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Cardiovascular Flashcards

1
Q

——— is the most posterior part of the heart

A

LA

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2
Q

Enlargement of the LA (eg, in ———) can lead to compression of the ——— (causing ———) and/or the ———, a branch of the ———, causing ——— (I.e., ——— syndrome)

A

- mitral stenosis

- esophagus

- dysphagia

- left recurrent laryngeal nerve

- vagus nerve

- hoarseness

- Ortner

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3
Q

——— is the most anterior part of the heart and most commonly ———

A

- RV

- injured in trauma

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4
Q

——— is about 2/3 and ———— is about 1/3 of the inferior (diaphragmatic) cardiac surface

A

- LV

- RV

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5
Q

Pericardium consists of what 3 layers (from outer to inner): ƒ

A

Fibrous pericardium ƒ
Parietal pericardium ƒ
Epicardium (visceral pericardium)

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6
Q

Pericardial space lies between ——— and ———

A

parietal pericardium and epicardium

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7
Q

Pericardium innervated by ———; thus, pericarditis can cause referred pain to the ———

A

- phrenic nerve

- neck, arms, or one or both shoulders (often left)

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8
Q

LAD and its branches supply what 3 areas:

A

- anterior 2/3 of interventricular septum

- anterolateral papillary muscle

- anterior surface of LV

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9
Q

PDA supplies what 3 areas:

A

- posterior 1/3 of interventricular septum

- posterior 2/3 walls of ventricles

- posteromedial papillary muscle

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10
Q

——— supplies AV node and SA node; thus, infarct may cause ——— (I.e., ——— or ———)

A

- RCA

- nodal dysfunction

- bradycardia or heart block

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11
Q

——— supplies RV

A

Right (acute) marginal artery

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12
Q

——— is the most commonly occluded coronary artery

A

LAD

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13
Q

Define right-dominant circulation (most common):

A

PDA arises from RCA

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14
Q

Define left-dominant circulation:

A

PDA arises from LCX ƒ

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15
Q

Define codominant circulation:

A

PDA arises from both LCX and RCA

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16
Q

Coronary blood flow to LV and interventricular septum peaks in ———

A

early diastole

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17
Q

Coronary sinus runs in the ——— and drains into the ———

A

- left AV groove

- RA

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18
Q

S1 is ——— and is loudest at ———area

A

- mitral and tricuspid valve closure

- mitral

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19
Q

S2 is ——— and is loudest at ———

A

- aortic and pulmonary valve closure

- left upper sternal border

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20
Q

S3 is ———, is associated with ———  (eg, as seen in conditions like ———), is caused by turbulence from ———, and is best heard at ———. S3 is more common in ——— (but can be normal in ———).

A

- in early diastole during rapid ventricular filling phase

- increased filling pressures

- MR, AR, HF, thyrotoxicosis

- blood from LA mixing with  increased ESV

- apex with patient in left lateral decubitus position

- dilated ventricles

- children, young adults, athletes, and pregnancy

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21
Q

S4 is in ———, is from turbulence caused by ———, and is best heard ———. S4 associated with ——— in atria and ——— in ventricle (eg, ———). S4 ——— if palpable. S4 common in ———.

A

- late diastole (“atrial kick”)

- blood entering stiffened LV

- at apex with patient in left lateral decubitus position

- high pressure

- noncompliance

- hypertrophy

- considered abnormal

- older adults

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22
Q

Kussmaul sign refers to ——— (normally, inspiration Žresults in ———pressure yielding increased ——— Ž  and decreased ———)

A

- Paradoxical increase in JVP on inspiration

- negative intrathoracic Ž

- venous return

- JVP

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23
Q

Kussmaul sign due to impaired Ž——— (I.e., cannot accommodate increased ——— during Ž———; thus, blood backs up into Ž———

A

- RV filling

- venous return

- inspiration

- vena cava

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24
Q

List 5 conditions associated with Kussmaul sign:

A

- constrictive pericarditis

- restrictive cardiomyopathy

- right HF

- massive pulmonary embolism

- right atrial or ventricular tumors

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25
List the 7 parts of cardiac conduction pathway:
- SA node - atria Ž - AV node Ž -bundle of His Ž - right and left bundle branches Ž(left bundle branch divides into left anterior and posterior fascicles) - Purkinje fibers Ž - ventricles
26
List in order speed of conduction of cardiac conduction system (fastest to slowest):
His-Purkinje > Atria > Ventricles > AV node (He Parks At Ventura AVenue)
27
Bundle branch block is an interruption of ———, which results in affected ventricle ———
- conduction of normal left or right bundle branches - depolarizes via slower myocyte-to-myocyte conduction from the unaffected ventricle, which depolarizes via the faster His-Purkinje system
28
Bundle branch block commonly due to ——— (eg, ——— or ———).
- degenerative changes - cardiomyopathy or infiltrative disease
29
Normally, ——— closure occurs just before ——— closure, and the combination of these sounds make up S2. A physiologic split S2 occurs when the ——— by a great enough distance to allow both sounds to be heard separately, which occurs during ——— when increased ——— delays the closure of the ———
- AV - PV - AV sound precedes PV sound - inspiration - venous return to the right side of the heart - pulmonic valve
30
In physiologic splitting of S2, ——— results in a Ždrop in ——— leading to increased ———, increased ———, Ž  increased ———, and increased ——— ; thus, there is delayed ———
- Inspiration - intrathoracic pressure - venous return Ž  - RV filling - RV stroke volume Ž  - RV ejection time - closure of pulmonic valve
31
Along with main cause physiologic splitting of S2, this phenomenon is also related to decreased pulmonary ——— (I.e., increased capacity of the ———) which also occurs during ———, and contributes to delayed closure of ———
- impedance - pulmonary circulation - inspiration - pulmonic valve
32
Wide splitting of S2 is seen in conditions that delay ——— (eg, ——— and ———), which causes delayed ——— (especially ———), with an exaggeration of normal splitting
- RV emptying - pulmonic stenosis and right bundle branch block - pulmonic sound - on pulmonic sound
33
Fixed splitting of S2 is heard in ——— because there is a Ž——— Žresulting in increased ——— volumes Žleading to increased flow through ——— Ž and delayed ——— (notably this is independent of ———)
- ASD - left-to-right shunt - RA and RV - pulmonic valve - pulmonic valve closure - respiration
34
Paradoxical splitting of S2 is heard in conditions that ——— (eg, ——— and ———)
- delay aortic valve closure - aortic stenosis and left bundle branch block
35
In paradoxical splitting of S2, the normal order of ——— is reversed: in paradoxical splitting ——— occurs before ———
- semilunar valve closure - P2 - A2
36
In paradoxical splitting of S2, what is observed on inspiration and what is observed on expiration?
- On inspiration: P2 closes later and moves closer to A2, “paradoxically” eliminating the split - On expiration: the split can be heard (opposite to physiologic splitting)
37
What systolic murmurs can best be heard in the aortic area?
- Aortic stenosis - Flow murmur (eg, physiologic murmur) - Aortic valve sclerosis
38
What systolic ejection murmurs can best be heard in the pulmonic area?
- Pulmonic stenosis - Atrial septal defect - Flow murmur (eg, physiologic murmur)
39
What systolic murmur can best be heard in the left sternal border area?
Hypertrophic cardiomyopathy
40
What diastolic murmurs can best be heard in the left sternal border area?
- Aortic regurgitation - Pulmonic regurgitation
41
What holosystolic murmurs can best be heard in the tricuspid area?
- Tricuspid regurgitation - Ventricular septal defect
42
What diastolic murmur can best be heard in the tricuspid area?
Tricuspid stenosis
43
What systolic murmurs can best be heard in the mitral area/apex?
- Mitral regurgitation - Mitral valve prolapse
44
What diastolic murmur can best be heard in the mitral area/apex?
Mitral stenosis
45
Describe the cardiovascular changes, murmurs that increase, and murmurs that decrease with Standing (abruptly) and Valsalva (strain phase)?
Cardiovascular changes: - decreased preload (decreased LV volume) Murmurs that increase: - MVP (decreased LV volume) with earlier midsystolic click - HCM (decreased LV volume) Murmurs that decrease: - Most murmurs (decreased flow through stenotic or regurgitant valve)
46
Describe the cardiovascular changes, murmurs that increase, and murmurs that decrease with passive leg raise?
Cardiovascular changes: - increased preload (increased LV volume) Murmurs that increase: - Most murmurs (increased flow through stenotic or regurgitant valve) Murmurs that decrease: - MVP (increased LV volume) with later midsystolic click - HCM (increased LV volume)
47
Describe the cardiovascular changes, murmurs that increase, and murmurs that decrease with squatting?
Cardiovascular changes: - increased preload, increased afterload (increased LV volume) Murmurs that increase: - Most murmurs (increased flow through stenotic or regurgitant valve) Murmurs that decrease: - MVP (increased LV volume) with later midsystolic click - HCM (increased LV volume)
48
Describe the cardiovascular changes, murmurs that increase, and murmurs that decrease with hand grip?
Cardiovascular changes: - increased afterload Žwith increased reverse flow across aortic valve (increased LV volume) Murmurs that increase: - Most other left-sided murmurs (AR, MR, VSD) Murmurs that decrease: - AS (decreased transaortic valve pressure gradient) - HCM (increased LV volume)
49
Describe the cardiovascular changes, murmurs that increase, and murmurs that decrease with inspiration?
Cardiovascular changes: - increased venous return to right heart, and decreased venous return to left heart Murmurs that increase: - Most right-sided murmurs Murmurs that decrease: - Most left-sided murmurs
50
Antiarrhythmics: sodium channel blockers (class ———) work by ———conduction (especially in ——— cells); result in a ——— slope of phase ——— depolarization
- I - slowing or blocking - depolarized - decreased - 0
51
Antiarrhythmics: sodium channel blockers have ——— action at ———; thus, as state dependent ——— leads to ——— diastole, Na+ channels spend ——- time in resting state (relative to these drugs, they ——— during this state), there is less time for drug to ———
- increased - faster HR - increase HR - shorter - less - dissociate - dissociate from receptor
52
Relative to sodium channel blockers state dependent effects: Effect most pronounced in ——— due to relative ———
- IC>IA>IB (Fast taxi CAB) - binding strength
53
Name the Class IA antiarrythmics:
Quinidine, procainamide, disopyramide (the QUeen PROClaims DISO’s PYRAMID)
54
The mechanism of Class IA antiarrythmics is ———. They result in ——— AP duration,  ——— effective refractory period (ERP) in ventricular action potential,  ——— QT interval, as well as some ——— blocking effects
- Moderate Na+ channel blockade - increased - increased - increased - K+ channel
55
The clinical use of Class IA antiarrythmics include both ———, especially ———
- atrial and ventricular arrhythmias - reentrant and ectopic SVT and VT
56
List 5 adverse effects of Class IA antiarrythmics (and specify particular drugs as applicable):
- cinchonism; ie, headache and tinnitus (quinidine) - reversible SLE-like syndrome (procainamide) - HF (disopyramide) - thrombocytopenia - torsades de pointes due to increased QT interval
57
Name the Class IB antiarrythmics:
Lidocaine, phenytoin, mexiletine. (I’d Buy (1B) LIDdy’s PHine MEXIcan tacos)
58
The mechanism of Class IB antiarrythmics is ———. They result in ——— AP duration, and preferentially affect ———
- Weak Na+ channel blockade - decreased - ischemic or depolarized Purkinje and ventricular tissue
59
The clinical use of Class IB antiarrythmics include both ———
- acute ventricular arrhythmias (especially post- MI) - digitalis-induced arrhythmias (IB is Best post-MI)
60
List 2 adverse effects of Class IB antiarrythmics:
- CNS stimulation/depression - cardiovascular depression
61
Name the Class IC antiarrythmics:
- Flecainide, propafenone (Can I have Fries, Please?)
62
The mechanism of Class IC antiarrythmics is ———. They result in ——— of ERP in AV node and accessory bypass tracts. They have ——— on ERP in Purkinje and ventricular tissue and ———- on AP duration.
- strong Na+ channel blockade - significantly prolongation - no effect - minimal effect
63
The clinical use of Class IC antiarrythmics is ———, including ———; only used as a last resort for
- SVTs, including atrial fibrillation - refractory VT
64
List a key adverse effect/contraindication of Class IC antiarrythmics:
- Proarrhythmic, especially post-MI (contraindicated) (IC is Contraindicated in structural and ischemic heart disease)
65
Name the Class II antiarrythmics:
β-blockers (class II) : Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol
66
Class II antiarrythmics ——— SA and AV nodal activity by ——— cAMP,  ———Ca2+ currents. Suppress abnormal pacemakers by ———. ——— node particularly sensitive, with ———
- decrease - decreasing - decreasing - decreasing slope of phase 4 - AV - increased PR interval
67
The clinical uses of Class II antiarrythmics are:
- SVT, ventricular rate control for atrial fibrillation and atrial flutter, prevent ventricular arrhythmia post-MI
68
List a 7 adverse effect of Class II antiarrythmics (and specific associated drug as applicable):
- impotence - exacerbation of COPD and asthma - cardiovascular effects (bradycardia, AV block, HF) - CNS effects (sedation, sleep alterations) - may mask the signs of hypoglycemia - dyslipidemia (Metoprolol) - exacerbate vasospasm in vasospastic angina (Propranolol)
69
β-blockers (except ———) cause unopposed ——— if given alone for ——— or for ——— (unsubstantiated)
- the nonselective α- and β-antagonists carvedilol and labetalol - α1-agonism - pheochromocytoma - cocaine toxicity
70
Treat β-blocker overdose with:
- saline, atropine, glucagon
71
Name the β-blocker that is very short acting:
Esmolol
72
Name the Class III antiarrythmics:
potassium channel blockers (class III) : Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
73
Class III antiarrythmics ———AP duration,  ———ERP,  and ——— QT interval (Markedly prolonged ———)
- increase - increase - increase - repolarization
74
The clinical uses of Class III antiarrythmics are:
- atrial fibrillation - atrial flutter - ventricular tachycardia (amiodarone, sotalol)
75
List 2 adverse effects of Sotalol:
- torsades de pointes - excessive β blockade
76
List an adverse effect of Ibutilide:
- torsades de pointes
77
List 7 adverse effects of Amiodarone:
- pulmonary fibrosis - hepatotoxicity -hypothyroidism or hyperthyroidism (amIODarone is 40% IODine by weight) - acts as hapten (corneal deposits, blue/gray skin deposits resulting in photodermatitis) - neurologic effects - constipation - cardiovascular effects (bradycardia, heart block, HF)
78
What tests need to be checked when using amiodarone?
PFTs, LFTs, and TFTs (Amiodarone is lipophilic and has class I, II, III, and IV effects.)
79
Name the Class IV antiarrythmics:
calcium channel blockers (class IV): Diltiazem, verapamil
80
Class IV antiarrythmics ———conduction velocity,  ——— ERP,  ——— PR interval. ——— rise of action potential and ——— repolarization (at AV node)
- decrease (Diltiazem, Verapamil = Decrease Velocity) - increase - increase - slow - prolong
81
The clinical uses of Class IV antiarrythmics are:
- prevention of nodal arrhythmias (eg, SVT), - rate control in atrial fibrillation
82
List an 4 adverse effects of Class IV antiarrythmics:
- constipation - flushing - edema -cardiovascular effects (HF, AV block, sinus node depression)
83
Adenosine function as an antiarrythmic by ——— , resulting in ——— the cell and ——— ICa, and thus, ——— AV node conduction
- increasing K+ out of cells - hyperpolarizing - decreasing - decreasing
84
Adensine is the drug of choice in diagnosing/terminating certain forms of ———
SVT
85
List 5 adverse effects of adenosine:
- flushing - hypotension - chest pain - sense of impending doom - bronchospasm
86
Adenosine is ——— acting
Very short (~ 15 sec)
87
Adenosine effects blunted by ——— and ——— (both are ———)
- theophylline - caffeine - adenosine receptor antagonists
88
Relative to acting as an antiarrhythmics, magnesium effective in treating ——— and ———
torsades de pointes and digoxin toxicity
89
What is the key ECG differentiator for SVT vs VT?
QRS complex duration

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