Shit - Cardio UWorld Flashcards
Epi vs. NE receptors
Epi b > a
NE a1 > a2 > b1
Beta blocker selectivity
A-M olol = b1
N-Z olol = b1 and b2
ilol/alol = a and b
*nebivolol = b1 block and b3 stimulate (activate NOS)
*sotalol = K+ and b blocker
Most common hear defect in turners
Bicuspid aortic valve (early systolic high-pitched click)
Effects of dobutamine:
Use:
1) Inotropic (increased contractility is most useful effect)
2) slight chronotropy (increases O2 consumption with inotropic, so bad, can cause ischemia)
3) increases conduction velocity (bad; arrythmyas)
Used for heart failure with decreased contractility i.e. MI cardiogenic shock
Front of heart =
Back of heart (against esophagus) =
front = right ventricle
back = left atrium
diastolic rumble with an opening snap
Mitral stenosis
Which vessel in the body has the lowest O2?
Coronary sinus (heart extracts 80-90% of the O2)
Rheumatic heart disease timeline post-strep throat
1-8 months
bounding pulses =
weak pulses =
(valve defects)
bounding = AR = Corrigan’s/water-hammer
Weak = AS = pulsus parvus et tardus
most important aspect of nitrates
decreased preload
MI collagen 1 w vs few months
1w = type III
months = type I
MCC NVBE and MV valve
MVP, mitral valve
Maintenance dose =
Cp x CL x dosage interval
DI i.e. ever 6 hours = 60min/hr x 6hrs
pulsus paradoxus: sign and mechanism and causes
> 10mmHg fall in SBP upon inspiration.
Mechanism: increase in RVP during inspiration (VR and pulmonary retrigrade flow) causes RVP>LVP → IVS pushed into LV decreasing filling → decreased CO and thus SBP
Causes: cardiac tamponade, asthma, OSA, pericaditis, croup
Hepatic Angiosarcoma
Vinyl chloride, arsenic, thorotrast
Daptomycin AE
Rhabdo and myopathy
Fates of embryonic veins:
Cardinal
Vitelline
Umbilical
Cardinal = systemic venous system
Vitellin = portal venous system
Umbilical = degenerate
highest oral bioavailable nitrate
isosorbide mononitrate
Biventricular pacemakers: path of LV lead
SVC, RA, coronary sinus (in A-V groove in post heart), LV
Blood supply to diaphragmatic part of the heart
posterior interventricular branch (85% of people via RCA)
AA creating NO
Arginine
Aortic arch baro-receptors to NTS via what nerve?
X (vagus)
carotid sinus baro-receptors to NTS via what nerve?
IX (glossopharyngeal)
[actually branch called hering’s nerve]
Sign of pulsus paradoxus
Lose pulse sounds with BP cuff during inspiration
Irreversible change associated with wide fixed splitting of S2
Pulmonary hypertension (via ASD)
Stable angina vessel profile
AS plaque obstructing >75% of lumen, no thombus
Decrease platelet aggregation AND vasodilate arteries: drug names and condition they treat
Cilostazole and dipyridamole. Intermittent claudication (PVD), angina, prevent stroke/TIA
CCB toxicity
flush, edema, AV block, constipation (verapamil)
Orthopnea specific for:
LHF (dyspnia while supine relieved by sitting up)
Could also be mitral stenosis
2 major regulators of coronary flow, and the vessel size they work best on
Adenosine = arterioles
NO = large arteries and pre-arteriolar
Dilated coronary sinus indicates:
Increased RAP i.e. RHF or pulmonary hypertension
Thiazide AE
Hyper GLUC (glycemia, lipidemia, uricemia, calcemia)
Cardiac structures anterior and posterior to esophagus
anterior = LA
posterior = descending aorta
phenoxybenzamine vs phentolamine
phenoxybenzamine = irreversible a-antag, for pheo
Phentolamine = reversible a-antag, for MAO pts with cheese reaction
effects of increased vs decreased baro-R firing:
Increased (i.e. HTN, valsalva, carotid massage) = slowed AV node by increasing refractory perior
Decreased (i.e. low BP or BV) = increase HR, BP, contractility, vasocontriction
Chronic pericarditis causes + key features
Causes: TB, radiation, cardiac surgery
Pericardial Knock: just after S2 (confused with MS opening snap), from chronic pericarditis
Sharp y-descent, depper/steeper with inspiration
What does b2 vs glucagon do to alter myocardial contractility
BOTH INCREASE cAMP!
(just have different receptors)
cause of janeway lesions
Septic emboli to cutaneous vessels
mutations in genetic DCM vs HCM
DCM = mitochondrial enzymes for ox phos and cardiac cytoskeletal element
HCM = beta myosin heavy chains
holosystolic murmur =
MR
TR
VSD
anti-hyperlipidemia drug causing flushing, warmth, and itching. What is drug and what mediates this AE?
Niacin (B3)
Prostaglandins (reduce with asprin)
Fenoldopam MOA
selective D1-agonist, causes arteriolar dilation and naturesis
Leads II, III and AvF
Specific s/s
RCA (inferior heart; inf wal of LV)
Bradycardia (RCA supplies SA and AV nodes)
Familial hyperchylomicronemia (type I hyperlipoproteinemia):
- Dx
- complications
LPLase deficiency, milky plasma on standing via chylomicrons
Hypertriglyceridemia, recurrent acute pancreatitis, lipidema retinalis, erruptive xanthomas
Nitroprusside action
VS BOTH arterioles and veins, so decreases preload AND afterload, maintaining SV
Diastolic HF: LVP, LVV, LVEF
LVP increased
LVV normal (increase pressure ot achieve normal volume)
LVEF normal
polymorphic QRS complexes (varying amplitude and cycle length) with prolonged QT =
causes =
torsades des pointes V tach
causes = class Ia + III (not amiodarone) antiarythmics + TCAs
substitute for asprin allergy in angina + MOA
Clopidogrel; irreversibly blocks platelet ADP-Rs
SCD: cause and predisposing factors
Cause = ventricular arrythmia
Predispose = CAD (70%), cardiomyopathies, channelopathies
Adenosine MOA
K+ efflux from nodal tissues (prolongs phase 4), as well as Ca++ influx (phase 0)
Small ventricular space, sigmoid shaped septum, brown pigments =
normal aging
Distance from A2 to OS: disease and what it tells you
Mitral stenosis Severity: decreased time = worse. Tighter stenosis = higher LAP needed to overcome it = LAP > LVP sooner (during LV isovolumetric relaxation) = valve opens sooner thus closer to aortic valve shutting
Calcific aortic stenosis via:
dystrophic calcification: abnormal organ calcification via damage (i.e. longterm hemodynamic stress os AS), with NORMOcalcemia
Hibernating myocardium
Ischemia so that myocardium doesn’t work, but they make enough ATP to survive. If oxygen is returned with CABG or angioplasty, the hibernating myocardium wakes up and s/s improve (overs hrs-months)
Myocardial stunning
Less severe version of hibernation. Ischemia
Anti-arythmic specific for rapidly depolarizing and repolarized myocytes (i.e. ischemic cells in v. tach)
Lidocaine
Best beta blocker for decreasing M/M in CHF; and its function
Carvedilol. B1, B2, A1 antagonist
Sotalol Special properties
Only class III (K+ blocker, prolong Q-T) with beta-antagonist effects (so will also cause bradycardia)
what part of the wave do beta blockers alter and how
Increased PR interval by slowing down AV node conduction
Drugs producing dilated cardiomyopathy
Anthracyclines = doxorubicin and daunorubucin. Prevent with dexrazoxane
Nesiritide
BNP analog
SVT DOC
Adenosine (especially paroxysmal SVT)
Adenosine AE
Flushing, burning chest pain, sense of impending doom, bronchospasm, hypotension
Drug for chemical stress test
Adenosine
HOCM heart changes (gross)
Asymmetrical septal hypertrophy, leading to systolic anterior motion (SAM) of anterior mitral valve leaflet
Class III antiarythmics
Amiodarone, Ibutilide, dofetilide, sotalol
how do vegetations form in bacterial endocarditis
Bug binds —> expresses tissue factor (thomboplastin/Factor III, extrinsic coagulation pathway)—> activates platelets and fibrin deposition —> vegetation
Osler-Weber-Rendu
Hereditary hemorrhagic telangectasias. AD. spider nevi with bleeds i.e. epistasis
Sturge-Weber
Facial, leptomeningeal, seizures, hemiplegia, skull tram track opacities
Conduction speed
Purkinje > atria > ventricles > AV
a fib ECG:
Lose P-waves, narrow QRS and irregularly spaced, variable RR
Hypercoaguable paraeoplastic: name, cause, s/s
Trousseau’s syndrome. Pancreatic, colon, lung adenocarcinomas. Make thromboplastin-like substance that causes migratory thrombophlebitis (and non-bacterial thrombotic endocarditis)
Aortic isthmus
tethered by ligamentum arteriosum, so injured during accel-deccel injuries
young woman with RVH
Cor pulmonale from primary pulmonary hypertension
What sets ventricle pace in 3rd degree block?
AV node = 45-55bpm
Coronary steal
giving adenosine or dipyridamole (coronary vasodilators) when there is a blocked vessel exacerbates it
Who has more compliant LA, chronic or acute MR?
Chronic; allows for room for blood to prevent acute pulmonary edema (seen in acute)
beck triad: what and when
What: severe hypotension, muffled heart sounds, distended neck veins. Via pericardial tamponade
Rx for AS with a fib
Cardioversion: they need the atrial kick to get blood into hypertrophied LV, and ot prevent acute pulmonary edema
Distance from A2 to OS: disease and what it tells you
Mitral stenosis
Severity: decreased time = worse. Tighter stenosis = higher LAP needed to overcome it = LAP > LVP sooner (during LV isovolumetric relaxation) = valve opens sooner thus closer to aortic valve shutting
Calcific aortic stenosis via:
dystrophic calcification: abnormal organ calcification via damage (i.e. longterm hemodynamic stress os AS), with NORMOcalcemia
Hibernating myocardium
Ischemia so that myocardium doesn’t work, but they make enough ATP to survive. If oxygen is returned with CABG or angioplasty, the hibernating myocardium wakes up and s/s improve (overs hrs-months)
Myocardial stunning
Less severe version of hibernation. Ischemia
Anti-arythmic specific for rapidly depolarizing and repolarized myocytes (i.e. ischemic cells in v. tach)
Lidocaine
Best beta blocker for decreasing M/M in CHF; and its function
Carvedilol. B1, B2, A1 antagonist
Sotalol Special properties
Only class III (K+ blocker, prolong Q-T) with beta-antagonist effects (so will also cause bradycardia)
what part of the wave do beta blockers alter and how
Increased PR interval by slowing down AV node conduction
Drugs producing dilated cardiomyopathy
Anthracyclines = doxorubicin and daunorubucin. Prevent with dexrazoxane
Nesiritide
BNP analog
SVT DOC
Adenosine (especially paroxysmal SVT)
Adenosine AE
Flushing, burning chest pain, sense of impending doom, bronchospasm, hypotension
Drug for chemical stress test
Adenosine
HOCM heart changes (gross)
Asymmetrical septal hypertrophy, leading to systolic anterior motion (SAM) of anterior mitral valve leaflet
Class III antiarythmics
Amiodarone, Ibutilide, dofetilide, sotalol
how do vegetations form in bacterial endocarditis
Bug binds —> expresses tissue factor (thomboplastin/Factor III, extrinsic coagulation pathway)—> activates platelets and fibrin deposition —> vegetation
Osler-Weber-Rendu
Hereditary hemorrhagic telangectasias. AD. spider nevi with bleeds i.e. epistasis
Sturge-Weber
Facial, leptomeningeal, seizures, hemiplegia, skull tram track opacities
Conduction speed
Purkinje > atria > ventricles > AV
a fib ECG:
Lose P-waves, narrow QRS and irregularly spaced, variable RR
Hypercoaguable paraeoplastic: name, cause, s/s
Trousseau’s syndrome. Pancreatic, colon, lung adenocarcinomas. Make thromboplastin-like substance that causes migratory thrombophlebitis (and non-bacterial thrombotic endocarditis)
Aortic isthmus
tethered by ligamentum arteriosum, so injured during accel-deccel injuries
young woman with RVH
Cor pulmonale from primary pulmonary hypertension
What sets ventricle pace in 3rd degree block?
AV node = 45-55bpm
Coronary steal
giving adenosine or dipyridamole (coronary vasodilators) when there is a blocked vessel exacerbates it
Who has more compliant LA, chronic or acute MR?
Chronic; allows for room for blood to prevent acute pulmonary edema (seen in acute)
beck triad: what and when
What: severe hypotension, muffled heart sounds, distended neck veins. Via pericardial tamponade
Rx for AS with a fib
Cardioversion: they need the atrial kick to get blood into hypertrophied LV, and ot prevent acute pulmonary edema
Functions of ANP
Kidney: dilates afferent arteriole, prevents Na+ resorption, inhibits renin secretion
Adrenal: restricts aldosterone secretion
Blood vessels: vasodilation and increases capillary permeability to decrease circulating BV
Pressures in the heart
Maneuvers for murmurs
Best way to hear S3
Lateral decubitus and exhaled to decrease lung volume and bring heart closest to chest
Resistance =
nL/r4
When is AS murmur the loudest?
When Aorta-LV pressure gradient is the largest, so mid-systole (hence the crescendo-decrescendo)
Response to arteriole vasodilators (minoxidil and hydralazine)
Decreased arterial BP causes baro-R firing causes increased SNS:
Reflex tachycardia/FOC
RAS causing fluid retention cuasing edema and Na+ retention
Congenital heart diseae causing toe cyanosis and clubbing
PDA
(deO2 blood from PA into descending aorta (past the 3 branches)
Signal for migration (and the proliferation) of smooth muscle cells into tunica intima
PDGF
From pletelets, endothelium, macrophages
Aortic aneurism vs aortic dissectoin major RF
aneurism = AS
dissection = HTN
effects of 5HT of the heart:
endocardial fibrosis
