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Flashcards in Cardiovascular Deck (214):
1

Truncus Arteriosus (TA) gives rise to?

Ascending aorta & Pulmonary Trunk

2

Bulbus Cordis gives rise to?

Smooth parts (outflow tract) of left and right ventricles

3

Primitive Ventricle gives rise to?

Trabeculated left and right ventricles

4

Primitive Atria gives rise to?

Trabeculated left and right atria

5

Left horn of sinus venosus (SV) gives rise to?

Coronary Sinus

6

Right horn of sinus venosus gives rise to?

Smooth part of right atrium

7

Right common cardinal vein and right anterior cardinal vein gives rise to?

SVC

8

Formation of Truncus Arteriosus?

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

Intraventricular Septum Development

1. Muscular ventricular septum forms. Opening is called intraventricular foramen
2. AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing IV foramen
3. Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum

10

Pathology of Intraventricluar Septum Development

-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

Interatrial Septum Development

1. Foarment primum narrows as septum grows toward endocardial cushions
2. Perforations in septum form foramen secundum (foramen primum disappears)
3. Foramen secundum maintains right-to-left shunt as septum secundum begins to grow
4. Septum secundum contains a permanent opening (foramen ovale)
5. Foramen secundum enlarges and upper part of septum primum degenerates
6. Remaining portion of septum primum forms valve of foramen ovale
7. Septum secundum & septum primum fuse to form the atrial septum
8.Foramen ovale ususally closes soon after birth because of inc. LA pressure

12

Pathology of Interatrial Septum Development

-patent foramen ovale: caused by failure of the septum primum and septum secundum to fuse after birth

13

Fetal Erythropoiesis

Yolk Sac: 3-10 weeks
Liver: 6wk - birth "Young Liver Synthesizes
Spleen: 15-30 weeks Blood"
Bone Marrow: 22wk-adult

14

Fetal Hemoglobin

alpha 2 gamma 2

15

Adult Hemoglobin

alpha 2 beta 2

16

Fetal Circulation

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

3 Shunts in Fetal Circulation

1. Blood entering the fetus through the umbilical vein is conducted via the ductus venosus into the IVC to bypass the hepatic circulation
2. Most oxygenated blood reaching the heat via the IVC is diverted through the foramen ovale & pumped out the aorta to the head & body
3. 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

Fetal-postnatal derivatives: Umbilical Vein

Ligamentum teres hapatis
(contained in falciform ligament)

19

Fetal-postnatal derivatives: Umilical Arteries

Medial umbilical ligaments

20

Fetal-postnatal derivatives: Ductus Arteriosus

Ligamentum Arteriosum

21

Fetal-postnatal derivatives: Ductus Venosus

Ligamentum Venosum

22

Fetal-postnatal derivatives: Foramen Ovale

Fossa Ovalis

23

Fetal-postnatal derivatives: Allantosis

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

Fetal-postnatal derivatives: Notochord

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)

157

Coronary Steal Syndrome

-Vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to area of higher perfusion

158

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

159

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

161

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

163

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

168

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)

169

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

171

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

176

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)

177

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)

178

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

179

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