Cv Pathology.

Front 1

Who is Grant's peedle?

Back 1

Megan

Front 2

Common Congenital Malformations

Back 2

1) Heart defects
2) Hypospadias
3) Cleft lip +/- cleft palate
4) Congenital hip dislocation
5) Spina bifida
6) Anencephaly
7) Pyloric stenosis (= often see projectile vomiting)

Front 3

Right --> Left Shunts

Back 3

= early cyanosis
= "blue babies"

Think--the 3 T's!
1) Tetralogy of Fallot (=most common cause of early cyanosis)
2) Transposition of the great vessels
3) Truncus arteriosus

**In this case, children may actually SQUAT to increase venous return.

Front 4

Left --> Right Shunts

Back 4

= late cyanosis
= "blue kids"

1) VSD (=most common congenital cardiac anomaly)
2) ASD (=loud S1; wide, fixed split S2)
3) PDA (=close w/ indomethacin)

Frequency: VSD > ASD > PDA

**Increased pulmonary resistance due to arteriolar thickening --> progressive pulmonary hypertension (=i.e. can progress to Eisenmenger's Syndrome)

Front 5

Eisenmenger's Syndrome

Back 5

**Uncorrected VSD, ASD, or PDA leads to progressive pulmonary HTN.

**As the pulmonary resistance increases, the shunt reverses from L --> R to R --> L.

= causes late cyanosis (=clubbing + polycythemia)

Front 6

Tetralogy of Fallot

Back 6

"Got something to PROVe"

1) Pulmonary stenosis (=MOST impt. determinant for prognosis)

2) Right Ventricular Hypertrophy (RVH)

3) Overriding aorta (=overrides the VSD)

4) VSD

3)

Front 7

What causes Tetralogy of Fallot?

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Anterosuperior displacement of the infundibular septum.

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Findings in Tetralogy of Fallot.

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1) Early cyanosis = due to the R --> L shunt across the VSD.

2) Patient suffers "cyanotic spells"

3) Boot-shaped heart on X-ray due to RVH

Front 9

Transposition of the Great Vessels

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= aorta leaves the RV (=anterior) + the pulmonary trunk leaves the LV (=posterior) --> SEPARATION OF THE SYSTEMIC + PULMONARY CIRCULATIONS

**This is NOT compatible w/ life UNLESS a shunt is present to allow adequate mixing of blood (= i.e. VSD, PDA, or patent foramen ovale)

**Without surgical correction, most infants die w/i the first few months of life.

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What causes transposition of the great vessels?

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Due to FAILURE of the aorticopulmonary septum to spiral.

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Coartation of the Aorta

Back 11

Male: Female, 3:1

**There are 2 types:
1) Infantile Type
2) Adult Type

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Infantile Type

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= aortic stenosis PROXIMAL to the insertion of the ductus arteriosus--PREductal

i.e. INfantile = IN close to the heart

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Adult Type

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= stenosis is DISTAL to the ductus arteriosus = POSTductal

**Associated with:
- Notching of the ribs
- HTN in upper extremities
- Weak pulses in lower extremities

SO, it is always VERY important to check FEMORAL PULSES on physical exam.

ADult: Distal to Ductus

Front 14

Patent Ductus Arteriosus

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= in the fetal period, the shunt is R --> L (=normal)

= in the neonatal period, lung resistance DECREASES + the shunt becomes L --> R w/ subsequent RVH + failure (=abnormal)

**Associated w/ a continuous MACHINE-LIKE MURMUR

Front 15

What could CLOSE a patent ductus arteriosus?

Back 15

Indomethacin

Front 16

What could be used to keep a PDA open and WHY might you want to do so?

Back 16

PGE
(+ the low O2 tension in the fetal period)

**Sometimes it might be necessary to keep the DA open to sustain life in conditions such as transposition of the great vessels.

Front 17

22q11 Syndromes

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- Truncus arteriosus
- Teralogy of Fallot

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Down Syndrome

Back 18

- ASD
- VSD

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Congenital Rubella

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- Septal defects
- PDA

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Turner's Syndrome

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Coarcation of the Aorta

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Marfan's Syndrome

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Aortic insufficiency

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Offspring of a diabetic mother

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Transposition of the great vessels

Front 23

HTN

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Defined as BP > 140/90

Front 24

Risk Factors

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- Increased age
- Obesity
- Diabetes
- Smoking
- Genetics
- Black > white > asian

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Types of HTN

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**90% of HTN is primary (=essential) + related to increased CO or TPR

**Remaining 10% is mostly secondary to renal disease

**MALIGNANT HTN is severe + rapidly progressing

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HTN predisposes you to

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- Atherosclerosis
- Stroke
- CHF
- Renal failure
- Retinopathy
- Aortic dissection

Front 27

Signs of Hyperlipidemia

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1) Atheromata
= plaques in blood vessel walls

2) Xanthoma
= plaques or nodules composed of lipid-laden histiocytes in the skin--especially the eyelids

3) Tendinous Xanthoma
= lipid deposit in tendon--especially Achilles

4) Corneal arcus
= lipid deposit in cornea

Front 28

Arteriosclerosis, Atherosclerosis + Monckeberg

= yes, they are all apparently different things

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1) Arteriolosclerosis
= hylanine thickening of small arteries in essential HTN
= you will get hyperplastic "ONION SKINNING" in malignant HTN

2) Atherosclerosis
= fibrous plaques and atheromas form in intima of arteries

3) Monckeberg
= calcification of the arteries--especially the radial or ulnar
= usually BENIGN

Front 29

Atherosclerosis Expanded

Back 29

= disease of elastic arteries + large and medium-sized muscular arteries

COLOR IMAGE 79

Front 30

Risk Factors

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1) Smoking

2) HTN

3) DM

4) Hyperlipidemia

5) FH

Front 31

Progression of Atherosclerosis

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Fatty streaks --> proliferative plaque --> complex atheromas

Front 32

Complications

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- Aneurysms
- Ischemia
- Infarcts
- Peripheral vascular disease
- Thrombus, emboli

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Location

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Abdominal aorta > coronary artery > popliteal artery > corotid artery

Front 34

Symptoms

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- Angina
- Claudication

**BUT can be asymptomatic

Front 35

Possible Manifestations of Ischemic Heart Disease

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1) Angina
2) Myocardial infarction
3) Sudden cardiac death
4) Chronic ischemic heart disease

Front 36

Angina

Back 36

**occurs w/ CAD narrowing >75%

Variants:

1) Stable
= mostly secondary to atherosclerosis
= will have retrosternal chest pain w/ exertion

2) Prinzmetal's Variant
= occurs at rest secondary to coronary artery spasm

3) Unstable/crescendo
= thrombosis but no necrosis (= worsening chest pain)

Front 37

Myocardial Infarction

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= most often acute thrombosis due to coronary artery atherosclerosis

**results in myocyte necrosis.

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Sudden Cardiac Death

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= death from cardiac causes within 1 hour of onset of symptoms

**most commonly due to a lethal arrhythmia

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Chronic Ischemic Heart Disease

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= progressive onset of CHF over many years due to chronic ischemic myocardial damage

Front 40

Red (=Hemorrhagic) Infarcts

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= occur in LOOSE tissues w/ COLLATERALS such as lungs, intestine, OR following reperfusion

(loose = blood spills out)

REd = REperfusion

Front 41

Pale Infarcts

Back 41

= occur in SOLID tissues w/ SINGLE blood supply such as the brain, heart, kidney, and spleen

Front 42

Immediate Cause of MI

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Coronary artery occlusion
= LAD > RCA > circumflex

Front 43

Symptoms

Back 43

- Diaphoresis
- Nausea, vomiting
- Severe retrosternal pain
- Pain in the left arm and/or jaw
- Shortness of breath
- Fatigue
- Adrenergic symptoms

COLOR IMAGE 80

Front 44

FIRST DAY

Back 44

**Occluded artery --> Infarct

Grossly:
= dark mottling
= PALE w/ tetrazolium stain

**Microscopic Changes:
= no visible change by light microscopy in first 2-4 hours
= coagulative necrosis
= contraction bands visible after 4h
= release of contents of necrotic cells into the bloodstream + the beginning of neutrophil emigration

Front 45

2 - 4 Days

Back 45

= HYPEREMIA grossly

= Tissue surrounding infarct shows ACUTE INFLAMMATION
= Dilated vessels (=hyperemia)
= Neutrophil emigration
= Muscle shows EXTENSIVE coagulative necrosis

Front 46

5 - 10 Days

Back 46

Gross:
= Hyperemic border
= Central yellow-brown softening
= MAXIMALLY yellow and soft by 10 days

= ingrowth of granulation tissue into the outer zone
= layer of macrophages
= layer of neutrophils

Front 47

7 Weeks

Back 47

**Recanalized artery
= gray-white scar
= contracted scar complete

Front 48

Diagnosis of MI

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**In the first 6h, ECG is the GOLD STANDARD.

Other Things to Look At:
- Cardiac troponin I
- CK-MB
- AST

Front 49

ECG Changes

Back 49

1) ST elevation (=transmural infarct)
2) ST depression (=subendocardial infarct)
3) Pathological Q waves (=transmural infarct)

Front 50

Transmural Infarct v. Subendocardial Infarct

Back 50

Transmural Infarct:
=involves the entire thickness of the left ventricular wall from the endocardium to the epicardium
=usually involves the anterior free wall + posterior free wall + septum w/ extension into the RV (15% of the time)

Subendocardial Infarct:
=multifocal areas of necrosis confined to the inner 1/3 - 1/2 of the left ventricular wall
=i.e. do NOT show the same changes as seen in a transmural MI

Front 51

Cardiac Troponin I

Back 51

=rises after 4 hours

=elevated for 7-10 days

**MORE SPECIFIC than other protein markers

Front 52

CK-MB

Back 52

=predominantly found in myocardium BUT can also be released from skeletal muscle

Front 53

AST

Back 53

=nonspecific --> can be found in cardiac, liver, and skeletal muscle cells

Front 54

MI Complications

Back 54

1) Cardiac arrhythmia
=impt. cause of death before reaching the hospital
=common in the first few days

2) LV failure + pulmonary edema

3) Cardiogenic shock
=occurs w/ LARGE infarcts
=high risk of mortality

4) Rupture of ventricular free wall, interventricular septum, papillary muscle (4-10 days post-MI), cardiac tamponade

5) Aneurysm formation
=dec. CO, risk of arrhythmia, embolus from mural thrombus

6) Fibrinous pericarditis
=evidenced by friction rub
=3-5 days post-MI

7) Dressler's Syndrome

Front 55

Dressler's Syndrome

Back 55

Autoimmune phenomenon resulting in fibrinous pericarditis

=occurs several weeks post-MI

Front 56

Cardiomyopathies

Back 56

1) Dilated (congestive) cardiomyopathy

2) Hypertrophic cardiomyopathy

3) Restrictive/obliterative cardiomyopathy

Front 57

Dilated (=congestive) Cardiomyopathy

Back 57

**Most common cardiomyopathy--90% of cases

**Heart DILATES + looks like a balloon on chest x-ray
=SYSTOLIC dysfunction ensues

Front 58

Etiologies of Dilated Cardiomyopathy

Back 58

Etiologies: (the ABCCCD)
-Alcohol abuse
-Beriberi
-Coxsackie B virus myocarditis
Chronic cocaine use
-Chagas' disease
-Doxorubicin toxicity

**can also have peripartum cardiomyopathy

**also seen in hemochromatosis

Front 59

Hypertrophic Cardiomyopathy

Back 59

**50% of cases are familial--AD
=cause of sudden death in young athletes

**Hypertrophy--often asymmetric--involving the interventricular septum
=DIASTOLIC dysfunction ensues

Front 60

Findings in Hypertrophic Cardiomyopathy

Back 60

1) Loud S4
2) Apical impulses
3) Systolic murmur

**Treat w/ B-blocker

Front 61

Restrictive/Obliterative Cardiomyopathy

Back 61

**Major Causes:
-Sarcoidosis
-Amyloidosis
-Postradiation fibrosis
-Endocardial fibroelastosis
-Endomyocardial fibrosis (=Loffler's)

Front 62

Mitral Regurgitation

Back 62

=Holosystolic high-pitched "blowing murmur"

=LOUDEST at apex

Front 63

Aortic Stenosis

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=Crescendo-decrescendo systolic ejection murmur following ejection click

=LV >> aortic pressure during systole

=Radiates to carotids/apex

**"Pulses parvus et tardus"
=pulses weak compared to heart sounds

Front 64

VSD

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Holosystolic murmur

Front 65

Mitral Prolapse

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=Late systolic murmur w/ MIDSYSTOLIC CLICK

**MOST frequent valvular lesion

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Aortic Regurgitation

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=Immediate high-pitched "blowing" diastolic murmur

=Wide pulse pressure

Front 67

Mitral Stenosis

Back 67

=Follows opening snap

=Delayed rumbling late diastolic murmur

=LA >> LV pressure during diastole

Front 68

How would you differentiate Tricuspid Stenosis from Mitral Stenosis?

Back 68

=Tricuspid Stenosis gets LOUDER w/ inspiration

Front 69

PDA

Back 69

Continuous machine-like murmur

**Loudest at the time of S2

Front 70

Most common primary cardiac tumor in adults

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Myxomas
=90% occur in the atria--usually LA
=described as a "BALL-VALVE" obstruction in the LA

**note: METASTASES are actually the most common heart tumor

COLOR IMAGE 88

Front 71

Most frequent primary cardiac tumor in children

Back 71

Rhabdomyomas
=associated w/ Tuberous Sclerosis

Front 72

Dyspnea on Exertion

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Failure of LV output to increase during exercise

Front 73

Cardiac Dilation

Back 73

Greater ventricular end-diastolic volume.

Front 74

Pulmonary edema, paroxysmal nocturnal dyspnea

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LV failure --> increased pulmonary venous pressure --> pulmonary venous distention + transudation of fluid

=will often see the presence of hemosiderin-laden macrophages (="heart failure cells")

Front 75

Orthopnea

Back 75

= shortness of breath when supine

=increased venous return in the supine position exacerbates pulmonary vascular congestion

Front 76

Hepatomegaly

Back 76

=i.e. often grossly a "nutmeg liver"

=increased central venous pressure --> increased resistance to portal flow

**rarely will lead to "cardiac cirrhosis"

Front 77

Ankle, sacral edema

Back 77

RV failure --> increased venous pressure --> fluid transudation

Front 78

Embolus Types

Back 78

"An embolus moves like a FAT BAT"

-Fat embolus
-Air embolus
-Thrombus
-Bacteria
-Amniotic fluid
-Tumor

Front 79

Fat Emboli

Back 79

=Associated w/ long bone fractures + liposuction

Front 80

Primary complication of amniotic fluid emboli

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=can lead to DIC--especially post-partum

Front 81

Symptoms of pulmonary emboli

Back 81

-Chest pain
-Tachypnea
-Dyspnea

**Approx. 95% of pulmonary emboli arise from DEEP LEG VEINS

Front 82

What predisposes you to deep venous thrombosis?

Back 82

**Virchow's Triad:
1) Stasis
2) Hypercoagulability
3) Endothelial damage

Front 83

What is cardiac tamponade?

Back 83

=compression of the heart by fluid (i.e. blood) in the pericardium

=leads to DECREASED CO

**equilibration of pressures in ALL 4 chambers.

Front 84

Findings in cardiac tamponade.

Back 84

1) Hypotension
2) Increased venous pressure (=JVD)
3) Distant heart sounds
4) Pulsus paradoxus

**ECG shows ELECTRICAL ALTERANS--> beat-to-beat alterations of QRS complex height

Front 85

Signs/Symptoms of Bacterial Endocarditis

Back 85

1) New murmur
=causes by valvular damage
2) Anemia
3) Fever
4) Osler's nodes
=tender raised lesions on finger or toe pads
4) Roth's spots
=round white spots on the retina surrounded by hemorrhage
5) Janeway lesions
=small erythematous lesions on palm or sole
6) Splinter hemorrhages on nail bed

Front 86

Diagnosis

Back 86

**Multiple blood cultures are necessary for diagnosis

COLOR IMAGE 82

Front 87

Etiology

Back 87

ACUTE
=S. aureus--HIGH virulence
=see large vegetations on previously normal valves

SUBACUTE
=Viridans streptococcus--LOW virulence
=see smaller vegetations on CONGENITALLY ABNORMAL or DISEASED valves
=more insidious onset
=often a sequela of dental procedures

**Endocarditis may ALSO be NONBACTERIAL
=secondary to metastasis or renal failure
=called NBTE (nonbacterial thrombotic endocarditis or marantic endocarditis)

Front 88

Which valve is most commonly involved?

Back 88

MITRAL VALVE

**Tricuspid valve endocarditis is associated w/ IV drug use.

Front 89

Complications

Back 89

-Chordae rupture
-Glomerulonephritis
-Suppurative pericarditis
-Emboli

Front 90

Think: Bacteria "FROM JANE"

Back 90

Fever
Roth spots
Osler's nodes
Murmur
Janeaway lesions
Anemia
Nail-bed hemorrhage
Emboli

Front 91

Libman-Sacks Endocarditis

Back 91

**Seen in SLE
=vegetations develop on BOTH sides of the valve (=mitral valve stenosis)
=BUT do NOT embolize

Front 92

Rheumatic Heart Disease

COLOR IMAGE 85

Back 92

**Sequelae of RHEUMATIC FEVER:
=Rheumatic fever is a consequence of pharyngeal infection w/ group A B-hemolytic strep

=SO, the late sequelae is rheumatic heart disease --> affects heart valves:

mitral > aortic >> tricuspid

=HIGH pressure valves affected most

**SO, rheumatic heart disease is IMMUNE-MEDIATED, not the DIRECT effect of bacteria!

Front 93

What would you expect to find in rheumatic heart disease?

Back 93

FEVERSS:

=Fever
=Erythema marginatum
=Valvular damage
=ESR increased
=Red-hot joints (migratory polyarthritis)
=Subcutaneous nodules
=St. Vitus' dance (=chorea)

**Also see:
-Aschoff bodies
-Elevated ASO titers

Front 94

What the hell is an Aschoff Body?

Back 94

**Aschoff bodies = granuloma w/ giant cells

SO, you will see Aschoff bodies and Anitschkow's cells (=activated histiocytes) in rheumatic heart disease

**Think of two RHussians w/ RHeumatic heart disease (=Aschoff and Anitschkow)

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Types of Pericarditis

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1) Serous
2) Fibrinous
3) Hemorrhagic

Front 96

Causes of Serous Pericarditis

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**Caused by:
=SLE
=Rheumatoid arthritis
=Infection
=Uremia

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Causes of Fibrinous Pericarditis

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=Uremia
=MI
=Rheumatic fever

Front 98

Causes of Hemorrhagic Pericarditis

Back 98

=TB
=Malignancy (i.e. melanoma)

Front 99

Findings in Pericarditis

Back 99

1) Pericardial pain
2) FRICTION RUB
3) ECG changes
=diffuse ST elevations in all leads
4) Pulsus Paradoxus
5) Distant heart sounds

Front 100

What the hell is pulsus paradoxus?

Back 100

=exaggeration of the normal variation in the pulse during respiratory inspiration
=Pulse becomes WEAKER as you inhale and STRONGER as you exhale

Front 101

Resolution of Pericarditis

Back 101

**can resolve WITHOUT scarring OR lead to chronic adhesive or chronic constrictive pericarditis

Front 102

Cause of Syphilitic Heart Disease

Back 102

=Tertiary syphilis DISRUPTS the vasa vasora of the aorta --> dilates the aorta and valve ring

**Often causes calcifications of the aortic root and ascending arch of the aorta
=which you can see on XRAY

Front 103

Complications:

Back 103

**Can result in ANEURYSM of the ascending aorta or aortic arch + AORTIC VALVE INCOMPETENCE