Vol. III - Cardiovascular and Pharm Flashcards
role of diuretics in HF
symptom management
high pitched “blowing” early diastolic decrescendo
aortic regurgitation
Left horn of sinus venosus becomes
coronary sinus
Use of Class IB anti-arrhythmics
Acute ventricular arrhythmias esp post MI
How do we prevent cerebral vasospasm in subarachnoid hemorrhage
Nimodipine
Class 3 anti-arrhythmic mechanism
K channel blockers –> increased Ap duration, ERP, and QT interval
Fixed splitting is heard in
ASD
3rd aortic arch becomes
Common carotid
treatment for primary hypertension
Thiazide diuretics, ACE-i/ARBs, Ca channel blockers
Pathology 2-several weeks post MI
contracted scar is complete
Continuous machine like murmur, loudest at S2
patent ductus arteriosus
Primitive pulmonary vein becomes
smooth part of left atrium
Causes of tricuspid regurgitation
RV dilation and Rheumatic fever
Drug induced long QT –> Torsades risk
ABCDEF: antiArrhythmics (Ia and III), antiBiotics (macrolides and fluorquinolones), Anti”C”ychotics (haloperidol, ziprasidone), antiDepressants (TCAs), antiEmetics (odansetron), antiFungals (azoles)
6th aortic arch becomes
proximal pulmonary arteries and ductus arteriosus
Abnormalities associates with failure of neural crest migration
Transposition of the great vessels
Tetralogy of Fallot
Persistent truncus arteriosis
Causes of mitral regurgitation
Ischemic heart disease post mI, LV dilation, Rheumatic fever
systolic crescendo-decrescendo that radiates to the carotids, loudest at base of heart
Aortic stenosis
Hypertrophic cardiomyopathy findings
S4, systolic murmur, possible mitral regurg
Frequency of left to right sunts
VSD > ASD > PDA
Pathology 1-3 days post MI
Coagulative necrosis and acute inflammation with neutrophils
late systolic crescendo with mid-systolic click, best heard over apex
Mitral valve prolapse
Opening snap followed by mid to late diastolic rumble
mitral stenosis
pacemaker action potential phases
0: voltage gated Ca
3: repolarization via K efflux
4: spontaneous depolarization b/c of funny Na/K channels
Things that increase contractility
Beta 1 activation by cathecholamines, increased Ca, decreased extracellular Na, Digoxin
right horn of sinus venosus becomes
smooth part of the right atrium
cardiovascular complication of syphilis
aortic atrophy and dilation, can lead to calcification
treatment for htn with diabetes
ACE-i/ARBs first line, Ca channel blockers, thiazides, Beta blockers (can mask hypoglycemia though)
Pathology 3-14 days post MI
macrophage infiltration followed by granulation tissue at the margins
Class IC anti-arrhythmics
Flecainide, propafenone
Use of Class IA anti-arrhythmics
both atrial and ventricular, esp. SVT and VT
2nd aortic arch becomes
Stapedial and hyoid arteries
Class IA anti-arrhythmics
Quinidine, procainamide, disopyramide
Pericardium is innervated by
Phrenic nerve
Fick principle
CO = rate of O2 consumption / (arterial O2 content - venous O2 content)
Rheumatic fever pathogenesis
Type II hypersensitivity - Ab to M protein cross react with self antigen, often myosin
Use of Class IC anti-arrhythmics
SVT, including afib, contraindicated post MI
Paradoxical splitting is heard in
Conditions that delay aortic valve closure (aortic stenosis and left bundle branch block)
Treatment for Torsades de pointes
magnesium sulfate
Dilated cardiomyopathy findings
HF, S3, systolic regurg murmur
Conduction pathway
SA node –> atria –> AV node –> bundle of His –> bundle branches –> purkinje fibers –> ventricles
Tetralogy of Fallot
most common cause of early childhood cyanosis
PROVe: Pulmonary stenosis, RVH, Overriding aorta, VSD
Class 4 anti-arrhythmic mechanism
Ca channel blockers –> decreased conduction velocity
S1 is
the mitral valve closing
Class 3 anti-arrhythmics
AIDS: amiodarone, ibutilide, dofetilide, sotalol
Right common and anterior cardinal vein becomes
SVC
Lithium exposure in utero causes
Ebstein anomaly: tricuspid valve is displaced down into RV
Things that decrease contractility
B1 blockade, HF with systolic dysfunction, acidosis, hypoxia, Ca channel blockers
Rhythm control in Torsades
Mg
Persistent truncus arteriosus
TA doesn’t divide into pulmonary trunk and aorta
Causes of aortic regurgitation
BEAR: Bicuspid valve, endocarditis, aortic root dilation, rheumatic fever
TAPVR
Pulmonary vein enters right heart, associated with ASD and PDA
Causes of aortic stenosis
age related calcification, or calcification of bicuspid aortic valve
Transposition of the great vessels
Not compatible with life without a shunt (circulations are separate)
Dressler syndrome
occurs several weeks post MI, autoimmune process resulting in fibrinous pericarditis
Pathology 0-24 hrs post MI
Wavy fibers or no change (0-4 hrs), early coag negrosis (4-24 hrs)
Digoxin antidote
slowly normalize K, cardiac pacer, anti-dig Ab fragments, Mg
Flow is proportional to
r^4
Congenital long QT syndromes
loss of K channel function
Which Ca channel blockers are cardioselective (nondihydropyrdines)
diltiazem and verapamil
Hypertrophic cardiomyopathy leads to
diastolic dysfunction
tachyphylactic means
there is an acute decrease in response to a drug after initial/repeated administration
treatment for htn with asthma
ARBs, Ca channel blockers, thiazides, cardioselective beta blockers
PDA is maintained by
PGE and low O2 tension
Mycoardial action potential channels per phase
0: Na
1: Na is inactivated, K opens
2: Ca influx balances K efflux
3: Massive K efflux via delayed rectifying channels
4: High K permeability maintains resting potential
4th aortic arch becomes
aortic arch, and proximal subclavian
Tricuspid atresia requires
ASD and VSD for viability
Class 1 anti-arrhythmic mechanism
Na channel blockers –> decrease slope of phase 0
Truncus arteriosus becomes
ascending aorta and pulmonary trunk
Umbilical vein becomes
Ligamentum teres
coronary blood flow to LV and septum peaks in
early diastole
Drugs that decrease HF mortality
ACE-Is or ARBs, beta blockers (not acute though), and spironolactone
holosystolic high pitched, “blowing murmur”
Mitral/tricuspid regurgitation (mitral also radiates to axilla
physiological S2 splitting is due to
delayed pulmonic valve closure (b/c of increased venous return on inspiration)
Class 2 anti-arrhythmic mechanism
beta blockers –> decrease SA and AV node via decreased cAMP and Ca
treatment for hypertension with HF
Thiazide diuretics, ACE-i/ARBs, beta blockers (compensated), aldosterone antagonists
Most common congenital cardiac anomaly
Ventricular septal defect
treatment for beta blocker overdose
saline, atropine, glucagon
in 1st order kinetics, half life =
0.7 x Vd / Cl
Class IB anti-arrhythmics
Lidocaine, phenytoin, mexiletine
Wide S2 splitting is seen in
conditions that delay RV emptying (pulmonary stenosis, and right bundle branch block)
Class 2 anti-arrhythmics (beta blockers)
metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol
Brugada syndrome
AD loss of function in Na channels –> ICD to prevent SCD
Medication to close a patent ductus arteriosus
Indomethacin
Hydralazine acts via
increased cGMP –> afterload reduction
Bacterial endocarditis presentation
FROM JANE: Fever, Roth Spots, Osler Nodes, Murmur, Janeway lesions. Anemia, Nail-bed hemorrhage, Emboli
holosystolic, harsh sounding murmur, loudest at tricuspid
Ventricular septal defect
Treatment of hypertrophic cardiomyopathy
stop high intensity workouts, beta-blockers or verapamil, avoid decreasing preload.
Use of class 2 anti-arrhythmic
SVT, rate control for a fib/flutter
Pericarditis causes referred pain to
neck, arms, or shoulders
treatment for htn in pregnancy
New Moms Love Hugs: Nifedipine, methyldopa, labetelol, hydralazine
JONES criteria for Rheumatic heard disease
Joints, heart, Nodules, Erythema marginatum, Sydenham chorea
S2 is
the aortic valve closing
Congenital right to left shunts
5 T’s: Truncus arteriosus, transposition, tricuspid atresia, tetralogy of fallot, TAPVR
1st aortic arch becomes
Maxillary artery
Treatment of type A aortic dissection
surgery (ascending aorta is involved in A)
Treatment of type B aortic dissecttion
Beta blockers for type B, then vasodilators (di-later-s)
Dilated cardiomyopathy leads to
systolic dysfunction
Wolff-Parkinson-White syndrome
most common ventricular pre-excitation syndrome, may cause SVT. Abnormal conduction bypasses AV node –> early ventricular depolarization (delta wave) –> wide QRS.
What type of muscle has Ca induced Ca release
Cardiac
Posterior, subcardinal, and supracardinal veins become
IVC
Treatment of dilated cardiomyopathy
Na restriction, ACE-I, spironolactone, digoxin
