CARDIOLOGY
Pulse pressure- difference btw systolc + diastolic pressure
Preload- amt of stretch the heart muscle undergoes to pump
Afterload- amt of resistance from aortic/arterial pressure
Stroke Volume- amt of blood ejected from left ventricle
Frank Starling- ability of heart to change it’s force of contraction s directly related to amt of stretch the heart has due to
the volume of blood
Athersclerosis (form of arteriosclerosis)
3 types of lesions:
1. Fatty Streak- thin, flat, yellow
2. Fibrous Plaque-grey/yellow, forms fibrous cap with collateral arteries
3. Advance Artheromatous plaque- scar tissue w/ ulceration which can rupture
**ASA inhibits thromboxane A-2 (which is secreted by platelets due to increase in plugging)
**Fibrinogen binds to Glycoprotein IIb/IIIa  causing platelet aggregaton
Myocardial Ischemia:
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Rsks: > 70 y/o, hx of MI, HTN, low HDL, high LDL, Dm, Marfans, smoking
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Classic Angina: responds to nitro-glycerin sx: SOB, sweating, N/V
o Dx: no ECG changes, T wave inversion, ST depression, No change in enzymes
o Tx: ASA, Nitro, B-blockers, PTCA, CABG
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Unstable Angina- pain at rest, not relieved by Nitroglycerin
o Chronic chest pan which radiates to neck/jaw/arm
o No change in enzymes, ST depresson, T wave inversion
o TX: MONA, heparin, glycoprotein IIb/IIIa inhibitors
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MI- infarction- ST elevation + change in cardiac enzymes
o Chest pain, intense/substernal/ radiates to neck, arm  “crushing/constricting”
o Levine’s sign- clenched fist against sternum
o Atypical sx: elderly, female, Dm
o MC injury- left ant. Descending wall
o Best Cardiac marker- Troponin I (not an enzyme, but a marker!)
o 2 types of MI:
 1. Non-ST elevaton
 II. ST elevaton- Q wave
o TX: MONA, heparin, PTCA, CABG
 Thrombolytics- if ST elevation > 1mm in 2 limbs or >2mm in 2 precordial
 CI: head trauma, brain tumor, surgery, recent CVA
o CX: Dressler’s Syndrome- immune rxn weeks post-MI: pericarditis/pleuritis, fever, malaise
Acute Arterial Occlusion- sudden embolic event  change in arterial blood flow
Sx: pallor, pistol shot, pulselessness, pain, paresthesia, paralysis, cyanosis, skin mottling, necrosis
Dx: angiography
tx: thrombolytics, anticoagulants
Peripheral Arterial Occlusive disease (chronic)
MC- lower limbs (gradual narrowing/plaques) caused by athersclerolosis in canals (mc at bifurcations)
Risks: smoking, hyperlipidemia, CVA, CAD, Dm, HTN, alcohol
Screening test: ABI
Sx: Intermittent Claudicaton in feet/calves, brittle toenails + loss of pretibial hair,
Leriche’s syndrome: impotence (iliac arteries involved), butt claudication, ED, absent femoral pulses
DX: Doppler US
TX: lifestyle modifications, HTN control
Thromboangitis Obliterans (Burger’s Disease)
C- chronic digital ulcers
R- Renyard’s phenomenon
I- idiopathic
S- superficial nodules phelbitis
P- pain
I- inflammatory vasculitis
G- gangrene
**involves distal arteries (migratory red tender nodules)
DVT
Virchow’s triad- venous stasis, endothelial injury, and hypercoaguable state
Sx: unilateral lower extremity edema/ palpable venous cord CX: PE
Homan’s sign- pain on dorsiflexion
dx: Duplex US
Tx: compression devices, anticoagulants, Green Field Filter
Varicose Veins (mc: saphenous veins)
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Primary varicose veins- weak valves
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Secondary varicose veins- due to DVT/ venous HTN
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MC in women b/c estrogen affects veins
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Sx: lower extremity edema, telangectasias, spider veins
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Dx: Dopler US TX: elastic stockings, leg elevaton, sclerotherapy; vein ligation (surgery)
Superficial Thrombophelbitis
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Blood clot in superficial vein
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Trousseau’s syndrome: migratory venous thrombus  sign of pancreatic cancer
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Sx: linear, tender, red induration within a warm vein, firm palpable cord
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Tx: NSAIDS, heat, elevation of limb
Chronic Venous Insufficiency- blood pools in lower limb
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MC risk- DVT
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Causes: obstruction, DVT, valve destruction
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“Bilateral edema”  causes stasis dermatitis (hyperpigmentation in ankles- hemosiderin)
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DX: US
Heart Failure
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Right Sided Heart Failure: edema, hepatomegaly, JVD
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Left Sided Heart Failure: pulmonary edema, SOB, DOE, diaphoresis
Hypotension (shock)- systolic BP < 90 (or drop of 30 systolic)
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Mcc- bleeding (hypovolemia)
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Sx: ↑HR, ↑PVR, ↑ catecholamines, ↑renin, ↑aldosterone, increase in blood volume
1. Hypovolemic Shock: GI bleed, internal bleed or loss of fluid, Mallory-Weiss tear, Borhaave’s Syndrome
a. Sx: N, dizziness, weak pulse
b. TX: vasopressin
2. Cardiogenic Shock
a. Decrease in heart function; mcc- MI
b. ↑ SNS  vasoconstriction/increased afterload  heart works harder
c. Myocardial stunning- post ischemis (dysfunction- area will restore itself)
d. Hibernating Myocardium- persistently impaired myocardium (decreased coronary blood flow)
e. DX: ECHO, EKG, cardiac enzymes
f. TX: MONA, heparin, glycoprotein IIb/IIIa inhibitors, vasopressors, PTCA, thrombolytics, CABG
3. Metabolic/Endocrine Shock
a. Ass. with change in body chemistry or failure of adrenal/thyroid/pit. Gland
4. Obstructive Shock
a. PERICARDIAL Tamponade- fluid in pericardial space
i. BECK’s triad: JVD, hypotension, muffled heart sounds
ii. DX: ECHO
iii. TX: pericardial centesis
b. Tension Pneumo
c. PE
d. Aortic Dissection- “ripping-tearing pain that radiates to back”
5. Distributive shock- decrease in vasomotor tone
a. SEPSIS- mcc (risk: cath, surgery, hx of infection)
i. TX: ICU, antibiotics + vasopressors
b. Anaphylaxis- allergic rxn Tx: EPI pen
c. Neurogenic- failure of nervous system to control blood vessels
i. Mcc- brain/spinal injury
ii. Sx: syncopy, hypotension, bradycardia, hypothermia
Myocarditis- inflammation of myocardium (infection, drugs, radiation)
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MCC: cocksackie B virus
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Increase in all cardiac enzymes
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CXR: pulmonary venous markings
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TX: digitalis, diuretics, vasodialators DX: Bx, US, Echo
Cardiomyopathy- primary heart disease
1. Dialated Cardiomyopathy- mc cardiomyopathy
a. Systolic dysfunction  Thin walls, abnormal systolic pump function
b. Causes: alcoholic, severe hypophosphatemis, cocaine
c. SX: SOB, DOE, orthopnea, pulmonary edema, JVD, hepatomegaly, PMI is displaced
d. DX: CXR; ECG-sinus tachycardia with enlargement; reduced ejection fraction
e. Common sx: mitral + tricuspid regurg
f. Angiography- dx of ejection fraction
g. TX: vasodilator  decreases preload/afterload; digitalis, diuretics, catecholamines, B-blockers
2. Hypertrophic Cardiomyopathy- IHSS
a. Mcc of sudden cardiac death in young adults who exercise
b. Diastolic dysfunction; asymmetric septal hypertrophy
c. Decrease blood into ventricle  increased obstruction of blood outflow (↓preload, ↓ afterload)
d. SX: Mitral Regurg; SOB, DOE, murmurs increase with Valsalva
e. DX: ECG, CXR, enlarged heart, ECHO
f. TX: b-blockers, surgery
3. Restrictive Cardiomyopathy
a. Diastolic dysfunction
b. Etiology: fibrosis of myocardium (sarcoidosis, amyloidosis)
c. Endocardium may be scarred/ thickened; valves are not involved
d. Sx: congestion  edema, SOB, hepatomegaly, DOE
e. DX: Bx is definitive
i. CXR: atrial enlargement with pulmonary venous congestion, edema
ii. EKG- sinus tachycardia
f. TX: no vasodialators, No digitalis, do not remove pericardium; only tx is transplant
g. NOTE: in pericarditis- you can remove the pericardium
Heart Murmurs + Valve Disease
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DX: ECHO, EKG, CXR
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TX: diuretics, digoxin, B-blocker
1. Mitral Stenosis- diastolic; “Opening Snap” at API; cause: Rheumatic Fever
2. Mitral Regurg- systolic; soft murmur at apex; causes: Marfan’s, mitral calcification
3. MVP- mc valve disorder; “MID-SYSTOLIC Click”
4. Aortic Stenosis- SAD: syncope, angina, DOE (radiates to neck)
5. IHSS- subaortic stenosis  increases with Valsalva
6. Aortic Regurg- best heard along left sternal border
a. Diastolic  produces LV hypertrophy
b. Causes: congenital, rheumatic fever
7. Graham Steel Murmur0 at 2nd ICS (pulmonic valve regurg)
8. Pericardial Friction Rub- grating noise from inflammation, heard best with experiation and PT leaning forward
Primary HTN: “essential HTN”- idiopathic
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Syndrome X- HTN, Dm, hyperlipidemia, obesity
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Mc presentation of HTN: asymptomatic
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MC sx: HA- suboccipital early in morning
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Cx: LV hypertrophy, MI, CHF, aortic aneursyms, S4 gallop, TIA, CVA, renal proteinuria, retinopathy
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Pre-HTN: 120-139/80-89
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STAGE 1: 140-159/90-99
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STAGE II: > 160/100
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Start drugs after 3 months of lifestyle modifications or immediately if they have:
o Dm, CAD, Renal Disease
o Initial tx: HCTZ
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HTN Emergency: DBP > 120-130 + end organ damage
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Dx: Ct, EKG, UA (microalbumnuria  Dm nephropathy)
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TX: IV nitroprusside
HTN Medications:
1. Diuretics: CHF, edema (CI: Dm, Gout, hyperlipidemia)
a. HCTZ: decrease Na/K/ Mg (increase glucose/ LDL/ Calcium) good for osteoporosis
b. Loop: decrease Na/K/Ca (increase glucose/uric acid)
c. K-sparing (decrease Na + increase K)
2. B-Blockers- MI, ischemia, migrane (CI: AV block, asthma, CHF, Dm)
3. Ace-Inhibitors- Dm nephropathy, CHF, MI (CI: bilateral renal artery stenosis + pregnancy)
a. Side effects- hyperkalemia, bronchospasm
4. ARBS (“sartan”)
5. CCBS (“dipine”)- CI: CHF, AV block (mc side effect: constipation)
6. alpha-blockers- for HTN + BPH
a. side effects: OH, bradycardia, dizziness
Secondary HTN:
1. Renal Parenchymal disease
a. Mcc- glomerulonephritis; also: Dm, chronic pyelonephritis, renal failure
b. Kidney can’t excrete NA  water retention
c. Tx: ACE inhibitor
2. Renal Artery Stenosis- due to athersclerosis, fibromusclar dysplasia in young women
a. Excessive rennin  increases angiotensin (↑ high rennin)
b. PE: epigastric/ renal artery bruits
c. DX: US, angiography
TX: stent, surgery
3. Primary Hyperaldosteronism (Conn’s disease)
a. Unilateral adrenal adenoma
b. Low rennin levels ; High aldosterone levels  increase in blood pressure
c. Sx: hyperkalemia (↑ K in urine and low rennin levels)
d. Dx: elevated adolesterone in urine/blood
e. Tx: K sparing diuretics
4. Pheochromocytoma  episodic HTN
a. Tachycardia, sweating, palps, feeling of impending doom
b. Dx: urinary vanillymandelic/ catecholamines
c. TX: alpha blockers, B-blockers, surgery
5. Cushing’s disease (because increase in ACTH)
a. HTN, truncal obesity, buffalo hump, moon face (facial plethora)
b. Dx: dexamethasone suppression test tx: surgery
6. Coarctation of Aorta
a. HTN is greater in Upper Extremities
CHD risk factors: HTN, low HDL, high LDL, family hx
CAD equivalents: Dm, HTN, AAA
Hyperlipidemia Tx:
1. HMG-CoA Reductase (Statins)  most powerful
2. Bile Acid sequestants (nyasin)  decreases LDL
3. Fibric Acid Derivatives  decreases TB
4. Ezetimbie (blocks absorption in intestine)
5. Probucol  decrease both LDL + HDL
6. Niacin  inhibits VLDL + LDL
a. Adr: pruritis, flushing, gout