Shit - Cardio Flashcards
bulbus cordis
smooth parts of ventricles (outflow tract)
primitive atria/ventricles
trabeculated part
primitive pulmonary veins
smooth part of LA
right horn of sinus venosus
smooth part of RA = sinus venarum (just incorporated into the atrium)
Left horn of sinus venosus
Coronary sinus: delivers deO2 blood from the heart into the RA
Right common cardinal vein and right anterior cardinal veins
SVC
How do you form the Membrnaous interventricular septum
From endocardial cushion
grows off muscular ventricular septum to join aorticopulonary septum (after it spirals)
Role of the endocardial cusions:
1) separate the atria from ventricles
2) Contribute to atrial septation
3) contribute to the membranous interventricular septum
4) Make all the valves (A,P,T,M)
3 fetal shuts: name, vessels, bypasses what
Ductus venosus: umbilical vein into IVC; bypasses liver
Foramen ovale: RA to LA; bypasses lungs
Ductus arteriosis: deO2 SV blood from head down into RV into pulmonary artery –> jump to descending aorta; bypasses lungs. [gives less oxygenated blood to extremities]
Fate of PDA
Close naturally via increased O2 and decreased plaental prostaglandins
Rx to close = indomethacin (NSAID, decrease PG)
Rx to keep open = PGE1 and PGE2
Allantois (urachus) becomes:
Median umbilical ligament
Umbilical arteries become;
MediaL umbilical ligaments
umbilical vein becomes:
ligamentum teres = round ligament (within falciform)
Which artery differ in supply with right and left dominant?
Posterior descending
Most common coronary artery occluded
LAD
Peak coronary flow in what part of cycle?
Early diastole
most posteriro part of heart?
Left atrium
Supply of AV and SA
RCA
CO =
= HR x SV
= MAP/TPR
= rate of O2 consumption/(Arterial O2 - Venous O2)
MAP =
= CO x TPR
= 2/3 diast + 1/3 syst.
PP =
= systolic - diastolic
= propotional to SV (systolic = full of blood, diastolic = empty)
= inversely proportional to arterial compliance (more compliant = more room for blood = lower systolic pressure because not pushing as hard on expanded walls, but roughly the same diastolic pressure)
SV =
EF =
SV = EDV - ESV
EF = EDV - ESV / EDV
EF = 55%
If HR increases, what will give to keep up withteh HR
Diastole
Therefore CO decreases (problem with v. tach)
Increase in PP via:
(see head bobbing)
Hyperthyroidism (increases beta-adrenergic, increases systolic)
Aortic regurgitation (leak back decreases distolic; then more to shoot out increases systolic)
Aortic stiffening (isolated systolic hypertension in elderly)
Obstructive sleep apnea (sympathetic tone)
Exercise (transient)
Decrease PP in:
Aortic stenosis - low S
Cardiogenic shock - low S
Cardiac tamponade - S and D equalize
Advanced heart failure (HF) - low S
Acidosis on contractility:
decreases
(H+ into cells, K+ out, increased Na//K; decreased Na//Ca)
ACE-I/ARB effect on preload and/or afterload
Decrease both:
Less AT-II on BV = vasodilation (arterial) = decreased afterload
Less aldosterone = less BV = decreased preload
Effects of systolic vs diastolic HF on EF
Systolic = decresed EF (<55%)
Diastolic = same EF (becasue same all relative to EDV; contractility is fine)
Resistance =
= 8 x viscosity x length / πr^4
= P/CO
Effect of organectomy on resistance and CO
Total body runs in parallel (1/R + 1/R); invidivual organs run in series (R+R)
So remove an organ will INCREASE TPR.
CO = P/R
with no change in P, CO will DECREASE
Inotrophy graph
+ = catecholamines, digoxin
- = uncomensated HF, Narcotic OD
Volume/venous tone graph
+ = fluid infusion, SNS
- = acute bleed, spinal anesthesia
TPR graph
- = exercise, AV shunt
+ = pressors
S3
SLOSH-ing-in
During late systole, when the ventricles are relaxing and atria are passively filling them with 80% of total blood volume (y-descent)
Physiological with high BV i.e. kids, pregnancy
Pathological with mitral regurg, HF, dilated ventricles
S4
a-STIFF-wall
Atrial kick
When atria contract against still ventricle to get last 20% of blood in (a-wave); i.e. ventricular hypertrophy
wide splitting via:
Delayed right ventricle emptying, delaying pulmonary valve closure
- RBBB
- pulmonary stenosis
Fixed splitting seen in:
why?:
ASD
Because left to right shunt .: always more blood in right (atrial and) ventricular system .: always takes longer to close pulmonary valve
Paradoxical splitting:
Seen in:
When A closes after P, so when you breathe in and P closes later, they end up closing closer together paradoxically eliminating the split
(inspiration normally enhances splits)
Seen when aortic closes later:
- LBBB
- Aortic stenosis
- HOCM
Where to listen for flow murmurs (physiological)
Pulonary and aortic areas
Aortic and pulonary regurg location:
left sternal boarder
hypertrophic cardiomyopathy: where to listen
left sternal boarder
Where to hear VSD and ASD
Tricuspid
Aortic regurg facts:
Diastolic, high-pitched, Blowing, Decrescendo
Associated with: (via inc. PP)
- Bounding (corrigan’s) pulse
- quinke’s sign = pulsating nails
- demuzzet’s sign = head bobbing
- Muller’s sign = uvula pulsation
Mitral stenosis facts:
Diastolic
Opening snap
rumbing
rheumatic fever
decreased S2-OS = increased severity
Aortic stenosis facts
- congenital, calcification, bicuspid
- Systolic, cesc-decres
- pulsus parvus et tardus (small and late)
- may have S4 from hypertrophy
- may have quiet/no S2
- can get paradoxical splitting
- complications = ASC (angina, syncope, CHF)
mitral regurg
Holosystolic, blowing, high-pitched
radiate to axilla
via ischemia (MI), MVP, LV dilation, RHD, Endocarditis
TR
High-pitched, blowing, holosystolic
loudest at tricuspic area, radiates to right sternal boarder
caused by RV dilation (also RHD or endocarditis)
VSD
holosystolic, harsh
tricuspid area
PDA
Continuous and machine-like, loudest at S2
Hear at left infraclavicular area
Bedside maneuvers
SNS activity on SA and AV nodes:
SA = chronotropy (HR)
AV = dronotropy (conduction velocity)
high-pitched “blowing murmur”
Any regurg
T inversion
recent MI
ST segment
flat = isoelectric = ventricles depolarized but not changing
Depressed = stable angina or subendocardial infarct
Elevated = pizmetal angina or transmural infarct
U-wave
via hypokalemia or bradycardia
Hyperkalemia and hypercalcemia effects on ECG
Both: decrease QT
HyperK+ inreases rate of repolarization (T-wave higher)
Hyper Ca++ also increases rate of repolarization somehow…
Torsades:
Long QT myocytes can pass their depolarization (+ charge) off onto neigbouring cells with normal QT that are already repolarizes → normal QT cells fire again .: ventricle cells all firing at different times (disorganized) = torsades
can become v.fib when the excessive repolarizations organize into loops (re-entry circuits)
Torsades ppt factors:
congenital: romero-ward, jervell and lange-nielsen - K+ ion channel defects, risk of SCD
Low K+, Mg++, Ca++
Drugs:
- Antiarrytmics (Ia + III - K+ blockers)
- antiBiotics (macro)
- antiCychotics (haloperidol)
- antiDepressants (TCA)
- AntiEmetics (ondansetron)
Romero-ward
Dominant
Jervell and lange-neilson
Recessive and sensorineural deafness
Brugada: disease and Rx
Adian males
AD
ST elevation in V1-V3 with pseudo-right bundle branch block
Risk of v. tachyarythmias and SCD
Rx = ICD
Wolf-Parkinson-White
bundle of kent; ventricles fire early
DELTA-wave .: decreases PR, wide QRS
can lead to re-entrant circuits = SVT [accessory path repols, so if it get depolarized again from the bottom (via another part of the ventricle that is still depolarized) the signal will travel UP the bundle into the atria cause a SUPRAventricular tachycardia]
TAPRV
Pulmonary veins drain into right heart
Congenital defects NEEDING other defects to survive:
Tranposition of great vessels (ASD, VSD, or PFO)
Tricuspid atresia (BOTH ASD and VSD)
TAPVR (ASD, sometimes PDA too)
Most common congenital defects: early and late cyanotic
Early = tetralogy
Late = VSD > ASD > PDA
ASD stethoscope
loud S1, fixed wide splitting of S2
ASD types and frequency
Osteum secundum = MC and isolated
Ostium primum = less common, associated with other defects i.e. in Downs
machinelike murmur
PDA
Late differential cyanosis
PDA (cyanosis in lower extremities)
Eisenmenger triad
Late cyanosis, clubbing, polycythemia
FAS heart:
ASD, VSD, PDA, Tetrallogy
Rubella heart:
septal defects, PDA, pulmonary artery stenosis
Diabetic mom, fetal heart
Transposition of great vessels
Marfans heart
MVP, cystic medial degeneration (thoaric AA and disection), aortic regurg
Prenatal lithium
Ebstein anomaly: low tricuspid with small RV
williams syndrome heart
supravalvular aortic stenosis
HTN in young woman: name and histo
Fibromuscular dysplasia of renal artery; string of beads
corneal arcus
lipids in cornea
old = arcus sinilis
young = hyperlipidemia
Smooth muscle migration signals in AS
PDGF, FGF
AS most common in what arteries (descending order)
Abdominal aorta > coronaries > popliteal/femoral > carotids > vertebrals
Abdominal vs throracic aortic aneurism risk factors:
abdominal = AS
thoracic = HTN, bicuspid aortic, CT disease, 3’ syphylis/temporal arteritis/takayasu
Unequal BP in arms with mediastinal widening =
aortic disection
ST depression can mean:
Stable angina
Unstable angina (with T inversion)
MI (NSTEMI, subendocardial, with biomarkers)
ST elevation can mean:
Prizmetal angina (transient)
MI (STEMI, transmural, with cardiac markers)
Prizmetal triggers
Tobacco, cocaine, triptans, ergots
MC arteries in MI
LAD > RCA > L circumflex
Complications post-MI by time:
0-4h; 4-24h, 1-3d, 3-14d, 2w+
0-4h = arrythmyas, HF, cardiogenic shock
4-24h = arrythmyas, HF, cardiogenic shock
1-3d = postinfarcting fibrinous pericarditis (frictoin rub)
3-14d = ruptures: tamponade, MR, VSD. pseudoaneurism via contained free-wall rupture
2+ weeks = real aneurism, Dresslers
contraction band: time and why
4-24h post-MI, via reperfusion injury
STEMI ECG
abnormal heart sounds in hypertrophic cardiomyopathy
S4
Systolic murmur (i.e. mitral regurg because can’t close)
causes of restrictive/infiltrative cardiomyopathy; ECG
sarcoidosis, amyloidosis, hemochomatosis, Loefflers (endomyocardial with eosinophils), endocardio fibroelastosis (young kids)
Diastolic dysfunction, low voltage ECG despite thick mycardium
Drugs that decrease mortality in HF:
ACE-I, ARB, b-blockers, spironolactone, hydralazine (also improves s/s)
bernheim and reverse berhheim
bernheim = LVF → LV enlargement → pushing into RV → obstructs flow → RHF s/s (liver, JVP, edema) but NO pulmonary edema
reverse bernheim = RVF pushing on LV
strep viridans endocarditis:
subacute
abnormal/diseased valves
dental procedures
Valve type and endocarditis:
- normal
- damaged
- prosthetic
- colon cancer
normal = s. aureus
damaged = s. viridans (mutans, sanguis)
prosthetic = s. epidermidis
colon cancer = s. bovis
ECG of acute pericarditis + causes
Wide and elevated S-T and/or PR depression
Causes = idiopathic, infection, radiation, autoimmune, uremia, CV (acute STEMI or dressler), neoplasia
Myxoma vs rhabdomyoma
Myxoma = LA, obstruct mitral, diastolic “tumour plop”, ground substance
Rhabdomyomas = ventricles, kids, with tuberous sclerosis
Kussmal sign: what and causes
Inspiration doesnt transmit to heart, so JVP
Constrictive pericarditis, restrictive cardiomyopathies, right-sided heart tumours
R-R of 5 little ECG boxes =
60bpm (0.2)
rate vs rhythm
rate = SA/AV Rhythm = myocardial AP
Arrythmya of binge drinking
A fib
Arrythmia of hyperthyroidism
a fib
Sawtooth arrythmya
A flutter
Completely erratic arrhythmia; fate
V fib. Death without CPR and defibrillation
A fib vs. a flutter Rx
A fib = antithombotic, rate, rhythm, cardioversion. A flutter = catheter ablation
constant but prolonged P-R
1st degree block
Regularly irregular
2nd degree, Mobitz I/Wenchebach
Random dropped beats (no warning)
2nd degree, Mobitz II. Need pacemaker
No link between atria and ventricles
3rd degree block
Micro cause of 3rd degree block
Lyme
Baro-R affect 4 things:
Contractility, HR, VC, BP
Cushing reaction
Triad: respiratory depression, bradycardia, hypertension
all via increased ICP
PCWP =
LAP
PCWP > LV diastolic P
Mitral stenosis
Irregularly irregular
a fib, no discrete (lose) P-waves
A fib causes:
binge drinking, hypertension, CAD, RHD, HF, valve disease, hyperthyroidism
R-R of 5 little ECG boxes =
60bpm (0.2)
rate vs rhythm
rate = SA/AV Rhythm = myocardial AP
Arrythmya of binge drinking
A fib
Arrythmia of hyperthyroidism
a fib
Sawtooth arrythmya
A flutter
Completely erratic arrhythmia; fate
V fib. Death without CPR and defibrillation
A fib vs. a flutter Rx
A fib = antithombotic, rate, rhythm, cardioversion. A flutter = catheter ablation
constant but prolonged P-R
1st degree block
Regularly irregular
2nd degree, Mobitz I/Wenchebach
Random dropped beats (no warning)
2nd degree, Mobitz II. Need pacemaker
No link between atria and ventricles
3rd degree block
Micro cause of 3rd degree block
Lyme
Baro-R affect 4 things:
Contractility, HR, VC, BP
Cushing reaction
Triad: hypertension, bradycardia, respiratory depression
PCWP =
LAP
PCWP > LV diastolic P
Mitral stenosis
Irregularly irregular
a fib, no discrete (lose) P-waves
A fib causes:
binge drinking, hypertension, CAD, RHD, HF, valve disease, hyperthyroidism
