Flashcards in Things to Remember Deck (55):
Cardiac tamponade sign where you have an accentuation/exaggeration of the normal drop in BP during inspiration to >10 mm Hg bc less blood to heart and less filling from inspiration and also tamponade pushing in on atria/ventricles
count heart beats and peripheral pulse rate doesn't match bc not every heart beat generates a strong peripheral beat bc not long enough time for diastolic filling in Afib
Pulsus Parvus et Tardus
Slow and Late Pulse associated with Aortic Stenosis bc harder to get aortic pressures up
HOCM and AR !!! Double beating arterial pulse bc squeeze a lot out initially and rapid rise in aortic pressure but then blood quickly bounces back and re-raises pressure again a little - returning waves from periphery
In Dilated Cardiomyopathy, how can you tell difference between Cardiogenic etiology and Volume overload etiology?
Poor pump = low EF
Volume overload = good EF
What EKG leads do you check to see if sinus rhythm?
P axis on Limb Lead I and avF p waves need to be upright from SA node
How do you count HR in EKG?
take 300 and divide by number of big boxes
normal is 3 (100 bpm) to 5 (60 bpm)
How would you see an LAD infarct on EKG?
Precordial leads V1-V5 and shows anterior wall infarct
How would you see a RCA infarct on EKG?
Leads 2, 3, avF and means Inferior wall infarct
How would you see a Left Circumflex infarct on EKG?
Leads I, avL and V6 and shows lateral wall infarct
What is a normal PR interval?
3-5 small blockes = 120-200 msec
What is First degree AV block?
PR interval longer than 5 blocks >.2 sec and slow conduction
What are the 2 types of Second degree AV block and how can you distinguish them?
Mobitz 1 - Weinkeback = PR widens prior to dropping a QRS
Mobitz 2 - PR unchanging and suddenly missing QRS ( worse)
What is 3rd degree AV block?
complete heart block where P wave completely divorced from QRS
Symptoms/Exam findings for Mitral Stenosis
Caused from Rhuematic Heart Disease and see Fish mouth fused commissures and hockey stick appearance to valves on Echo
Symptoms arise from increased pressure gradient from LA and LV - like CHF and increased Atrial pressure is the cause! Can get RHF and pulmonary edema
Signs are mitral facies, Loud P2 as mitral slams shut, RV heave from dilatoin, Large A wave in JVP
Auscultation - opening snap!!! Diastolic low pitched rumble murmur with presystolic accentuation and Loud S1 when it shuts
Radiology LAE - see double density, upliting L main bronchus, and enlarged posterior area on lateral
Tx - control HR - allow more diastolic filling, Diureses (less volume) manage Atrial Fibrillation
Symptoms, cause, clinical findings treatment etc for Mitral Regurgitation
Cause - valve pathology (ex papillary rupture or myxomatous) or LV dilation
Acute - BAD - rupture, endocarditis, trauma and no time to dilate so pulmonary edema!
Patho- LA dilation, reduced outflow, LV dilation (both get big) leading to LHF and see good EF
1) Holosystolic murmur high intensity
2) S3 "Slushing In" extra volume reverberating
3) Hyperdynamic apex with thrill to back and axilla
Tx- AFterload reduction!!!
usually asymptomatic but can see palpitations, chest pain, fatigue syncope - REgurgitation!
posterior valve leaflestts enalred, change collagen, myomatous material, Marfans
Mid to late systolic click and late systolic murmur and changes with manuver
Bicuspid, Senile, Rheumatic
thicker hypertrophic ventricle with increased pressure - like systemic HTN = Concentric LV hypertrophy = CHF and Angina
CHF bc high diastolic pressure
Get HF, Syncope and angina!!!! (cant increase CO with exercise - syncope on exertion) can get arrhythmias
1) Crescendo-decrescendo systolic flow murmur
2) Ejection Click - bicuspid valve after S1 opening of aortic
3) Pulsus Parvus et Tardus harder to raise aortic pressure
4) S4 gallop = "A stiff wall" bc atrial kick onto stiff wall
Bicuspid valve - accellerated degeneration process and likely to see aoric dilation, aneurism and disssection
Valve leaky from congenital, rhumatic, endoc OR Root dilation from dissection or syphilis or marphans
Chronic AR - Wide Pulse Pressure!!!!! eccentric LVH changes in caivty side and wall stress -- results in CHF and angina
1) wide PP - head bob, uvula etc
3) early diastolic high pitched blowing decrescendo murmur
3) Pulsus Bisferience (like HOCM) 2 beats in periphery
Acute - emergency and massive pulmonary edema, no wide PP - same volume overload but no dilation
Treatment - Diuretics - decrase diastolic in ventricle to stop flooding lungs and AFterload decreasing to encourage forward flow
AS vs AR
AS - pressure overload and systolic problem - LV hypertrophy
AR - volume overload and diastolic problem - LV dilation
Drugs to use for HTN in pregnancy
MethylDopa!!!! (central A2 agonist that doesnt change CO to placenta)
Hydralazine - for preecclampsia
Only 1 beta blocker - lobatolol?
when do you hear S3?
vibration of a distended ventrile during filling "from volume overload in CHF or MR"
whats the first step and subsequent steps in atheroma formation?
LDL OXIDATION!!! then endothelial dysfunction then monocyte activation and VCAM1 to recruit them to eat the LDL and create foam cells that then cause SM proliferation and creation of plaqe
What drugs cause INCREASED mortality after MI?
Class Ic propafenone and flecanide - only used for VTACh or SVT
positive inotrope that has high toxicity but when used at lower levels increases parasympathatic responses and slows HR but can lead to AV block if already have bradycardia
How do Fibrates work? what are tey?
act tio DECREASE TG by increasing LPL through PPAR
What do you do to treat salycylate OD?
Urine Trap with Bicarbonate!
How do you treat Iron overload?
what is reverse use dependence?
K+ channel blockers (Class 3) bind better and Prolong QT more in bradycardia and slower rhythms so pace people to keep HR up
how do you treat torsade?
regular - irregular 300 bpm with 2-4 conduction
GIVE BB/CCB/Dig for rate control
no heart disease can use 1c or 3
Use Rhythm control when rate control doesnt work OR on bypass tracts (class 3 or class 1c if no heart damage)
SE Asian men (sleep like women at night)
Na channel deficit LONG QT3 bc they die in their sleep
What should you DEFINITELY use CCB for?
Prinzmetals!!! coronary spasm use DHP long term
What is Ritrodine?
Beta 2 agonist used for tocolysis to relax sm
What should you not give in WPW?
BB, CCB, Dig - nothing to slow AV node!
Long QT 2?
Herg Channel - die in emotional or startle OR drug induced
Die in exercise - pool
Die in sleep
2 drugs taht can give lupus?
A2 and insulin and clonidine
Clonidine is an A2 agonist and so will decrease insulin release
Statins - Discuss
Decrease LDL and cholesterol - INCREASE LDLR and decrease Isoprenylation of proteins and inflammation
GIVE WITH CoQ10 for Ubiquinone
Side Effects = Hepatitis, Rhadmyalisis/Myositis, Teratogenic, Polyneuropathy
CYPS reaction so don't give with Warfairin or CCBs or Clopidogrel
Bile Resins - discuss
Cholestyramine and they block reuptrake of bile acids and so then get activation of FXR which acts to increase Bile Acid PRoduction
Stop cholesterol uptake!
NPC1L - take up plant sterol and cholesterol
sitosterolemia blocks ABCG5/8 so hyperabsorption
receptor on fat cells to stop lypolysis and decrase FFA and TG syntehstsis and decrease LDL/VLDL and increase ApoA thereofre less THa nd increase HDL
BUT causes GI distress, liver problems, flush -- beta arrestin pathway
Gemfibrozil and Fenofibrate
Decrese TG and Increase HDL with PPAR to decrease LPL and ApoC to increase lipolysis
Stopes PDE and stops platelets
When do you not use prasugrel?
Prior stroke, >75 or low weight
what GP2a3b agents are there and when do you use them?
Abciximab, Tirofiban and Eptifiatide
use for PCI so like UA and NSETMI
LDL receptor defect or polygenic
Xanthomas and corneal arcus
Familial Combined Hyperlipidemia
RRD Remnant Removal Disease = Type 3 Hyperlipidemia
ApoE 2 cant take up IDL from liver and lots of remantns - YELLOW PALMAR STREAKS and xanthomas
lots of VLDL and increased TG
CeTP makes it so when more FFA and TG then added to decraese HDL and excreted and increase LDL so smaller and denser and can oxidze easier/greater affinity for monocytes
NO LPL!!! so increase VLDL and TG
Tangeers = no ABCA1 so increased cholesterol in macrophages bc not going to APOa1 and yellow throwat
or bad LCAT and so CE in HDL free and goes to eyes and kidneys - EYES AND KINDEYS
= TC - HDL - TG/5