Atrial & Venous Disease Flashcards

1
Q

normal BP response on standing

A

upon standing, 500-1000mL of blood pools in legs/abdomen –> 5-10mmHg fall in SBP –> compensatory reflex by baroreceptors and medulla oblongata –> pulse increases 10-25bpm

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2
Q

orthostatic hypotension

A

significant reduction in BP upon standing

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3
Q

etiology of orthostatic hypotension

A

-neurogenic
-non-neurogenic
-40% idiopathic

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4
Q

neurogenic etiology of orthostatic hypotension

A

baroreflex dysfxn d/t Parkinson’s, Lewy Body Dementia, DM, Age

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5
Q

non-neurogenic etiology of orthostatic hypotension

A

-volume depletion (diuretics, hyperglycemia, V/D, hemorrhage)
-adverse medication effects (Beta blockers, TCAs)

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6
Q

meds that can induce orthostatic hypotension,

A

antihypertensives (incl diuretics)
vasodilators (nitrates)
alpha-blocking agents (terazosin, doxazosin, prazosin)
AD (TCAs, SSRIs, MAOIs)
Atypical AP
PD drugs (Levodopa)
PDE-5 inhibitors

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7
Q

orthostatic hypotension epidemiology

A

25% of pts >65yo

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8
Q

Sx of orthostatic hypotension

A

*occur upon standing or w/ prolonged standing; also w/ exertion or after meals (blood drawn to GI)

-weakness
-dizzy/lightheadedness
-blurry/darkened vision
-posterior neck pain/HA (“coat-hanger HA”)
-syncope

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9
Q

Signs (PE) of orthostatic hypotension

A

5 minutes supine, take BP; stand 2-5 minutes then repeat BP
*reduction of 20mmHg+ SBP or 10mmHg+ DBP

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10
Q

dx tests for orthostatic hypotension

A

-EKG
-HCT, electrolytes, BUN, Cr, glucose
-Plasma norepinephrine level can guide med selection

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11
Q

Tx of orthostatic hypotension

A

-d/c exacerbating meds (if able to)
-non-pharm: increase salt & water intake (risky if pt has HTN), modify daily activities, diet, body positioning, compression stocking & abdominal binder
-if not improved or partially improved start med

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12
Q

POTS

A

*postural orthostatic tachycardia syndrome
-MC in younger to middle age females
-tachycardia, lightheaded/dizzy, and palpitations on standing; chronic fatigue, anxiety

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13
Q

vasovagal hypotension

A

acute, transient hypotension d/t particular triggers (emotional distress, pain, heat)
-increase in sympNS which is overcompensated by increased parasympNS –> syncope

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14
Q

what is the MC cause of syncope across all ages

A

vasovagal hypotension

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14
Q

vasovagal hypotension sx

A

prodrome:
-dizziness
-epigastric pain or nausea
-palpitations
-blurry or dark vision

post-syncope fatigue is common

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14
Q

PE for vasovagal hypotension
*if syncopal episode occurred do full syncope workup

A

-orthostatic vital signs
-check for neurological deficits

CV exam:
-delayed carotid upstroke (AV stenosis)
-abnormal PMI or S3 (cardiomyopathy)
-irregular or bradycardic rhythm
-midsystolic murmur (aortic stenosis, HCM)
-Holosystolic murmur (mitral regurgitation)

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14
Q

diagnostic tests for vasovagal hypotension

A

EKG - usually normal if vasovagal is the cause (BBB, Q waves, LVH, long QT, delta waves suggest something much worse)

Other tests:
-if suspicious of cardiac causes order echo, coronary angiography, stress EKG, holter monitor
-if suspicious of neurologic causes order brain CT or MRI, carotid doppler, EEG

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14
Q

Tx of vasovagal hypotension

A

*no tx consistently prevents vasovagal syncope
-d/c or minimize meds that may induce volume depletion
-avoid triggers
-drink lots of fluids (1.5-3L daily)
-6-10g Na daily
-compression garments (stocking, abd binder)
-counterpressure maneuvers (leg crossing w/ tensing of leg, abd, and butt; handgrip; arm tensing)

15
Q

orthostatic hypotension v. vasovagal hypotension

A

Orthostatic hypotension:
-elderly
-chronic
-BP regularly decreases upon standing

Vasovagal hypotension:
-younger, healthy
-likely to improve spontaneously
-stress, pain, heat cause hypotension

16
Q

Printzmetal’s Angina (vasospastic angina)

A

-spasm of smooth m. layer of a coronary a., resulting in high-grade obstruction, potentially cardiac arrest

17
Q

Does Printzmetal’s angina always occur at site of atherosclerotic plaque?

A

No, commonly it does but it can also occur in (angiographically) normal coronaries

18
Q

does Printzmetal’s angina occur with or without exertion?

A

it can occur w/ or w/o an increase in myocardial oxygen demand

19
Q

Unstable angina vs. Printzmetal’s angina

A

Unstable angina typically lasts longer and can result in cardiac damage

-both can occur with or without exertion

20
Q

Printzmetal’s angina RF

A

CIGARETTE SMOKING
genetics
insulin resistance (diabetes)
recreational drug use (cocaine)

21
Q

Sx of Printzmetal’s angina

A

-identical to “typical” angina (chest pressure) but context of pain is different
-occurs predominantly AT REST (midnight-early AM is MC)
-episodes last 5-15mins (STEMI angina is >15min)

Sx:
tachycardia, HTN, diaphoresis
**bradycardia & hypotension may be present if sinus nodal, AV nodal, and R ventricle arteries (r coronary) are involved

22
Q

Printzmetal’s angina: PE & Dx

A

-no specific PE or dx tests (troponin should be normal bc Printzmetal doesn’t typ last long enough to cause cell death)
-EKG is usu normal btwn episodes (if during an acute episode, maybe transient ST elevation or depression in multiple leads)
-If EKG is normal do exercise stress test
-If stress test is normal, do coronary angiography

23
Q

Printzmetal angina: Tx

A

-sublingual NTG prn
-smoking cessation
-CCB to promote vasodilation (Diltiazem or amlodipine)

24
Q

Drugs to avoid in a pt w/ Printzmetal angina

A

-nonselective B-blockers (propanolol)(exacerbates vasospasm if it blocks B2 receptors)
-high doses of prostacyclin inhibitors (ASA - blocks COX-2, prostaglandin, and prostacyclin)(prostacyclin induces vasodilation so we don’t want to block that!)
-Triptans (cause vasoconstriction, used in tx of migraines)
-5-FU (fluorouracil)(chemo)

25
Q

Varicose veins

A

-visibly dilated, tortuous LE veins that permit reverse flow of blood

26
Q

Venous HTN caused by one of 3 things:

A
  1. valvular incompetence - collagen failure
  2. obstruction - thromboses, anatomy
  3. calf-muscle pump failure - anything that promotes immobility (age, stroke, neuromuscular conditions, arthritis, trauma)
27
Q

Varicose Veins: RF

A

FH
female
increased age
pregnancy (current or multiple) - typ temporary
standing for long periods
obesity
hx of DVT

28
Q

varicose veins sx

A

may be asymptomatic or cause aching, swelling or “heaviness”

29
Q

signs of varicose veins

A

-spider veins (flat)(early signs)
-bulging, blue veins of LE
-more severe dz, pt may have skin color changes d/t degraded Hgb (degraded from fluid/pressure build up), may even have weeping &/or ulcers

30
Q

Varicose veins: Dx

A

usu clinical
can use US to guide tx

31
Q

Varicose vein Tx

A

initial tx is conservation (elevation, exercise, and compression therapy)
-if sx persist, then may be candidate for superficial venous ablation

32
Q

phlebitis

A

inflammation of a vein

33
Q

thrombophlebitis

A

inflammation of a vein d/t a thrombus (clot)

34
Q

RF of thrombophlebitis

A

-varicose veins
-abnormal coagulation
-malignancy
-infection
-venous stasis (bad valves -> pooling, sim to varicose v.)
-IV therapy
-IV drug abuse

35
Q

Presentation of thrombophlebitis

A

-tenderness, induration (firmness), and erythema along the known course of a superficial v.
-involved v. could be an inch below the surface of normal-appearing skin (esp in obese pts)

36
Q

phlebitis vs. cellulitis vs. “red streaking” (don’t need to know)

A

Phlebitis: inflammation along v., not necessarily an infection

Cellulitis: spreads like a blanket, is an infection tx w/ Abx, lots of swelling

“Red streaking”: lymphangitis, determined through pt hx (typ of a dirty, invasive wound), typ true infection so would likely have a fever & high WBC

37
Q

Thrombophlebitis: Dx tests

A

Perform US if:
-you suspect a thrombosis (clot) of the great saphenous or small saphenous veins (because it can embolize and travel into femoral v. and up to the lungs -> PE)
-there is LE swelling that’s greater than would be expected from thrombophlebitis alone
-evidence of clinical progression during a period f/u

*remember femoral v. dumps into great saphenous v., travels medially down leg behind the knee to become the popliteal vein and then branches into small saphenous v. that travels posteriorly down the calf)

38
Q

Thrombophlebitis: Tx

A

-symptomatic care: elevate LE, warm or cool compress (whichever feels better), compression stockings, pain management (NSAIDs)
-repeat PE w/in 7-10 days
-AC based on pt risk

39
Q

if the pt has a clot in the great saphenous vein near the femoral vein (upper third of thigh) should you start the pt on AC?

A

yes, to reduce risk of PE

40
Q

Thrombophlebitis: VTE risk flowchart

A

Superficial VTE –> r/o DVT/PE –> distance from saphenofemoral junction & thrombosis RFs & length of clot will determine tx (therapeutic AC x6wks vs. prophylactic AC x2-6wks vs. no tx)