Cardiovascular Flashcards
(214 cards)
1
Q
Truncus Arteriosus (TA) gives rise to?
A
Ascending aorta & Pulmonary Trunk
2
Q
Bulbus Cordis gives rise to?
A
Smooth parts (outflow tract) of left and right ventricles
3
Q
Primitive Ventricle gives rise to?
A
Trabeculated left and right ventricles
4
Q
Primitive Atria gives rise to?
A
Trabeculated left and right atria
5
Q
Left horn of sinus venosus (SV) gives rise to?
A
Coronary Sinus
6
Q
Right horn of sinus venosus gives rise to?
A
Smooth part of right atrium
7
Q
Right common cardinal vein and right anterior cardinal vein gives rise to?
A
SVC
8
Q
Formation of Truncus Arteriosus?
A
Neural crest migration - truncal and bulbar ridges that spiral & fuse to form the aorticopulmonary (AP) septum - ascending aorta & pulmonary trunk
-transposition of great vessels (failure to spiral), tetralogy of Fallot (skewed AP septum development), persistent TA (partial AP septum development)
9
Q
Intraventricular Septum Development
A
- Muscular ventricular septum forms. Opening is called intraventricular foramen
- AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing IV foramen
- Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum
10
Q
Pathology of Intraventricluar Septum Development
A
- improper neural crest migration into the TA can result in transposition of the great arteries or a persistent TA
- membranous septal defect causes an initial left-to -right shunt, which later reverses to a right-to-left shunt due to the onset of pulmonary HTN (Eisenmenger’s syndrome)
11
Q
Interatrial Septum Development
A
- Foarment primum narrows as septum grows toward endocardial cushions
- Perforations in septum form foramen secundum (foramen primum disappears)
- Foramen secundum maintains right-to-left shunt as septum secundum begins to grow
- Septum secundum contains a permanent opening (foramen ovale)
- Foramen secundum enlarges and upper part of septum primum degenerates
- Remaining portion of septum primum forms valve of foramen ovale
- Septum secundum & septum primum fuse to form the atrial septum
- Foramen ovale ususally closes soon after birth because of inc. LA pressure
12
Q
Pathology of Interatrial Septum Development
A
-patent foramen ovale: caused by failure of the septum primum and septum secundum to fuse after birth
13
Q
Fetal Erythropoiesis
A
Yolk Sac: 3-10 weeks
Liver: 6wk - birth “Young Liver Synthesizes
Spleen: 15-30 weeks Blood”
Bone Marrow: 22wk-adult
14
Q
Fetal Hemoglobin
A
alpha 2 gamma 2
15
Q
Adult Hemoglobin
A
alpha 2 beta 2
16
Q
Fetal Circulation
A
Blood in umbilical vein has a PO2 of = 30mmHg & is ~80% saturated with O2
- umbilical arteries have low O2 saturation
- at birth, infant takes breath, dec. resistance in pulmonary vasculature causes inc. left atrial pressure vs. right atrial pressure, foramen ovale closes (fossa ovalis)
- inc. in O2 leads to dec. in prostaglandins, causing closure of ductus arteriosus
- indomethacin helps close PDA
- Prostaglandins E1 & E2 keep PDA open
17
Q
3 Shunts in Fetal Circulation
A
- Blood entering the fetus through the umbilical vein is conducted via the ductus venosus into the IVC to bypass the hepatic circulation
- Most oxygenated blood reaching the heat via the IVC is diverted through the foramen ovale & pumped out the aorta to the head & body
- Deoxygenated blood entering the RA from the SVC enters the RV, is expelled into the pulmonary artery, and then passes through the ductus arteriosus into the descending aorta
18
Q
Fetal-postnatal derivatives: Umbilical Vein
A
Ligamentum teres hapatis
contained in falciform ligament
19
Q
Fetal-postnatal derivatives: Umilical Arteries
A
Medial umbilical ligaments
20
Q
Fetal-postnatal derivatives: Ductus Arteriosus
A
Ligamentum Arteriosum
21
Q
Fetal-postnatal derivatives: Ductus Venosus
A
Ligamentum Venosum
22
Q
Fetal-postnatal derivatives: Foramen Ovale
A
Fossa Ovalis
23
Q
Fetal-postnatal derivatives: Allantosis
A
Urachus-median umbilical ligament
(the urachus is the part of the allantoic duct b/w the bladder and the umbilicus)
-urachal cyst or sinus is a remnant
24
Q
Fetal-postnatal derivatives: Notochord
A
Nucleus pulposus of intervertebral disc
25
Coronary Artery Anatomy
-SV & AV nodes normally supplied by RCA
-Right-dominant circulation = 85%
PD arises from RCA
-Left-dominant circulation = 8%
PD arises from LCX
-Codominant circulation 7% PD arises from both LCX and RCA
-Coronary occlusion most commonly occurs in the LAD
26
Coronary Arteries fill during?
diastole
27
Most posterior part of the heart?
left atrium
- enlargement can cause dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve (from vagus))
- transesophageal echocardiography is useful for diagnosing left atrial enlargement, aortic dissection, and thoracic aortic aneurysm
28
Cardiac Output (CO)
stroke volume (SV) x heart rate (HR)
29
Fick principle
CO = rate of O2 consumption/ (arterial O2 content - venous O2 content)
30
Mean arterial pressure (MAP)
CO X total peripheral resistance
or
2/3 diastolic pressure + 1/3 systolic pressure
31
Pulse Pressure
systolic pressure - diastolic pressure
| proportional to stroke volume
32
SV
CO/HR
| EDV-ESV
33
Early stages of exercise, CO is maintained by?
inc. HR & inc. SV
34
Late stages of exercise, CO is maintained by?
inc. HR only (SV plateaus)
35
What happens if HR is to high?
-diastolic filling is incomplete & CO dec.
| centricular tachycardia
36
Stroke Volume is Affected by?
- Contractiligy
- Afterload
- Preload
inc. SV when inc. preload, dec. afterload, or inc. contractility
SC CAP
37
Contractility (and SV) increases with?
- catacholamines (inc. activity of Ca2+ pump in sarcoplasmic reticulum)
- inc. intracellular Ca2+
- dec. extracellular Na+ (dec. activity of Na/Ca exchanger)
- Digitalis (blocks Na/K pump, inc. intracellular Na, dec. Na/Ca exchanger, inc. intra Ca)
38
Contractility (and SV) decreases with?
- beta-blockade (dec. cAMP)
- heart failure (systolic dysfunction)
- acidosis
- hypoxia/hypercapnea (dec. PO2/inc. PCO2)
- non-dihydropyridine Ca2+ channel blockers
39
Stroke Volume increases?
in anxiety, exercise, & pregnancy
| -a failing heart has dec. SV
40
Myocardial O2 demand is inc. by:
- inc. afterload (proportional to arterial pressure)
- inc. contractility
- inc. heart rate
- inc. heart size
41
Preload
ventricular EDV
| venodilators decrease preload (nitroglycerin)
42
Afterload
mean arterial pressure (proportional to peripheral resistance)
vasodilators decrease afterload (hydralazine)
43
Preload increases with?
- exercise (slightly)
- inc. blood volume (overtransfusion)
- excitement (inc. sympathetic activity)
44
Starling Curve
Force of contraction is proportional to end-diastolic length of cardiac muscle fiber (preload)
- inc. contractility with sympathetic stimulation, catecholamines, digoxin
- dec. contractility with loss of myocardium (MI), beta-blockers, calcium channel blockers
45
Ejection Fraction
EF= SV/EDV = (EDV-ESV)/EDV
- index of ventricular contractiligy
- normally >55%
- EF dec. in systolic heart failure
46
Change in pressure
=Q x R
(like Ohm's law) change in V=IR
-pressure gradient drives flow from high pressure to low pressure
47
Resistance
(driving pressure)/(flow(Q))=(8 viscosityxlength)/pi r^4
- resistance is directly proportional to viscosity and vessel length & inversly proportional to the radius to the fourth power
- arterioles account for most of total peripheral resistance - regulate capillary flow
48
Total Resistance of Vessels in series
= R1 + R2 + R3...
49
1/total Resistance of Vessels in Parallel
=1/R1 + 1/R2 + 1/R3
50
Viscosity depends mostly on?
hematocrit
51
Viscosity increases in?
- polycythemia
- hyperproteinemic states (multiple myeloma)
- hereditary spherocytosis
52
Viscosity decreases in?
anemia
53
Cardiac & Vascular Function Curves
1. Operating point of heart (cardiac output & venous return are equal)
2. dec. TPR (exercise, AV shunt)
3. inc. TPR (hemorrhage before compensation can occur)
4. As in heart failure, narcotic overdose
5. X-intercept of venous return curve = mean systemic filling pressure
54
S1
mitral valve & tricuspid valve closure (loudest at mitral area)
55
S2
aortic & pulmonary valve closure (loudest at left sternal border)
56
S3
in early diastole during rapid ventricular filling phase
-associated with increased filling pressure (mitral regurg, CHF) and more common in dilated ventricles (but normal in children and pregnant women)
57
S4
"atrial kick"
- in late diastole
- high atrial pressure
- associated with ventricular hypertrophy, left atrium must push against stiff LV wall
58
Jugular Venous Pulse (JVP)
a wave: atrial contraction
c wave: RV contraction (closed tricuspid valve bulging into atrium)
x descent: atrial relaxation & downward displacement of closed tricuspid valve during ventricular contraction
v wave: inc. right atrial pressure due to filling against closed tricuspid valve
y descent: blood flow from RA to RV
59
Normal Splitting
Inspiration - drop in intrathoracic pressure - inc. venous return to the RV - inc. RV stroke volume - inc. RV ejection time - delayed closure of pulmonic valve.
Dec. pulmonary impedance (inc. capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve
60
Wide Splitting
- Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block)
- Delay in RV emptying causes delayed pulmonic sound (regardless of breath)
- an exaggeration of normal splitting
61
Paradoxical Splitting
- Seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block)
- Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound
- Therefore on inspiration, P2 closes later and moves closer to A2, thereby "paradoxically" eliminating the split
62
Fixed Splitting
-Seen in ASD, ASD - left-to-right shunt - inc. RA & RV volumes - inc. flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
63
Auscultation of the Heart: Aortic Area
-systolic murmer
aortic stenosis
flow murmur
aortic valve sclerosis
64
Auscultation of the Heart: Left sternal Boarder
```
-Diastolic murmur
Aortic regurgitation
Pulmonic regurgitation
-Systolic murmur
Hypertrophic cardiomyopathy
```
65
Auscultation of the Heart: Pulmonic Area
-Systolic Ejection Murmur
Pulmonic stenosis
Flow murmur (atrial septal defect, patent ductus arteriosus)
66
Auscultation of the Heart: Tricuspid Area
```
-Pansystolic Murmer
tricuspid regurgitation
ventricular septal defect
-Diastolic murmur
tricuspid stenosis
atrial septal defect
```
67
Auscultation of the Heart: Mitral Area
-Systolic Murmur
mitral regurgitation
-Diastolic murmur
mitral stenosis
68
Bedside Maneuver: Inspiration
inc. intensity of right heart sounds
69
Bedside Maneuver: Expiration
inc. intensity of left heart sounds
70
Bedside Maneuver: Hand grip (inc. systemic vascular resistance)
inc. intensity of MR, AR, VSD, MVP murmurs
| dec. intensity of AS, hypertrophic cardiomyopathy murmurs
71
Bedside Maneuver: Valsalva (dec. venous return)
dec. intensity of most murmurs
| inc. intensity of MVP, hypertrophic cardiomyopathy murmurs
72
Bedside Maneuver: Rapid Squatting
inc. venous return, inc. preload, inc. afterload with prolonged squatting
dec. intensity of MVP, hypertrophic cardiomyopathy murmurs
73
Systolic Heart Sounds
- aortic/pulmonic stenosis
- mitral/tricuspid regurgitation
- ventricular septal defect
74
Diastolic Heart Sounds
- aortic/pulmonic regurgitation
| - mitral/tricuspid stenosis
75
Heart Murmurs: Mitral/Tricuspid Regurgitation (MR/TR)
SYSTOLIC
Holosystolic, high-pitched "blowing murmur"
Mitral: loudest at apex & radiates toward axilla, enhanced by maneuvers that inc. TPR (squatting, hand grip) or LA return (expiration), MR is often due to ischemic heart disease, MVP, or LV dilation
Tricuspid: loudest at tricuspid area & radiates to right sternal border. Enhanced by maneuvers that inc. RA return (inspiration). TR can be caused by RV dilation
-Rheumatic fever & infective endocarditis can cause either MR or TR
76
Heart Murmurs: Aortic Stenosis (AS)
SYSTOLIC
Crescendo-decrescendo systolic ejection murmur following ejection click (EC; due to abrupt halting of valve leaflets)
LV >> aortic pressure during systole
-radiates to carotids/heart base "pulsus parvus et tardus" - pulses are weak with a delayed peak.
-can lead to Syncope, Angina, & Dyspnea on exertion (SAD)
-often due to age-related calcific aortic stenosis or bicuspid aortic valve
77
Heart Murmurs: VSD
SYSTOLIC
- Holosystolic, harsh-sounding murmur
- loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload
78
Heart Murmurs: Mitral Valve Prolapse (MVP)
SYSTOLIC
- late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae)
- most frequent valvular lesion. Best heard over apex. Loudest at S2. Usually benign. Can predispose to infective endocarditis.
- Can be caused by myxomatous degeneration, rheumatic fever, or chordae rupture
- Enhanced by maneuvers that dec. venous return (standing or valsalva)
79
Heart Murmurs: Aortic Regurgitation (AR)
DIASTOLIC
- intermediate high-pitched "blowing" diastolic decrescendo murmur
- wide pulse pressure when chronic; can present with bounding pulses & head bobbing
- often due to aortic root dilation, bicuspid aortic valve, endocarditis, or rheumatic fever
- inc. murmur during hand grip.
- Vasodilators dec. intensity of murmur
80
Heart Murmurs: Mitral Stenosis (MS)
DIASTOLIC
- follows opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips)
- delayed rumbling late diastole murmur
- LA > LV pressure during diastole
- often occurs secondary to rheumatic fever
- chronic MS can result in LA dilation, enhanced by maneuvers that inc. LA return (expiration)
81
Heart Murmurs: PDA
CONTINUOUS
- continuous machine-like murmur
- loudest at S2, often due to congenital rubella or prematurity
- best heard at left infraclavicular area
82
Electrocardiogram: P wave
atrial depolarization
| atrial repolarization is masked by QRS complex
83
Electrocardiogram: PR interval
conduction delay through AV node (normally <200 msec.)
84
Electrocardiogram: QRS Complex
ventricular depolarization (normally < 120msec)
85
Electrocardiogram: QT interval
mechanical contraction of the ventricles
86
Electrocardiogram: T wave
ventricular repolarization, T-wave inversion may indicate recent MI
87
Electrocardiogram: ST segment
isoelectric, ventricles depolarized
88
Electrocardiogram: U wave
caused by hypokalemia, bradycardia
89
Speed of Conduction
Purkinje > atria > Ventricles > AV node
90
Pacemakers
SA > AV > bundle of His/Purkinje/Ventricles
91
Conduction Pathway
SA node - atria - AV node - common bundle - bundle branches
92
SA node
"pacemaker" inherent dominance with slow phase of upstroke
93
AV node
-100 msec delay - atrioventricular delay; allows more time for ventricular filling
94
Torsades de Pointes
- Ventricular Tachycardia, characterized by shifting sinusoidal waveforms on ECG, can progress to ventricular fibrillation
- anything that prolongs the QT interbal can predispose to torsades de pointes
- treatment: Magnesium sulfate
- congenital long QT syndromes are most often due to defects in cardiac sodium or potassium channels, can present with severe congenital sensorineural deafness (Jervell & Lange-Nielsen Syndrome)
95
Atrial Fibrillation
- chaotic & erratic baseline (irregularly irregular) with no discrete P waves in b/w irregularly spaced QRS complexes
- can result in atrial stasis and lead to stroke
- treatment includes rate control, anticoagulation, and possible cardioversion
96
Atrial Flutter
- a rapid succession of identical, back-to-back atrial depolarization waves
- the identical appearance accounts for the "sawtooth" appearance of the flutter waves
- pharmacologic conversion to sinus rhythm: class IA, IC or III antiarrhythmics
- Rate control: beta-blocker or calcium channel blocker
97
Ventricular fibrillation
a completely erratic rhythm with no identifiable waves & defibrillation
98
1st degree AV Block
- the PR interval is prolonged (>200msec)
| - asymptomatic
99
2nd degree AV Block: Mobitz Type I (Wenckebach)
- Progressive lengthening of the PR interval until a beat is "dropped" (a P wave not followed by a QRS complex)
- usually asymptomatic
100
2nd degree AV Block: Mobitz Type II
- Dropped beats that are not preceded by a change in the length of the PR interval (type I)
- Abrupt, nonconducted P waves result in a pathologic condition
- Often found as 2:1 block, which there are 2 or more P waves to 1 QRS response, may progress to 3rd degree block
- Treated with pacemaker
101
3rd degree AV Block: Complete
- atria & ventricles beat independently of each other
- both P waves bear no relation to the QRS complex
- atrial rate is faster than ventricular rate, usually treated with pacemaker
- Lyme disease can cause this
102
Atrial Natriuretic Peptide
- released from atrial myocytes in response to inc. blood volume & atrial pressure
- causes generalized vascular relaxation and dec. Na+ reabsorption at the medullary collecting tubule
- constricts efferent renal arterioles & dilates afferent arterioles (cGMP mediated), promoting diuresis & contributing to the "escape from aldosterone" mechanism
103
Receptors: Aortic Arch
Transmits via vagus nerve to solitary nucleus of medulla (responds only to inc. BP)
104
Receptors: Carotid Sinus
Transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to inc. & dec. BP)
105
Baroreceptors: Hypotension
- dec. arterial pressure - dec. stretch - dec. afferent baroreceptor firing - inc. efferent sympathetic firing & dec. efferent parasympathetic stimulation - vasoconstriction, inc. HR, inc. contractility, inc. BP
- important in the response to severe hemorrhage
106
Baroreceptors: Carotid Massage
inc. pressure on carotid artery, inc. stretch, inc. afferent baroreceptor firing, dec. HR
107
Baroreceptors: Contributes to Cushing reaction
Triad: hypertension, bradycardia, respiratory depression
-inc. intracranial pressure constricts arterioles, cerebral ischemia & reflex sympathetic inc. in perfusion pressure (hypertension), inc. stretch, reflex baroreceptor induced-bradycardia
108
Peripheral Chemoreceptors
-carotid & aortic bodies are stimulated by dec. PO2 (<60mmHg), inc. PCO2, & dec. pH of blood
109
Central Chemoreceptors
- are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2
- do not directly respond to PO2
110
Organ with Largest Blood Flow?
Lung
111
Organ with Largest share of systemic cardiac output?
Liver
112
Organ with highest blood flow per gram of tissue?
Kidney
113
Organ with largest arteriovenous O2 difference?
Heat
114
Pulmonary Capillary Wedge pressure
- good approximation of left atrial pressure
- in mitral stenosis, >LV diastolic pressure
- measured with pulmonary artery catheter (Swan-Ganz catheter)
115
Autoregulation of the Heart
- Local Metabolic (vasodilatory) - CO2, adenosine, NO
- pulmonary vasculature is unique in that hypoxia causes vasoconstriction so that only well-ventilated areas are perfused
- other organs (hypoxia causes vasodilation)
116
Autoregulation of the Brain
-local metabolites (vasodilatory) CO2 (pH)
117
Autoregulation of Kidneys
Myogenic & Tubuloglomerular feedback
118
Autoregulation of Lungs
Hypoxia causes vasoconstriction
119
Autoregulation of Skeletal Muscles
Local Metabolites - lactate, adenosine, K+
120
Autoregulation of Skin
Sympathetic stimulation most important mechanism - temperature control
121
Capillary Fluid Exchange
Starling forces determine fluid movement through capillary membranes
Pc = capillary pressure: pushes fluid out of capillary
Pi=interstitial fluid pressure: pushes fluid into capillary
pic=plasma colloid osmotic pressure: pulls fluid into capillary
pii=interstitial fluid colloid osmotic pressure: pulls fluid out of capillary
Pnet = [(Pc-Pi)-(pic-pii)]
Kf=filtration constant (capillary permeability)
Jv=net fluid flow = Kf(Pnet)
122
Edema is caused by?
- inc. capillary pressure (inc. Pc heart failure)
- dec. plasma proteins (dec. pic, nephrotic syndrome, liver failure)
- inc. capillary permeability (inc. Kf, toxins, infections, burns)
- inc. interstitial fluid colloid osmotic pressure (inc. pii, lymphatic blockage)
123
Congenital Heart Disease: Right to left shunts
"Blue babies"
1. Tetralogy of Fallot: most common cause of early cyanosis
2. Transposition of the great vessels
3. persistent Truncus arteriosus: failure of truncus arteriosus to divide into pulmonary trunk & aorta, most patients have accompanying VSD
4. Tricuspid atresia: characterized by absence of tricuspid valve & hypoplastic RV, requires both ASD & VSD for viability
5. Total anomalous pulmonary venous return (TAPVR): pulmonary veins drain into right heart circulation (SVC, coronary sinus), associated with ASD & sometimes PDA to allow for right-to-left shunting to maintain CO
124
Congenital Heart Disease: Left-to-Right Shunt
"blue kids"
- VSD (most common congenital cardiac anomaly)
- ASD (loud SI, wide, fixed split S2)
- PDA (close with indomethacin)
VSD>ASD>PDA
125
Eisenmenger's Syndrome
- uncorrected VSD, ASD, or PDA causes compensatory pulmonary vascular hypertrophy, which results in progressive pulmonary HTN
- as pulmonary resistance inc. the shunt reverse from left-to-right to right-to-left, which causes late cyanosis, clubbing, & polycythemia
126
Tetralogy of Fallot
-caused by anterosuperior displacement of the infundibuar septum
1. Pulmonaryinfundibular stenosis (most important determinant for prognosis)
2.RVH
3. Overriding aorta (overrides the VSD)
4. VSD
-early cyanosis "tet spells" caused by a right-to-left shunt across the VSD, isolated VSDs usually flow left to right (acyanotic)
-in tetralogy, pulmonary stenosis forces right-to-left (cyanotic) flow & causes RVH (on x-ray, boot-shaped heart)
PROVe
-older patients historically learned to squat to relieve cyanotic symptoms, this reduced blood flow to the legs, inc. peripheral vascular resistance (PVR), & thus dec. the cyanotic right-to-left shunt across the VSD
Treatment: early, primary surgical correction
127
D-transposition of great vessels
- aorta leaves RV (anterior) & pulmonary trunk leaves LV (posterior) - separation of systemic & pulmonary circulations
- not compatible w/life unless a shunt is present to allow adequate mixing of blood (VSD, PDA, patent forament ovale)
- due to failure of aorticopulmonary septum to spiral
- w/o surgical correction, most infants die w/in first few months of life
128
Coarctation of the aorta
can result in regurgitation
129
Coarctation of the aorta: Infantile Type
- aortic stenosis proximal to insertion of ductus arteriosus (preductal)
- associated with Turner syndrome
- Infantile: In close to the heart
- check femoral pulses on physical exam
130
Coarctation of the aorta: Adult Type
-stenosis is distal to ligmentum arteriosum (postductal)
-associated with notching of ribs (due to collateral circulation), HTN in upper extremities, weak pulses in lower extremities
Distal to Ductus
-most commonly associated with bicuspid aortic valve
131
Patent Ductus Arteriosus
- in fetal period, shunt is right to left (normal)
- in neonatal period, lung resistance dec. & shunt becomes left to right with subsequent RVH or LVH & failure (abnormal)
- Associated w/continuous, "machine-like" murmur
- patency is maintained by PGE synthesis & low O2 tension
- uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis)
- normal in utero and normally closes only after birth
132
Endomethacine
(indomethacin) ends patency of PDA
| PGE kEEps it open (may be necessary to sustain life in conditions such as transposition of the great vessels)
133
22q11 syndrome causes?
| cardio
Truncus arteriosus, tetralogy of Fallot
134
Down Syndrome causes?
| cardio
ASD, VSD, AV septal defect (endocardial cushion defect)
135
Congential Rubella causes?
| cardio
Septal defects, PDA, pulmonary artery stenosis
136
Turner Syndrome causes?
| cardio
coarctation of aorta (preductal)
137
Marfan's Syndrome causes?
| cardio
aortic insufficiency & dissection (late complication)
138
Infant of Diabetic Mother causes?
| cardio
transposition of great vessels
139
HTN
defined as BP > 140/90 mmHg
- Risk factors: inc. age, obesity, diabetes, smoking, genetics, black > white > asian
- Features: 90% of HTN is primary (essential) & related to inc CO or inc. TPR, remaining 10% mostly secondary to renal disease, malignant HTN is severe (>180/120) & rapidly progression
- Predisposes to: atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, aortic dissection
140
Atheromas
plaques in blood vessel walls
141
Xanthomas
plaques or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids (xanthelasma)
142
Tendinous Xanthoma
lipid deposit in tendon, especially Achilles
143
Corneal Arcus
lipid deposit in cornea, nonspecific (arcus senilis)
144
Arteriosclerosis: Monckeberg
- Calcification in the media of the arteries, especially radial or ulnar
- usually benign "pipestem" arteries
- does not obstruct blood flow, intima not involved
145
Arteriosclerosis: Arteriolosclerosis
-2 types: hyaline (thickening of small arteries in essential hypertension or diabetes mellitus) & hyperplastic ("onion skinning" in malignant HTN)
146
Arteriosclerosis: Atherosclerosis
- Fibrous plaques & atheromas form in intima of arteries
| - disease of elastic arteries & large and medium-sized muscular arteries
147
Atherosclerosis: Risk Factors
Modifiable: smoking, HTN, hyperlipidemia, diabetes
| Non-Modifiable: age, gender (men, postmenopausal women), family history
148
Atherosclerosis: Progression
Inflammation
Endothelial cell dysfunction - macrophage & LDL accumulation - foam cell formation - fatty streaks - smooth muscle cell migration (involves PDGF & FGF), proliferation, & extracellular matrix deposition - fibrous plaque - complex atheromas
149
Atherosclerosis: Complications
aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
150
Atherosclerosis: Location
abdominal aorta > coronary artery > popliteal artery > carotid artery
151
Atherosclerosis: Symptoms
angina, claudication (but can be asymptomatic)
152
Aortic Aneurysms
localized pathologic dilation of blood vessel
153
Abdominal Aortic Aneurysms
associated with atherosclerosis
| occurs more frequently in hypertensive male smokers > 50 years of age
154
Thoracic Aortic Aneurysm
associated with HTN, cystic medial necrosis (Marfan's Syndrome) & historically tertiary syphilis
155
Aortic Dissection
- Longitudinal intraluminal tear forming false lumen
- Associated with HTN, bicuspid aortic valve, cystic medial necrosis, & inherited connective tissue disorders (Marfan's syndrome)
- presents with tearing chest pain radiating to the back, CXR shows mediastinal widening
- false lumen can be limited to the ascending aorta, propagate from the descending aorta
- can result in pericardial tamponade, aortic rupture, & death
156
Angina
CAD narrowing > 75%, no myocyte necrosis
Stable-mostly secondary to atherosclerosis, ST depression on ECG (retrosternal chest pain with exertion)
Prinzmenta's Variant-Occurs at rest secondary to coronary artery spasm, ST elevation of ECG
Unstable/Crescendo-thrombosis with incomplete coronary artery occlusion, ST depression on ECG (worsening chest pain at rest or with minimal exertion)
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Coronary Steal Syndrome
-Vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to area of higher perfusion
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Myocardial Infarction
-most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery & myocyte necrosis, ECG initially shows ST Depression progression to ST elevation with continued ischemia & transmural necrosis
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Sudden Cardiac Death
- death from cardiac causes w/in 1 hr on onset of symptoms, most commonly due to a lethal arrhythmia (ventricular fibrillation)
- associated with CAD (up to 70% of cases)
160
Chronic ischemic heart disease
-progressive onset of CHF over many years due to chronic ischemic myocardial damage
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Evolution of MI
coronary artery occlusion LAD>RCA>circumflex
| symptoms: diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, SOB, fatigue
162
MI: 0-4 hr
risk: arrhythmia, CHF exacerbation, cardiogenic shock
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MI: 4-12 hr
Gross: infarct, dark mottling, pale with tetrazolium stain
Microscopic: early coagulative necrosis, edema hemorrhage, wavy fibers
Risk: arrhythmia
164
MI: 12-24 hr
Gross: infarct, dark mottling, pale with tetrazolium stain
Microscope: contraction bands from reperfusion injury, release of necrotic cell content into blood, beginning of neutrophil migration
Risk: arrhythmia
165
MI: 1-3 days
Gross: Hyperemia
Microscope: extensive coagulative necrosis, tissue surrounding infarct shows acute inflammation, neutrophil migration
Risk: fibrinous pericarditis
166
MI: 3-14 days
Gross: hyperemic border, central yellow-brown softening-maximally yellow & soft by 10 days
Microscope: macrophage infiltration followed by granulation tissue at the margins
Risk: free wall rupture leading to tamponade, papillary muscle rupture, ventricular aneurysm, interventricular septal rupture due to macrophages that have degraded important structural components
167
MI: 2 weeks to several months
Gross: recanalized artery, gray-white
Microscope: contracted scar complete
Risk: Dressler's Syndrome
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Diagnosis of MI
- in first 6 hrs., ECG is the gold standard
- Cardiac troponin I rises after 4 hrs & is elevated for 7-10 days, more specific than other protein markers
- CK-MB is predominantly found in myocardium but can also be released from skeletal muscle. Useful in diagnosing reinfarction following acute MI b/c levels return to normal after 48hrs
- ECG changes: ST elevation (transmural infarct), ST depression (subendocardial infarct), pathologic Q waves (transmural infarct)
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Transmural Infarct
inc. necrosis
affects entire wall
ST elevation of ECG, Q waves
170
Subendocardial Infarct
due to ischemic necrosis of <50% of ventricle wall
- subendocardium especially vulnerable to ischemia
- ST depression on ECG
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ECG: Anterior wall (LAD) leads?
V1-V4
172
ECG: Anteroseptal (LAD) leads?
V1-V2`
173
ECG: Anterolateral (LCX) leads?
V4-V6
174
ECG: Lateral Wall (LCX) leads?
I, aVL
175
ECG: Inferior Wall (RCA) leads?
II, III, aVF
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MI Complications?
1. Cardiac arrhythmia-important cause of death b/f reaching hospital; common in first few days
2. LV failure & pulmonary edema
3. Cardiogenic Shock (large infarct-high risk of mortality)
4. Ventricular Free wall rupture: cardiac tamponade, papillary muscle rupture, severe mirtral regurg. & interventricular septum rupture-VSD
5. Ventricular aneurysm formation: dec. CO, risk of arrhythmia, embolus from mural thrombus, greatest risk approx. 1 week post-MI
6. Postinfarction fibrinous pericarditis: friction rub (1-3days post MI)
7. Dressler's Syndrome: autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI)
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Dilated (congestive) Cardiomyopathy
-most common (90%)
-often idiopathic (50% familial)
-or Alcohol abuse, wet Beriberi, Coxsacki B virus myocarditis, chronic Cocaine use, Chagas' disease, Doxorubicin toxicity, hemochromatosis, & peripartum cardiomyopathy
-S3, dilated heart on ultrasound, balloon appearance on x-ray
Treatment: Na+ restriction, ACE inhibitors, diuretics, digoxin, transplant
-systolic dysfunction ensues
-eccentric hypertrophy (sarcomeres added in series)
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Hypertrophic Cardiomyopathy
-hypertrophied interventricular septum is too close to mitral valve leaflet, leading to outflow tract obstruction
-60-70% familial, autosomal dominant (beta-myosin heavy chain mutation)
-associated with Friedreich's ataxia, disoriented, tangled, hypertrophied myocardial fibers
-cause of sudden death in young athletes
-Findings: normal-sized heart, S4, apical impulses, systolic murmur
Treatment: B-blocker or non-dihydropyridine calcium channel blocker
-diastolic dysfunction ensues, asymmetric concentric hypertrophy (sarcomeres in parallel)
-proximity of hypertrophied interventricular septum to mitral leaflet obstructs outflow tract, resulting in systolic murmur & syncopal episodes
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Restrictive/Obstructive Cardiomyopathy
-major causes include sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler's syndrome (endomyocardial fibrosis w/a prominent eosinophilic infiltrate), & hemochromatosis (dilated cardiomyopathy can also occur)
180
CHF
- a clinical syndrome that occurs in patients with an inherited or acquired abnormality of cardiac structure or function, which is characterized by a constellation of clinical symptoms (dyspnea, fatigue) and signs (edema, rales)
- right heart failure most often results from left heart failure, isolated right heart failure is usually due to cor pulmonale
- ACE inhibitors, B-blockers (not acute decompenstated HF), angiotensin receptor antagonists, & spironolactone reduce mortality. Thiazide or loop diuretics are mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms & mortality in select patients
181
Cause of Cardiac Dilation
greater ventricular end-diastolic volume
182
Casse of Dyspneal on Exertion
failure of cardiac output to inc. during exercise
183
Left Heart Failure
Pulmonary edema, Paroxysmal Nocturnal dyspnea:
-inc. pulmonary venous pressure - pulmonary venous distention & transudation of fluid.
-presence of hemosiderin-laden macrophages ("heart failure" cells) in the lungs
Orthopnea (Shortness of breath when supine):
-inc. venous return in supine position exacerbates pulmonary vascular congestion
184
Right Heart Failure
```
Hepatomegaly (nutmeg liver):
-inc. central venous pressure-inc. resistance to portal flow, rarely leads to "cardiac cirrhosis"
Peripheral Edema:
-inc. venous pressure-fluid transudation
Jugular Venous Distention:
-inc. venous pressure
```
185
Bacterial Endocarditis
Fever (most common)
Roth's Spots (round white spots on retina surrounded by hemorrhage)
Osler's nodes (tender raised lesions on finger or toe pads)
new Murmur
Janeway lesions (small, painless, erythematous lesions on palm or sole)
Anemia
Splinter hemorrhages on nail bed
-blood culture necessary
Acute: S. aureus (high virulence), large vegetations on previously normal valves, rapid onset
Subacute: Viridans streptococci (low virulence), smaller vegetations on congenitally abnormal or diseased valves, sequela of dental procedures, more insidious onset
-may also be nonbacterial secondary to malignancy, hypercoagulable state, or lupus (marantic/thrombotic endocarditis) S. bovis is present in colon cancer, S. epi on prostetic valves
-mitral valve is most frequent
-tricuspid valve associated with IV drug use (S. aureus, pseudomonas, candida)
186
Complications of Bacterial Endocarditis
chordae rupture
glomerulonephritis
suppurative pericarditis
emboli
187
Rheumatic Fever
- a consequence of pharyngeal infection with group A beta-hemolytic streptococci. Early deaths due to myocarditis. Late sequelae include rheumatic heart disease, which affects heart valves-mitral>arotic>> tricuspid (high-pressure valves affect most). Early lesion mitral valve regurgitation, late lesion in mitral stenosis. Associated with Aschoff bodies (granuloma with giant cells), Anitschkow's cells (activated histiocytes), elevated ASO titers
- immune mediated (type II hypersensitivity) not a direct effect of bacteria, abs to M protein
188
Acute Pericarditis
- sharp pain, aggravated by inspiration, & relieved by sitting up & leaning forward, presents with friction rub, ECG changes include widespread ST-segment elevation and/or depression
- Fibrinous: caused by dressler's syndrome, uremia, radiation, presents with loud friction rub
- Serous: viral pericarditis (often resolves spon), noninfectious inflammatory diseases (rheumatoid arthritis, SLE)
- Suppurative/purulent: usually caused by bacterial infections (pneumococcus, streptococcus), rare now
189
Cardiac Tamponad
- compression of heart by fluid (blood effusions) in pericardium, leading to dec. CO
- equilibration of diastolic pressures in all 4 chambers
- Finding: hypotension, inc. venous pressure (JVD), distant heart sounds, inc. HR, pulsus paradoxus
190
Pulsus Paradoxus
dec. in amplitude of systolic BP by >10mmHg during inspiration
- seen in severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, & croup
191
Syphilitic Heart Disease
- tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of the vessel wall & dilation of the aorta & valve ring
- may see calcification of the aortic root & ascending aortic arch, leads to "tree bark" appearance of aorta
- can result in aneurysm of the ascending aorta or aortic arch & aortic insufficiency
192
Cardiac Tumors: Myxomas
most common primary cardiac tumor in adults
- 90% occur in atria (mostly left atrium)
- usually described as a "ball valve" obstruction in the left atrium (associated w/multiple syncopal episodes)
193
Cardiac Tumors: Rhabdomyomas
most frequent primary cardiac tumor in children (associated with tuberous sclerosis)
-most common heart tumor is a metastasis (from melanoma, lymphoma)
194
Kussmauls' Sign
inc. in JVP on inspiration instead of a normal dec.
- inspiration-negative intrathoracic pressure not transmitted to heart-imparired filling of right ventricle-blood backs up into vena cavae- JVD
- may be seen with constrictive pericarditis, restrictive cardiomyopahties, right atrial or ventricular tumors, or cardiac tamponade
195
Raynaud's Phenomenon
- dec. blood flow to the skin due to arteriolar vasospasm in response to cold temp. or emotional stress
- most often found in fingers & toes
- disease when primary, syndrome when secondary to mixed connective tissue disease, SLE, or CREST
196
Temporal (Giant Cell) Arteritis
Large-Vessel Vasculitis
- elderly females, unilateral headache (temporal artery), jaw claudication, may lead to irreversible blindness due to ophthalmic artery occlusion, associated with polymyalgia rheumatica
- most commonly affects branches of carotid artery
- focal granulomatous imflammation, inc. ESR
- treat with high-dose corticosteroids
197
Takayasu's Arteritis
Large-Vessel Vasculitis
- asian females (weak extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
- granulomatous thickening of aortic arch, proximal great vessels, Inc. ESR, treat with corticosteroids
198
Polyarteritis Nodosa
Medium-Vessel Vasculitis
- young adults, hep. B seropositivity (30%), fever, weight loss, malaise, headache, abdominal pain, melena, HTN, neurologic dysfunction, cutaneous eruptions, renal damage
- typically involves renal & visceral vessels, not pulmonary arteries, immune-complex mediated, transmural inflammation of the arterial wall with fibrinoid necrosis, lesions are of different ages, many aneurysms & constriction on arteriogram, treat w/corticosteroids, cyclophosphamide
199
Kawasaki Disease
Medium-Vessel Vasculitis
- asian children <4, fever, cervical lymphadenitis, conjunctival injection, strawberry tongue (oral lip mucosa), hand-foot erythema, desquamating rash
- may develop coronary aneurysms - MI rupture, treat with IV Ig & aspirin
200
Buerger's Disease (thromboangiitis obliterans)
Medium-Vessel Vasculitis
- heavy smokers s phenomenon is often present
- segmental thrombosing vasculitis, treat with smoking cessation
201
Microscopic Polyangiitis
Small-Vessel Vasculitis
- necrotizing vasculitis commonly involving lung, kidney, & skin with pauci-immune glomerulonephritis & palpable purpura
- no granulomas, p-ANCA, treat with cyclophosphamide & corticosteroids
202
Wegener's granulomatosis (granulomatosis with polyangiitis)
Small-Vessel Vasculitis
- upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
- lower respiratory tract: hemotysis, cough, dyspnea
- Renal: hematuria, red cell casts
- tirad: focal necrotizing vasculitis, necrotizing granulomas in the lung & upper airway, necrotizing glomerulonephritis
- cANCA, x-ray: large nodular densities
- treat with cyclophosphamide, corticosteroids
203
Churg-Strauss Syndrome
Small-Vessel Vasculitis
- asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop)
- can also involve heart, GI, kidneys (pauci-immune glomerulonephritis)
- granulomatous, necrotizing vasculitis w/eosinophilia
- pANCA, elevated IgE level
204
Henoch-Schonlein Purpura
Small-Vessel Vasculitis
- most common childhood systemic vasculitis
- often follows URL
triad: skin: palpable purpura on buttocks/legs, arthralgia, GI: abdominal pain, melena, multiple lesions of same age
- vasculitis secondary to IgA complex deposition, associated with IgA nephropathy
205
Strawberry Hemangioma
benign capillary hemangioma of infancy, appears in first few weeks of life (1/200 births), grows rapidly and regresses spontaneously at 5-8 years of age
206
Cherry Hemangioma
benign capillary hemangioma of elderly, does not regress, freq. inc. with age
207
Pyogenic Granuloma
polypoid capillary hemangioma that can ulcerate & bleed, associated with trauma & pregnancy
208
Cystic Hygroma
Cavernous Lymphangioma of the neck, associated with Turner syndrome
209
Glomus Tumor
benign, painful, red-blue tumor under fingernails, arises from modified smooth muscle cells of glomus body
210
Bacillary Andiomatosis
benign capillary skin papules found in AIDS paitents
| -caused by Bartonella henselae infections, frequently mistaken for Kaposi's sarcoma
211
Angiosarcoma
rare blood vessel malignancy typically occuring in the head, neck, & breast areas, associated with patients receiving radiation therapy, especially for breast cancer and Hodgkin's lymphoma, very aggressive & difficult to resect due to delay in diagnosis
212
Lymphangiosarcoma
lymphatic malignancy associated with persistent lymphedema (post radical mastectomy)
213
Kaposi's Sarcoma
-endothelial malignancy most commonly of the skin , but also of mouth, GI tract, & respiratory tract, associated with HHV-8 & HIV, frequently mistaken for bacillary angiomatosis
214
Sturge-Webber Disease
- congenital vascular disorder that affects capillary-sized blood vessels. Manifests with port-wine stain (nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, & early-onset glaucoma
- affects small vessels
