Cardiology 5

temporal arteritis (if extracranial branches of carotid involved)

Systemic panarteritis affecting med- lg vessels in pts >50

polymyalgia rheumatica

Giant Cell Arteritis

Blindness due to opthalmic artery occlusion

High ESR, CRP & Interleukin-6 ; mild norm/norm anemia w/ thrombocytosis; temporal art bx is diagnostic

prevention of blindness, Prednisone 60 mg ASAP & cont for 1-2 mos before taper dosage

Thoracic aortic aneurysms are 17X more frequent

Raynaud Phenomenon

Primarily affects young women

pallor

cyanosis then rubor (white to blue to red)

Lifestyle changes (gloves), CCB/ nitrates for chronic vasodilation; tx underlying condition

primary or secondary to other disease states (scleroderma/SLE)

CHD

1 in 5

70% women & 80% of men under 65 will die within 8 years

increases risk x8

1 in 4

(II, III, aVF); RCA; left circumflex if left dominant

(V2-V5); LAD

(I, aVL, V5-V6); Left circumflex

(II, III, aVF, I, aVL); Large RCA, or Left dominant Left circumflex

(V4-V6, I, aVL); Left circumflex

Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy (diastolic non-compliant CHF more common in hypertension than Systolic (end stage hypertensive dz))

myocardial dz; pericardial dz

Cardiomyopathy; myocarditis

dilated; hypertrophic; restrictive

infectious; toxic; idiopathic

Pericarditis; Pericardial effusion / tamponade; Pericardial constriction

At risk without known disease

Heart disease-asymptomatic

Prior or current symptoms

Advanced or refractory

Age; Hypertension; Tobacco abuse; Diabetes mellitus; Obesity; ETOH/Substance abuse

Coronary artery dz/MI; Valvular or congenital heart dz; Hypertension….diastolic dysfn; ETOH/substance abuse; Viral Infxns; PG; Idiopathic

1 plaque rupture; 2 plt activation aggregation; 3 fibrin generation; 4 thrombus formation

Progressive intraluminal narrowing; Sudden disruption/fissuring of plaques

to produce collateral blood supply & more likely to cause worsening stable/unstable angina (>75%)

to rupture, causing ACS (Acute Coronary Syndrome) or Acute MI (25-75%)

2x risk for 1/2 to 1 pack/day; 3x risk for > 1 pack/day; risk declines 50% after one year of tobacco cessation

Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy

Diastolic more than Systolic (end stage hypertensive dz)

Coronary artery dz/MI (ischemia induced); congenital; anything that causes CHF

Chest pain/pressure/tightness; Jaw/ neck/ throat/scapular/ arm pain; SOB/ Dyspnea on exertion; N&V; Diaphoresis; Fatigue

the coronary sinus & thebesian veins

Anomalous coronary arteries (4-15% of young people with sudden cardiac death); 1-2% of population

AV valves do; semilunar valves do not

systole

diastole

preload

afterload

myocardial contractility

sympathetic stimulation/action

myocardial injury

blood volume/viscosity; resistance in aorta & other peripheral vessels

inspiration or increasing venous return to right heart)

end systolic volume

80

EDV (end diastolic volume) – ESV (end systolic volume)

HR x SV (normal about 5 L/min)

SV=70ml, EDV=135ml, ESV=65ml, CO=5L total blood

Cardiac output

Stroke volume

SV increases as the EDV increases

EF% = SV/EDV

Ejection Fraction

67% (at DUMC: >55%)

fibrous ring surrounding each of the 4 cardiac valves; fn: to provide structural support to the heart

Stenosis

Regurgitation / Insufficiency

Mitral (Systole)

Aortic valve closing (diastole)

CHF (sounds like: Ken-Tuc-Key)

HTN or CAD (sounds like: Tenn-es-see)

S4

Sinuses of Valsalva

LAD; Left circumflex

Distal branches from RCA (supply the septum 70%)

Distal branches from LCx (supply the septum 20%)

RCA 60% of the time & by LCX 40% of the time

dominant artery (RCA or LCx)

Collateral Vessels

Nonfunctional because no pressure gradient is present

palpitations; dizziness; presyncope/ syncope

Cardiomyopathy; Myocarditis

1. Plaque rupture; 2. Plt activation/aggregation; 3. Fibrin generation; 4. Thrombus formation

Age; Gender ? FH; Sedentary Lifestyle; Tobacco; HTN; DM/insulin resistance; Hyperlipidemia

Diffuse dz; small vessel dz; CHF & death rates post MI; death or MI post CABG & PCI

Devoted exercise 30 min/day, 5 d/wk; initially under med supervision

Atherosclerosis; Vasospastic disorders; stenosis or HCM; Coronary thrombosis/ embolization; Acute aortic dissection

Pericarditis; myocarditis; MVP; chostocondritis; C- or T-spine dz/thoracic outlet; GI/gall bladder; PE; pneumonia; pneumothorax

risk of non-diabetic with prior MI

coronary atherosclerosis & superimposed coronary thrombosis

Fibrinolytics, anticoagulants, antiplatelet drugs

STEMI only

Acute: UFH, LMWH, DTIs; chronic: warfarin

UFH > LMWH

Hypotension; Decrease HR, heart block; May worsen HF symptoms; CNS (fatigue, malaise, depression); Bronchospasm (use ß1 selective agents)

Clopidogrel

Prior hemorrhagic CVA; any cerebrovascular events < 1 year; active internal bleeding; Known intracranial neoplasm; suspected aortic dissection

BP > 180/110; Use of anticoags w/ INR > 2; Noncompressible vascular punctures; Prolonged CPR (> 10 minutes); PG or Menstruation; Trauma < 2-4 weeks prior; Major surgery < 3 weeks prior

bleeding

Both STEMI and NSTEMI

Factor II (thrombin)

Factor Xa

Bleeding, HIT, osteoporosis

UFH

LMWH

Fondiparinux

UFH / LMWH

pts w/ USA or NSTEMI w/anticoag indication (to maintain INR 2.0-3.0)

usu loading & maint doses

Bleeding; Thrombocytopenia; Leukopenia; TTP

All STEMI/NSTEMI (2-4 wks to 1 yr)

STEMI pts going for PCI

PCI is not planned

Serum conc of chylomicrons elevated; trigs are elevated to >99th percentile

Serum LDL chol elevated; the total chol is >90th percentile. Triglyceride and/or apolipoprotein B may also be ≥ 90th percentile

Serum LDL & VLDL elevated; TC and/or trigs may be ≥ 90th percentile and apolipoprotein B ≥ 90th percentile

Anti-atherogenic (reduced atherosclerosis progression; regression of existing dz)

High chol & CHD are common; rel btw TC & LDL & risk of CHD & coronary mortality; lowering LDL in mod/hi risk pt => few CV events; dyslipidemia (not LDL) common in early onset CHD; screen tests commonly avail

Endothelial damage; changes in vasc tone; Monocyte/ macrophage recruitment; increased LDL uptake by macrophages (foam cell formation); Induction of GF; Increased plt aggregation; Formation of auto-Abs to oxidized LDL

Reverse chol transport; antioxidation; protection vs thrombosis; maintenance of endothelial fn; maintenance of low blood viscosity thru permissive action on red cell deformability

Reverse cholesterol transport

Wt reduction & inc physical activity; LDL-C is primary target of tx; Non-HDL-C is secondary target of tx (if trigs ³200 mg/dL); consider nicotinic acid or fibrates

Serum VLDL remnants & chylomicrons elevated; TC & trigs >90th percentile

Serum VLDL elevated; TC may be >90th percentile & may also see trigs >90th percentile or low HDL

Elevated serum chylomicrons & VLDL; triglycerides >99th percentile

Accumul of chylomicron remnants & VLDL remnants; generation of small, dense LDL-C; assoc w/ low HDL-C; increased coagulability (inc plasminogen activator inhibitor (PAI-1); inc factor VIIc; activation of prothrombin to thrombin

LDL < 160 & 0-01 risk factor; or LDL <130 & >1 risk factor: rescreen in 5 yrs

1. Fasting lipid level

2. determine CHD equivalents

3. Major CHD factors other than LDL

4. If >1 non-LDL CHD factor (in pt w/o CHD or equivalent): use modified Framingham criteria

5. Detn risk category to establish LDL goal, when to initiate tx lifestyle changes, & when to consider drug tx

3 of 5: abd obesity (waist men >40 in & women >35 in; trigs ≥150 or tx for hi trigs; HDL <40 (M) & <50 (F) or tx for low HDL; BP ≥130/85 or tx for hi BP; FPG ≥100 or tx

Inc waist girth plus any 2: 1. Trigs >150 or tx; HDL <40 (M) & <50 (F) or tx; SBP >130, DBP >85, or HTN tx; FPG >100 or prior dx type 2 DM

Type I: hi trigs & HTN; Type 2: dyslipid, HTN, ins resistance, obesity, FH atherosclerosis; SMK NOT risk factor for I or 2

Primary: remove risk factors; secondary: early detection & tx; tertiary: reduce complications

A. Saturated & trans fat; B. monounsaturated & polyunsaturated fat

energy utilization; lipid deposition; steroid hormone prodn; bile acid formation

esterified & unesterified chol, trigs, phospholipids, & protein

apolipoproteins or apoproteins.

cofactors for enzymes and ligands for receptors

abnormalities in lipid handling

chylomicrons

Apolipoproteins (including A-I, A-II, A-IV, B-48, C-I, C-II, C-III, and E)

cholesterol esters

apolipoprotein B-100.

cholesterol esters

apolipoproteins A-I, A-II, C-I, C-II, C-III, D, and E

oxidative modification

endogenous trigs (& to a lesser degree chol)

B-100, C-I, C-II, C-III, and E

chol esters & triglycerides

apolipoproteins B-100, C-III, and E

transfers oxidized lipids from LDL to HDL

HDL apolipoproteins

Liver takes up reduced lipids from HDL more rapidly than from LDL

Low serum HDL; assoc w/ increased risk of overt CHD

MI risk increases by 25 percent for every 5 mg/dL decrement in HDL below median values

SMK; sedentary;obese; insulin resistant/ DM; hypertriglyceridemia; chronic inflammatory dz

>60 mg/dL (>75 assoc w/ longevity syndrome)

Increase apo A-I prodn; promote reverse chol transport; delay HDL catabolism

increases

Lower LDL; increase HDL

Fredrickson phenotypes III, IV, & V

atherothrombosis

fibrinogen, clotting factors VII & X, & blood viscosity

<150

150-199

200-499

=/> 500

Metabolic syndrome

CHD

pancreatitis

at least every 5 yrs for pts 20 or older

within 1-2 yrs

Age, TC, HDL, BP, & SMK

TC (but LDL is primary tx target)

r >20%, 10-20%, and <10%

LDL-C is Low

dyslipidemia, hypertension, type 2 DM

Detect & stage HTN severity; detect TOD; assessing overall CV risk; detect secondary causes of HTN

1 in 3 in US = HTN; 66 mil in US 20 yo & older; 95% are essential HTN; 2005 in US, direct & indirect cost of HTN = $59.7 Billion

63% aware of the dx; only 45% receiving tx; 34% under ctrl using a threshold criterion of 140/90

Genetic defect, inc dietary Na intake, intrinsic renal differences, stress, obesity, drug or substance abuse

Variable plasma renin activity; variable symp n.s. response & catecholamines; insulin resistance & DM; inadequate dietary K+ & Ca+ ; resistant vessels

Excessive renin release in response to decrease in renal blood flow & perfusion pressure

85% atherosclerosis of proximal renal arteries (pts usu also have CAD); 15% fibromuscular dysplasia (esp in F 15–50 yrs; genetic predisposition)

fibrous thickening of the intima, media, or adventitia of the renal artery

Coarctation of the Aorta

Rare (1:10,000) & usually accompanies other abnormalities such as bicuspid aortic valve or Turner Syndrome

unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia

Outpouring of catecholamines during unrelated surgical/ radiologic procedure can lead to severe, abrupt hypertensive crisis & mortality rate over 80%

HTN = response to chronic, intermittent hypoxia during nocturnal apneic episodes

HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)

HTN is second most common cause of chronic kidney disease (> 25% of cases)

HTN

vasoconstriction at the level of the resistance arterioles

BP of 160/60 (pulse pressure of 100 mmHg) carries 2x the risk of fatal coronary heart dz as 140/110 (pulse pressure of 30 mmHg) (PP = SBP – DBP)

Peaks in the early 50’s, then declines for men and women (Systolic BP continues to rise for both throughout life)

Defined as persistence of BP > 140/90 despite tx with full doses of 3 or more different classes of meds in rational combination (& including a diuretic); important to know pt is compliant

Pseudoresistance; Inadequate medical regimen; Nonadherence or ingestion of pressor substances; secondary HTN

Usually caused by white coat effect superimposed on chronic HTN that is well controlled with meds outside the office

Absence of appropriate diuretic; Renal fn impairment which affects drug clearance; monotherapy or inadequate dosing of meds

a. Medication nonadherence; b. Lifestyle modification noncompliance; obesity, high salt diet, excessive alcohol intake; c. Habitual use of tobacco, cocaine, meth, phenylephrine or NSAIDS (cause renal Na+ retention)

If you’ve exhausted the first 3 categories, time to look for secondary cause of HTN

Chronic kidney dz & primary aldosteronism

Severe elevation of BP; No evidence of progressive TOD; benefit from BP lowering in a few hrs; absence of raised intracranial pressure

Acute, severe elevation in BP; evidence of rapidly progressive TOD (eg, MI, pulmonary edema or renal failure); requires immediate, gradual reduction of BP (NOT to the normal range); always look for secondary causes

Controlled, gradual lowering of BP; 10% decrease in first hour, then 15% over next 3–12 hrs to BP of no less than 160/110; rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia

Type of Hypertensive Emergency; usually accompanied by other end organ damage

Young adults, prior renal dz, AA males, PG, or collagen vascular dz

CHF; High Coronary Dz Risk; Chronic Kidney Dz; DM; Post-MI; Recurrent Stroke Prevention

Blockade of parts of the symp NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin

Normally stims release of Na+-retaining hormone aldosterone (adrenal corticol cells); normally amplifies vasoconstriction (systemic and renal)

Cough; Angioedema; Hyperkalemia; Rash; CI in PG; use cautiously in renal artery stenosis (RAS)

Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs

Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS

Act to block Na+ (and K+) from being absorbed, thus increasing urine Na+. Water follows Na+ out of the body. Blood volume is less (lowering BP)

Hypokalemia; Volume depletion; Gout; increased insulin resistance; hyponatremia; increased chol levels

Blocks vascular smooth mx contractility (resulting in vasodilatation & afterload reduction). Also result in coronary vasodilatation & are used in coronary artery spasm

DHPs more vascular selective; nonDHPs are more cardio-selective with more inhibitory effects on the SA/AV node

CO X PVR

established primary HTN

elevated peripheral vascular resistance

variations in ECF volume, heart contractility, & vascular tone

SBP over 140 &/or DBP over 90

of 130/80 mmHg.

DM, chronic kidney dz, CV or Cerebrovascular dz, or LVH on EKG

ECF volume, heart contractility, or vascular tone

30% M & 20% F

Chronic renal dz (proteinuria, high creat)

85%