Cardiology Flashcards
1
Q
Embryology: Truncus arteriousus
A
ascending aorta and pulmonary trunk
2
Q
Embryology: Bulbus cordi
A
smooth parts (outflow tract) of left and right ventricles
3
Q
Embryology: endocardial cushion
A
atrial septum, membranous interventricular septum, AV and semilunar valves
4
Q
Embryology: primitive atrium
A
trabeculated part of left and right atria
5
Q
Embryology: primitive ventricle
A
trabeculated part of left and right ventricles
6
Q
Embryology: primitive pulmonary vein
A
smooth part of left atrium
7
Q
Embryology: left horn of sinus venosus
A
coronary sinus
8
Q
Embryology: right horn of sinus venosus
A
smooth part of right atrium (sinus venarum)
9
Q
Embryology: right common cardinal vein and right anterior cardinal vein
A
Superior vena cava
10
Q
Heart beats by what week?
A
4 weeks
11
Q
cardiac looping
A
primary heart tube loops to establish left-right polarity; begins in week 4 of gestation
problems with cardiac looping cause a defect in left-right dynein (involved in LR asymmetry) can lead to dextrocardia, as seen in kartagener syndrome (primary ciliary
12
Q
______is a rare heart condition in which your heart points toward the right side of your chest instead of the left side.
A
Dextocardia
13
Q
which two structures fuse to form the foramen ovale
A
septum secundum and septum primum fuse
soon after birth the foramen ovale closes due to increased left atrial pressure
14
Q
Septation of the chambers
A
1) septum primum grows towards the endocardial cushions, narrowing foramen primum
2) foramen secundum forms in septum primum. Foramen primum disappears
3) septum secundum develops as foramen secundum maintains right to left shunt
4) septume secundum expands and covers most of the foramen secundum. The residual foramen is the foramen ovale
5) remainder of septum primum forms valve of foramen ovale
15
Q
Ventricles morphogenesis
A
1) muscular interventricular septum forms. Opening is the interventricular foramen
2) aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing the interventricular foramen
3) growth of the endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portions of the interventricular septum
16
Q
Most common congenital cardiac anomaly?
A
Ventricular septal defect
17
Q
Aortic/pulmonary valves are derived from
A
endocardial cushions of outflow tract
18
Q
mitral/tricuspid valves are derived from
A
fused endocardial cushions of the AV canal
19
Q
Fetal circulation
A
From placenta –> umbilical vein (PO2 of 30 mmHg and is 80% saturated with O2) –> liver OR ductus venosus –> ductus venosus bypasses hepatic circulation –> IVC –> foramen ovale –> aorta –> head and body
Deoxy blood from SVC goes from RA to RV –> main pulmonary artery –> ductus arteriosus (connecting the main pulmonary artery to the proximal descending aorta.) –> descenting aorta
shunt is due to high fetal pulmonary artery resistance due to low O2 tension.
20
Q
Why does the ductus arteriosus close
A
Increase in O2 due to respiration and decrease in prostaglandins from placental separation causes closure of ductus arteriorsus
Indomethacin helps close PDA/patent ductus arteriosus –> ligamentum arteriosum
Prostaglandins E1 and E2 keep the PDA open
21
Q
Why does the foramen ovale close
A
At birth –> take breathe –> decreases resistance in pulmonary vasculature –> increases left atrial pressure vs right atrial pressure–> foramen ovale closes (now fossa ovalis)
22
Q
Fetal postnatal derivatives: Allantois–> urachus
A
Median umbilical ligament
23
Q
Fetal postnatal derivatives: ductus arteriosus
A
ligamentum arteriosum
24
Q
Fetal postnatal derivatives: ductus venosum
A
ligamentum venosum
25
Fetal postnatal derivatives: foramen ovale
fossa ovalis
26
Fetal postnatal derivatives: notochord
nucleus pulposus
27
Fetal postnatal derivatives: umbilical arteries
medial umbilical ligaments
28
Fetal postnatal derivatives: umbilical vein
ligamentum teres hepatis (round ligament). contains the falciform ligament
29
What artery supplies the lateral and posterior walls of the left ventrical and anterolateral papilalry mm
left circumflex coronary artery
30
What artery supplies anterior 2/3 of interventricular spetum, anterolateral papilalry muscle, and anterior surface of left ventricle
Left anterior descending artery
31
What artery supplies the right ventricle
Right(acute) marginal artery
32
What artery supplies the AV node, posterior 1/3 of interventricular septum, posterior 2/3 walls of ventricles and posteromedial papilalry mm
posterior descending/interventricular artery (PDA)
33
What supplies the SA node
RCA
34
what supplies the AV node
PDA
35
Right vs left dominant circulation
Right dominant circulation (85%) = PDA arises from RCA
Left dominant circulation (8%) = PDA arises from LCX
Codominant circulation = PDA from both LCX and RCA
36
Where does coronary artery occlusion most commonly occur?
Left anterior descending artery (LAD)
37
When does coronary blood flow peak?
in early diastole
38
What is the most posterior part of the heart? Its enlargement causes what problems?
Left atrium
causes dysphagia due to compression of the esophagus
Causes hoarseness due to compression of the left recurrent laryngeal nerve
39
The layers of the pericardium and its innervation
1) (outer) Fibrous pericardium
2) Parietal layer of serous pericardium
- ---pericardial cavity---
3) Visceral layer of serous pericardium
Innervation is phrenic nerve. Referred pain to shoulder
40
Cardiac output
CO= SV x HR
during early exercise: CO maintained by increase HR and SV
during late exercise: CO maintained by only increase HR and SV plateaus
41
Ficks principle of Cardiac Output
CO=rate of O2 consumption/ (arterial O2 content-venous O2 content)
42
Mean arterial pressure
MAP = CO x Total Peripheral resistance (TPR)
MAP at resting HR= 2/3 diastolic pressure + 1/3 systolic pressure
43
Pulse pressure
Pulse pressure = systolic pressure - diastolic pressure
proportional to SV
Inversely proportional to arterial compliance
increases in hyperthyroidism, aortic regurg, aortic stiffening(isolated systolic hypertension), obstructive sleep apnea (increased sympathetic tone), anemia, exercise
decreases in aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF
44
Stroke volume
SV= EDV-ESV
affected by contractility, afterload, and preload
SV increase with increase contractility, increased preload (i.e. early pregnancy), and decreased afterload
45
What happens to diastole as HR increases?
shortened because less filling time and drop in CO
46
What effect does Catecholamine stimulation have on stroke volume? contractility? How?
Increases stroke volume and contractility via stimulation of β1 receptor.
Ca channels are phosphorylated --> increases Ca entry --> increases Ca induced Ca release and Ca storage in sarcoplasmic reticulum
phospholamban (membrane protein that regulates the Ca2+ pump in cardiac muscle cells) phosphorylation --> active Ca ATPase --> increases Ca storage in sarcoplasmic reticulum
47
What effect does Digitalis have on stroke volume? contractility? How?
Increases stroke volume and contractility by blocking Na/K pump
This increases intracellular Na --> decrease Na/Ca exchanger activity --> increases intracellular Ca
note: decrease in extracellular Na causes increase in SV and Contractility by decreasing activity of Na and Ca exchanger
48
Preload
preload is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand.
depends on venous tone and circulating blood volume. If you use vasodilators it decreases your preload.
49
Afterload
Afterload is the pressure against which the heart must work to eject blood during systole (systolic pressure). The lower the afterload, the more blood the heart will eject with each contraction.
50
What determines afterload
It is approximated by MAP
Increase in afterload -> increase in pressure --> increase wall tension per Laplace law. The left ventrical will compensate for this by thickening the wall muscle and thus decreasing wall tension
51
What effect does ACE inhibitors and ARBs have on preload? afterload?
Decrease both
52
Wall tension
follows Laplace's law
Wall tension = pressure x radius
53
Wall stress
Wall stress=(pressure x radius)/(2*wall thickness)
54
Ejection fraction
Index of ventricular contractility
EF= SV/EDV=(EDV-ESV)/EDV
55
Starlings curve
y axis: SV or CO
X axis: Ventricular EDV or preload
force of contraction is proportional to end diastolic length of cardiac mm fiber (preload)
56
How does the starling curve shift with exercise
Left (increased contractility/inotropy)
57
How does the starling curve shift with HF+digoxin? HF alone?
Both shift right (decreased contractility/inotropy)
58
How does the starling curve shift with catecholamines, positive inotropes like digoxin?
Left (increased contractility/inotropy)
59
How does the starling curve shift with loss of myocardium (MI), beta blockers, non-dihydropyridine Ca blockers, dilated cardiomyopathy, narcotic overdose, HF with reduced EF, sympathetic inhib?
shift right (decreased contractility/inotropy)
60
Resistance, pressure, and flow equations
ΔP=change in pressure= Q x R
Q=volumetric flow rate= flow velocity(v) x cross sectional area (A)
R=ΔP/Q= 8ηL/πr^4
η=viscosity which depends on hematocrit
61
Total resistance of vessels in series
R1 +R2 etc
62
Total resistance of essels in parallel
1/R1 + 1/R2 etc
63
What has the lowest flow velocity?
Capillaries due to high cross sectional area
64
What accounts for most of total peripheral resistance (TPR)?
Arterioles
65
Compliance
= ΔV/ΔP
66
In the cardiac and vascular fx curves, what does the intersection of the two curves mean?
operating point of the heart
venous return=CO
67
S1 heart sound
mitral and tricuspid valve closure.
Loudest at mitral area
68
S2 heart sound
aortic and pulmonary valve closure
loudest and left upper sternal border
69
S3 heart sound
S2 S3 S1
early diastole
Rapid ventricullar filling phase
associated with increased filling pressures (mitral regurg or HF or dialted ventricles)
Can be normal in children, young adults, pregnant women
70
S4 heart sound
S4 S1 S2
late diastole
best heart at apex with patient in left lateral decubitus position
Due to high atrial pressure or ventricular noncomplaince because left atrium must push against stiff LV wall.
always abnormal
71
Jugular venous pulse (JVP) - a wave
atrial contraction
absent in a fib
72
Jugular venous pulse (JVP) - c wave
RV contraction
closed tricuspid valve bulging into atrium
73
Jugular venous pulse (JVP) - x descent
downward displacement of closed tricuspid valve during rapid ventricular ejection phase
reduced or absent in tricuspid regurg and right HF because pressure gradients are reduced
74
Jugular venous pulse (JVP) - v wave
increase in RA pressure due to filling against closed tricuspid valve
think "villing"
75
Jugular venous pulse (JVP) - y descent
RA emptying into RV
prominent in constrictive pericarditis
absenct in cardiac tamponade
76
Why does normal splitting occur
on Inspiration
drop in intrathoracic pressure which increases venous return and RV filling. This causes an increase in RV SV and RV ejection time. There is a delay in the closure of pulmonic valve
S2 (aortic and pulmonic valve) --> now A2 and delayed P2
77
Why does wide splitting occur
Conditions that delay RV emptying (pulmonic stenosis, RBBB)
exaggeration of normal splitting where S2 has a normal A2 but an exaggerated delay in P2.
there is normally a delay on inspiration but now its exaggerated
78
Why does fixed splitting occur
Atrial septal defect
ASD there is a left to right shunt which increases RA and RV volumes. This increase in volume also increases the flow through the pulmonic valve, such that regardless of inspiration or expiration...there is a greatly delayed pulmonic valve closure
Sa --> A2 ---------> P2
79
Why does paradoxical splitting occur?
Conditions that delay aortic valve closure ( aortic stenosis, LBBB). A split that is heard on expiration but reduced on inspiration.
normal order is reversed and P2 sounds occur before delayed A2 sounds. Therefor when on inspiration --> there is a delay in P2 sounds which bring P2 closer to the A2. Thereby paradoxically eliminating the split.
80
Murmur heard at Aortic area? conditions that could cause it?
Systolic murmur
Aortic senosis
Flow murmur
Aortic valve sclerosis
81
Murmur heard at the Pulmonic area? conditions that cause it?
Systolic ejection murmur
pulmonic stenosis
flow murmur
atrial septal defect
82
Murmur heard at tricuspid area? conditions that cause it?
Holosystolic murmur due to tricuspid regurg and ventricular septal defect
Diastolic murmur due to tricuspid stenosis
83
Murmur heard at mitral area? conditions that cause it?
Holosystolic murmur due to mitral regurg
Systolic murmur due to mitral valve prolapse
Diastolic murmur due to mitral stenosis
84
What is a holosystolic murmur?
A holosystolic murmur begins at the first heart sound (S1) and continue to the second heart sound (S2)
85
Heart murmur related to aortic stenosis?
- crescendo-decrescendo systolic ejection murmur
- soft S2 (ejection click may be present)
- LV pressure > aortic pressure during systole
- Loudest at heart base and radiates to the carotids
- "pulsus parvus et tardus" - pulses are weak with a delayed peak
- SAD --> syncope, angina, dyspnea
- mostly due to calcification of bicuspid aortic valve
S1 /\/\/\/\/\/~~~~~S2
86
what is a crescendo-decrescendo murmur?
crescendo—decrescendo murmurs (diamond or kite-shaped murmurs), a progressive increase in intensity is followed by a progressive decrease in intensity.
87
Heart murmur related to mitral/tricuspid regurg?
- Holosystolic, high pitched "blowing murmur"
- Both can be due to rheumatic fever and infective endocarditis
- Mitral regurg is loudest at apex and goes to axilla. Usually due to ischemic heart dz post MI, mitral valve prolapse, LV dilation
- Tricuspid regurg is loudest at tricuspid area. Usually due to RV dilation
S1/\/\/\/\/\/\/\/\/\/\/\S2
88
Heart murmur associated with mitral valve prolapse?
Most frequent valvular lesion and best heard over apex. Usually benign
Late systolic crescendo (high intensity just before S2) murmur with midsystolic click due to sudden tensing of chordae tendineae
can be due to myxomatous degeneration ( due to marfan or ehlers danlos syndrome), rheumatic fever, chordae rupture
S1---------CLICK-/\/\/\/\/\/\/\ S2
89
Heart murmur associated with ventricular septal defect?
holosystolic, harsh sounding murmur
loudest at tricuspid
S1/\/\/\/\/\/\/\/\/\/S2
90
Heart murmur associated with aortic regurg?
High pitched blowing
Early long diastolic decrescendo (low intensity) murmur
hyperdynamic pulse
Head bobbing when severe and chronic
wide pressure pulse
due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever. Progresses to left HF
S1 S2 /\/\/\/\/~~~~~~~~~~~~~~~
91
Heart murmur associated with mitral stenosis?
Follows an opening snap due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips
mid to late diastolic murmur.
Decreased delay between S2 and snap means greater severity
LA >>>> pressure than LV
Due to rheumatic fever. Can also get because chronic MS can result in LA dilation --> compress esophagus and L recurrent laryngeal nerve --> dysphagia and hoarseness
S1 S2 SNAP ~~~~~~~~
92
Heart murmur associated with patent ductus arteriosus?
continuous machine like murmur
best heard at left infraclavicular area
loudest at S2
due to congenital rubella or prematurity
S1 ~~~~~/\/\/\/\S2\/\/\/\~~~~~~
93
Mycocardial AP phases 0-4
0) voltage gated Na channels open (rapid upstroke and depolarization)
1) Inactivation of voltage gated Na channels and voltage gated K channels begin to open. (Initial repolarization)
2) Calcium influx through voltage gated Ca channels balances K+ efflux. Ca influx triggers Ca release from sarcoplasmic reticulum and myocyte contraction. (Plateau)
3) massive K+ efflux due to opening of voltage gated slow K+ channels and closure of voltage gated Ca channels (rapid repolarization)
4) High K+ permeability through K+ channels (resting potential (-85 mV)
94
Hand grip
Increases afterload
Increases intensity of mitral regurg, aortic regurg, and ventricular septal defect murmurs
decreases hypertrophic cardiomyopathy and aortic stenosis murmurs
Later onset of click/murmur for mitral valve prolapse
95
Valsalva (phase II)
| Standing up
standing up decreases preload
decreases intensity of most murmurs
increases intensity of hypertrophic cardiomyopathy murmur
Mitral valve prolapse has an earlier onset of click
96
Rapid squatting
Increases venous return
which increases preload
Which increases afterload
Decreases intensity of hypertrophic cardiomyopathy murmur
Increases intensity of AS, MR, and VSD murmur
Mitral valve prolapse has a later onset of click
97
Cardiac vs skeletal mm AP differences
Cardiac mm AP has a plateau which is due to Ca influx and K efflux
Cardiac mm contraction requires Ca influx from ECF to induce Ca release from SR
Cardiac myocytes are electrically coupled to each other by gap junctions
98
Pacemaker action potential
SA and AV nodes
phase 4: slow spontaneous diastolic depolarization due to If (funny current) from If channels. If channels are slow mixed Na/ K inward current, they are what causes the automaticity of SA and AV nodes. The slope is in the SA node and determines HR.
Phase 0: upstroke - opening of the voltage gated Ca channels. Fast voltage gated Na channels are premanently inactivated. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles
Phase 1: absent
Phase 2: absent
Phase 3: re-polarization due to inactivation of the Ca channels and increase activation of K+ channels which increases K+ efflux
99
Conduction pathway in the heart
SA node --> atria --> AV node --> bundle of his --> right and left bundle branches --> purkinje fibers --> ventricles
100
What is the pacemaker of the heart?
SA node
101
Where is the AV node and why is it important?
interatrial septum
blood supply usually the RCA
100msec delay that allows for the ventricular filling before contraction
102
Speed of conduction in the heart (greatest to lowest?
purkinje>atria>ventricles>AV node
103
P wave?
QRS interval?
T wave?
U wave?
P wave - atrial depolarization
QRS interval - venricular depolarization
T wave - ventricular repolarization (inversion may indicate ischmia or recent MI)
U wave? prominent in hypUkalemia. Smal wave after T wave
104
Torsades de pointes
polymorphic ventricular tachycardia
From: long QT interval
Becomes: v fib
causes? drugs, low potassium, low Mg,
Tx? magnesium sulfate
105
Drugs that induce long QT?
```
A - antiArrhythmics (classIA and III)
B- antiBiotics
C - antiCychotics
D- antiDepressants
E-antiEmetics
```
106
Congenital syndromes that can cause a long QT?
Romano-ward syndrome-autosomal dominant, pure cardiac phenotype with no deafness
Jervell and Lange-nielsen syndrome - autosomal recessive, sensorineural deafness
107
The most common type of ventricular preexcitation syndrome? with characteristic delta wave?
Wolff-parkinson white syndrome
abnormal fast accessory conduction pathway from atria to ventricle (bundle of kent) bypasses the rate slowing AV node
ventricles begin to partially depolarize earlier causing the delta wave with widened QRS complex and shortened PR interval
may result in reentry circuit --> supraventricular tachycardia
108
What ECG tracing causes irregularly irregular heartbeat?
Atrial fibrillation
Can lead to stroke
109
What ECG tracing causes a sawtooth patttern?
Atrial flutter
back to back depolarization
definitive treatment is catheter ablation
110
What ECG tracing has no discernible rhythm and need immediate CPR and defib?
V fib
111
Which block pattern has a prolonged PR?
First degree AV block
prolonged but same PR interval for each
benign and no tx needed
112
Which block pattern has a progressive lengthening of PR intervals until a beat is dropped?
Mobitz type I (wenckebach)
113
Which block pattern has dropped beats without a change in the PR interval length?
Mobitz type II
Treat with pacemaker or it will progress to a type III
114
Which block pattern shows atria and ventricles beating independently of eachother?
third degree (complete) AV block
arial rate> ventricular rate
needs pacemaker
can be caused by lyme disease
115
What peptide is released in response to increased blood volume and atrial pressure?
atrial natriuretic peptide (ANP) is released from the atrial myocytes
acts via cGMP to cause vasodilation and decrease Na reabsorption at the renal collecting tubules
It also contributes to the aldosterone escape mechanism by dialating afferent renal arteriolsies and constricting efferent arterioles thus promoting diuresis
116
What peptide is released in response to increased tension?
B type (brain) natriuretic peptide is released by the ventricular myocytes
similar to ANP except longer half life
117
What peptide is a good blood test for diagnosing HF?
BNP has a very good negative predictive value
can also be used for treatment in HF via recombinant form (nesiritide)
118
How do the receptors in the aortic arch transmit information? and to where?
via vagus nerve to the solitary nucleus of medulla
119
How do teh receptors in the carotid sinus transmit information? and to where
via glossopharyngeal nerve to solitary nucleus of medulla
120
What does the carotid massage do and how does it happen?
The carotid massage decreases HR
By pushing down on the carotid --> increase pressure --> increases the signals back to the solitary nucleus via glossopharyngeal --> ultimately causes an increase in the AV node refractory period --> decreases HR
121
The cushings reflex
triad of HTN, bradycardia, and respiratory depression
The increase in the intracranial pressure constrict arterioles and causes cerebral ischemia. This causes an increase in the partial pressure of pCO2 and decrease pH
This results in the central reflex --> increase in sympathetics --> increase in perfusion pressure (HTN) --> increase stretch --> peripheral reflec baroreceptors induce bradycardia
122
peripheral chemoreceptors
carotid and aortic bodies respond to high pCO2, low pO2, low pH
123
central chemoreceptors
stimulated by changes in pH and pCO2 in brain which depends on arterial pCO2 levels
DO NOT directly respond to pO2
124
Pulmonary capillary wedge pressure
Left atrial pressure
measured by a pulm artery catheter (swan-Ganz catheter)
125
Autoregulation in the heart
Vasodilatory via adenosine, NO, CO2 (pH), decrease O2
126
Auto regulation in the brain
vasodilatory via CO2 (pH)
127
Autoregulation via in the lungs
the pulmonary vasculatory is unique because hypoxia causes vasoconstriction so that only well ventilated areas are perfused
128
Net fluid flow equation for capillary fluid exchange
Jv=net fluid flow= Kf[(Pc-Pi)-σ(πc-πi)]
kf=capillary permeability
Pc=capillary pressure
Pi=interstitial pressure
σ= reflection coefficient that measures capillary permeability to protein
πc=plasma oncotic pressure pulls fluid into capillary
πi=interstitial fluid oncotic pressure pulls floid out of capillary
129
Right to left shunts have ____ babies? What anomalies cause it? how to treat it?
Blue babies - think "eaRLy" cyanosis tx with maintenance of PDA via prostaglandin administration
5 Ts:
1) Truncus arteriosus ( 1 vessel)
2) Transposition ( 2 switched vessels)
3) Tricuspid atresia (3=tri)
4) Tetralogy of fallor (4=tetra)
5) TAPVR (5 letters)
130
Persistent truncus arteriosus
fails to divide into pulm trunk and aorta
R-->L
blue baby
131
D transposition of great vessels
Aorta leaves RV and pulmn trunk leaves LV
systemic and pulmonary circulation is seperated
fatal - needs surgery or VSD/PDA/patent foramen ovale
R--> L blue baby
132
Tricuspid atresia
absent tricuspid and RV hypoplastic
needs both ASD and VSD
R--> L blue baby
133
Tetralogy of fallot
MOST COMMON cause of cyanosis/ blue baby. R--> L
caused by the anterosuperior displacement of the infundibular septum
Think PROVe
1) Pulm infundibular stenosis - important for prognosis because it forces the R-->L flow across the VSD and causes RVH
2) RV hypertrophy --> boot shape
3) Overriding aorta
4) VSD
pt has "tet spells" - crying, fever, exercise due to exacerbation of RV outflow obstruction.
R--> L blue baby
134
How does squatting help with tet spells in tetralogy of fallot?
Squatting increases SVR which then causes a decrease in the R--> L shunt and improves cyanosis
135
Total anomalous pulmonary venous return
pulmonary veins drain into right heart circulation
normally pulmonary veins drain into the left atrium and bring oxygenated blood from the lungs
R-->L blue baby
136
Ebstein anomaly
Displacement of tricuspid valve leaflets downward into RV causing tricuspid regurg, accessory conduction pathways, and right sided HF
lithium exposure in utero
R---> L blue baby
137
Left to right shunt have ______ babies? what congenital conditions?
think L--> R as LateR cyanosis. Babies are acyanotic on presentation
1) VSD
2) ASD
3) PDA
4) Eisenmenger syndrome
138
What is the most common congenital cardiac defect?
Ventricular septal defect - increase O2 saturdation in RV and Pulm artery
VSD>ASD>PDA
139
Atrial septal defect
wide split fixed S2
ostium secundum defect is most common
O2 saturation increases in RA,RV, and pulmonary artery
may lead to paradoxical emboli- systemic venous emboli bypass lungs and become systemic arterial emboli
140
Patent ductus arteriousus
machine like continuous mumur
Maintain patency with PGE and low O2 tension. This is important in conditions like transposition of the great vessels.
Indomethancin (think ENDomethacin) ends patency
141
What syndrome do we worry about in an uncorrected L--> R shunt that can become a R-->L shunt pathologically?
Eisenmenger syndrome
uncorrected left to right shunt causes increase in pulmonary blood flow--> pathological remodeling of vasculature --> pulmonary arterial HTN --> RVH to compensate --> now a right to left shunt
signs: late cyanosis, clubbing, polycythemia
142
Coarctation of the aorta
Aortic narrowing near insertion of ductus arteriosus
HTN in UE and weak delayed pulse in LE
Associated with turners syndrome and HF, increased risk of berry aneurysm, aortic rupture, endocarditis
143
Primary (essential hypertension)
due to increased CO or increased TPR
most HTN cases
144
Secondary HTN
renal/renovascular dz related such as fibromuscular dysplasia ( string of beads appearance of renal artery)
145
HTN urgency? emergency?
urgency is >= 180/120 but no end organ damage
| Emergency is HTN with end organ damage
146
pt presents with hypercholesterolemia and are at risk of ____ affecting their eye?
Corneal arcus
elderly pt
147
Two types of arteriolosclerosis (small vessels and arterioles)
1) hyaline - thickening of vessel walls in essential HTN or DM
2) hyperplastic - onion skinning in severe HTN with proliferation of smooth MM cells
148
Arteriosclerosis that affects medium sized vessels. Internal elastic lamina and media of arteries are calcified
Monckeberg sclerosis (medial calcific sclerosis)
vascular stiffening without obstruction
pipestem appearance on xray
149
Atherosclerosis is
a type of arteriosclerosis caused by buildup of cholesterol plaques
Abdominal aorta> coronary artery>poplitieal artery>carotid artery
150
pathogenesis of atherosclerosis
inflammation important
endothelial cell dysfunction --> macrophage and LDL accumulation --> foam cell formation --> fatty streaks --> smooth mm cell migration, proliferation, and extracellular matrix deposition --> fibrous plaque --> complex atheromas
151
Aortic aneurysm
abdominal infrarenal typically associated with atherosclerosis
thoracic ones are associated with cystic medial degeneration. CT diseases are a risk factor (i.e marfan which also has risk of aortic dissection) and tertiary syphilis
trauma related is mostly at aortic isthmus
152
pt with back pain that has different BP in arms
aortic dissection!
Stanford type A: proximal. Ascending aorta. Can result in aortic regurg or cardiac tamponade. Needs surgery
Stanford type B: distal. descending aorta Below ligamentum arteriosum. give Beta blockers then vasodilators
153
Chest angina
Chest pain due to ischemia secondary to coronary artery narrowing or spasm
stable: pain on exertion, ST depression
unstable: pain at rest, ST depression and or T wave inv
vasospastic: coronary artery spasm, transient ST elevation
154
Pt has coronary stenosis and is resulting in maximally dilated vessels distal to the stenosis. Think pharmacologic stress test.
Coronary steal syndrome
give vasodilators --> dilation --> so blood is shunted toward well perfused areas but then ischemia in myocardium perfused by stenosed vessels
155
NSTEMI
subendocardial infarct
subendocardium (inner 1/3) especially vulnerable to ischemia
ST depression on ECG
156
STEMI
Transmural infarct
fullthickness of myocardial wall involved
ST elevation
Q waves
157
Pt has a ruptured coronary artery atherosclerotic plaque that has caused acute thrombosis.
MI
elevated CK-MB and Troponins are diagnostic
158
What is the order of arteries most common sclerosed in an MI
LAD>RCA>circumflex
159
0-24 hrs after an MI
early coagulative necrosis , wavy fibers, neutrophils
reperfusion injury concern
160
1-3 days after an MI
extensive coagulative necrosis
Hyperemia
tissue surrounding infarct has acute inflammation with neutrophils
postinfarction fibrinous pericarditis --> friction rub
161
3-14 days after an MI
hypereremic border, central yellow brown softening.
macrophages then granulation tissue at margins
free wall rupture can result in cardiac tamponade
papillary muscle rupture can cause mitral regurg
interventricular septal rupture due to macrophage mediated structural degradation
LV pseudo aneurysm due to a contained free wall rupture
162
2 wks to several months after an MI
Now gray white
contracted scar complete
True ventricular aneurysm
Dressler syndrome - autoimmune phenomenon resulting in fibrinous pericarditis "dress for your heart"
163
DX of MI in first 6 hours
first 6 hours: ECG gold standard
164
When is cardiac troponin begin to rise? peak? how long does it remain high?
cardiac troponin rises at 4 hours and peaks at 24 hours and is high for 7-10 days
165
When is CK-MB begin to rise? peak? how long does it remain high?
rises after 6-12 hours
peaks at 16-24 hours
returns to normal at 48 hours
good for acute MI
166
Anteroseptal leads and what is their blood supply
V1-V2
LAD
167
Anteroapical leads and bloody supply
V3-V4
distal LAD
168
Anterolateral leads and blood supply
V5-V6
LAD or LCX
169
Lateral leads and blood supply
I, aVL
LCX
170
Inferior leads and blood supply
II,III,aVF
RCA
171
Posterior leads
V7-V9
PDA
172
What is a pt with an MI likely to die from before reaching the hospital and within the first 24 hours post MI?
cardiac arrhythmia
173
Unstable angina/NSTEMI treatment
```
Anticoagulation (heparin)
Anti platelet therapy (aspirin)
ADP receptor inhibitors
Beta blockers
ACEi
Statins
SX control with nitroglycerin and morphine
```
174
STEMI tx
```
Anticoagulation (heparin)
Anti platelet therapy (aspirin)
ADP receptor inhibitors
Beta blockers
ACEi
Statins
SX control with nitroglycerin and morphine
Reperfusion therapy is most important - percutaneous coronary intervention preferred over fibrinolysis
```
175
Most common cardiomyopathy that present swith HF, S3, systolic regurg murmur
Dilated cardiomyopathy --> balloon appearance of heart on CXR. Leads to a systolic dysfunction and has eccentric hypertrophy. Sarcomeres are added in series.
```
Chronic alcohol abuse
Wet beriberi
Coxsackie B viral myocarditis
Chronic cocaine use
Chagas disease
Doxorubicin toxicity
```
tx: Na restriction, ACE inhib, beta blockers, diuretics, digoxin, ICD, heart transplant
176
pt presents with ventricular apical balloon after a stressful situation
Takotsubo cardiomyopathy
broken heart syndrome
177
Pt is a young athlete that was exercising and experienced a syncope. Physical exam findings included a S4 and systolic murmur. Mitral valve closure was also impaired. Pt was pronounced dead later.
Hypertrophic obstructive cardiomyopathy - a diastolic dysfunction. most commonly due to mutations in genes encoding sarcomeric proteins such as myosin binding protein C and beta myosin heavy chain. Sarcomeres are added in parallel.
death due to ventricular arrhythmia
cease high intesity exercise, beta blockers, or non dihydropyridine Ca channel blockers.
178
Physiology behind hypertrophic obstructive cardiomyopathy
asymmetric septal hypertrophy and systolic anterior motion of mitral valve. This causes an outflow obstruction and ultimately dyspnea and syncope. An arrhythmia can cause death in these patients
179
Type of restrictive/infiltrative cardiomyopathy with hypereosinophilic syndrome
Loffler endocarditis
histology shows eosinophilic infiltrates in myocardium
180
What is the most likely cause of RHF
LHF
cor pulmonale though refers to an isolated cause due to pulmonary cause
181
systolic vs diastolic dysfunction
systolic: reduced EF and increased EDV. Decreased contractility
diastolic: preserved EF, normal EDV, decreased compliance(increased end diastolic pressure)
182
Signs of left heart failure
orthopnea (SOB when supine)
paroxysmal nocturnal dyspnea ( breathlessness waking you up)
Pulmonary edema (increase in pulm VP --> venous distention and transudation of fluid)
presence of hemosiderin laden macrophages in lungs
183
Presence of hemosidern laden macropages in the lungs indicates
Left HF
184
Signs of right heart failure
Hepatomegaly (nutmeg liver)
Jugular venous distention
Peripheral edema
185
Obstructive shock
cardiac tamponade
pulmonary embolism
tension pneumothorax
186
Distributive shock
sepsis
anaphylaxis
CNS injury
compared to other forms of shock (cold and clammy), distributive can be warm or dry. If its warm then there is deceased preload, increased CO, and decreased afterload/SVR. If it is dry then its decreased preload, decreased CO, decreased afterload/SVR.
187
Symptoms of bacterial endocarditis
FROM JANE
```
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail bed hemorrhage
Emboli
```
188
Acute vs subacute bacterial endocarditis
Acute is caused by S aureus with high virulence. It results in large vegetaions on previously normal valves. Rapid onset.
subacute- viridans strep with low virulence. smaller vegetation on congenitally abnormal or diseased valves.
189
What are you at risk for due to dental procedures
subacute bacterial endocarditis
190
What valve is most commonly involved in bacterial endocarditis
mitral valve
191
What valve is most commonly involved in IV drug users
tricuspid valve
"dont tri drugs"
192
A consequence of pharyngeal infection with group A beta hemolytic infection
Rheumatic fever --> rheumatic heart dz affecting mitral >aortic>tricuspid
early: mitral regurg
late: mitral stenosis
193
This is associated with aschoff bodies (granuloma with giant cells), anitschkow cells (enarged macrophages with ovoid,wavy,rod like nucleus), increase in antistreptolysin O titers
Rheumatic fever
J<3NES criteria
```
J-joints (migratory polyarthritis)
<3 carditis
N-nodules (subq)
E-erythema marginatum (evanescent rash with ring margin)
S-sydenham chorea
```
194
PT presents with a sharp chest pain that is worse on inspiration. He improves when sits up and leans forward
acute pericarditis
often complicated by pericardial effusion
presents with friction rub
195
What causes widespread ST segment elevation and or PR depression
acute pericarditis
196
What is a major cause of sudden cardiac death in adults < 40 yo
myocarditis- global enlargement of heart and dilation of chambers due to inflmmation of myocardium
197
Pt presents with hypotension, distended neck veins, and distant heart sounds. ECG shows electrical alternans
Cardiac tamponade - becks triad
electrical alternans due to swinging movement of heart in large effusion
Also has pulsus paradoxus which is a decrease in amplitude of systolic BP by >10 mm Hg during inspiration
Pulses paradoxus. High yield caused by croup. Tamponade. Copd. Asthma. Restrictive lung disease. Sleep Apnea
198
What conditions can you see pulsus paradoxus
cardiac tamponade, asthma, obsructive sleep apnea, pericarditis, croup
a decrease in amplitude of systolic BP by >10 mm Hg during inspiration
199
syphilitic heart dz
disrupts vasa vasorum of the aorta --> atrophy of BV--> dilation of aorta and valve ring
calcification of aortic root, ascending arch, and thoracic aorta
leads to tree bark appreance of aorta
200
Pt is a 70 yo woman complaining about a unilateral headache and pain in her jaw (jaw claudication). What are you most worried about?
Giant cell (Temporal)
involves the temporal artery. may lead to irreversible blindness due to ophthalmic artery occlusion
Most commonly affects branches of the carotid artery
associated with polymyalgia rheumatica
focal granulomatous inflammation
201
Pt is an asian female presenting with fever, night sweats, arthritis, myalgia, and weak UE pulses
Takayasu arteritis
also see skin nodules and ocular disturbances
granulomatous thickening and narrowing of aortic arch and proximal great vessels
202
Pt is a 45 yo man that recently tested positive for Hep B, he complains of a fever, weight loss, malaise and headache. What are you most worried about?
Polyarteritis nedosa
can also see abd pain and melena. HTN, neurological dysfx, cutaneous eruptions, renal damage
on labs you see transmural inflammation of the arterial wall with fibrinoid necorsis (usually renal and visceral). Also innumerable renal microaneurysms and spasms on angiogram
203
A 3 yo asian child with high fever and a strawberry tongue. what are you most worried about?
kawasaki disease (mucocutaneous lymph node syndrome)
asian kids <4 yo
think CRASH and burn your motorcycle
```
C-conjunctival inhection
R-rash (polymorphous --> desquamating)
A-adenopathy (cervical)
S- strawberry tongue
H-hand foot changes (edema and erythema)
```
burn=fever
204
pt is a 35 yo male with a strong history of smoking. what are you most worried about?
Buerger disease or thromboangiitis obliterans
intermittent claudication --> gangrene
Raynaud phenomenon
segmental thrombosing vasculitis with vein and nerve inolvement
205
Pt presents with a saddle nose and red urine and couging up blood
Wegeners (granulomatosis with polyangiitis)
triad: focal nectrotizing vasculitis, necrotizing granulomas in lung and upper airway, necrotizing glomerulonephritis
UR tract - perforation of nasal septum , chronic sinusitis, otitis media, mastoiditis
Renal - hematuria and red cell casts
c-ANCA/PR3-ANCA
206
Microscopic polyangiitis
Necrotizing vasculitis commonly involving the lungs, kidneys, skin with pauci immune glomerulonephritis and palpable purpura
similar to wegners except no nasopharyngeal involvement
No granulomas
p-ANCA/MPO-ANCA
207
p-ANCA?
anti myeloperoxidase
208
c-ANCA?
anti proteinase 3
209
Behcet syndrome
Turkish and eastern mediterranean descent
immune complex vasculitis
recurrent aphtous ulcers, genital ulcerations, uveitis, erythema nodosum
related to HSV or parvo virus
HLA-B51
210
Churg strauss
Eosinophilic granulomatosis with polyangitis
granulomatous necrotizing vasculitis with eosinophilia
pANCA and increase IgE levels
asthma, sinusitis, skin nodules or purpura, peripheral neuropathy resulting in wrist and foot drop
211
Henoch-Schonlein purpura
Immunoglobulin A vasculitis
Following an URI in children
classic triad: palpable purpura on buttocks and legs, arthralgia, abdominal pain associated with intssusception
212
Most common cardiac tumor
metastasis
213
most common primary cardiac tumor in adults
myxoma commonly in the left atrium
"ball valve" obstruction in left atrium . early diastolic tumor plop sound
multiple syncopal episodes
on histology there are gelatinous material, myxoma cells immersed in glycosaminoglycans
214
most common primary cardiac tumor in children
rhabdomyomas
associated with tuberous sclerosis
on histology there are hamartomatous growth
215
Kussmaul sign
increase JVP on inspiration instead of decrease
inspiration: negative intrathroacic pressure not transmitted to heart --> impiared filling of RV --> blood backs up into vena cava --> JVD
constrictive pericarditis, restricive cardiomyopathies, right atrial and ventricular tumors
216
Osler Weber Rendu syndrome
Hereditary hemorrhagic telangiectasia is an inhereted disorder of BVs
blanching lesions or telangiectasia on skin and mucous membranes
```
recurrent epistaxis
skin discoloration
AV malformation
GI bleeding
Hematuria
```
217
Hypertrophic cardiomyopathy mutation
missense mutation in beta mysoin heavy chain
and
myosin binding protein C
