Shit - Cardio Flashcards
(134 cards)
1
Q
bulbus cordis
A
smooth parts of ventricles (outflow tract)
2
Q
primitive atria/ventricles
A
trabeculated part
3
Q
primitive pulmonary veins
A
smooth part of LA
4
Q
right horn of sinus venosus
A
smooth part of RA = sinus venarum (just incorporated into the atrium)
5
Q
Left horn of sinus venosus
A
Coronary sinus: delivers deO2 blood from the heart into the RA
6
Q
Right common cardinal vein and right anterior cardinal veins
A
SVC
7
Q
How do you form the Membrnaous interventricular septum
A
From endocardial cushion
grows off muscular ventricular septum to join aorticopulonary septum (after it spirals)
8
Q
Role of the endocardial cusions:
A
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)
9
Q
3 fetal shuts: name, vessels, bypasses what
A
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]
10
Q
Fate of PDA
A
Close naturally via increased O2 and decreased plaental prostaglandins
Rx to close = indomethacin (NSAID, decrease PG)
Rx to keep open = PGE1 and PGE2
11
Q
Allantois (urachus) becomes:
A
Median umbilical ligament
12
Q
Umbilical arteries become;
A
MediaL umbilical ligaments
13
Q
umbilical vein becomes:
A
ligamentum teres = round ligament (within falciform)
14
Q
Which artery differ in supply with right and left dominant?
A
Posterior descending
15
Q
Most common coronary artery occluded
A
LAD
16
Q
Peak coronary flow in what part of cycle?
A
Early diastole
17
Q
most posteriro part of heart?
A
Left atrium
18
Q
Supply of AV and SA
A
RCA
19
Q
CO =
A
= HR x SV
= MAP/TPR
= rate of O2 consumption/(Arterial O2 - Venous O2)
20
Q
MAP =
A
= CO x TPR
= 2/3 diast + 1/3 syst.
21
Q
PP =
A
= 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)
22
Q
SV =
EF =
A
SV = EDV - ESV
EF = EDV - ESV / EDV
EF = 55%
23
Q
If HR increases, what will give to keep up withteh HR
A
Diastole
Therefore CO decreases (problem with v. tach)
24
Q
Increase in PP via:
(see head bobbing)
A
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)
25
Decrease PP in:
Aortic stenosis - low S
Cardiogenic shock - low S
Cardiac tamponade - S and D equalize
Advanced heart failure (HF) - low S
26
Acidosis on contractility:
decreases
(H+ into cells, K+ out, increased Na//K; decreased Na//Ca)
27
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
28
Effects of systolic vs diastolic HF on EF
Systolic = decresed EF (\<55%)
Diastolic = same EF (becasue same all relative to EDV; contractility is fine)
29
Resistance =
= 8 x viscosity x length / πr^**4**
= P/CO
30
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
31
Inotrophy graph
+ = catecholamines, digoxin
- = uncomensated HF, Narcotic OD
32
Volume/venous tone graph
+ = fluid infusion, SNS
- = acute bleed, spinal anesthesia
33
TPR graph
- = exercise, AV shunt
+ = pressors
34
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
35
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
36
wide splitting via:
Delayed right ventricle emptying, delaying pulmonary valve closure
- RBBB
- pulmonary stenosis
37
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
38
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
39
Where to listen for flow murmurs (physiological)
Pulonary and aortic areas
40
Aortic and pulonary regurg location:
left sternal boarder
41
hypertrophic cardiomyopathy: where to listen
left sternal boarder
42
Where to hear VSD and ASD
Tricuspid
43
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
44
Mitral stenosis facts:
Diastolic
Opening snap
rumbing
rheumatic fever
decreased S2-OS = increased severity
45
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)
46
mitral regurg
Holosystolic, blowing, high-pitched
radiate to axilla
via ischemia (MI), MVP, LV dilation, RHD, Endocarditis
47
TR
High-pitched, blowing, holosystolic
loudest at tricuspic area, radiates to right sternal boarder
caused by RV dilation (also RHD or endocarditis)
48
VSD
holosystolic, harsh
tricuspid area
49
PDA
Continuous and machine-like, loudest at S2
Hear at left infraclavicular area
50
Bedside maneuvers
51
SNS activity on SA and AV nodes:
SA = chronotropy (HR)
AV = dronotropy (conduction velocity)
52
high-pitched "blowing murmur"
Any regurg
53
T inversion
recent MI
54
ST segment
flat = isoelectric = ventricles depolarized but not changing
Depressed = stable angina or subendocardial infarct
Elevated = pizmetal angina or transmural infarct
55
U-wave
via hypokalemia or bradycardia
56
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...
57
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)
58
Torsades ppt factors:
congenital: romero-ward, jervell and lange-nielsen - **K+ ion channel defects**, risk of **SCD**
Low K+, Mg++, Ca++
Drugs:
* **A**ntiarrytmics (Ia + III - K+ blockers)
* anti**B**iotics (macro)
* anti**C**ychotics (haloperidol)
* anti**D**epressants (TCA)
* Anti**E**metics (ondansetron)
59
Romero-ward
Dominant
60
Jervell and lange-neilson
Recessive and sensorineural deafness
61
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
62
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]
63
TAPRV
Pulmonary veins drain into right heart
64
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)
65
Most common congenital defects: early and late cyanotic
Early = tetralogy
Late = VSD \> ASD \> PDA
66
ASD stethoscope
loud S1, fixed wide splitting of S2
67
ASD types and frequency
Osteum secundum = MC and isolated
Ostium primum = less common, associated with other defects i.e. in Downs
68
machinelike murmur
PDA
69
Late differential cyanosis
PDA (cyanosis in lower extremities)
70
Eisenmenger triad
Late cyanosis, clubbing, polycythemia
71
FAS heart:
ASD, VSD, PDA, Tetrallogy
72
Rubella heart:
septal defects, PDA, pulmonary artery stenosis
73
Diabetic mom, fetal heart
Transposition of great vessels
74
Marfans heart
MVP, cystic medial degeneration (thoaric AA and disection), aortic regurg
75
Prenatal lithium
Ebstein anomaly: low tricuspid with small RV
76
williams syndrome heart
supravalvular aortic stenosis
77
HTN in young woman: name and histo
Fibromuscular dysplasia of renal artery; string of beads
78
corneal arcus
lipids in cornea
old = arcus sinilis
young = hyperlipidemia
79
Smooth muscle migration signals in AS
PDGF, FGF
80
AS most common in what arteries (descending order)
Abdominal aorta \> coronaries \> popliteal/femoral \> carotids \> vertebrals
81
Abdominal vs throracic aortic aneurism risk factors:
abdominal = AS
thoracic = HTN, bicuspid aortic, CT disease, 3' syphylis/temporal arteritis/takayasu
82
Unequal BP in arms with mediastinal widening =
aortic disection
83
ST depression can mean:
Stable angina
Unstable angina (with T inversion)
MI (NSTEMI, subendocardial, with biomarkers)
84
ST elevation can mean:
Prizmetal angina (transient)
MI (STEMI, transmural, with cardiac markers)
85
Prizmetal triggers
Tobacco, cocaine, triptans, ergots
86
MC arteries in MI
LAD \> RCA \> L circumflex
87
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
88
contraction band: time and why
4-24h post-MI, via reperfusion injury
89
STEMI ECG
90
abnormal heart sounds in hypertrophic cardiomyopathy
S4
Systolic murmur (i.e. mitral regurg because can't close)
91
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
92
Drugs that decrease mortality in HF:
ACE-I, ARB, b-blockers, spironolactone, hydralazine (also improves s/s)
93
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
94
strep viridans endocarditis:
subacute
abnormal/diseased valves
dental procedures
95
Valve type and endocarditis:
- normal
- damaged
- prosthetic
- colon cancer
normal = s. aureus
damaged = s. viridans (mutans, sanguis)
prosthetic = s. epidermidis
colon cancer = s. bovis
96
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
97
Myxoma vs rhabdomyoma
Myxoma = LA, obstruct mitral, diastolic "tumour plop", ground substance
Rhabdomyomas = ventricles, kids, with tuberous sclerosis
98
Kussmal sign: what and causes
Inspiration doesnt transmit to heart, so JVP
Constrictive pericarditis, restrictive cardiomyopathies, right-sided heart tumours
99
R-R of 5 little ECG boxes =
60bpm (0.2)
100
rate vs rhythm
rate = SA/AV Rhythm = myocardial AP
101
Arrythmya of binge drinking
A fib
102
Arrythmia of hyperthyroidism
a fib
103
Sawtooth arrythmya
A flutter
104
Completely erratic arrhythmia; fate
V fib. Death without CPR and defibrillation
105
A fib vs. a flutter Rx
A fib = antithombotic, rate, rhythm, cardioversion. A flutter = catheter ablation
106
constant but prolonged P-R
1st degree block
107
Regularly irregular
2nd degree, Mobitz I/Wenchebach
108
Random dropped beats (no warning)
2nd degree, Mobitz II. Need pacemaker
109
No link between atria and ventricles
3rd degree block
110
Micro cause of 3rd degree block
Lyme
111
Baro-R affect 4 things:
Contractility, HR, VC, BP
112
Cushing reaction
Triad: respiratory depression, bradycardia, hypertension
all via increased ICP
113
PCWP =
LAP
114
PCWP \> LV diastolic P
Mitral stenosis
115
Irregularly irregular
a fib, no discrete (lose) P-waves
116
A fib causes:
binge drinking, hypertension, CAD, RHD, HF, valve disease, hyperthyroidism
117
R-R of 5 little ECG boxes =
60bpm (0.2)
118
rate vs rhythm
rate = SA/AV Rhythm = myocardial AP
119
Arrythmya of binge drinking
A fib
120
Arrythmia of hyperthyroidism
a fib
121
Sawtooth arrythmya
A flutter
122
Completely erratic arrhythmia; fate
V fib. Death without CPR and defibrillation
123
A fib vs. a flutter Rx
A fib = antithombotic, rate, rhythm, cardioversion. A flutter = catheter ablation
124
constant but prolonged P-R
1st degree block
125
Regularly irregular
2nd degree, Mobitz I/Wenchebach
126
Random dropped beats (no warning)
2nd degree, Mobitz II. Need pacemaker
127
No link between atria and ventricles
3rd degree block
128
Micro cause of 3rd degree block
Lyme
129
Baro-R affect 4 things:
Contractility, HR, VC, BP
130
Cushing reaction
Triad: hypertension, bradycardia, respiratory depression
131
PCWP =
LAP
132
PCWP \> LV diastolic P
Mitral stenosis
133
Irregularly irregular
a fib, no discrete (lose) P-waves
134
A fib causes:
binge drinking, hypertension, CAD, RHD, HF, valve disease, hyperthyroidism
