CV- FA Flashcards
C-ANCA targets what? what about P-ANCA?
C-ANCA: neutrophil proteniase 3
P-ANCA: neutrophil myeloperoxidase
weak pulse, fever, night sweats, myalgia, ocular disturbances. Diagnosis?
Takayasu
- Takayasu: PULSLESS disease
Rapid acting beta blokcer?
esmolol
Brugada syndrome
- inheritance pattern
- most commonly affected group
- ECG findings
- autosomal dominant
- asian male
- ST elevation on V1-V3, pseudo right bundle branch block
Aortic stenosis vs. Aortic regurgitation: at which location is murmur heard?
- AS: aortic area, RIGHT 2nd intercoastal
- AR: LEFT sternal border, 3rd/4th intercoastal
- this rule applies same for PS and PR
- PS: pulmonic area, LEFT 2nd intercoastal
- PR: left sternal border
Three heart manifestations of Marfan
- Aortic dissection
- Thoracic aortic aneurysm
- MVP
What is dextrocardia?
Heart in right side of chest
Kartgener syndrome
Ranolazine
- MOA
- indication
- major side effect
- inhibit late stage Na+ channel -> decrease wall tension, no effect on contractility or HR
- refractory angina
- QT prolongation
- BUT does NOT cause Torsades (this is UWORLD question)
BNP (B type natriuretic peptide)
- where is it released? in response to what?
- How is it used clinically
- What is name of recombinant form?
- BNP is released from VENTRICLE in response to increased VENTRICULAR TENSION (HF)
- BNP test can be used for HF diagnosis.
Very good NEGATIVE predictive value, meaning
negative BNP test means no HF (ruling out) - HF -> increased ventricular volume -> increased BNP
- Nesiritide (recombinant form) can be used for HF patient
- diuresis -> reduce congestion
MI diagnosis
- what is gold standard for first 6 hrs
- troponin I
- CK-MB
- ECG gold standard for first 6 hrs
- Troponin I: specific, peaks at 24 hrs, last 7-10 days
- CK-MB: less specific, peaks at 16-24 hrs, last only for two days => useful for re-infarction
Pt with osteopenia wants to avoid development of osteoporosis. what lipid lowering drug should be avoided?
cholestyramine
GI upset and malabsorption of fat soluble viatamins
-> less vitamin D -> less Ca2+ absorption
Kussmaul signs vs. Kussmaul respiration
- how is it different?
- example for each? 3 for Kussmaul signs and 1 for Kussmaul repisration
- Kussmaul sign: increase in JVP in respiration, meaning that there is defect in heart filling
=> constrictive heart pathology
1. pericarditis
2. cardiac temponade
3. RA or RV tumors (bulky tumors inhibiting filling) - Kussmaul respiration:
rapid/deep breathing= hyperventilation
seen in DKA
Three drugs that increase digoxin toxicity? by what mechanism?
- Quinidine
- Amiodarone
- Verapamil
Decrease renal clearance of digoxin
- Antiarrythmics; 1A, 3, 4
Hydralazine is co-administered with what drug? why?
to prevent reflex tachy, beta blocker is given
Contraindications for hydralazine? why?
angina and CAD
reflex tachy will overload heart
- hydralazine is normally indicated for
- hypertension
- HF
Triad of Cushing reaction? explain why
- hypertension
- bradycardia
- respiratory depression
increased ICP -> CNS vascular constriction
- > brain ischemia -> pCO2 -> central chemoreceptor to increase perfusion-> increased blood pressure
- > increased blood pressure sensed by baroreceptor
- > reflex bradycardia and respiratory depression
What cardiac condition show PR depression on ECG?
pericarditis (I have no fucking clue)
In pericarditis, widespread ST elevation will be also seen
Describe how cardiac output is changed over the course of exercise
- early phase
- late phase
- early phase: both HR and SV increases
- late phase: only HR is increased, while SV stays constant
- SV plateaus
What does inverted T wave on ECG mean?
recent MI
What two heart sounds are present in dilated cardiomyopathy? explain
- Systolic regurgitant murmur: dilated ventricle, blood flows back to atrium during systole
- S3: same reason of regurgitant murmur. Dilated ventricle, blood flows back to atrium during systole. In next round of filling, extra blood in atrium makes S3 sound
What causes closure of foramen ovale after birth?
increased LA pressure
Which two beta blockers are safe for treating pheocytochroma? Why?
carvedilol and labetalol
- these are non-selective alpha and beta blocker.
Other beta blockers are not safe for pheo, as selective beta blockade can result in unopposed alpha stimulation.
- Pheocytochroma is treated with alpha antagonist first (Phenoxybenzamine, irreversible alpha antagonist), followed by beta blocker (non-selective) to suppress reflex tachy
An infant is found to have a PDA and tetralogy of Fallot at birth. What treatment would you recommend until surgery is possible?
Prostaglandins E1 and E2 to keep PDA opened
=> Keeping PDA opened will reduce pulmonary stenosis effect in tetralogy of Fallot
*this is also true for transposition of great vessels. keeping PDA opened will allow communication between pulmonary artery and aortic artery.
Which class of antiarrhythmics can be used to treat digitalis (digoxin) induced arrythmia?
class 1B
- class 1B is also used for post MI ventricular arrythmia
Tricuspid pressure wave- x descent and y descent
- in which condition is X descent prominent? what about the condition where X descent is absent?
- in which condition is y descent prominent? what about the condition where y descent is absent?
- prominent x descent
1. tricuspid valve insufficiency: blood leaking into ventricle, more dramatic decrease in x descent
2. right HF: less RV pressure, more downward shift of tricuspid valve leaflet - absent x descent: tricuspid valve regurgitation
- prominent y descent: constrictive pericarditis
=> more squeezing, more RA emptying into RV - absent y descent: cardiac temponade
=> less RA blood initially, thus less RA emptying into RV
Familial hypertrophic cardiomyopathy
- inheritance pattern
- what gene is associated?
- autosmal dominant
- beta-myosin heavy chain mutation
cyanotic lower extremities, while upper extremities are normal. diagnosis?
PDA
: PDA inserts into aorta after 3 branches for upper extremities and brain
- this is called differential cyanosis
Ebstein anomaly: explain how tricuspid is messed up
tricuspid VALVE DISPLACEMENT
: valve leaflets DOWNWARD into RV, atrializing ventricle
Explain histologic finding on Buerger disease
segmental THROMBOSING vasculitis
- way to remember: another name for Buerger is thromboangitis obliterans. so THROBOSING
ECG finding of atrial fibrillation?
no p wave, irregular RR interval
FA p.278
Define Monckeberg sclerosis
calcification in MEDIA and INTERNAL ELASTIC LAMINA
intima NOT affected. Thus, NO OBSTRUCTION (clinically silent). just vascular stiffening.
X-ray: calcified blood vessels
Which pressure parameter is useful for estimating preload?
PCWP (also good indicator of LA pressure)
Which coronary arteries are susceptible to obstruction? ( from most likely to least likely) - circumflex - left anterior descending - right coronary artery
LAD >RCA > circumflex
- this makes sense: the bigger artery is, the more likely it is going to be obstructed.`
What two congenital heart defects are associated with DiGeorge syndrome?
- truncus arteriosus
- tetralogy of Fellot
Which nucleus of medulla receives vagus nerve signal from aortic baroreceptor?
solitary nucleus
What step in embryology is impaired in
- tetralogy of Fellot
- transposition of great vessels
- truncus arteriosus
- tetralogy of Fellot: deviation of intrafundibular septum
- transposition of great vessels: impaired spiraling of aorticopulmonary septum
- truncus arteriosus: absence of aorticopulmonary septum
List all vasculitis that show granuloma
- giant cell
- takayasu
- wegner (granulomatosis with polyangitis)
- churg-strauss (eosiniphilic granulomatosis with polyangitis)
- note that none of medium sized vasculitis (PAN, kawasaki, buerger) show granuloma
ECG finding in cardiac temponade?
low voltage QRS with electrical alterations (heart swinging within pericardial fluid)
Which ion can be infused to reverse digoxin toxicity?
Mg2+
Dihydropyridine (amlodipine) side effect on mouth?
gingival hyperplasia
What is direct effect of ANP on renal tubule?
it inhibits Na+ reabsorption
*also vasodilation in general
Compare order of pacemaker rates of
- SA node
- AV node
- bundle of His/Purkinje/ventricles
SA > AV> bundle of His/Purkinje/ventricles
- this is pacemaker rates, not conduction rate
- this makes sense that bundle of His/Purkinje/ventricles rarely (or very slowly) produce own pacemaker
Right sided HF may show what finding in physical exam?
hepatomegaly (nutmeg liver)
may also show cardiac cirrhosis (rare, extreme case)
In patient with aortic stenosis, how splitting is affected during inspiration?
aortic stenosis -> LEFT SIDE problem -> pardoxical
PARADOXICALLY, inspiration DECREASES split time
How does valvular defect changes in rheumatic fever over time?
early lesion: mitral regurgitation
late lesion: mitral stenosis (kinda like old and tear principle)
maternal diabetes. what congenital heart defect?
transposition of great vessels
What general condition results in decreased pulse pressure? examples (4)?
decreased blood pumped by LV
- aortic stenosis
- cadiogenic shock
- HF
- cardiac temponade
What condition results in increased pulse pressure? examples?
aortic regurgitation
blood flowing back during systole, resulting in great decrease in diastolic pressure
What is Williams syndrome? what congenital cardiac defect is associated with it?
“elfin” facial characteristics and exhibits an unusually cheerful demeanor
supravalvular aortic stenosis
ECG findings in
- subendocardial infarction
- transmural infarction
- subendocardial infarction: ST depression
- transmural infarction: ST elevation
How is cardiac contractility affected by metabolic acidosis?
decreased
- this makes sense: acidosis -> more H+ into cell, more K+ pumped out to cell -> prolonged hyperpolarized state
Patient with hypertension in upper extremities and weak pulses in lower extremieties. What imaging study will be helpful? why
chest x-ray for notched ribs
aortic coarctation -> blood back up and collateral arteris erdode ribs
Signs of atrial fib is noticed on ECG. What medication is promptly needed? why?
warfarin: LONG TERM anticoagulation
a fib, predisposes to cardiac embolism (stasis), which leads to systemic embolism (may be fatal embolic stroke)
most common infection in culture negative bacterial endocarditis?
coxiella burnetii (most common)
also HACEK H- Hemophilus A- Aggregatibacter C- Cardiobacterium E- Eikenella K- Kingella
How is pressure-volume loop is affected with increased contractility?
increased contractility means stronger squeezing force.
=> less ESV (end systolic volume)
first line for supraventricular tachy?
adenosine
Describe how VSD and MR/TR murmur is similar and different
BOTH are holocystolic murmur
MR/TR: high pitched, blowing murmur
VSD: harsh-sounding murmur
median umbilical ligament is derived from what prenatal structure? what about medial umbilical ligament?
mediaN umbilical ligament: derived from allaNtosis
mediaL umbilical ligament: derived from umbiLical artery
Which parts (2) of aorta is susceptible to calcification/ aneurysm?
- ascending aorta
- aortic arch
given systolic pressure and diastolic pressure, how to calculate MAP?
MAP= 1/3 systolic P + 2/3 diastolic P
Which type of cardiomyopathy is peripartum cardiomyopathy?
dilated cardiomyopathy
- peripartum: last month of pregnancy to up to 6 months postpartum
- think like this: womb gets dilated during pregnancy, so does heart
nucleus pulposus is derived from what embryological structure?
Notochord
- Notochord -> Nucleus pulposus
- nucleus pulposus is inner core of vertebral disc
patient with angina takes a vasodilator. How may this actually aggravate his ischemia?
coronary steal syndrome
: vasodilation shunts blood to well perfused area, reducing blood flow to post-stenotic region
- refer to note p.43
Which hematologic/GI disorder can cause both dilated and restrictive cardiomyopathy?
hemochromatosis
which beta blocker can cause dyslipidemia
metoprolol
What congenital heart defects are associated with alcohol exposure in utero?
- ASD
- VSD
- PDA
- tetralogy of Fallot
Which beta blocker should be avoided in prinzmetal angina? why?
propanolol
=> it may exacerbate vasospasm
verapamil vs. diltiazem: both are non-dihydropyridines. which one has more specificity to cardiac muscle?
verapamil
How does hypoxia/hypercapnia change heart contractility?
decrease
just like effect of acidosis
hypercapnea/hypoxia -> acidotic state
-> more K+ flux out of cell -> hyperpolarization
chest X-ray finding in tetralogy of Fellot?
boot shaped heart due to RV hypertrophy
Diastolic heart dysfunction: how below values get changed?
- EF (ejection fraction)
- EDV (End diastolic volume)
- EDP (End diastolic pressure)
- EF (ejection fraction): no change
- EDV (End diastolic volume): no change
- EDP (End diastolic pressure): increased
Which two heart valves are derived from the endocardial cushions of the outflow tract?
aortic and pulmonic
- focus on word OUTFLOW TRACT
Catchecoleamine increased HR by changing slope of which phase of pacemaker action potential?
phase 4, which gives automaticity through funny current
Aortic dissection: How to treat type A and type B differently?
type A: involve ascending aorta (also may be arch), needs surgery
type B: only involve descending aorta, sugery is not indicated. Just treat with B-blocker and then vasodilators (to reduce pressure that can further damage dissection)
Down syndrome: what congenital cardiac defect?
endocardial cushion defect
: ASD, VSD
widened S1/S2 split vs. fixed split: compare etiology
widened: delaying RV emptying- pulmonary stenosis, right bundle branch block
* unlike fixed, widened one still has more delayed splitting during inspiration.
fixed: ASD
*ASD is the only condition that gives S1/S2 split.
VSD is holocystolic murmur
Transposition of great vessels is incompatible with life unless
unless there are shunts present
- PDA, VSD, ASD, patent ovale
Location of infarct?
- V1-V2
- V3-V4
- V5-V6
- I, aVL
- II,III,aVF
- V7-V9
- V1-V2: LAD
- V3-V4: LAD (distal)
- V5-V6: LAD and LCX
- I, aVL: LCX
- II,III,aVF: RCA
- V7-V9: PDA
Four arteries most susceptible for artherosclerotic burden (most common to less common order)
abdominal aorta > coronary artery > popliteal > carotid
Edema and wavy fibers can be seen in histology how long after MI?
4-12 hrs
How exactly S.epidermis forms vegetation on prosthetic valves or IV catheters
biofilms
: EXTRACELLULAR POLYSACCHARIDE matrix
How exactly S. virdians form vegetation in subacute bacterial endocarditis?
DEXTRANS (from sucrose) binds to fibrin-platelet aggregates on PREVIOUSLY DAMAGED valves
MOA of nitrate?
nitrate is converted to NO
NO -> increased cGMP -> increased MLCP (myosin light chain phosphatase) -> vasodilation
Is Turner syndrome associated with MVP?
nope
Turner is bicuspid aortic valve and coarctation of aorta
- Diseases I need to think for MVP is connective tissue diseases- Marfan and Ethlers-Danlos
evolocumab and alirocumab
- MOA
- indication
- side effects
- PCSK9 inhibitor -> inhibition of LDL receptor degradation
- effective LDL lowering
- neurocognitive effects: dementia, derilum
Effect of cholestyramine in
- LDL
- HDL
- triglyceride
- LDL: low
- HDL: slightly high
- triglyceride: slightly HIGH
Two medication options for HCM?
- beta-blocker
- verapamil (non-dihydropyridine CCB)
- bottomline: to reduce work stress for thickened cardiac muscle
Three medications for antianginal therapy?
- beta blocker
- note: pindolol and acebutolol has partial beta agonist activity, so these are contraindicated
- nitrate
- verapamil
- bottomline: decrease heart work (so myocardial O2 consumption)
- hydralazine is NOT indicated (due to reflex tachy)
What is target of fibrates?
upregulates lipoprotein lipase: increase TG clearance
vs. niacin: which targets hormone sensitive lipase to inhibit lipolysis
how to treat two types of aortic dissection differently?
A type
B type
- A type: surgery
- B type: medication, beta-blocker then vasodilators
=> to reduce pressure
