by JMMeis

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Timeframe for angina

Cause of the pain
Increases in intensity for 2-3 min. Usually gone within 30

Bradykinins and adenosine cause pain
Cutoff for definition of blockage
70% blockage
Who supplies blood to the left ventricle?

Where does it end up after the great, small and middle cardiac veins get a hold of it?
Mainly the anterior descending and circumflex arteries (branches of the left)

cardiac sinus (other veins drain directly into the rt. atrium)
Prinzmental Angina

3 characteristics
What do you treat it with?
What do you NOT treat it with?
CP of vasospasm. No precipitating factors. Not associated with stenosis.

Usually happens in morning, more often women and assoc. with ST segment elevation

CCBs, nitrates

NOT with B-blockers, they increase the spasm
What Framingham risk score is a CAD equivalent?
20%; 15 points
ankle brachial index: the ratio of blood pressure in the brachial and dorsalis pedis. Use dopplar. Should be 1.0. If higher, it's a venous problem, if lower, arterial. <0.6 is serious disease, <0.5 is ischemic
5 Ps of PAD
Pulselessness: late sign
Pain: especially ischemic rest pain
Pallor: compare with back of your hand.
Blackish wound. Common in arterial insufficiency (on extremities), not so much with venous insufficiency
Endovascular aneurysm repair:

This is basically a catheter put through an aneurysm. Less invasive than a full stent.
Carotid endarectomy cleans out the plaque with open procedure.

Indication: >70% blockage
Imaging venous insufficiency

Dopplar ultrasound
Contrast venography
  • Photoplethysmography: Noninvasive, uses light and sound to graph valvular function
  • Doppler ultrasound: Noninvasive, used to identify obstructions such as DVT or venous reflux.
  • Contrast venography: Gold standard--use of contrast injected into distal pedal vein to visualize venous system (good for pre-op venous stripping)
Invasive treatments for venous insufficiency
  • Radiofrequency closure: Cath to injured vein and RF waves make it closed
  • Endovenous laser therapy: Scar vein closed with cath to bad spot
  • Venous stripping
Tietze's syndrome
Costochondral tenderness associated with chest pain. Tender to palpation. Movement of chest wall influences pain
Predictive values of ACS

ECG with 1mm ST elevation or new Q wave in =>2 leads

ECG with 1mm new ST depression in =>2 leads

ST changes indicative of ischemia/strain


what do Kerley B lines mean and what are they?
They mean CHF and they're parallel lines seen at periphery of lung in X-ray
ACS and Troponin levels (I vs T)

2-6 hours increasing to peak @12

I more indicative than T
I normalizes in 7 days, T 10

CK-MB increases 4-6 hours to peak @ 18-24. normalizes in 2 days
Indications for stress IMAGING study (4)
  • Abnormal baseline ECG
  • Inadequate exercise capacity=Pharmacologic stress¬† imaging study
  • Localize ischemia
  • Equivocal prior treadmill exercise test
Rule of thumb for pulse
220 - age
atrium contracting against high pressure: HTN, lv hypertrophy. Just before S1 (diastolic). Can also be aortic stenosis.
Which sound could be intensified by anemia or exercise?
Rapid filling of ventricles. Can be innocent in younger individuals but almost certainly patho in adults (CHF)
What are the indications for prophylactic ABX with heart condition
  • NOT mitral prolapse with regurg
  • Prosthetic heart valves, including bioprosthetic and homograft valves.¬†
  • Prosthetic material used for cardiac valve repair
  • A prior history of IE.
  • Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits.
  • Completely repaired congenital heart defects with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first six months after the procedure.
  • Repaired congenital heart disease with residual defects at the site or adjacent to the site of the prosthetic device.
  • Cardiac "valvulopathy" in a transplanted heart. Valvulopathy is defined as documentation of substantial leaflet pathology and regurgitation
7 qualities of a murmur
Shape (e.g. crescendo)
Pitch (high or low)
Quality (machine, blowing)
3 causes of physiological murmurs and what happens with resolution?
Contraindication #1 for ETT
aortic stenosis
what 7 things mean bacterial endocarditis?
  • fever
  • new murmur
  • Janeway lesions
  • Osler nodes (nodules on tips of fingers)
  • roth spots (pale retinal lesions with a peripheral area of hemorrhage, usually near optic disc)
  • splinter hemorrhages (on fingertips)
  • IV drug use
What percent of PEs come from the calf?

Usually they're from the proximal leg (which tend to be asymptomatic)

20% of folks with thrombophlebitis also have occult DVT
What measurement of asymmetry is significant?

Where do you measure from?
>3 cm measured 10 cm below tibial tuberosity
What's the best test for diagnosing PE?
D-dimer (rule it out) and color-flow duplex ultrasound (rule it in)
Protein S, C and aT3
Anticoagulant proteins. They're good tests to do for recurrent DVTs.

Also used when transferring someone from heparin to coumadin (wait for certain levels)
Initial non-pharmacologic treatment for DVT
  • bed rest: 1-4 days
  • Pt education on anti-coagulant therapy (interactions, foods, length of time, etc.)
  • Labs to monitor INR, etc.
Diagnostic imaging for workup of PE (3)
Gold standard: Pulmonary angiography (but not done all that often due to mortality rate and cost)

Spiral (helical) CT: requires IV contrast. Standard approach when paired with the D Dimer.

VQ scan: good but not great. Cheap and available but ~75% are "indeterminate"
Treatment of HTN in these individuals is best with diuretic monotherapy:
Treatment of HTN in someone with DMII?
ACE inhibitor
Produced by myocardial cells in times of stress.

Direct vasodilator.
Most important physiological factor in systolic BP?
Alpha blockers are indicated to treat HTN with what other condition?
first line therapy for pts with HTN and CHF?
ACE inhibitor
when do you use an ACE inhibitor as first line therapy for HTN?
diabetes, CHF
main physiological response responsible for lowering BP with longstanding diuretic use?
Initially it's loss of volume but longstanding effects come from vasodilatory effects. Takes around a month to see all the effects- so that's when you follow up.
Stage I HTN?
Stage II?
the "canary in the cole mine" for CAD for men
what are renal indications for HTN?
microalbuminuria or estimated GFR <60 ml/min
what's a drug induced cause for 2ndry HTN?
oral contraceptives, NSAIDs, sympathomimetics, illicit drugs
resistant hypertension and unexplained hypokalemia
primary hyperaldosteronism
Isolated diastolic HTN?
indications for Lasix?
Usually used to treat edema, CHF, etc. and decrease in BP is more of a 2ndry effect.
why is hypokalemia no-so-good?
It will predispose the pt to ventricular arrhythmias.
What CCBs are best for treatment of hypertension?

Which are best for angina or cardiac dysrhythmias?
Dihydropyridines: amlodipine, nifedipine & felodipine

Verapamil and diltiazem

One thing to note is that reflex tachycardia is common with the dihydropyridines and pairing them with a B-blocker is a good method for keeping this to a minimum (but you'd better not even think about combining one with verapamil or diltiazem). Also, the fast-acting dihydropyridines are SO '90s (and also SO deadly).
ACEs and ARBs beneficial effects (4)
  • prevent vasoconstrion
  • decrease smooth and cardiac muscle hypertrophy
  • reduce aldosterone secretion
  • reduce production of reactive oxygen species known to decrease the dilating impact of endothelial factors
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