CARDIOLOGY Flashcards
In 70% of patients, the posterior descending artery derives from what?
Right coronary artery.
In 70% of patients, the posterior descending artery derives from what?
Right coronary artery.
Coronary arteries fill during which stage of cardiac cycle?
Diastole. Therefore, conditions or drugs that reduce disastolic filling allow less coronary perfusion.
LAD supplies?
Anterior wall of LV. Septal branch of LAD supplies anterior 2/3 of IV septum.
Circumflex branch supplies?
LA, lateral wall of LV, posterior wall of LV
PDA supplies?
Inferior wall of LV, posterior 1/3 of IV septum
Marginal branch supplies?
RA, RV
SA, AV nodal branches supply
SA and AV nodes. Duh.
Acidosis causes what effect on SV?
Decreases.
Hypoxia causes what effect on SV?
Decreases.
CO increases during exercise initially due to? Later due to?
Increasing SV, THEN increasing HR.
MAP = ?
CO x TPR aka diastolic arterial pressure + 1/3 pulse pressure
Pulse pressure = ?
SBP - DBP
Vitamins that apparently help prevent CAD
Vitamins E and C as well as beta carotene
STrongest predictor for stroke?
HTN
HDL > 60 cancels how many risks?
1
HMG-CoA reductase inhibitors site of action
Liver
Ezetimibe MOA
Cholesterol absorption inhibitor.
Ezetimibe ONLY affects which cholesterol?
LDL
Fibric acids site of action
Blood, as they stimulate lipoprotein lipase
Fibric acids greatest effect on? Least effect on/
Greatest effect on triglycerides. Then LDL, then HDL.
Bile acid sequestrates have no effect on ?
HDL. May or may not actually RAISE triglycerides.
Niacin site of action
Liver
Niacin has the least effect on which lipid?
Triglycerides.
Niacin has been shown to exacerbate which disease?
Gout
Niacin has what effect on insulin?
Insulin resistance.
Increased LFTs can be seen in which classes of lipid lowering anents?
Statins, cholesterol absorption inhibitors, fibric acids, and niacin.
Nitroglycerin may also reduce effects of which 2 cause of chest pain?
GERD, esophageal spasm.
Electrolytes to keep an eye on during treatment of unstable angina
Potassium to keep K+ levels >4 mEq/L. Magnesium to keep levels >2 mEq/L.
When os CABG considered?
Left am stenosis >50%, 3 vessel disease, or history of CAD and DM.
2 vessels most commonly used in CABG
Saphenous vein and internal mammary artery
ST elevation in V2-V4 indicates which artery is occluded?
LAD. Anterior area of infarct.
ST elevation in V1-V3 indicates which artery is occluded?
LAD. Septal area of infarct.
ST elevation in II, III, and aVF indicates which artery is occluded?
either posterior descending or marginal branch. Inferior area of infarct.
ST elevation in I, aVL, V4-V6 indicates which artery is occluded?
LAD or circumflex. Lateral area of infarct.
ST elevation in V1 and V2 indicates which artery is occluded?
PDA. Posterior area of infarct.
Greatest risk of sudden cardiac death is how long post-MI?
First few hours from tach, fib, or cariogenic shock.
Which types of heart block get ventricular pacemaker?
Mobitz II or complete/third-degree block
PDA supplies?
Inferior wall of LV, posterior 1/3 of IV septum
Marginal branch supplies?
RA, RV
CO increases during exercise initially due to? Later due to?
Increasing SV, THEN increasing HR.
Vitamins that apparently help prevent CAD
Vitamins E and C as well as beta carotene
2 vessels most commonly used in CABG
Saphenous vein and internal mammary artery
Greatest risk of ventricular wall rupture is how many days post-MI?
4-8 days.
PR interval in first degree heart block
> 0.2 sec
Second degree heart block Type I is caused by?
InTRAnodal or His bundle conduction defect, , drug effects (.eg., B-blockers, digoxin, CCB) or increased vagal tone.
Second degree heart block Type II is caused by?
InFRAnodal conduction problem (bundle of His, parking fibers).
Which types of heart block get ventricular pacemaker?
Mobitz II or complete/third-degree block
Narrow QRS not associated with p waves, rate of 60
3rd degree block (junctional rhythm)
Wide QRS not associated with p waves, rate >40 but
accelerated ventricular rhythm
Narrow QRS not associated with p waves, rate >100
junctional tachycardia
Wide QRS, not associated with p waves, rate 20-40
ventricular rhythm
Wide QRS, not associated with p waves, rate >100
ventricular tachycardia
Narrow QRS not associated with p waves, rate >60 but
accelerated junctional rhythm
Difference between wandering pacemaker and Multifocal atrial tacky?
> 3 diff p wave morphologies but wandering pacemaker is ventric rate of 100.
Treatment for PACs?
None
Drug of choice in PSVT?
IV adenosine
Scenarios you’d see Kussmaul’s sign
Increased JVD with inspiration is seen in right ventricular infarct, massive PE, constrictive pericarditis, restrictive cardiomyopathy, and rarely, cardiac tamponade.
When might a subclinical mitral stenosis from rheumatic heart disease become clinically apparent?
Volume overload state, such as pregnancy.
Diastolic murmur heard best in left lower sternum that increases with inspiration
Tricuspid stenosis
Late diastolic murmur with an opening snap (no change with inspiration)
Mitral stenosis
Systolic murmur heard best in the second right IC space
Pulmonic stenosis
Systolic murmur heard best in the second left IC space
Aortic stenosis
Late systolic murmur best heard at the apex
MVP
Diastolic murmur with a widened pulse pressure
AR
Holosystolic murmur that is louder wit inspiration at the left lower sternum
Tricispid regurg
Holosystolic murmur heard at the apex and radiates to the axilla
MR
When do PVCs become concerning for development of other ventricular arrhythmias?
> 3 PVC/min
Anti-arrhythmic commonly used in Vtach?
Lidocaine or tocainamide, type IB.
Causes of sytstolic dysfunction
Caused by decreased contractility, increased preload, increased after load, HR abnormalities, or high output conditions such as anemia, hyperthyroidism
Causes of diastolic dysfuntion
Hypertrophy or restrictive cardiomyopathy.
Chronic constrictive pericarditis is most commonly caused by?
Radiation, heart surgery
Pathophys of Brugada Syndrome
Mutation in the gene that encodes for sodium ion channel in the cell membranes of the myocytes. Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization. The transmural dispersion underlies ST-segment elevation and the development of a vulnerable window across the ventricular wall, whereas the epicardial dispersion of repolarization facilitates the development of phase 2 reentry, which generates a phase 2 reentrant extrasystole that captures the vulnerable window to precipitate ventricular tachycardia and/or fibrillation that often results in sudden cardiac death.
Genetics of Brugada syndrome
AD, more common in males and higher prevalence in Asians
ECG of Brugada syndrome
Persistent ST elevations in V1-V3 with right BBB with or without terminal S waves. Prolongation of PR interval is also sometimes seen.
Why is there an elevated pulse pressure in aortic regurg:
Due to insufficiency of aorta, blood flows back into LA, lowering DBP. This widens the pulse pressure.
Treatment of AR
Decrease after load with a vasodilator like an ACE-I or CCB like nifedipine.
High levels of what are associated with 3x risk of atherosclerosis
Homocysteine
Unique symptoms of inferior wall MI
Bradycardia, diarrhea, lightheadedness.
Inferior wall MI is caused by infarction of posterior descending artery. The supply of PDA is posterior (duh) heart, and when this is irritated, it irritates the surrounding structures which happen to include the left vagus nerve. This is why you see vagal sx.
Pt is in vtach and pulseless
Non-synchronized CVN / defibrillation
Arrhythmia + no pulse.
Pt has PEA or asystole
Give 1 mg of IV epi during CPR.
NYHA Class I CHF
HF with no limitations on physical activity and no symptoms, even with exertion
NYHA Class II CHF
Slight limitations on physical activity and symptoms of heart failure with physical activity.
NHA Class III CHF
Symptoms such as angina, SOB and palpitations qitth physical exertion
NYHA Class IV heart failure
sx of heart failure even at rest
what is Heyde’s syndrome
Combo of calcific aortic stenosis and GI bleeding due to colonic angiodysplasia. It is thought that aortic stenosis causes type 2 von willebrand syndrome which results in inefficient hemostasis in high flow areas. This results in bleeding from angiodysplastic lesions.
Medical treatment of PAD
Cilostazol to improve flow to LE and decrease claudication. CONTRAINDICATED IN HEART FAILURE.
Second line medical treatment of PAD
Pentoxifylline, also contraindicated in CHF. Ginko biloba. Thats fun.
When are compressing stockings effective in post op prevention of DVT?
In low risk post op general surgery or neurosurgery pts.
Where is the rash in Kawasakis
Truncal
Tx of Kawasakis
IVIG and high dose ASA. Echo in acute phase and 6-8 weeks later.
When is anticoag considered in superficial thrombophlebitis
In lower extremity or extension into femoral vein
Tx of small VSD
Monitor/reassurance. 40% close by 3 years and 75% close by 10 yrs
Tx of large VSD
Monitor nutirtion and weight gain due to higher risk of FTT
Treat CHF with ACE, diuretics, digoxin
Influenza vaccine and winter pavlivizumab if younger than 2 for RSV prevention
When are large VSD surgically repaired
Medical management fails
Signs of pHTN at
When is endocarditis ppx indicated in VSD patients
If it was surgically repaired
Common defect in pts with abstains anomal
PFO with R – > L shunt. Also can have dilated RA giving increased risk of SVT and WPW
Tx of Abstains anomaly
PGE
Digoxin
Diuresis
PRopranolol for SVT
Next step in management of congenital heart disease with early cyanosis
PGE (keep it open!!!!)
6 week old infant presents to meds ER for irritability and is found to have signs of left sided heart failure. An EKG is interpreted as a left sided MI. What is most likely dx?
Anomalous origin of Left coronary artery (from pulm rather than aorta)
What class of meds is indicated in pts wit ha hereditary prolongation of QT interval in order to prevent v fib
Beta blockers
Weak pulses in upper extremities – which vasculitis?
Takayasu
Which vasculitis has necrotizing granulomas of lung and necrotizing GN
WEgeners
Which vasculitis has necrotizing immune complex inflammation of visceral and renal vessels
Poly arteritis nodosa
Which vasculitis is the most common
Temporal arteritis
Which vasculitis is associated with Hep B
Polyarteritis nodosa
Which vasculitis a/w perf of nasal septum
Wegeners
Defects that comprise ToF
Overriding aorta
Pulm stenosis
VSD
RVH
What are classic findings of HSP?
Recent uri Abdominal pain Arthritis Renal disease LE purpura
Persistent ST elevations in anterior leads 5 weeks after an MI
Ventricular aneurysm
Tx of Prinzmetal angina
CCB, nitrates.
Contraindicated in prinzmetals angina
Beta blockers (non selective) because of unopposed alpha receptor vasoconstriction which can worsen sx cause death.
When should you consider 2 drug therapy in hypertension
When BP is more than 20/10 mmHg above goal.
Goal BP in pts >60
Combo therapy of choice in htn
ACE/ARB in concert with long acting dihydropyridine CCB.
ACE/ARB + diuretic can also be used but may be less beneficial.
Initial mono therapy for HTN in blacks
Thiazide or long acting CCB
Initial mono therapy in pts who have diabetic nephropathy or non diabetic CKD and proteinuria with HTN
ACE or ARB
Initial mono therapy in pt with ischemic heart disease or CHF with decreased EF along with HTN
Beta blocker
Goal BP in pts with diabetes or CKD without proteinuria
Define proteinuria
> 500-1000 mg/day
HbA1C diagnostic of DM
> 6.5%
Goal HbA1C for diabetics
