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Internal Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Benefit of digoxin in CHF

A
  • decreases hospitalization
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2
Q

Fibromuscular dysplasia

A
  • Renal artery stenosis in a young adult

Symptoms: headache, elevated BP, and renal bruit

Treatment: percutaneous angioplasty w/ stent placement

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3
Q

Orthostatic hypotension

A
  • Drop in systolic BP >20 mmHg from lying down to standing.

- Prolonged recumbence increases the risk.

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4
Q

Treatment for PSVT

A
  • Valsalva maneuver, carotid massage, cold water immersion —–>increase vagal tone ——> decreased conduction through AV node
  • Adenosine is another AV nodal blocker that can be used.
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5
Q

Hepatojugular reflux

A
  • Useful in differentiating between liver pathology and heart pathology; specific for heart path
  • Reflects a failing right ventricle.

Due to: constrictive pericarditis, right ventricular infarction, and restrictive cardiomyopathy

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6
Q

Constrictive pericarditis

A

Signs: Kussmaul’s sign - lack of decrease or an increase in JVD during inspiration, pericardial knock, and pericardial calcifications on CXR

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7
Q

Side effect of amlodipine

A

Lower extremity edema

  • Due to preferential dilation of the precapillary arterioles.
  • Seen more with dihydropyridine CCB more so than with non-DHP CCBs
  • Addition of and ACE inhibitor or ARB can reduce this side-effect.
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8
Q

Amiodarone toxicity

A
  • contraindicated in lung disease due to pulmonary toxicity.
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9
Q

Beta-blockers in lung disease

A

Contraindicated in obstructive lung disease (COPD and asthma), but not in restrictive lung disease

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10
Q

Aortic regurgitation

A

Common causes: aortic root dilation, post-inflammatory, and congenital bicuspid aortic valve

Clinical features: diastolic decrescendo murmur, widened pulse pressure (collapsing/water hammer pulse), uncomfortable awareness of heart beat while in left lateral decubitus position

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11
Q

Nitroglycerin

A

Used to treat angina
Acts by converting to nitric oxide and causing vasodilation of the blood vessels
Secondary effects: increased contractility and reflex tachycardia caused by baroreceptor firing in response to decreased blood pressure

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12
Q

Pathologic Q waves

A

Possibly indicates previous MI

  • > 40 ms (1mm) wide
  • > 2mm deep
  • > 25% depth of QRS
  • seen in leads V1-3
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13
Q

ST depression

A

> or= .5 mm depression in 2 or more contiguous leads

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14
Q

Dobutamine

A

sympathomimetic drug which acts on the beta-1 adrenoreceptors on the heart, increasing contractility, heart rate, and CO
- Can cause vasodilation, leading to hypotension

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15
Q

Dipyradimole -thallium

A

Phosphodiesterase inhibitor that increases cAMP and cGMP

- Cuases vasodilation of the blood vessels

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16
Q

Conditions that may confound results of perfusion imaging

A

Left bundle branch block and ventricular pacer

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17
Q

Adenosine (stress test)

A

causes vasodilation of the coronary vasculature

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18
Q

Aliskiren

A

direct renin inhibitor

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19
Q

grade I or II midsystolic ejection murmur

A

innocent flow murmur of childhood - no workup necessary

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20
Q

Potential side effects of statins

A

muscle damage, hepatotoxicity

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21
Q

Possible side effects of ARBs

A

hyperkalemia, hypotension, and renal failure

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22
Q

Aortic stenosis

A

Crescendo-decrescendo systolic ejection murmur, loudest at the right sternal border, radiating to the carotids

  1. Diminished and delayed carotid pulse (pulsus parvus and tardus) due to blood flow obstruction
  2. Mid to late (if severe enough to cause symptoms) peaking systolic murmur from turbulence due to stenosis
    - Early peaking is seen in milder, asymptomatic disease.
  3. Presence of soft and single second heart sound
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23
Q

Mitral stenosis

A

Mid-to-late (if mild) diastolic murmur following an opening snap, heard best at the apex

  • If severe, the diastolic murmur will start closer to the opening snap
  • Typically have a loud S1
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24
Q

S3

A

Heard in people with chronic severe mitral or aortic regurgitation, heart failure and sometimes in high output states such as pregnancy or thyrotoxicosis

  • Heard after S2, in early diastole during the rapid ventricular filling phase.
  • Due to increased filling pressures and dilated ventricles
25
Q

Symptomatic AVF

A

Congenital - patent ductus arteriosos, angiomas, pulmonary AVF, CNS AVF
Acquired - trauma, iatrogenic, atherosclerosis, cancer
- Decreases systemic vascular resistence because the blood bypasses the capillaries (resistence vessels)
Symptoms: widened pulse pressure

26
Q

Causes of high-output heart failure

A

AVF, thyrotoxicosis, Paget’s disease, anemia, and thiamine deficiency

27
Q

Right ventricular MI

A

In addition to normal MI treatment, fluids may be needed to increase preload
- Avoid nitrates and diuretics

28
Q

ECG changes in PE

A

tachycardia, nonspecific ST segment and T wave abnormalities, new onset RBBB, S1Q3T3 pattern - large S wave in lead I, a Q wave in lead III, and a inverted T wave in lead III

29
Q

RBBB

A 
wide QRS (>120 ms)
V1(M), V6 (W)
30
Q

Beta-blocker overdose

A

Symptoms: bradycardia, AV block, hypotension, diffuse wheezing, hypoglycemia, seizures
- Beta 2 receptors also cause increased insulin release which in overdoses can cause hypoglycemia
- Calcium channel bloackers, digoxin, and cholinergic agents can cause similar findings, but the wheezing is specific for beta blockers
Treatment: secure an airway, give fluids, IV atropine
- in patients with profound hypotension, IV glucagon is then given —-> increases intracellular cAMP (helpful in CCB overdose too)
Additional therapies: IV calcium, vasopressors, high dose insulin and glucose, and IV lipid emulsion therapy

31
Q

Aminophylline

A 
methylxanthine in the same class as theophylline
inhibits phosphodiesterase leading to increased cAMP ---> bronchodilation, positive inotropic and chronotropic effects
32
Q

Digoxin overdose

A

Symptoms: fatigue, anorexia, nausea, blurred vision, disturbed color perception, and cardiac arrhythmias

33
Q

Normal JVP

A
34
Q

Common signs of end organ damage seen in preeclampsia

A

proteinuria, thrombocytopenia, transaminitis, elevated creatinine, pulmonary edema, headache, visual changes

35
Q

Effects of progesterone on vasculature

A

rising progesterone during early pregnancy causes vasodilation —> 5-10 mmHg decrease in BP
- typically returns to normal during the third trimester

36
Q

Pregnancy-related risks with HTN

A

superimposed preeclampsia, postpartum hemorrhage, preterm delivery, gestational diabetes, abruptio placentae, C-section, oligohydramnios, fetal growth restriction, mortality to newborn

37
Q

Placenta accreta risk factors

A

previous C-section, uterine curettage

38
Q

How does aortic rupture cause hypertension

A

visceral afferent reflexes cause a hypertension or a pseudocoarctation response

39
Q

Treatment for reversible exercise-induced ischemia

A

Aspirin, beta-blockers and lifestyle modification

40
Q

Albuterol

A

B2>B1

- B1 activity can cause tachycardia, hypertension and arrythmias in pts w/ CAD

41
Q

Erythropoeitin

A

contraindicated in pts with CAD due to possible thromboembolic events and stroke

42
Q

Metformin

A

Can cause lactic acidosis in pts predisposed to hypoxia (CAD, CKD)

43
Q

Lesser known characteristics of Turner syndrome

A

narrow, high-arched palate, cubitis valgus, aortic root dilation putting the patient at risk for aortic dissection

44
Q

Patent ductus arteriosis

A

can present asymptomatically or with symptoms of extertional dyspnea or CHF
- seen in congenital rubella syndrome and Char syndrome

45
Q

Char syndrome

A

facial anomolies, patent ductus arteriosis, and limb abnormalities

46
Q

Restrictive cardiomyopathy

A

right-sided heart failure is more prominent

47
Q

Clopidogrel, prasugrel, ticagrelor, ticlopidine

A

ADP receptor inhibitors (ADP binding to P2y12 receptor induces GpIIb/IIIa expression on the platelet surface —> fibrinogen binds here —>platelet aggregate)

48
Q

Drug-eluting stents

A

DAPT recommended in all pts for at least 12 months following placement

49
Q

Direct factor Xa inhibitor

A

apixiban

- Used for nonvalvular a fib, DVT and PE

50
Q

Postinfarction pericarditis

A

NSAIDs and sometimes cholchicine inhibitors

51
Q

Milrinone

A

selective phosphodiesterase inhibitor that increases cardiac contractility (increased cAMP)
- Increases mortality in CHF pts

52
Q

CYP450 inhibitors

A

SICKFACES.COM
Sodium valproate, Isoniazid, Cimetidine, Ketaconazole, Fluconazole, Alcohol, Chloramphenicol, Erythromycin, Sulfonamides, Ciprofloxacin, Omeprazole, Metronidazole, Grapefruit juice
- also NSAIDs and acetaminophen, amiodarone, cranberry juice, Ginko balboa, vitamin E, thyroid hormone, SSRIs

53
Q

CYP450 inducers

A

CRAP GPS induce me to madness
Carbamazipines, rifampicin, chronic alcohol, phenytoin, griseofulvin, phenobarbitol, sulfonylureas
- Also ginseng, greens, oral contraceptives, St. John’s wort

54
Q

Tetrology of Fallot

A

Infundibular spasm can be induced by exertion or agitation, causing blood to flow from right to left across VSD

  • Oxygen can be given to cause vasodilation of the pulmonary vasculature and and vasoconstriction of the systemic vasculature
  • ductal dependent pulmonary blood flow
55
Q

Transposition of the great vessels

A
  • Most common form of cyanotic CHD presenting in the first 24 hrs of life
  • Pulmonary and systemic circuits are in parallel rather than series.
  • PFO is necessary for survival
    Three variants:
    1) TGA with intact ventricular septum
    2) TGA with VSD
    3) TGA with VSD and pulmonic stenosis

Clinical manifestations:
- Cyanosis present from birth
- Loud single S2
- Mild cardiomegaly, increased pulmonary vascular markings.
- Egg-shaped cardiac silhouette (narrow mediastinum)
ECG - right ventricular hypertrophy and right axis deviation

Treatment: PGE1 to increase aorta to pulmonary artery shunting via the ductus arteriosus

  • ductal independent mixing lesions
56
Q

Tricuspid atresia

A
  • Severe hypoplasia or absence of the right ventricle
    Two types:
    1) with normally related great arteries
    2) with TGA
  • Usually have PFO and VSD and pulmonary stenosis or atresia
  • Degree of pulmonary stenosis dictates the severity of cyanosis - patency of the ductus arteriosus becomes important here
  • If pulmonary atresia is present, severe cyanosis can occur with closure of the ductus arteriosis
    ECG: left axis deviation, right atrial enlargement and left ventricular hypertrophy
  • Minimal pulmonary blood flow, single S2
    -ductal dependent pulmonary blood flow
57
Q

Truncus arteriosis

A

VSD is always present

  • Associated with DiGoeorge syndrome
  • CHF develops due to increased pulmonary blood flow that develops due to decreased pulmonary vascular resistence, and decreased systemic blood flow.
  • Single S2, nonspecific systolic ejection murmur
  • Widended pulse pressure and bounding arterial pulses
  • Cardiomegaly, increased pulmonary vasculature
58
Q

Total anomolous pulmonary venous connection

A

4 variants:

1) Supracardiac - blood drains via a vertical vein into the innominate vein or directly into the SVC
2) cardiac - blood drains into the coronary sinus or directly into the R atrium
3) infradiaphragmatic - blood drains via a vertical vein into the portal or hepatic veins
4) Mixed - combination of above

  • Presence of pulmonary venous obstruction dicatates cyanosis
  • ASD or PFO must be present
  • leads to CHF
  • Typically severe cyanosis and respiratory distress
    Chest XR - pulmonary edema and “snowman sign” (enlarged supracardiac veins and SVC)

Internal Medicine (12 decks)

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