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Warfarin Excess
- INR > 10 and not bleeding: Vitamin K at least 3mg S/Q or slow IV.
- INR > 10 and bleeding: Vitamin K 10mg slowly IV, fresh frozen plasma 15ml/kg,
optionally also add 50 units of prothrombin complex concentrate.
Basic
- cardiac
cycle.pdf
- axes: 0.2s horizontal blocks, 0.5mv vertically
- Rate: 300, 150, 100, 75, 60, 50 (pacemakers atria 75, AVN 60, Vent 30-40)
- Rhythm: PR 0.11-0.22, QRS < 0.1, normal QT is 0.4*RRinterval
- Axis: QRS above I, AVG
- Hypertrophy in V1: P < 0.11, R wave for RVH, V1 S wave + V5 R wave > 35mm ->
LVH
- Infarction: Q in absence of LBBB - > 0.4s or greater than 1/3 of QRS
in lead III, inverted T, elevated ST (if also elevated T then suspect pericarditis).
Following localizations are somewhat unreliable, vascularity varies greatly:
- anterior (anterior descending branch of left coronary artery): Q in V1-V4
- lateral (circumflex branch of left coronary artery): Q in I and AVL
- posterior (posterior descending artery, usually off right coronary): large R in V1,
significant Q wave in V6, R/S ratio >= 1 in V2
- inferior (variable, may be right or left or both coronary arteries): Q in II, III, AVF
Pediatric (esp. < 8 yo)
- see Harriet-Lane Handbook
- T wave may always be inverted in V5-V6, even by age 5 may have inversion in V1-V2.
Before age 5 may have R > S in V1. Adult pattern emerges @ age 5-8.
Rhythm
- Washington
Manual
- Varying: sinus (sick sinus syndrome), wandering, atrial fib
- Extra: paroxysmal (atrial, nodal, ventricular), atrial flutter,
ventricular flutter, atrial fib, vfib, pvc
WPW or Wolff-Parkinson-White
- accessory bundle of Kent -> ventricular pre-excitation, shortened PR and longer
appearing QRS, delta wave swoop (nike) between P and QRS.
- Most common tachycardia has narrow QRS, but may have rate-related BBB with wider QRS.
Major risk is that AFib may induce VFib in pts with WPW since auxiliary pathway doesn't
block. Usual pattern is orthodromic -- antegrade through AV node, retrograde through
accessory pathway.
- familial variant has no gender predominance, sporadic 2:1 male
- 7-20% have Ebstein's
anomaly (tricuspid valve malformation) or other defect
- Cannot interpret exercise stress test and thallium scan can have false positive,
difficult to assess symptoms.
- Usually refer to cardiologist, treat if symptomatic with arrhythmias. Radiofrequency
ablation is @85% successful, EKG normalizes.
Block
- SA: miss 1-2 cycle but return in step
- AV block
- Primary: PR more than 0.2 second
- Secondary (2:1, 3:1, 4:1, etc)
- Mobitz Type I (Wenckebach): PR progressively increases then drop QRS
- Mobitz Type II: drop QRS abruptly -- greater risk of complete block.
- Complete: ventricular pacemaker gives erratic rate of 20-40
- BBB QRS > 0.11s, cannot assess for LVH, if LBBB cannot assess for Q
wave.
- RBBB: rabbit ears -- RsR' in V1 or V3, wide S in V5-V6
- LBBB: mountain -- RR' in V5 or V6, wide S in V1-V2
Miscellaneous
- large pulmonary infarction RV strain/ischemia pattern: S1Q3, inverted T
waves V1-V4, ST depressed II, transient RBBB
- LV aneurysm: anteroseptal infarct on EKG with persistent ST elevation.
- electrolytes: U wave with low K, short QT with high Ca, long QT with low Ca
- dig toxicity
- short QT, inverted T
- PAT with block (>1 P for each QRS), AV block, multifocal tachycardia
- quinidine: long QT syndrome/roller coaster
Valsalva test
- 90% specific, useful if suspect CHF but not confident enough to order ECHO.
- inflate cuff to 15mm above systolic then pt performs Valsalva
- Positive findings: maintain beats throughout Valsalva (abnormal persistence of increased
BP) and failure of beats to reappear after Valsalva ended (but cuff still on; BP once down
fails to jump up again)
Physiology
- volume depletion -> incr renin & decr renal perfusion -> incr Cr, BUN and
SIADH -> hyponatremia. If add ACE may get sudden decr BP.
- hyponatremia is marker for hi renin state and poor prognosis. Rx with ACE over 8 days.
Watch for incr K, BUN, Cr. in this setting. Alternative is hydralazine
Activity and Symptoms: In class IV failure
- activity > decr. renal perfusion > incr. Na/fluid retention >
increased failure sx.
- good day followed by bad days due to overactivity.
- titrate diuretics and teach adjusting of activity/meds/diet.
Therapies
- Angiotensin II receptor blockers (Teveten/eprosartan, Micardis/telmisartan,
Cozaar/losartan, Diovan/valsartan and about a hundred other "sartans") may be of
use, studies pending.
Systolic failure
Desired BP with CHF: sysolic 110. Desire minimal orthostatic Sx if pt class IV.
- ACE inhibitors (first line)
- digoxin for symptomatic relief (fatigue)
- has 2 phase distribution: may be best given in evening and levels done in am.
- diuretic for symptomatic relief (congestion), thiazide 2-3 times/week for mild CHF,
otherwise avoid diuretics if mild
- beta blockers (not class IV) - carvedilol (Coreg) is a now popular beta blocker/alpha-1
antagonist added to ACE, digoxin, diuretics. usually can't go above 12.5 mg BID. Can cause
fluid retention, require more diuretics.
- spironolactone (aldosterone receptor antagonist): one large good study showed major
benefit in class III/IV when added to ACE inhibitor. 12.5-25 mg qD. Significant
hyperkalemia risk. Note Indocin and other NSAIDs can increase K.
- older: isordil (160 mg) + hydralazine (300 mg) -- titrate to target dose
- fluid restriction: 1500 ml/day (old?)
Diastolic Failure
- if CHF and EF on U/S > 40% Rx as diastolic
- avoid digoxin (contrary to old habits)
- ACE, cardevilol, spironolactone? maybe diuretic
- fasting serum homocysteine of 12 umol/l -> odds ratio 4.8
- can also do 4 hour methionine load test if IHD without other risk factors
- Rx. with 1 mg of folic acid day
Urgent Care Evaluation: New BP Elevation
- NSAID, other meds
- fundi, heart
- Cr, K, Uric, BUN, Na, Glu
- EKG, CXR
Supplemental Hypotensive agents
- OS Cal 800 mg qD
- Micro K 30-40 mEq Daily
Diet
- low salt
- regular salt + Ca blocker?
Special cases
- age < 40: ternormin
- difficult HTN in younger person: prazosin/doxazosin + diuretic
- older: diuretic
- alcoholic, tobacco addict: clonidine
- NSAIDS (block many agents)
- greatest increase in BP: indocin, naprosyn, piroxicam
- least incr in BP: ibuprofen, aspirin, sulindac
- (3)
- supplement, esp. renin dependent: clonidine
- resistant HTN
- tenormin or lopressor + HCTZ + Hydralazine (<200 mg/day)
- lopressor or labetolol + Lasix + Minoxodil
NHLBI Guidelines
- Hyperlipidemia
The NHLBI Guidelines page
has the best references, but in general the "guidelines" on hyperlipidemia are
confusing. A better approach would be to use a risk factor calculator to
estimate a 10 year risk of ischemic event, then base interventions on a risk benefit model
adjusted for age (years of life gained). In general incorporation of age and family
history isn't handled very elegantly by the current guidelines. (If I get time, maybe I'll
write a paper on this!)
The guidelines are really written for persons < 65 yo (to some extent, age 45-65). For
persons older than 65 there's a serious "clinical judgement" component.
- risk factors
As of 2/2003 I suspect obesity will eventually be incorporated as an independent risk
factor, perhaps expressed as abdominal girth parameters. My other hunch is that peripheral
testosterone activity will one day be considered a finer disriminant risk factor than
gender. Xanthelasmas and xanthomas aren't formally part of risk factor assessment, but in
the presence of elevated triglycerides they should probably prompt testing for a familial
hyperlipidemia disorder and may indicated more aggressive therapy. Homocystine levels are
falling out of favor as unoficial risk factors.
- HDL < 40 (used to be < 35)
- Hypertension
- Family History
CHD in 1st degree male relative age < 55, female age <65
- Smoking
- Age
men < 45, women < 55
- Goals
LDL < 100 is desired universally. Initiate dietary therapy when exceed the goal level
(but this almost always fails, or only works for a year or two). The gap between
initiating dietary therapy vs. initiating drug therapy is a cost/benefit issue. The meds
have more known toxicity than diet, and we can be sure that not all the long term
toxicities (or benefits) are fully known. Presumably if the meds were 100% safe and
totally free there would be no diet/drug "gap". Clinical judgement (assess
individual risk factors for drug side-effects, consider informal risk factors such as
abdominal girth, etc) may operate within this "gap", but doing nothing is
certainly supported, perhaps along with yearly monitoring.
Note that all the recommendations are really optimized for patients age 45-65, outside
that range things are trickier.
- 0-1 risk factors
- Diet if > 160
- Drugs if > 190
if 10 year risk is > 10% using risk calculatory, I'd say use drugs when LDL > 160
- 2 or more risk factors
All men over age 45 and women over 55 have one risk factor, and most of this population
with LDL > 130 will also have HDL < 40. So most healthy men with good lifestyles and
elevated lipids over age 45 fall into this group.
A 10 year risk calculation is
used to guide interventions, so it makes more sense to just use the Framingham Risk
Calculator approach from the start!. As age increases the point at which to initiate drug
therapy falls, though one may mitigate the decision based on estimates of drug toxicity,
drug interactions, etc. Since the risk calculators just work off risk factors, and since
these goals also incorporate risk factors, this could probably have been more simply
expressed as a age-cutoff.
- diet if > 130
- 10 year risk > 10%: drugs at > 130
- 10 year risk < 10%: drugs at > 160
- CHD/Diabetes, lots of risk factors
- diet if > 100
- drugs if > 100-130
- Some comments on therapy
- Hyperlipidemia and Dementia
There may be a significant relationship between cellular cholesterol metabolism and
Alzheimer's. There is a relationship between vascular disease and dementia. It is not
known whether treating hyperlipidemia with a statin reduces or increases one's risk of
Alzheimer's disease or other dementias.
- ASA 75 mg/qD for 5 year risk of at least 3%
General Guidelines
These are old. As of 2003 it's statins all the way, and their effect is only partly due
to lowering LDL.
- Beware drug interactions and pregnancy
- Many require monitoring of CBC, LFT, a few CK. Typically q2-6 months.
- Beware muscle pain. It's not clear that we fully understand the effect of statins on
muscles, and, incidentally, on the CNS.
Names and classes
Bile Acid Sequestrants
Expensive, taste awful, GI problems, cause vit K and folate deficiency (beware use with
Coumadin). Give with vitamins. Must mix with juice.
- Cholestyramine: Cholybar, Questran, Questran Light.
Try: Questran Lite, 2 scoops in 8 oz water by bedside. Take before bedtime.
- Colestipol: Colestid (monitor LFT, CBC)
HMG CoA Reductase Inhibitors (Statins)
Give with evening meal or at bedtime.
Monitor LFTs +/- CK q6w fo 3 mo, then q8w for 1st year then q6months.
Avoid use with erythromycin, warfarin
Triglyceride Metabolism Modifiers
Nicotinic Acid (Niacin)
Do not substitute, avoid sustained release preparations. Rarely used any more. Very
poorly tolerated.
- GI upset, rash, hepatoxic, increased glucose and urea
- ASA 325 mg qD will decrease flushing
- a niacin dose of less than 1000 mg total daily is not worth continuing
- regimen: 100 mg and 500 mg tabs available
- 100 mg BID x 1 wk
- 200 mg BID x 1 wk
- 300 mg BID x 1 wk
- 500 mg BID x 1 wk (check chem 26, +/- CK)
- 1000 mg BID (ck chem 26 in 6 weeks, aim for 750-1000mg BID)
- monitor LFT, glucose +/- CK
Fibric Acids
Lopid (gemfibrozil). Very rarely used.
- gallstones, rhabdomyolysis with Mevacor
- need low HDL-cholesterol, elevated LDL-cholesterol, and elevated triglycerides to merit
use (per Parke-Davis and FDA)
- baseline LFT then q6-12 months
Dangerous Combinations
- mevacor and lopid (rhabdomyolysis)
- mevacor and niacin (maybe muscle injury)
Effective Combinations
(These are old combinations.)
- lower the LDL: Questran and Niacin or Questran and Mevacor
- lower TRIG: Lopid and Niacin (watch LFTs!)
- Niacin and Colestid
- Lopid and Colestid
- Mevacor and Colestid
Dosages
- Niacin: 3-12 gm qD
- Questran or Questran Light
- 5 gm = 1 packet = 1 scoop
- 1-6 times per Day (TID)
- Colestid
- 5 gm = 1 packet = 1 scoop
- 3-6 times per Day (TID)
- Lopid
- 600 mg, 1 tab 30 minutes before breakfast and supper
Markers
- myoglobin: early marker, can be used in d/dx in ED
- troponin I or T: Become elevated in 3-12 hours, remain elevated 7-10 days. Can show a
recent MI has occurred. Elevation related to worse prognosis. Has largely replaced CK-MB.
afterload and preload reduction: HTN, pulmonary edema
a) intravenous medications:
- NTG: IV 0.2 -20 mcg/kg/min; esp. dec PL, less dec AL. Good if angina.
- NIPRIDE: IV 0.5-10 mcg/kg/min; esp. dec AL, less dec PL. (check thiocynate levels) Onset
3s, durn 3m.
- diazoxide: 50-150 mg IV q5m or 7.5-30 mg/min (onset 5m, durn 4-24h); esp dec AL. Do not
need art line, often with beta-blocker and diuretic. (reflex inc HR). Dangerous if aortic
dissection, angina, MI. Always give with strong diuretic.
- isosorbide dinitrate 3mg bolus IV q5min has been used in some trials for acute pulmonary
edema with improved results (1998)
b) oral medications (or both)
- captopril 6.5-13 mg PO q8h. onset 15m; durn 4-6h. Sublingual Captopril 12.5 repeat in 60
minutes is being used @1997.
- prazosin: 2-5 mg PO q6h; balanced dec PL and AL.
- terazosin
- good with BPH
- less s/e than prazosin
- doxazosin
- good with BPH
- less s/e than prazosin
- hydralazine: 50-100 mg PO q6h or 10-20 mg IV (onset 10-30 min, durn 2-4 h); esp dec AL,
often use with beta blocker (reflex tach).
management of hypertension (not preload/afterload)
a) labetolol (Trandate, Normodyne)
- initial dose 20 mg IV then 20-40 mg q10-30 minutes to pressure better or max 300 mg
- IV infusion: 200 mg in 200 ml D5 at 2 mg/min (stop when BP ok)
- Onset 10-30 min, durn. 3-6h. May continue PO.
b) propranolol: beta block; 1-10 mg IV then 3 mg/hr. Total blockade with 0.1 mg/kg. PO
80-640 mg qD; onset 2h durn 12h.
inotropes and vasopressors
a) DOPAMINE: beta 1 and alpha. typical use 500-1500 mcg/min. At 2-5 mcg/kg/min may have
renal vasodilatation (renal dose), at > 15 mcg/kg/min effect is predominantly alpha
(vasoconstriction). Esp. good for septic shock. (dopamine = norepinephrine + dobutamine)
b) DOBUTAMINE: beta 1 >> beta 2. typical use 800-2000 mcg/min. In range 5-15
mcg/kg/min greatest affect on CO, small chg PVR (up or down). Esp. for cardiogenic shock,
CHF, post MI.
- physiology: abnormal pressure + norepinephrine > increased
trophic hormone release from vessel wall > macrophage migration into endothelium
> macrophage uptake of small LDL (oxidized, hyrolyzed) > fatty
deposition of obese macrophages and vessel wall damage.
- keep diabetic BP < 120/80
- use qD meds at bedtime
- NAS diet: 2 gm/day
- favored BP meds (lipid effects)
- clonidine TTS
- ACE inhibitors
- alpha blocker: doxazosin
General
Mitral Valve Regurgitation
Author: John G. Faughnan.
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