UWorld Targeted Review: Cardio Flashcards
primary cause of morbidity in acute rheumatic fever?
heart failure from severe pancarditis
[mitral stenosis develops years/decades later]
what 2 features will ECG of patients with WPW show?
WPW = Wolff-Parkinson-White triad
- shorted PR interval
- delta wave: slope in beginning of QRS (—> widened QRS complex)
caused by accessory bypass tract (bundle of Kent) connecting atria and ventricles
ECG shows narrow QRS complex tachycardia with regular rhythm and non-visible P waves
paroxysmal supra-ventricular tachycardia (PSVT): episodic arrhythmia originating at/above the AV node (why QRS are narrow)
most common type is AV nodal reentrant tachycardia (AVNRT) - due to 2 distinct AV nodal conduction pathways (fast + slow)
describe the cause of AVNRT
AVNRT = AV nodal reentrant tachycardia: affects otherwise healthy young patients
due to 2 distinct AV nodal condition pathways: fast pathway (long refractory period) and slow pathway (short refractory period)
normally works fine because they meet and cancel out, but if there is a premature atrial contraction (PAC) while the fast tract is still refractory, the impulse may reach the bottom but then be carried upwards by the fast pathway (now not refractory) —> reentrant circuit with rapid conduction is created
cause of WPW vs AVNRT
WPW = accessory bypass tract (bundle of Kent) connects atria and ventricles, triggered by reentry of impulses through accessory pathway
AVNRT = fast + slow dual conduction pathways, triggered by premature atrial contraction (PAC) allowing fast pathway to creating a reentrant circuit
[most common type of supraventricular tachycardia]
which of the following describes the effect of clonidine?
a. decreased presynaptic release of ACh
b. decreased presynaptic release of NE
c. blockage of beta1 receptors in SA node
d. blockage of Ca2+ channels in AV node
e. blockage of K+ channels in AV node
clonidine = alpha2 agonist, stimulates presynaptic receptors in the rostral ventrolateral medulla (area responsible for basal and reflex control of SNS activity) —> decreased NE release, subsequent bradycardia and decreased vascular resistance
b. decreased presynaptic release of NE
where does atrial fibrillation most often arise?
near the pulmonary veins
what is the greatest determinant of the severity of Tetralogy of Fallot?
degree of RV outflow tract obstruction
TOF: RV outflow tract obstruction + large VSD + overriding aorta + RV hypertrophy
[VSD size isn’t determinant because it is always large]
how does Tetralogy of Fallot affect the following?
a. RV pressure
b. pulmonary artery pressure
c. LA pressure
a. RV pressure - INCREASE (due to RVOT obstruction)
b. pulmonary artery pressure - DECREASE (blood is obstructed from entering, so there’s a lower volume)
c. LA pressure - DECREASE (receiving less blood from lungs)
how would bicuspid aortic valve vs pulmonic stenosis affect cardiac auscultation?
bicuspid aortic valve —> narrowed/paradoxical split of S2
pulmonic stenosis —> widely split S2
[it goes A2, then P2 - like the alphabet]
pt experiencing palpitations is given rapid IV administration of a drug that causes short-lived flushing, burning in the chest, and SOB - what is the dx and what was the drug given?
paroxysmal supraventricular tachycardia (PSVT) - treated with adenosine
adverse effects include flushing, hypotension, bronchospasm, high-grade AV block
what are the phases and ions being moved in each phase for pacemakers vs non-pacemaker cardiomyocytes?
pacemakers:
4: Na+ in
0: Ca2+ in
3: K+ out
non-pacemakers:
4: resting
0: Na+ in
1: K+ out
2: Ca2+ in / K+ out
3. K+ out
QRS complex duration is typically reduced during exercise. However, a patient’s QRS duration is measured normal at rest and prolonged at near-maximal heart rate. They take a drug to treat their atrial fibrillation. What drug are they taking?
flecainide: class Ic anti-arrhythmic used to treat supraventricular tachycardias (such as a-fib)
Class Ic have strong use dependence (slowest to dissociate) and therefore prolong the QRS complex (Na+ blocking effects intensify as HR increases)
Class Ic bind fast Na+ channels responsible for phase 0 depolarization, blocking inwards Na+ current
which medications should be avoided in patients with hypertrophic cardiomyopathy?
HCM severity is determined by degree of LV outflow tract obstruction, which is lessened by more volume in the heart (puts pressure on the walls to open up the chambers)
therefore, drugs that decrease LV blood volume should be avoided, including:
1. nitrates, diuretics - reduce preload
2. hydralazine (arterial dilator) - reduces afterload
3. dihydropyridine Ca2+ channel blockers, ACEi - combined venous/arterial dilators
instead, tx w/ beta blockers and non-dihydropyridine Ca2+ channel blockers (verapamil)
what is the most common congenital cardiac anomaly associated with Down syndrome?
complete atrioventricular (AV) canal defect: compromised of atrial septal defect + ventricular septal defect + common AV valve
due to failure of endocardial cushion fusion —> ostium primum ASD + VSD + common AV valve
L to R shunting and AV valve regurgitation cause excessive pulmonary blood flow and heart failure —> auscultation will reveal hyperdynamic precordium + mid-diastolic rumble at LSB (increased pulmonary venous return) + holosytolic murmur in apex that radiates to the axilla (AV valve regurgitation)
what heart defect is seen with the following genetic conditions?
a. DiGeorge
b. Marfan
c. Friedreich ataxia
d. tuberous sclerosis
e. Turner’s
a. DiGeorge (22q11.2 deletion) - tetralogy of Fallot, truncus arteriosus, transition of great arteries (stuff affecting top of heart)
b. Marfan (fibrillin-1) - dissecting aortic aneurysms, aortic valve regurgitation (via cystic medial necrosis)
c. Friedreich ataxia (frataxin) - hypertrophic cardiomyopathy
d. tuberous sclerosis (tuberin, hamartin) - cardiac rhabdomyomas in ventricle and AV valves
e. Turner’s (45,X) - bicuspid aortic valve, aortic coarctation
differential cyanosis (involving lower extremities but not upper extremities) is suggestive of…
ductus arteriosus - suggests pattern of R to L shunting distal to the branch point of the arteries supplying the head/upper extremities
what is cardiac index
cardiac output per body surface area
therefore, cardiac index is increased with sympathetic activation
what does pulsus alternans vs electrical alternans indicate, respectively?
pulsus alternans: beat to beat variation in pulse amplitude (systolic BP), due to LV systolic dysfunction
electrical alternans: beat to beat variation in QRS complex on ECG, due to cardiac tamponade (heart swinging in pericardial fluid)
pulse with 2 distinct peaks =
dicrotic pulse: 2 distinct peaks, during systole and other during diastole
occurs in patients with severe systolic dysfunction and high SVR
rapidly rising pulse with high amplitude =
hyperkinetic pulse: rapidly rising amplitude due to rapid ejection of a large SV against decreased afterload
occurs with aortic regurgitation and high-output heart failure (thyrotoxicosis, AV fistula)
of which aortic arch is the ductus arteriosus a derivative?
sixth aortic arch on the left
[on the R —> proximal pulmonary arteries]
what is derived from the following embryonic structures?
a. bulbus cordis
b. primitive atria
c. sinus venosus
c. sinus venosus = receives blood from vena cava in embryonic heart, later forms smooth portion of R atrium called sinus venarum
b. primitive atria = receives blood from sinus venosus in embryonic heart and transmits to primitive ventricle, later forms rough portions of L/R atria
a. bulbus cordis = beginning of ventricular outflow tract in embryonic heart, later forms smooth portions of L/R ventricles adjacent to the aorta/pulmonary artery
from which aortic arch is the carotid artery derived?
third aortic arch - forms common carotid + proximal internal carotid arteries
from which embryonic aortic arch is the aortic arch derived?
fourth aortic arch
left —> aortic arch
right —> proximal right subclavian artery
which antihypertensive medications may cause peripheral edema?
dihydropyridine Ca2+ channel blockers - amlodipine and nifedipine
may also cause headache, flushing, dizziness
[remember the kid sitting on the floor of the ice cream shop in Sketchy!!]
which anti-arrhythmic drug causes prolonged PR interval, QRS duration, AND QT interval?
amiodarone
—> Class I effect inhibits fast Na+ channels, prolonging QRS interval
—> Class II/IV effect inhibits slow L-type Ca2+ channel, prolonging PR interval
however, risk of torsade de pointes is lower than with other class III drugs
the preferred anti-HTN drugs for decreasing risk of progression of diabetic nephropathy in patients with proteinuria are ______
ACEi and ARBs - have anti-proteinuric effects independent of effects on BP
(patients with increased urinary albumin excretion)
what effect do beta-blockers have on RAAS?
inhibit renin release
what are the most common pathogens causing purulent pericarditis in the following scenarios?
a. patients with portal from skin (ex, tunneled catheter)
b. patients with adjacent pneumonia
c. patients with total parenteral nutrition (TPN) or immunosuppression
a. patients with portal from skin (ex, tunneled catheter) = Staph. aureus
b. patients with adjacent pneumonia = Strep. pneumoniae
c. patients with total parenteral nutrition (TPN) or immunosuppression = Candida
which congenital heart defect creates the appearance of a narrow mediastinum on CXR?
transposition of the great arteries (TGA)
oxygen administration will not improve cyanosis, often there is no murmur
which class of anti-arrhythmics causes slowing of phase 0 depolarization AND prolongation of phase 3 repolarization?
Class 1A: (intermediate binding) slow phase 0 depolarization AND prolong phase 3 repolarization (prolong AP duration)
Class 1B: (weak binding) shorten phase 3 repolarization (decreasing action potential duration)
Class 1C: (strong binding) slow phase 0 depolarization (do not affect AP duration)
where should ablation be performed to treat atrial flutter vs a-fib?
flutter = area between the tricuspid valve and IVC in the R atrium
fibrillation = ostia of the pulmonary veins in the L atrium
ACE inhibitors affect the ______ arterioles
EFFERENT arterioles - this will DECREASE GFR
and this is a problem in people with renal stenosis because they really relied on efferent constriction to maintain a normal-ish GFR!
which of the following would NOT be useful in treating a patient with concurrent BPH and HTN?
a. doxazosin
b. tamsulosin
c. prazosin
d. terazosin
non-specific alpha1 blockers: doxazosin, prazosin, terazosin
uroselective alpha1 blocker: tamsulosin
why are beta blockers useful for hypertrophic cardiomyopathy?
beta blockers reduce HR and LV contractibility - this keeps more blood in the LV
higher blood volume in LV helps decrease outflow obstruction
