Cardiovascular Flashcards

1
Q

Determine axis of EKG:
normal?
LAD?
RAD?

A
Normal = +QRS in leads 1 and avF (0-90*)
LAD = +QRS in lead 1, and -QRS in avF
RAD = -QRS in lead 1, and +QRS in avF
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2
Q

What does a LBBB look like?

A

a QRS >120msec, no R wave in V1, tall R waves in 1, V5, and V6

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3
Q

What does a RBBB look like?

A

QRS >120msec, RSR complex with a wide R wave in V1, wide S wave in 1, V5, and V6

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4
Q

What is Kussmauls sign?

A
Increased JVP with inspiration. Could mean:
ventricular infarction
postoperative cardiac tamponade
tricuspid regurg
constrictive pericarditis

I.E. = something is pushing the blood out of the RA up into the neck!

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5
Q

What does a mitral valve prolapse murmur sound like?

A

A midsystolic or late systolic murmur with a preceding click

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6
Q

Diastolic murmurs are always abnormal.

A

They include aortic regurg or mitral stenosis.

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7
Q

A college age male “passes out” while playing basketball w/ no prodromal symptoms or seizure activity. His cardiac exam is normal. EKG shows slurred upstroke of the QRS. What do you do?

A

This is WPW.

Advise against exercise and tx the arrhythmia with procainamide and refer for electrophysiology study.

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8
Q

What does an S3 mean?

S4?

A

S3: dilated cardiomyopathy, mitral valve disease or a floppy ventricle (Slosh-ing in.) Can be normal in pregnancy or high flow state.

S4: caused by HTN, stiff ventricle (A-stiff heart), or aortic stenosis. Often normal in young patients and athletes

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9
Q

What causes pulsus paradoxis? What does it indicate?

A

Caused by a decreased systolic BP when inspiration. Due to pericardial tamponade, asthma, COPD, tension PNX, or FOB in airway

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10
Q

What causes pulsus alternans?

A

=alternating weak and strong pulses.

Due to cardiac tamponade, LVHF

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11
Q

What causes pulsus parvus et tardus?

A

=weak or delayed pulses

Due to Aortic Stenosis

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12
Q

A man with CHF is taking lasix and metoprolol, what else should he be on?

A

an ACE-I

They have a +mortality benefit when used with BB’s in class 2-4 CHF patients

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13
Q

Describe Second degree heart blocks?

A

Type 1 (wenckebach) = progressive PR lengthening until beat is dropped

Type 2 = unexpected drops in beat w/o PR lengthening. more dangerous type, can lead to type 3 block. NEEDS PACEMAKER

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14
Q

What are cannon A waves seen with?

A

Type 3 block (complete dissociation between P and QRS)

NEEDS PACEMAKER

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15
Q

What is the most common indication for a pacemaker?

A

SSS (sick sinus syndrome)

This is a combo of SVT and bradyarrythmias. Can present as syncope, palpitations, TIA, stroke…

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16
Q

When do you anticoagulate a patient with Afib?

A

Use the CHADS2 score and anticoagulate if they are >2 or if it has been >48h since afib

If cardiovert them (If TEE shows no clot, or else you have to have 3-6 warfarin therapy with INR of 2-3)

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17
Q

What is the atrial and ventricular rates in aflutter?

A

atrial rate = 240-320

ventricular rate = 150

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18
Q

What type of arrhythmia occurs when the “P wave is buried in the QRS.”

A

Atrioventricular Nodal Reentry Tachycardia (AVNRT)

Occurs when a reentry circuit in the AV node depolarizes the atrium and ventricle simultaneously.

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19
Q

What type of arrhythmia occurs when there is a “retrograde P wave after a normal QRS”

A

Atrioventricular Reciprocating Tachycardia (AVRT)

WPW is a particular form of these that will have a DELTA WAVE

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20
Q

How do you treat symptomatic PVCs?

A

BB’s

21
Q

How do you treat torsaddes de point?

A

Give magnesium and cardiovert.

Correct hypokalemia, withdraw offending drugs that may be lengthening the QT (haldol)

22
Q

When should BBs be started in a patient with CHF?

A

when the patient is no longer volume overloaded (euvolemic)

23
Q

What drugs that we give CHF patients have no mortality benefit?

A

Dig and diuretics, these provide symptom relief only

24
Q

How does diastolic CHF differ from systolic HF?

A

The LVEDP is elevated, but the CO and the EF are normal.

This type almost always happens to really old people with long standing HTN

Digoxin does NOT work in these patients!

25
Q
Side effects of diuretics?
loops
thiazides
k sparing
CA inhibitors
osmotic agents
A

loops = ototoxicity, met alkalosis, hypo-kalemia, calcemia, gout
thiazides = hyper-glucose, lipid, uric acid, calcium (GLUC)
k sparing = hyperkalemia, gynecomastia, sex dysfunction
CA inhibitors = hypercholermic metabolic acidosis, NH3 toxicity, sulfa allergy
osmotic agents = pulmonary edema, contraindicated in CHF

26
Q

What will increase the murmur in HOCM?

A

a decrease in preload (valsalva or standing) will increase the sound of the HOCM murmur

an increase in preload (passive leg raise) will decrease the sound of a HOCM murmur

27
Q

22 yo woman with chest pain in the early morning and has ST elevation on EKG w/o cardiac enzyme elevations?

A

Prinzmetals angina (due to vasospasm of coronary vessels)

28
Q

What 2 meds are the only ones shown to have a mortality benefit in treating angina?

A

ASA and beta blockers

29
Q

Only difference between Unstable angina and NSTEMI?

A

NSTEMI has leak of cardiac enzymes, unstable angina does not

30
Q

What is the first cardiac enzyme to become elevated after a STEMI?

A

Myoglobin, short duration (1 hour)

CK-MB - catches the 1-2 hour

31
Q

State which leads you will see the following infarction in?
RCA infarct
anterior MI (LAD)
lateral infarct (LCA)

A
RCA = leads 2,3 ,avF
LAD = V1-V4
LCA = 1, avL, V5-6
32
Q

Woman has pulseless electrical activity on hospital day 7 after a lateral wall STEMI, what is the dx?

A

infarct was probably the LCA

Now she probably experienced a LV free wall rupture and has acute cardiac tamponade. Do a paricardiocentesis

33
Q

What is the most common cause of death after an MI?

A

arrhythmia

34
Q

What is dressler’s syndrome?

A

an autoimmune process that occurs 2-10 weeks after MI - patient will present with fever, pericardits, pleural effusion, leukocytosis, and elevated ESR

35
Q
Post MI complications:
First day:
2-4 days:
5-10 days:
weeks-months:
A

First day: HF
2-4 days: arrhythmia, pericarditis
5-10 days: LV wall rupture, papillary muscle rupture
weeks-months: ventricular aneurysm, Dressler’s syndrome

36
Q
Side effects of lipid medications:
Statins (HMG CoA reductase):
Fibrates:
Cholesterol absorption inhibitors:
Niacin:
BABR:
A

Statins (HMG CoA reductase): increase LFT’s, myositis, warfarin potentiation
Fibrates: GI upset, cholelithiasis, myositis, increase LFT’s
Cholesterol absorption inhibitors: D/Ab pain, angioedema
Niacin: skin flushing (block w/ aspirin), parasthesias, pruritis, GI upset, increased LFT’s
BABR: GI/Constipation, decrease absorption of drugs in the SI, increase LFT’s

37
Q

Diffuse ST segment elevation and PR segment depressions followed by T-wave inversions =

A

Pericarditis

Patient will have CP that worsens in the supine position and with inspiration.

38
Q

What antihypertensive medication can cause hirsutism?

A

Minoxidil

39
Q

Why avoid corticosteroids within a few days of M.I. because…

A

They can predispose to ventricular wall rupture

40
Q

What is Becks triad? What disease?

A

Cardiac Tamponade:

Triad is JCD, hypotension, and distant (muffled) heart sounds.

Look for decreased ventricular preload in these pts due to septum deviation!

41
Q

What type of valve disease will you see a head bob with each heart beat and a water hammer pulse?

A

Aortic Regurg. This is called musset’s sign and a corrigan sign and they are due to the widened pulse pressure.

42
Q

What type of medication provides symptom relief in MV stenosis?

A

anti-arrythmics

43
Q

All men age 65-75 with a history of smoking should be screened once in their lives for?

A

AAA by U/S

44
Q

What is the #1 risk factor for:

AAA?
Aortic Dissection?

A

AAA = atherosclerosis

Aortic Dissection = HTN

45
Q

You can see neurological deficits with aortic dissections if the aortic arch or the spinal arteries are involved

A

yep

46
Q

What ankle brachial index is associated with rest pain?

A
47
Q

Milroy’s disease:

A

Congenital malformation of the lymphatic system which results in lymphedema in childhood

48
Q

Down syndrome cardio abnormality?

A

Atrioventricular cushion defect