gated Ca2+ chnls balances K+ efflux.
Ca2+ coming in triggers rls of even more Ca2+ from SR- this causes myocyte contraction.

78
Q

Ventricular AP: Phase 3

A

Rapid repolarization

Massive K+ efflux d/t opening of volt-gated slow K+ chnls and closure of Ca2+ chnls

79
Q

Ventricular AP: Phase 4

A

Resting potential

High K+ permeability through K+ chnls (“leak” current is K+ efflux)

80
Q

What are the leak currents?

A

K+ going out
Na+ coming in
Ca2+ coming in

81
Q

What are the pumps/exchgrs?

A

Na+/K+ pump (Na+ out / K+ in)
note: the leak channels go in the opp direction

Na+ in, Ca2+ out
note: Ca2+ leak chnl is back in
Na+ leak chnl is in tho, bc of the Na+/K+ pump

82
Q

Where does the ventricle AP also occur?

A

bundle of His and purkinje fibers

83
Q

How is cardiac musc contraction different than skeletal musc?

A

Cardiac musc AP has a plateau (d/t Ca2+ influx)
Cardiac nodal cells spontaneously depolarize, resulting in automaticity d/t I(f) channels
Cardiac myocytes are electrically coupled to each other by gap jns

84
Q

If the mbr were freely permeable to each of these (individually) what would the voltage be?
K+, Na+, Ca2+

A

K+ -75mV
Na+ +55mV
Ca2+ +20mV

85
Q

How do anti-arrhythmics slow down the heart rate?

A

By increasing ERP- effective refractory period.

During ERP, another AP can’t occur. (another contraction can’t occur)

86
Q

What drugs prolong phase 3 (ventricular AP)?

A

K+ chnls blockers

87
Q

Which phase do Na+ chnl blockers prolong?

A

Phase 0 (ventricular AP)

88
Q

Pacemaker AP- where does this take place?

A

In the pacemakers- SA and AV nodes.

In contrast to the ventricular AP, which occurs in the ventricles

89
Q

Pacemaker AP- what are the phases?

A

Phase 0, 3, 4

90
Q

Pacemaker AP: phase 0

A

Upstroke = opening of volt-gated Ca2+ chnls
Ca2+ comes in
Unlike ventricular myocytes, the pacemaker cells don’t have fast volt-gated Na+ chnls.
Thus, there is a slow conduction velocity- this allows the AV node to prolong the transmission from atria to ventricles (to allow for filling)

91
Q

Pacemaker AP: phase 3

A

Inactivation of Ca2+ chnls

Increased activation of K+ chnls, so increased K+ efflux

92
Q

Pacemaker AP: phase 4

A

Slow diastolic depolarization- the mbr potential spontaneously depolarizes as Na+ conductance increases. Accounts for automaticity of SA and AV node.

93
Q

What part of the pacemaker AP determines the HR?

A

the slope of phase 4 (slow depolarization)
ACh decreases the rate of diastolic depolarization and so decreases HR
Catecholamines increase depolarization and therefore increase HR.
Sympathetic stimulation increases the chance that the I(f) Na+ chnls are open (so makes depol faster)

94
Q

Which drugs inhibit phase 0 of the pacemaker AP?

A

Ca2+ chnl blockers

95
Q

How do beta blockers affect the pacemaker AP?

A

They decrease the slope of phase 4 (and thus reduce HR)

96
Q

Mne for anti-arrhythmics

A 
No Bad Boy Keeps Clean
I- Na+ blockers
II- B-blockers
III- K+ blockers
IV- Ca2+ blockers
97
Q

How do Na+ chnls blockers work on the myocyte AP?

A

They decrease the slope of phase 0, thereby prolonging the ERP.

98
Q

What are the Na+ chnl blockers

A

PDQ TLM FPE
Police Dept Questioned The Little (pudgy) Man For Pushing Ecstacy

Class I-A:
Procainamide
Disopyramide
Quinidine (not quinine!)

Class I-B:
Tocainide
Lidocain
(Phenytoin)
Mexiletine

Class I-C:
Flecainide
Propafenone
Encainide

99
Q

Procainamide

A

Class IA anti-arrythmic (Na+ chnl blocker)
Used for WPW
Can cause drug-induced SLP (shipP, anti-histone Ab)

100
Q

What is WPW?

A 
abnormal electrical pathway bt atria and ventricles- bundle of Kent.
can stimulate ventricles to contract too early, causing atrioventricular reciprocating tachycarding- a type of SVT.
EKG: short PR interval and delta waves
Rx: Procainamide (class 1a) or amiodarone (class III)
101
Q

Effect of Class Ia anti-arrhythmics

A

Increase AP duration, so increase ERP
EKG: increased QT interval
affect both atrial and ventricular arrhythmias, esp re-entrant and ectopic supraventricular or ventricular tachycardia.

102
Q

Side effects of quinidine

A

Cinchonism: headache and tinnitus
Thrombocytopenia
Torsades de pointes d/t increased QT interval

103
Q

Effect of class I-B ant-arrhythmics

A

I-B = tocainide, lidocaine, (pheytoin), mexiletine
Decrease the AP duration. (yes, decrease)
Preferentially affect ischemic or depolarized purkinje and ventricular tsu
useful in acute ventricular tachy-arrythmias (esp post-MI) and in arrythmias caused by digitalis

104
Q

Toxicity of class 1-B

A

Local anesthetic (lidocaine!)
CNS stim/deprsn
CV deprsn

105
Q

Effect of class 1-C

A

Flecainide, Propafenone, Encainide

Have no effect on AP duration (really)
Useful in V-tach that progresses to VF, and in intractible SVT.
Usu last resort.
For pts w/o structural abn.

106
Q

Toxicity of Class 1c

A

pro-arrythmic, esp post-MI (contraindicated)

Signif prolongs the refactory period in the AV node.

107
Q

Which of the Na+ blocking classes is best post-MI? worst?

A 
Best = 1B
Contraindicated = 1C
108
Q

What electrolyte imbalance increases toxicity for all class 1 drugs?

A

Hyperkalemia

109
Q

Class II anti-arrythmics

A

Beta-blockers
Propranolol, esmolol (short acting), metoprolol, atenolol, timolol
Mech: decrs cAMP (bc B receptors are Gs- so if you block them, will decrs it) and decrs Ca2+ currents
They suppress abn pacemakers by decreasing the slope of phase 4
EKG: increased PR interval (AV node is esp sensitive)
Use for v-tach, SVT, slowing ventricular rate during a-fib and a-flutter

110
Q

Toxicity of Class 2 anti-arrythmics

A 
Impotence
Exacerbation of asthma
CV: bradycardia, AV block, CHF
CNS: sedation, sleep alteration
Can mask signs of hypoglycemia, so be careful in diabetic pts
Metoprolol can cause dyslipidemia
Treat OD w glucagon.
111
Q

Class III anti-arrhythmics

A 
K+ channel blockers
Sotalol, amiodarone, ibutilide, bretylium, dofetilide
Increase AP duration, so increase ERP.
Used when other anti-arrhythmics fail.
EKG: increased QT interval
112
Q

What is sotalol used for?

Toxicity?

A

rhythm control for a-fib

tox: torsades de pointes (incrsd QT), excessive Beta-block

113
Q

Toxicity of ibutilide (class 3)

A

torsades de pointes (increased QT)

114
Q

Toxicity of bretylium

A

new arrythmias, hypotension

note: guanethidine and bretylium are the drugs that inhibit NE rls from adrenergic (sympathetic) neurons

115
Q

Toxicity of amiodarone

A

Pulmonary fibrosis,
hepatotoxicity,
hypo- or hyperthyroidism (amiodarone is 40% iodine by weight. only organ in body that uses iodine is thyroid!)
Check PFTs, LFTs, TFTs when using amiodarone
Also, corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF)

116
Q

What is unique about the effects of amiodarone on the ventricular AP?

A 
It has class I, II, III, and IV effects bc it alters the lipid mbr
Mostly class III, but used to be listed as class Ia
117
Q

What phase of the ventricular AP do the K+ chnl blockers affect?

A

Class 3 = Phase 3 effects

118
Q

What drugs cause photosensitivity?

A

SAT for a photo:
Sulfonamides
Amiodarone (class III anti-arrythmic)
Tetracycline

119
Q

What are the 2 kinds of Ca2+ chnl blockers?

A

dihydropyridine- these work at the vessels

non-dihydropyridine- these work at the heart (these are the anti-arrhythmics)

120
Q

Class IV anti-arrhythmics

A

Ca2+ channel blockers (non-dihydropyridine)
Verapamil, diltiazem
Primarily affect AV nodal cells
Decrease conduction velocity (decrease slope of phase 0 in pacemaker AP), increase ERP
EKG: increased PR interval
Used to prevent nodal arrhythmias (eg SVT)

121
Q

Toxicity of Class IV

A

constipation, flushing, edema, CV effects (CHF, heart block, sinus node deprsn)
Get heart block if you combine them w other anti-arrythmics, esp B-blockers

122
Q

Which anti-arrhythmics increase the QT interval?

A 
Class Ia (Na+ blockers)
Class III (K+ blockers)
Increasing QT means at risk for torsades de pointes
123
Q

Which anti-arrhythmics increase the PR interval?

A 
Class II (beta-blockers)
Class IV (Ca2+ blockers)
124
Q

Other than the 4 classes, what are the other anti-arrythmics?

A

Adenosine, K+, Mg2+

125
Q

Adenosine

A

Antiarrhythmic
Increases K+ efflux out of cells, leading to hyperpolarization of the cell and decreased inward Ca2+.
Drug of choice for dx’ing or abolishing SVT
V short acting (~15 sec!)
Toxicity: flushing, hypotension, chest pain- these effects are blocked by theophylline (methylxanthine bronchodilator)

126
Q

K+ as an anti-arrhythmic

A

Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)

127
Q

Mg2+ as an anti-arrhythmic

A

Effective in torsades de pointes (long QT) and digoxin toxicity

* DIT each session (34 decks)

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