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MEDICINE 2 Subject CORONARY ARTERY DISEASE, HYPERTENSION, HYPERLIPIDEMIA Topic

Doc Bernie “we’re not worthy” Morantte Jr Lecturer2nd Shifting 03-sept-08 Shifting /Date

goLdi and her still invisible frends Trans group

classmates, ung me mga * un po ung mga side comments ni Doc..

Regulation of coronary blood flow

• Aortic driving pressure which is affected by the presence stenosis in the coronary arteries

• LVED pressure• Heart rate and diastolic filling time• Coronary vascular resistance _ from the

contraction and relaxation of the smooth muscles• Endothelium derived vasodilator substance which

is affected by the presence of atherosclerosis• Myocardial oxygen demand

TYPES OF CADI Congenital Anomalous origin from the pulmonary artery Anomalous origin from other coronary arteries

• Hypoplastic artery• Myocardial bridging• Coronary AV or sinus fistulas

2. Atherosclerotic – most common3. Non-atherosclerotic Embolus – Atrial fibrillation, endocarditis, post cardiac

valve replacement, atrial myxoma Drug-induced – ex. cocaine Vasculitides Kawasaki Aortic Dissection Iatrogenic

ATHEROMA

AtheromaAtheroma

Plaque

Cross section of an artery

Foam cells

Macrophages

Smooth muscle proliferation and migration

Fibroblast

calcification

*Atheroma narrows the lumen and degree of narrowing determines if that part of the artery will experience arterial insufficiency

MYOCARDIAL BRIDGING

intramyocardial segment not important unless tachycardia develops Tx: β-blockers to prevent tachycardica and advise

patients to refrain from strenuous activities

MYOCARDIAL ISCHEMIAIs the imbalance between the oxygen supply and the myocardial demand for oxygen resulting in some reversible cellular changes in the sarcolema.

CLINICAL SYNDROMES OF CAD1. CLASSIC ANGINA (Angina pectoris) chest discomfort resulting from myocardial ischemia d/t

coronary blood flow insufficiency related to physical exertion and relieved by rest

most common presentation is transient ST depression in EKG

2. VARIANT ANGINA chest discomfort characteristic of angina occurring at

rest associated with transient ST elevation in EKG

3. UNSTABLE ANGINA new onset, prolonged chest pain (20-30 mins),

acceleration of angina, failure to respond to medical therapy

4. ACUTE MYOCARDIAL INFARCTION ischemia irreversible angina-like chest discomfort lasting for > 30 mins assoc. w/ sustained EKG changes & enzymatic evidence

of myocardial necrosis ST and Non-ST MI

5. SUDDEN DEATH SYNDROME- sudden CV collapse with loss of BP and heart beat

P.E. FINDINGS- transient disappears when angina resolves- coincides w/ anginal attack- transient murmurs in mitral regurgitation- if did not disappear heart attack

HEART ATTACK infarction

necrosis necrotic area will heal (fibrosis)

rupture dead tissue (no impulse)

cardiac tamponade

heart does not function properly

* clear, shrap, tearing pain Aortic Dissection* constricting, heavy, preasure-like heart attack* usually, if patient goes to clinic and angina is already

resolved, EKG would most likely be normal so do Exercise Test then check EKG

Old Heart Attack- only an abnormal Q wave is seen (permanent)- Long Time accdg to doc morantte is 2 mos or longer

*it takes ST waves 2 mos to normalize!*cardiac enzymes should go up to 2x the normal value* frequency of heart attack depends on the status of the

coronary artery

INCOMPLETE HEART ATTACK- C.A. stenotic by 75% but goes into spasm

may be prolonged necrosis

RISK FACTORSMAJOR

HyperlipidemiaHPNDMCigarette smoking

OthersObesityC-reactive proteinphysical inactivityhypothyroidism(+) Family HxAcromegalyHomocysteinuria/HomocystenemiaHypertriglyceridemia

*CAD begins at 40…. in males*35 y/o pt with chest pain = 5% probability of IHD

DIFFERENTIAL DIAGNOSIS OF AMI Does the patient with chest pain need to be in the hospital?Patients with Unstable Angina and AMI need not be hospitalized

Hospitalization Outpatient Work-up1. Pulmonary emboli 2. Aortic dissection 3. Acute myopericarditis

with arrhythmia 4. Serious trauma

Acute pericarditisHOCMProlapse of MVCostochondritis ( Tietze’s syndrome)Reflux esophagitis /Esophageal spasmDrug induced myocardial

ischemiaAortic stenosis

Mild chest trauma

Are the diagnostic test you are contemplating available on an outpatient basis?

NB: After 3 days:CPK (normal) CPK increases w/in the 1st 6 hrs, Peaks at 24-48 hrs, then decreases by the 3rd dayTroponin (elevated) Troponin I increases w/in the 1st 6hrs and STAYS ELEVATED FOR 1 WEEK

After 1 week both markers will be NORMAL

DIAGNOSTICS CHRONIC STABLE ANGINA EKG (70% accurate) CXR to know if there is cardiomegaly w/c is a risk

factor for CHF Lipid Chemistry Panel Echocardiogram for those w/ heart murmur Exercise Testing with or without Myocardial Perfusion

Scan

UNSTABLE ANGINA Above test except for exercise testing Cardiac enzymes CPK isoenzymes Troponin I Persantine technitium or thallium scans Coronary angiogram

ACUTE MYOCARDIAL INFARCTION EKG Chest x-ray Cardiac enzymes

CPK isoenzymnes Troponin I

Coronary angiogram if acute intervention is planned

Chest CT scan to exclude aortic dissection if suspected.

**Presentation of Heart Attack (in 50%) pressure feeling in the chest constricting arms feel heavy choking in the neck

*DM due to peripheral neuropathy (decreased ability to sense pain) may have a heart attack without chest pain*Unstable Angina no exercise Test

RISK STRATIFICATION of CAD common denominator of patients with high risk for MI and Sudden death1. Significant multivessel CAD2. Impaired left ventricular function.

Myocardial Perfusion Scans – multiple perfusion defectsDIAGNOSTICS

HIGH RISK LOW RISKTreadmill Findings1. 2mm of ST depression at low level exercise

normal

2. ST segment elevation3. Ventricular Tachycardia <2mm of ST depression at

high level exerciseEchocardiography1. EF < 50%with wall motion abnormalities

EF > 50% with normal wall motion

2. Radionuclide Left Ventriculography*wall motion abnormalities

normal wall motion

3. Coronary Arteriography*significant mutivessel disease EF< 50%

Single vessel disease and normal EF except for LAD

TREATMENT of CHRONIC STABLE ANGINAI. Risk factors modificationII. Medical RxA. Nitrites

1. Sublingual nitroglycerin – 0.2 – 0.6 mg2. Nitro spray3. Oral

a. Isosorbide dinitrate (5-20 mg q 4h off 8h)b. Isosorbide mononitrate (20 mg BID 7h apart)

4. Nitroglycerin ointment ½ inch – 2 in q 6h off at night5. Nitro Patch (0.1 – 0.6 mg/h off at night)

B. β-Blockers1. Metoprolol (25 – 50 mg BID to 400 mg daily)2. Atenolol (25 – 100 mg daily)3. Acebutalol (200 mg up to 1200 mg4. Pindolol (5mg – 40mg BID)5. Betaxolol (5 mg – 40 mg daily)6. Bisoprolol (50 mg - mg daily )

C. Calcium-channel blockers – available in sustained release forms1. Diltiazem_ 30 mg TID up to 360 mg / day2. Verapamil _ 80 mg TID : start at 40 mg when EF is low3. Bipridil _ 200- 400 mg.: watch for QT prolongation

D. Anti-platelet drugs - Aspirin or clopidogrel

Therapy in Unstable Angina1. Supportive Rx

a) mild sedationb)oxygen for hypoxemia

2. IV nitroglycerin3. IV Heparin ( UHF) or LMWH4. Anti-platelet Rx

a) ASAb)Abicisimab 0.25 mg/ kg bolus then

c. 0.125 mg / kg for 12 hours5. Betablockers6. Anti-arrhythmic therapy for A-fib, SVT and V-tach7. which may include DC cardioversion8. Followed by diagnostic work up for risk stratification

which may include coronary angiography.

INVASIVE TECHNIQUES1. Percutaneous Interventions Balloon Angioplasty (PTCA) Coronary Stent Atherectomy Lasers

2. Coronary Artery Bypass Surgery Thoracotomy

Saphenous vein grafts Internal mammary artery graft

one of the most effective bypass procedure esp in LAD

Other arterial conduits

Closed angioscopically guided bypass surgery

ACUTE MYOCARDIAL INFARCTIONI. Window of OpportunityA. Thrombolytic Rx – w/in 6 hrs Any of the ff:1. TPA 100 mg IV in 3 divided doses, 15 mg IV bolus, then 50 mg over 30 mins, then 35 mg over 1 hr2. Reptelase 10 units IV bolus, then 10 units in ½ hr3. Tenecteplase 40 mg IV bolus Single Dose4. IV Streptokinase drip

B. Primary PTCA or PCI – 4 hrs maximum benefit is obtained when performed within 1 hr of chest pain

II. Medical TherapyIII. ACE-inhibitors for ventricular IV. Hemodynamic monitoringV. Treatment of complications such asVI. Cardiac rehabilitation and risk factor Rx

COMPLICATIONS OF AMI and THERAPY1. Hypotension – IV inotropic agents (IV DRIP)Dobutamine, Dopamine generally usedAmrinone2. CHF – IV Furosemide3. Bradycardia – Atropine and temporary pacemaker4. 2nd & 3rd degree AV block – temporary pacemaker5. Acute pulmonary edema – assisted ventilation and IV Furosemide6. Cardiogenic shock – Intra-aortic balloon pump to relieve the workload on the heart while it is recovering7. RV infarction – IV fluids hydration

8. Acute Pericarditis / Dressler’s Syndrome* – NSAID / Prednisone*autoimmune response to MI necrosis/ damage9. Ventricular Aneurysm and Systemic Embolization – IV heparin followed by Coumadin10. Ruptured papillary muscle – acute MR11. Acute Ventricular Septal Defect (VSD)12. Cardiac rupture*ung last 3 alang therapy na nakaindicate..*Bypass surgery a.k.a. Saphenous Vein Bypass Graft (double bypass, triple bypass, quadruple bypass)

--------end of CAD lecture-------

HYPERTENSION

FLUID BALANCE• Water excretion is dependent on the heart because it

controls hydrostatic pressures.• Water conservation is controlled by the adrenal gland

and the pituitary by their role in osmotic pressure regulation.

• Normal kidneys respond to changes in both the hydrostatic and osmotic pressures

DEFINITION: BP > 140/90 at rest x 4Questions:1. What type of hypertension?

SystolicDiastolic

2. Is ir transient or sustained?3. Is it reversible or irreversible?4. Is it primary or secondary?

SYSTOLIC HYPERTENSION• High cardiac output conditions:

a. Severe anemia b. Arterio-venous fistulas c. Hyperthyroidism d. Fever e. Paget’s disease f. PDA

SEVERITY OF HYPERTENSION• Diastolic pressures: Borderline 86 – 90 mm Hg. Stage I Mild 91- 105 Stage II Moderate 106- 115 Stage III Severe > 115

TRANSIENT REVERSIBLE HYPERTENSION1. Stress induced2. White coat syndrome3. Initial response to dehydration or loss of blood

volume4. Sympathomimetic drugs

REVERSIBLE HYPERTENSION1. Congenital a. Coarctation of the aorta b. Renal artery stenosis ( fibromuscular)2. Drug induced - amphetamines, cocaine3. Tumors of the thyroid, adrenal, and pituitary glands4. Pre-eclampsia / eclampsia 5. Renal insufficiency in children

HypertensionPrimary ( Unknown) - Essential 92- 94 % of patientsSecondary

a. Renal - Parenchymal Renovascular_ atherosclerotic

b. Adrenal - Primary aldosteronism Cushing’s syndrome Pheochromocytoma

c. Pituitary - Acromegalyd. Hyperthyroidsime. Hyperparathyroidism f. Miscellaneous - oral contraceptives

drugs - amphetamines, cocaine Immune connective tissue diseases

g. Neurogenic - increased intracranial pressure, psychogenicHISTORY

1. Duration of hypertension2. Use of illicit drugs and alcohol3. Identify transient causes of hypertension4. Other risk factors for vascular disease5. Prior History of CVA, MI6. Family history7. Prior medicines including oral contraceptives8. Allergies and side effects

PHYSICAL EXAMINATIONAim or Goal: To find signs of reversible causes of hypertension such as:

a. bruits b. difference in BP in the 4 extremities c. systolic murmur along the aorta d. physical signs of endocrinopathy2. Assess the severity 3. To determine target organ damage a. Presence of retinopahty. b. Cardiomegaly c. Signs of water retention4. Others such as signs of connective tissue disease

DIAGNOSTIC STUDIESTo determine cause:

1. Renal Parenchymal: Urinalysis_ microalbuminuria, electrolytes

2. Renovascular: Renal scan to determine difference in kidney size, renin levels, aortography3. Pheochromocytoma : 24 hour urine for

cathecholamine levels4. Aldosteronism: serum electrolytes and aldosterone

levels5. Cushings: cortisol level and dexamethasone

suppression test6. Thyroid: T3, T4, TSH 7. Hyperparathyroidism: serum calcium8. Acromegaly: GH level following glucose load

Diagnostic tests to determine target organ damage1. Serum BUN and creatinine, glucose2. EKG3. Chest x-ray4. Echocardiography

* The above test are used to follow the success of the therapy

THERAPY FOR ESSENTIAL HYPERTENSIONNon-pharmacologic:

1. Salt restriction - benefits 30% of patients2. Stop cigarette smoking3. Weight reduction ( achieve normal BMI)4. Stress reduction and lifestyle changes

5. Preferably no alcohol

Pharmacologic I. Monotherapy - thiazide diuretics , β-blockers

II. Others: a. Alpha blockers - Prazocin, Terazocin, Doxasocin b. ACE inhibitors - Catopril, Enalopril. Lisinopril c. Angiotensin receptor blockers Losartan,Candesartan, Irbesartan d. Calcium channel blockers - Diltiazem, Verapamil e. Dihydropyridines - Nifedipine, Amlodipine, Filodipine, Isradipine f. Centrally acting agents - Clonidine (transdermal), Guanabenz and Methyldopa g. Peripheral dilators - Hydralazine, Minoxidil h. Potassium sparing diuretics - Aldactone, TriamtereneIII. For hypertensive crisis - IV nitroprusside Sublingual nifidipine

Choice of Antihypertensive medications:1. Presence of contraindications2. Cost3. Ease of taking the medications4. Development of side effects

*most common cause of Hypertensive crisis is SUDDEN WITHDRAWAL FROM HPN MEDS*Diabetes mellitus is the #1 cause of kidney failure*acute renal failure causes BP to increase

--------end of HPN lecture-------yey.. last lec na.. weee..

HYPERLIPIDEMIA

FACTORS AFFECTING LIPID LEVELS:a. Dietary intakeb. Lipid absorption in the GITc. Clearing of chylomicronsd. activity of lipoprotein lipasee. endogenous production of lipids by the liverf. reverse transport by HDLg. LDL receptors in the liver

CRITERIA:1. Total Cholesterol > 200 mg/dL2. LDL > 100 mg/dL3. HDL < 55mg/dL females ; <40 mg/dL in males4. TG > 200 mg/dL

* 2 samples are required*samples taken during stressful situations such as trauma, AMI, abnormal hydration status, cannot be used as baseline.

FORMULA: LDL = TOTAL CHOLESTEROL – HDL – TG/5

TYPES: (based on lipid molecule)1. Chylomicrons2. VLDL3. IDL4. LDL5. Triglycerides6. Lipoprotein A*for blood that is sitting for some time, the serum will be cloudy/milky d/t chylomicrons

CONDITIONS THAT CAUSE ELEVATED LIPIDS1. obesity VLDL is 2. OCP VLDL is 3. alcohol VLDL is

ACQUIRED CAUSES of HYPERLIPIDEMIAHYPOTHYROIDISM LDL NEPHROTIC SYNDROME

LDL

RHEUMATIC FEVER VLDL LDL ACUTE HEPATITIS VLDL ACUTE PANCREATITIS VLDL PRIMARY BILIARY CIRRHOSIS

VLDL

HISTORY and P.E.1. Family Hx of Hyperlipidemia2. Presence of xanthomas3. Arcus senelis4. Xanthelasmas (low specificity)5. bruits6. diminished peripheral pulses suggests vascular dse7. gangrene

THERAPYGoal: LOWER: LDL < 100 mg/dL for Px w/ MI, CVD LDL < 130 mg/dL for Px w/ one risk factor LDL < 160 mg/dL Px w/ No risk factor TG to < 200 mg/dL INCREASE HDL to NORMAL

NON-PHARMACOLOGIC1. Diet Therapy: 200 mg cholesterol / day

Saturated fat < 7% Polyunsaturated fat to 10% Monosaturated fat 20%

2. Weight reduction (achieve normal BMI)3. Exercise Program4. Treat risk factors for CVD

PHARMACOLOGIC 1. Bile Acid sequestration – Cholestyramine, Colestipol (*side effect: constipation)

2. Niacin3. Fibric Acid – Gemfibrozil (eto ung mga Lipigem Lipizile, Lopid), Fenofibrate (Fenogal, Lipanthyl)4. HMG-CoA reductase (statins)side ffects: drug-induced hepatitis, myalgia, myositis5. Esitimibe (eto ung nakalagay sa lec ni doc) pero di ko cya mahanap.. kaya feeling ko EZETIMIBE ung drugEZETIMIBE – brand name: Ezetrol; alone or in combination w/ statins or fenofibrate for the reduction of total or LDL cholesterol.. aun lng..

-----Owari-----

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