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103 Cards in this Set

  • Front
  • Back
Who is Grant's peedle?
Common Congenital Malformations
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)
Right --> Left Shunts
= 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.
Left --> Right Shunts
= 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)
Eisenmenger's Syndrome
**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)
Tetralogy of Fallot
"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

What causes Tetralogy of Fallot?
Anterosuperior displacement of the infundibular septum.
Findings in Tetralogy of Fallot.
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
Transposition of the Great Vessels
= 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.
What causes transposition of the great vessels?
Due to FAILURE of the aorticopulmonary septum to spiral.
Coartation of the Aorta
Male: Female, 3:1

**There are 2 types:
1) Infantile Type
2) Adult Type
Infantile Type
= aortic stenosis PROXIMAL to the insertion of the ductus arteriosus--PREductal

i.e. INfantile = IN close to the heart
Adult Type
= 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
Patent Ductus Arteriosus
= 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
What could CLOSE a patent ductus arteriosus?
What could be used to keep a PDA open and WHY might you want to do so?
(+ 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.
22q11 Syndromes
- Truncus arteriosus
- Teralogy of Fallot
Down Syndrome
Congenital Rubella
- Septal defects
Turner's Syndrome
Coarcation of the Aorta
Marfan's Syndrome
Aortic insufficiency
Offspring of a diabetic mother
Transposition of the great vessels
Defined as BP > 140/90
Risk Factors
- Increased age
- Obesity
- Diabetes
- Smoking
- Genetics
- Black > white > asian
Types of HTN
**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
HTN predisposes you to
- Atherosclerosis
- Stroke
- Renal failure
- Retinopathy
- Aortic dissection
Signs of Hyperlipidemia
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
Arteriosclerosis, Atherosclerosis + Monckeberg

= yes, they are all apparently different things
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
Atherosclerosis Expanded
= disease of elastic arteries + large and medium-sized muscular arteries

Risk Factors
1) Smoking

2) HTN

3) DM

4) Hyperlipidemia

5) FH
Progression of Atherosclerosis
Fatty streaks --> proliferative plaque --> complex atheromas
- Aneurysms
- Ischemia
- Infarcts
- Peripheral vascular disease
- Thrombus, emboli
Abdominal aorta > coronary artery > popliteal artery > corotid artery
- Angina
- Claudication

**BUT can be asymptomatic
Possible Manifestations of Ischemic Heart Disease
1) Angina
2) Myocardial infarction
3) Sudden cardiac death
4) Chronic ischemic heart disease
**occurs w/ CAD narrowing >75%


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)
Myocardial Infarction
= most often acute thrombosis due to coronary artery atherosclerosis

**results in myocyte necrosis.
Sudden Cardiac Death
= death from cardiac causes within 1 hour of onset of symptoms

**most commonly due to a lethal arrhythmia
Chronic Ischemic Heart Disease
= progressive onset of CHF over many years due to chronic ischemic myocardial damage
Red (=Hemorrhagic) Infarcts
= occur in LOOSE tissues w/ COLLATERALS such as lungs, intestine, OR following reperfusion

(loose = blood spills out)

REd = REperfusion
Pale Infarcts
= occur in SOLID tissues w/ SINGLE blood supply such as the brain, heart, kidney, and spleen
Immediate Cause of MI
Coronary artery occlusion
= LAD > RCA > circumflex
- Diaphoresis
- Nausea, vomiting
- Severe retrosternal pain
- Pain in the left arm and/or jaw
- Shortness of breath
- Fatigue
- Adrenergic symptoms

**Occluded artery --> Infarct

= 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
2 - 4 Days
= HYPEREMIA grossly

= Tissue surrounding infarct shows ACUTE INFLAMMATION
= Dilated vessels (=hyperemia)
= Neutrophil emigration
= Muscle shows EXTENSIVE coagulative necrosis
5 - 10 Days
= 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
7 Weeks
**Recanalized artery
= gray-white scar
= contracted scar complete
Diagnosis of MI
**In the first 6h, ECG is the GOLD STANDARD.

Other Things to Look At:
- Cardiac troponin I
ECG Changes
1) ST elevation (=transmural infarct)
2) ST depression (=subendocardial infarct)
3) Pathological Q waves (=transmural infarct)
Transmural Infarct v. Subendocardial Infarct
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
Cardiac Troponin I
=rises after 4 hours

=elevated for 7-10 days

**MORE SPECIFIC than other protein markers
=predominantly found in myocardium BUT can also be released from skeletal muscle
=nonspecific --> can be found in cardiac, liver, and skeletal muscle cells
MI Complications
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
Dressler's Syndrome
Autoimmune phenomenon resulting in fibrinous pericarditis

=occurs several weeks post-MI
1) Dilated (congestive) cardiomyopathy

2) Hypertrophic cardiomyopathy

3) Restrictive/obliterative cardiomyopathy
Dilated (=congestive) Cardiomyopathy
**Most common cardiomyopathy--90% of cases

**Heart DILATES + looks like a balloon on chest x-ray
=SYSTOLIC dysfunction ensues
Etiologies of Dilated Cardiomyopathy
Etiologies: (the ABCCCD)
-Alcohol abuse
-Coxsackie B virus myocarditis
Chronic cocaine use
-Chagas' disease
-Doxorubicin toxicity

**can also have peripartum cardiomyopathy

**also seen in hemochromatosis
Hypertrophic Cardiomyopathy
**50% of cases are familial--AD
=cause of sudden death in young athletes

**Hypertrophy--often asymmetric--involving the interventricular septum
=DIASTOLIC dysfunction ensues
Findings in Hypertrophic Cardiomyopathy
1) Loud S4
2) Apical impulses
3) Systolic murmur

**Treat w/ B-blocker
Restrictive/Obliterative Cardiomyopathy
**Major Causes:
-Postradiation fibrosis
-Endocardial fibroelastosis
-Endomyocardial fibrosis (=Loffler's)
Mitral Regurgitation
=Holosystolic high-pitched "blowing murmur"

=LOUDEST at apex
Aortic Stenosis
=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
Holosystolic murmur
Mitral Prolapse
=Late systolic murmur w/ MIDSYSTOLIC CLICK

**MOST frequent valvular lesion
Aortic Regurgitation
=Immediate high-pitched "blowing" diastolic murmur

=Wide pulse pressure
Mitral Stenosis
=Follows opening snap

=Delayed rumbling late diastolic murmur

=LA >> LV pressure during diastole
How would you differentiate Tricuspid Stenosis from Mitral Stenosis?
=Tricuspid Stenosis gets LOUDER w/ inspiration
Continuous machine-like murmur

**Loudest at the time of S2
Most common primary cardiac tumor in adults
=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

Most frequent primary cardiac tumor in children
=associated w/ Tuberous Sclerosis
Dyspnea on Exertion
Failure of LV output to increase during exercise
Cardiac Dilation
Greater ventricular end-diastolic volume.
Pulmonary edema, paroxysmal nocturnal dyspnea
LV failure --> increased pulmonary venous pressure --> pulmonary venous distention + transudation of fluid

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

=increased venous return in the supine position exacerbates pulmonary vascular congestion
=i.e. often grossly a "nutmeg liver"

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

**rarely will lead to "cardiac cirrhosis"
Ankle, sacral edema
RV failure --> increased venous pressure --> fluid transudation
Embolus Types
"An embolus moves like a FAT BAT"

-Fat embolus
-Air embolus
-Amniotic fluid
Fat Emboli
=Associated w/ long bone fractures + liposuction
Primary complication of amniotic fluid emboli
=can lead to DIC--especially post-partum
Symptoms of pulmonary emboli
-Chest pain

**Approx. 95% of pulmonary emboli arise from DEEP LEG VEINS
What predisposes you to deep venous thrombosis?
**Virchow's Triad:
1) Stasis
2) Hypercoagulability
3) Endothelial damage
What is cardiac tamponade?
=compression of the heart by fluid (i.e. blood) in the pericardium

=leads to DECREASED CO

**equilibration of pressures in ALL 4 chambers.
Findings in cardiac tamponade.
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
Signs/Symptoms of Bacterial Endocarditis
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
**Multiple blood cultures are necessary for diagnosis

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

=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)
Which valve is most commonly involved?

**Tricuspid valve endocarditis is associated w/ IV drug use.
-Chordae rupture
-Suppurative pericarditis
Think: Bacteria "FROM JANE"
Roth spots
Osler's nodes
Janeaway lesions
Nail-bed hemorrhage
Libman-Sacks Endocarditis
**Seen in SLE
=vegetations develop on BOTH sides of the valve (=mitral valve stenosis)
=BUT do NOT embolize
Rheumatic Heart Disease

**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!
What would you expect to find in rheumatic heart disease?

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

**Also see:
-Aschoff bodies
-Elevated ASO titers
What the hell is an Aschoff Body?
**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)
Types of Pericarditis
1) Serous
2) Fibrinous
3) Hemorrhagic
Causes of Serous Pericarditis
**Caused by:
=Rheumatoid arthritis
Causes of Fibrinous Pericarditis
=Rheumatic fever
Causes of Hemorrhagic Pericarditis
=Malignancy (i.e. melanoma)
Findings in Pericarditis
1) Pericardial pain
3) ECG changes
=diffuse ST elevations in all leads
4) Pulsus Paradoxus
5) Distant heart sounds
What the hell is pulsus paradoxus?
=exaggeration of the normal variation in the pulse during respiratory inspiration
=Pulse becomes WEAKER as you inhale and STRONGER as you exhale
Resolution of Pericarditis
**can resolve WITHOUT scarring OR lead to chronic adhesive or chronic constrictive pericarditis
Cause of Syphilitic Heart Disease
=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
**Can result in ANEURYSM of the ascending aorta or aortic arch + AORTIC VALVE INCOMPETENCE