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
STEMI ECG
