USMLE - Cardiology Part 2

Isoelectric

| Ventricles Depolarize

HypoK, Bradycardia

SA --> Atria --> AV --> Common Bundle --> Bundle Branches --> Purkinje Fibers --> Ventricles

100 msec delay allows for ventricular filling

Can progress to Vfib

Long QT interval predisposes towards it

Treatment is Magnesium Sulfate

Defect in cardiac Na or K channels

| Can present with congenitcal sensorineural deafness (Jervell and Lang Nielsen Syndrome)

Irregularly irregular with no discrete P wave between irregularly spaced QRS

Can result in atrial stasis which leads to stroke

Treatment: anticoagulants, β Blockers, cardioversion, Ca Channel Blockers, Digoxin

Back to back P waves (sawtooth)

| IA, IC, II, III, IV

Erratic rhythm with no identifiable waves

| Fatal without CPR and Defib

PR interval prolonged (>200 msec)

| Asymptomatic

Wenckenbach

Progressive lengthening of PR interval until a beat is dropped

Usually asymptomatic

Extra P waves

Treat with pacemaker

Can progress to 3rd degree black

A and V beat independently

Treat with pacemaker

Can be caused by Lyme Disease

Released by atrial myocytes in response to ↑ vol and atrial pressure.

Leads to vascular relaxation and ↓ Na reabsorption in medullary collecting tubule.

Constricts EA and dilates AA (via cGMP)

Transmit via Vagus nerve to NTS in medulla and respond to ↑ BP only

Transmits via glossopharyngeal nerve to NTS and responds to any change in BP

↓ BP --> ↓ stretch --> ↓ afferent baroreceptor firing --> ↑ efferent sympathetic firing and ↓ efferent parasympathetic firing --> vasoconstriction, ↑ HR, ↑ contractility, ↑ BP

↑ pressure on carotid artery --> increase stretch --> ↑ afferent firing --> ↓ HR

HTN, Bradycardia, Respiratory Depression

↑ ICP constricts arterioles --> cerebral ischemia --> reflex HTN --> ↑ stretch --> Reflex baroreceptor induced bradycardia

Carotid and Aortic bodies stimulated by ↓ PO2 (< 60mmHg), ↑ PCO2, and ↓ pH

Stimulated by change in pH and PCO2 of brain interstitial fluid

Do not directly respond to PO2

Liver

Kidney

Heart

| ~80%. ↑ O2 demand must be met with ↑ blood flow

RA: less than 5

RV: 5-25

PA: 25-10

LA: less than 12

LV: 130-10

Aorta: 130-90

PCWP measured with Swan-Ganz catheter

Local metabolites - CO2, Adenosine, NO

Local metabolites - CO2, pH

Myogenic and tubuloglomerular feedback

Hypoxia vasoconstriction

Local metabolites - lactate, adenosine, K

Sympathetic stimulation for temperature control

J = K[(Pc-Pi)-(πc-πi)]

↑ Pc pushes fluid out of capillaries

↓ πc

↑ K

| Toxins, Infections, Burns

πi

| Caused by lymphatic blockage

R-L shunt

Tetralogy of Fallot (most common)

Transposition of the great vessels

Persistent Truncus arteriosus (with PDA)

Tricuspid atresia

Total Anomalous Pulmonary Venous Return

PDA

ASD and sometimes PDA to allow for R-L shunt to maintain CO

L-R shunt

| VSD > ASD > PDA

Uncorrected VSD, ASD, PDA causes compensatory pulmonary vascular hypertrophy --> PHTN

As pulmonary resistance ↑, the shunt reverses and becomes R-L

Presents as Cyanosis, Clubbing, Polycythemia

Caused by anterosuperior displacement of infundibular septum

PROV

Pul stenosis, RVH, Overriding Aorta (overrides VSD), VSD

R-L shunting --> cyanosis

Boot-shaped heart on XR

Surgery

Squatting --> ↓ blood flow to legs --> ↑ Resistance --> ↓ R-L shunt across VSD

Only compatible with life if there is a VSD, PDA, or PFO

Due to failure of the aorticopulmonary septum to spiral

Surgery

Aortic Regurgitation

Stenosis proximal to ductus arteriosus

Associated with Turners Syndrome

Check femoral pulses

Stenosis distal to ligamentum arteriosum

Associated with bicuspid aortic valve

On Physical Exam: Notching of the ribs due to collateral circulation, HTN in upper extremities, Weak pulses in lower extremities

Cyanosis in the lower extremities (differential cyanosis)

L-R shunt --> RVH and/or LVH and failure

Truncus arteriosus and ToF

ASD, VSD, AVSD (endocardial cushion defect)

Septal defects, PDA, Pulmonary artery stenosis

Preductal coarctation of the aorta

Aortic insufficiency and dissection (late)

Transposition of the great vessels

Pulmonary veins drain into R heart

140/90

Age, diabetes, obesity, smoking, genetics

Black > White > Asian

90% primary. 10% Secondary

Related to ↑ CO and TPR

Renal disease

180/120 and rapidly progressing

Aterosclerosis, LVH, Stroke, CHF, Renal Failure, Retinopathy, Aortic Dissection

Lipid plaques in blood vessel walls

Plaques or nodules composed of lipid laden histiocytes in the skin. Found on eyelids (xanthelasma), tendons (Tendinous Xanthomas) (esp Achilles tendon)

Lipid deposits in cornea.

| Nonspecific (arcus senilis)

Calcification of media of arteries. Especially radial or ulnar. Usually benign and does not obstruct blood flow. Only involves media, not intima

Hyaline: Thickening of small arteries seen in essential HTN and DM

Hyperplastic: "onion skinning" seen in MHTN

Fibrous plaques and atheromas for in the intima of elastic arteries and large/medium muscular arteries.

Smoking, HTN, Hyperlipidemia, Diabetes

Age, Male, Postmenopausal women, family history

Endothelial cell dysfunction --> macs and LDL accumulation --> Foam cells --> Fatty streaks --> SM migration (PDGF and FGF), proliferation, and ECM deposition --> Fibrous plaque

Aneurysm, ischemia, infarcts, peripheral vascular disease, thrombus, emboli

Abdominal Aorta > coronary arteries > Popliteal arteries > carotid arteries

angina, claudication, but may be asymptomatic

Atherosclerosis in Male smoker >50 with HTN

HTN, Marfan's (Cystic Medial Necrosis), and Tertiary Syphilis

Longitudinal tear forms false lumen

Associated with HTN, Bicuspid Aortic Valve, Cystic Medial Necrosis, Connective Tissue Disorder (i.e. Marfan's)

Presents with tearing chest pain radiating to the back

CXR shows mediastinal widening with false lumen larger than true lumen

Can result in pericardial tamponade, aortic rupture

75% but this does not produce myocyte necrosis

Retrosternal chest pain with exertion Mostly secondary to atherosclerosis ST depression on ECK

Secondary to coronary artery vasospasms

| ST elevation on EKG

Worsening chest pain at rest or with minimal exertion. Caused by thrombosis with incomplete coronary artery occlusion. ST depression on ECK

Vasodilators aggravate ischemia by shunting blood from affected area to region of higher perfusion

Complete occulsion of coronary artery producing myocyte necrosis.

Most often due to thrombosis

ST depression progressing to ST elevation

Subendocardial wall damage

Transumarl wall damage

Death from cardiac cause within 1 hour of symptom onset Most commonly due to lethal arrhythmia (Vfib) Associated with CAD

Chronic ischemic myocardial damage. Progresses to CHF

Diaphoresis, naseau, vomiting, retrosternal pain, pain in left arm and/or jaw, dyspnea, fatigue

Gross: none LM: none Risk: Arrhythmias, CHF exacerbation, shock

Gross: Dark mottling. Pale with tetrazolium stain LM: Early coagulative necrosis, edema, hemorrhave, wavy fibers Risk: Arrhythmias

Gross: Dark mottling. Pale with tetrazolium stain LM: Contraction bands from reperfusion injury, Release of necrotic cell contents into blood, Beginning of neutrophil migration Risk: Arrhythmias

Gross: hyperemia LM: Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation. Neutrophil migration Risk: Fibrinous pericarditis

Gross: Hyperemic border with centrally yellow-brown softening (maximally yellow at day 10) LM: Macs. Granulation tissue at margins Risk: Free wall rupture --> tamponade, Papillary muscle rupture, Aneurysm, IV septal rupture

Gross: Gray-white tissue | Dresslers syndrome

EKG is gold standard in the first 6 hours. Troponin I rises after 4 hours and is elevated for 7-10 days (specific). CKMB predominantly found in myocardium but also skeletal muscle. Useful in diagnosing reinfarction because returns to normal after 48 hours

ST elevation. Pathological Q wave

ST depression. Necrosis of <50% of ventricle wall