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Memay.Pau.Rachelle.Esther.Joel.Glenn.Toni
MEDICINE 2 Subject
CORONARY ARTERY DISEASE, HYPERTENSION, HYPERLIPIDEMIA Topic
Doc Bernie “we’re not worthy” Morantte Jr Lecturer
2nd Shifting 03-sept-08 Shifting /Date
goLdi and her still invisible
frends Trans group

classmates, ung me mga * un po ung mga side comments I Congenital

ni Doc..  Anomalous origin from the pulmonary artery
 Anomalous origin from other coronary arteries
Anatomy of the Coronary Arteries • Hypoplastic artery
Aorta LCA
• Myocardial bridging
LMCA Left anterior
desc ending
• Coronary AV or sinus fistulas
RCA
SA nodal
artery
Circumflex
Diagonal
Anomalous Origin of the Coronary
RV branch
Septal
perforator
Bx
Arteries
Aorta LCA Left anterior
LMCA
descending
Obtuse marginal RCA
LV SA nodal
branch Postero-lateral Circumflex
artery Diagonal
Septal Bx
Posterior desc ending RV branch perforator
Posterior circumflex
branch

Obtuse marginal
LV
branch Postero-lateral

Posterior descending
Physiology of Coronary Circulation branch
Posterior circumflex

• Myocardial perfusion occurs mainly in

diastole BP 120/60 2. Atherosclerotic – most common
Epic ardium
Epicardial artery
3. Non-atherosclerotic
 Embolus – Atrial fibrillation, endocarditis, post
Subendocardium
Endocardium
Intramural arteries cardiac valve replacement, atrial myxoma
 Drug-induced – ex. cocaine
LV
 Vasculitides
LV pressure 120 /10
 Kawasaki
Diastolic pressure gradient = 50 mm HG Atheroma
 Aortic Dissection
 Iatrogenic
< 40 mm mean aortic pressure
coronary flow is zero.
ATHEROMA
Regulation of coronary blood flow
Foam cells
• Aortic driving pressure which is affected Macrophages
by the presence stenosis in the coronary Plaque Smooth muscle
arteries proliferation and
migration
• LVED pressure
Fibroblast
• Heart rate and diastolic filling time
calcification
• Coronary vascular resistance _ from the
contraction and relaxation of the smooth Cross section of an artery
muscles *Atheroma narrows the lumen and degree of
• Endothelium derived vasodilator narrowing determines if that part of the artery
substance which is affected by the will experience arterial insufficiency
presence of atherosclerosis
• Myocardial oxygen demand MYOCARDIAL BRIDGING
TYPES OF CAD
 4. ACUTE MYOCARDIAL INFARCTION
Myocardial Bridging  ischemia irreversible
Left anterior
 angina-like chest discomfort lasting for > 30
descending
mins
Epicardium Intramyocardial segment
 assoc. w/ sustained EKG changes &
Endocardi um enzymatic evidence of myocardial necrosis
LV
 ST and Non-ST MI

5. SUDDEN DEATH SYNDROME

in
tramyocardial segment Clinical Syndromes of Coronary artery
 not important unless tachycardia develops disease (CAD) Mechanism
 Tx: β-blockers to prevent tachycardica and Chronic
Chronic stable >> 50 % stenosis
s tenosis (x
(x--area)
area)
•• Angina Variant angina ( Prinzmetal)
Prinzmetal) ccoronary
oronary spasm
advise patients to refrain from strenuous
activities •• Unstable Angina ( Pre-
Unstable Pre-infarction
infarction angina)
angina) plaque
plaque rupture
rupture
•• dissec tion, hemorrhage
dissection,
non -Q wave MI
non- MI
(subendocardial or
or non-
non- STEMI)
•• Ac ute MI
Acute

Aortic dissection Q wave

wave MI ( transmural
transmural or
STEMI
ST EMI )
or thrombosis
thrombosis
total occlusion
Aorta LCA
LMCA Left anterior sudden
sudden death syndrome
syndrome
desc ending acute pulmonary edema (( Killip’ss class
class III)
RCA
cardiogenic shock ( Killips
Killips class
class IV)
SA nodal
Circumflex cardiac rupture
artery
D iagonal
Septal Bx
RV branch perforator

Obtuse marginal - sudden CV collapse with loss of BP and heart

LV
branch Postero-lateral
beat

Posterior desc ending

Posterior circumflex
branch

MYOCARDIAL ISCHEMIA P.E. FINDINGS

Is the imbalance between the oxygen supply - transient  disappears when angina resolves
and the myocardial demand for oxygen resulting - coincides w/ anginal attack
in some reversible cellular changes in the - transient murmurs  in mitral regurgitation
sarcolema. - if did not disappear  heart attack
CLINICAL SYNDROMES OF CAD HEART ATTACK
1. CLASSIC ANGINA (Angina pectoris) infarction
 chest discomfort resulting from myocardial
ischemia d/t coronary blood flow insufficiency necrosis
related to physical exertion and relieved by necrotic area will heal (fibrosis)
rest
most common presentation is transient ST rupture dead tissue (no
depression in EKG impulse)

2. VARIANT ANGINA
 chest discomfort characteristic of angina
occurring at rest Chest pain
associated with transient ST elevation in EKG
EKG

3. UNSTABLE ANGINA
normal ST depression ST elevation
new onset, prolonged chest pain (20-30
Non-c ardiac transient persistent transient persistent
mins), acceleration of angina, failure to Subendocardial
or angina Variant or Ac ute MI
respond to medical therapy Angina infarction
Prinzmetal

Subacute

old
cardiac tamponade 1. Pulmonary Acute pericarditis
emboli HOCM
2. Aortic dissection Prolapse of MV
heart does not function properly 3. Acute Costochondritis
myopericarditis ( Tietze’s
* clear, shrap, tearing pain  Aortic Dissection with syndrome)
* constricting, heavy, preasure-like  heart arrhythmia Reflux esophagitis
attack 4. Serious trauma /
* usually, if patient goes to clinic and angina is Esophageal spasm
already resolved, EKG would most likely be Drug induced
normal so do Exercise Test then check EKG myocardial
ischemia
Old Heart Attack Aortic stenosis
- only an abnormal Q wave is seen (permanent)
- Long Time  accdg to doc morantte is 2 mos Mild chest trauma
or longer
Are the diagnostic test you are contemplating
available on an outpatient basis?

*it takes ST waves 2 mos to normalize! NB:

*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
After 3 days:
CPK (normal)
 CPK increases w/in the 1st 6 hrs, Peaks at 24-
48 hrs, then decreases by the 3rd day
Troponin (elevated)
 Troponin I increases w/in the 1st 6hrs and
STAYS ELEVATED FOR 1 WEEK
After 1 week  both markers will be NORMAL

DIAGNOSTICS
RISK FACTORS
 CHRONIC STABLE ANGINA
MAJOR
Hyperlipidemia  EKG (70% accurate)
HPN CXR  to know if there is cardiomegaly w/c is
DM a risk factor for CHF
Cigarette smoking  Lipid Chemistry Panel
Others Echocardiogram for those w/ heart murmur
Obesity  Exercise Testing with or without Myocardial
C-reactive protein Perfusion Scan
physical inactivity
hypothyroidism  UNSTABLE ANGINA
(+) Family Hx  Above test except for exercise testing
Acromegaly
 Cardiac enzymes
Homocysteinuria/Homocystenemia
 CPK isoenzymes
Hypertriglyceridemia
 Troponin I
*CAD begins at 40…. in males  Persantine technitium or thallium scans
*35 y/o pt with chest pain = 5% probability of  Coronary angiogram
IHD
 ACUTE MYOCARDIAL INFARCTION
DIFFERENTIAL DIAGNOSIS OF AMI  EKG
 Does the patient with chest pain need to be  Chest x-ray
in the hospital?  Cardiac enzymes
Patients with Unstable Angina and AMI  need • CPK isoenzymnes
not be hospitalized • Troponin I
 Coronary angiogram if acute intervention is
Hospitalization Outpatient Work-up • planned
 Chest CT scan to exclude aortic dissection if
• suspected.
 2. Atenolol (25 – 100 mg daily)
**Presentation of Heart Attack (in 50%) 3. Acebutalol (200 mg up to 1200 mg
 pressure feeling in the chest 4. Pindolol (5mg – 40mg BID)
 constricting 5. Betaxolol (5 mg – 40 mg daily)
 arms feel heavy 6. Bisoprolol (50 mg - mg daily )
 choking in the neck
C. Calcium-channel blockers – available in
*DM due to peripheral neuropathy (decreased sustained release forms
1. Diltiazem_ 30 mg TID up to 360 mg / day
ability to sense pain)  may have a heart attack
2. Verapamil _ 80 mg TID : start at 40 mg when
without chest pain
EF is low
*Unstable Angina  no exercise Test
3. Bipridil _ 200- 400 mg.: watch for QT
prolongation
RISK STRATIFICATION of CAD
 common denominator of patients with high D. Anti-platelet drugs - Aspirin or
risk for MI and Sudden death clopidogrel
1. Significant multivessel CAD
2. Impaired left ventricular function Therapy in Unstable Angina
. 1. Supportive Rx
Myocardial Perfusion Scans – multiple perfusion a) mild sedation
defects b) oxygen for hypoxemia
DIAGNOSTICS 2. IV nitroglycerin
3. IV Heparin ( UHF) or LMWH
HIGH RISK LOW RISK
4. Anti-platelet Rx
Treadmill Findings
a) ASA
1. 2mm of ST depression normal
b) Abicisimab 0.25 mg/ kg bolus then
at low level exercise
2. ST segment elevation c. 0.125 mg / kg for 12 hours
3. Ventricular <2mm of ST depression 5. Betablockers
Tachycardia at 6. Anti-arrhythmic therapy for A-fib, SVT and V-
high level exercise tach
Echocardiography 7. which may include DC cardioversion
1. EF < 50% EF > 50% with normal 8. Followed by diagnostic work up for risk
with wall motion wall motion stratification which may include coronary
abnormalities angiography.
2. Radionuclide Left normal wall motion
Ventriculography INVASIVE TECHNIQUES
*wall motion 1. Percutaneous Interventions
abnormalities
 Balloon Angioplasty (PTCA)
3. Coronary Single vessel disease
Arteriography and normal EF except for  Coronary Stent
*significant mutivessel LAD  Atherectomy
disease EF< 50%  Lasers

TREATMENT of CHRONIC STABLE ANGINA 2. Coronary Artery Bypass Surgery

I. Risk factors modification  Thoracotomy
II. Medical Rx • Saphenous vein grafts
A. Nitrites
• Internal mammary artery graft
1. Sublingual nitroglycerin – 0.2 – 0.6 mg
2. Nitro spray  one of the most effective bypass
3. Oral procedure esp in
a. Isosorbide dinitrate (5-20 mg q 4h off LAD
8h) • Other arterial conduits
b. Isosorbide mononitrate (20 mg BID 7h
apart)  Closed angioscopically guided bypass
surgery
4. Nitroglycerin ointment ½ inch – 2 in q 6h off
at night ACUTE MYOCARDIAL INFARCTION
5. Nitro Patch (0.1 – 0.6 mg/h off at night) I. Window of Opportunity
A. Thrombolytic Rx – w/in 6 hrs
B. β-Blockers Any of the ff:
1. Metoprolol (25 – 50 mg BID to 400 mg daily)
1. TPA 100 mg IV in 3 divided doses, 15 mg IV
bolus, then 50 mg over 30 mins, then 35 mg
over 1 hr
2. Reptelase 10 units IV bolus, then 10 units in
½ hr
3. Tenecteplase 40 mg IV bolus Single Dose
4. IV Streptokinase drip
I ntake Fluid Balance
B. Primary PTCA or PCI – 4 hrs
GI TRACT WATER EXCRETION
 maximum benefit is obtained when
thirst PATHWAY
performed within 1 hr of chest pain osmolality vein
Intravascular
volume

II. Medical Therapy Hypothalamus

cathecolamine ANF
III. ACE-inhibitors for ventricular adrenal
Heart
IV. Hemodynamic monitoring RH
glocucorticoid
Angiotensin I I
CO
V. Treatment of complications such as aldosterone ACE
ACTH Angiotensin I
VI. Cardiac rehabilitation and risk factor Rx Liver
Pituitary
AVP Na/ K angiotensinogen
COMPLICATIONS OF AMI and THERAPY VR artery
1. Hypotension – IV inotropic agents (IV DRIP) Kidney Renin
WATER CONSERVATI ON
Dobutamine, Dopamine  generally used PATHWAY
Amrinone Urine output
2. CHF – IV Furosemide
3. Bradycardia – Atropine and temporary FLUID BALANCE
pacemaker • Water excretion is dependent on the heart
4. 2nd & 3rd degree AV block – temporary because it controls hydrostatic pressures.
pacemaker • Water conservation is controlled by the
5. Acute pulmonary edema – assisted ventilation adrenal gland and the pituitary by their
and IV Furosemide role in osmotic pressure regulation.
6. Cardiogenic shock – Intra-aortic balloon pump • Normal kidneys respond to changes in
to relieve the workload on the heart while it is both the hydrostatic and osmotic pressures
recovering
7. RV infarction – IV fluids hydration
8. Acute Pericarditis / Dressler’s Syndrome* –
NSAID / Prednisone DEFINITION: BP > 140/90 at rest x 4
*autoimmune response to MI necrosis/ damage Questions:
9. Ventricular Aneurysm and Systemic 1. What type of hypertension?
Embolization – IV heparin followed by Coumadin Systolic
10. Ruptured papillary muscle – acute MR Diastolic
11. Acute Ventricular Septal Defect (VSD) 2. Is ir transient or sustained?
12. Cardiac rupture 3. Is it reversible or irreversible?
*ung last 3 alang therapy na nakaindicate.. 4. Is it primary or secondary?
*Bypass surgery a.k.a. Saphenous Vein Bypass
Graft (double bypass, triple bypass, quadruple SYSTOLIC HYPERTENSION
bypass) • High cardiac output conditions:
a. Severe anemia
--------end of CAD lecture------- b. Arterio-venous fistulas
c. Hyperthyroidism
d. Fever
e. Paget’s disease
HYPERTENSION
f. PDA

SEVERITY OF HYPERTENSION
Hypertension • Diastolic pressures:
Borderline 86 – 90 mm Hg.
Blood Pressure
Stage I Mild 91- 105
Arterial vascular resistance Stage II Moderate 106- 115
Cardiac output Stage III Severe > 115

Stroke volume and heart rate TRANSIENT REVERSIBLE HYPERTENSION

Ventricular contractility
Preload
 1. Stress induced 4. Others such as signs of connective tissue
2. White coat syndrome disease
3. Initial response to dehydration or loss of
blood volume DIAGNOSTIC STUDIES
4. Sympathomimetic drugs To determine cause:
1. Renal Parenchymal: Urinalysis_
REVERSIBLE HYPERTENSION microalbuminuria, electrolytes
1. Congenital 2. Renovascular: Renal scan to determine
a. Coarctation of the aorta difference in kidney size, renin levels,
b. Renal artery stenosis ( fibromuscular) aortography
2. Drug induced - amphetamines, cocaine 3. Pheochromocytoma : 24 hour urine for
3. Tumors of the thyroid, adrenal, and cathecholamine levels
pituitary glands 4. Aldosteronism: serum electrolytes and
4. Pre-eclampsia / eclampsia aldosterone levels
5. Renal insufficiency in children 5. Cushings: cortisol level and
dexamethasone suppression test
Hypertension 6. Thyroid: T3, T4, TSH
Primary ( Unknown) - Essential 92- 94 % of 7. Hyperparathyroidism: serum calcium
patients 8. Acromegaly: GH level following glucose
Secondary load
a. Renal - Parenchymal
Renovascular_ atherosclerotic Diagnostic tests to determine target organ
b. Adrenal - Primary aldosteronism damage
Cushing’s syndrome 1. Serum BUN and creatinine, glucose
Pheochromocytoma 2. EKG
c. Pituitary - Acromegaly 3. Chest x-ray
d. Hyperthyroidsim 4. Echocardiography
e. Hyperparathyroidism
f. Miscellaneous - oral contraceptives * The above test are used to follow the success
drugs - amphetamines, of the therapy
cocaine
Immune connective tissue THERAPY FOR ESSENTIAL HYPERTENSION
diseases Non-pharmacologic:
g. Neurogenic - increased intracranial 1. Salt restriction - benefits 30% of patients
pressure, 2. Stop cigarette smoking
psychogenic 3. Weight reduction ( achieve normal BMI)
HISTORY 4. Stress reduction and lifestyle changes
1. Duration of hypertension 5. Preferably no alcohol
2. Use of illicit drugs and alcohol
3. Identify transient causes of hypertension Pharmacologic
4. Other risk factors for vascular disease I. Monotherapy - thiazide diuretics , β-
5. Prior History of CVA, MI blockers
6. Family history II. Others:
7. Prior medicines including oral a. Alpha blockers - Prazocin, Terazocin,
contraceptives Doxasocin
8. Allergies and side effects b. ACE inhibitors - Catopril, Enalopril.
Lisinopril
PHYSICAL EXAMINATION c. Angiotensin receptor blockers
Aim or Goal: To find signs of reversible causes Losartan,Candesartan,
of hypertension such as: Irbesartan
a. bruits d. Calcium channel blockers - Diltiazem,
b. difference in BP in the 4 Verapamil
extremities e. Dihydropyridines - Nifedipine, Amlodipine,
c. systolic murmur along the aorta Filodipine,
d. physical signs of endocrinopathy Isradipine
2. Assess the severity f. Centrally acting agents - Clonidine
3. To determine target organ damage (transdermal),
a. Presence of retinopahty Guanabenz and
. b. Cardiomegaly Methyldopa
c. Signs of water retention g. Peripheral dilators - Hydralazine, Minoxidil
 h. Potassium sparing diuretics - Aldactone, 2. OCP VLDL is 
Triamterene 3. alcohol VLDL is 
III. For hypertensive crisis - IV nitroprusside
Sublingual nifidipine ACQUIRED CAUSES of HYPERLIPIDEMIA
HYPOTHYROIDISM LDL 
Choice of Antihypertensive medications: NEPHROTIC LDL 
1. Presence of contraindications SYNDROME
2. Cost RHEUMATIC VLDL LDL 
3. Ease of taking the medications FEVER 
4. Development of side effects
ACUTE HEPATITIS VLDL

*most common cause of Hypertensive crisis is
SUDDEN WITHDRAWAL FROM HPN MEDS ACUTE VLDL
*Diabetes mellitus is the #1 cause of kidney PANCREATITIS 
failure PRIMARY BILIARY VLDL
*acute renal failure causes BP to increase CIRRHOSIS 

--------end of HPN lecture------- HISTORY and P.E.

yey.. last lec na.. weee.. 1. Family Hx of Hyperlipidemia
2. Presence of xanthomas
HYPERLIPIDEMIA 3. Arcus senelis
4. Xanthelasmas (low specificity)
FACTORS AFFECTING LIPID LEVELS: 5. bruits
a. Dietary intake 6. diminished peripheral pulses suggests
b. Lipid absorption in the GIT vascular dse
c. Clearing of chylomicrons 7. gangrene
d. activity of lipoprotein lipase
e. endogenous production of lipids by the liver THERAPY
f. reverse transport by HDL Goal:
g. LDL receptors in the liver LOWER: LDL < 100 mg/dL for Px w/ MI, CVD
LDL < 130 mg/dL for Px w/ one risk
CRITERIA: factor
1. Total Cholesterol > 200 mg/dL LDL < 160 mg/dL Px w/ No risk
2. LDL > 100 mg/dL factor
3. HDL < 55mg/dL females ; <40 mg/dL in TG to < 200 mg/dL
males INCREASE HDL to NORMAL
4. TG > 200 mg/dL
NON-PHARMACOLOGIC
* 2 samples are required 1. Diet Therapy: 200 mg cholesterol / day
*samples taken during stressful situations such Saturated fat < 7%
as trauma, AMI, abnormal hydration status, Polyunsaturated fat to 10%
cannot be used as baseline. Monosaturated fat 20%

FORMULA: 2. Weight reduction (achieve normal BMI)

LDL = TOTAL CHOLESTEROL – 3. Exercise Program
HDL – TG/5 4. Treat risk factors for CVD

PHARMACOLOGIC
1. Bile Acid sequestration – Cholestyramine,
TYPES: (based on lipid molecule)
Colestipol
1. Chylomicrons
(*side effect: constipation)
2. VLDL
2. Niacin
3. IDL
3. Fibric Acid – Gemfibrozil (eto ung mga
4. LDL
Lipigem Lipizile, Lopid), Fenofibrate (Fenogal,
5. Triglycerides
Lipanthyl)
6. Lipoprotein A
4. HMG-CoA reductase (statins)
*for blood that is sitting for some time, the
side ffects: drug-induced hepatitis, myalgia,
serum will be cloudy/milky d/t chylomicrons
myositis
CONDITIONS THAT CAUSE ELEVATED LIPIDS
1. obesity VLDL is 
5. Esitimibe (eto ung nakalagay sa lec ni doc)
pero di ko cya mahanap.. kaya feeling ko
EZETIMIBE ung drug
EZETIMIBE – brand name: Ezetrol; alone or in
combination w/ statins or fenofibrate for the
reduction of total or LDL cholesterol.. aun lng..

-----Owari-----

This is the beginning of a new day. You have been

given this day to use as you will... You can waste it or
use it for good. What you do today is important
because you are exchanging a day of your life for it.
When tomorrow comes, this day will be gone forever.
In its place is something you have left behind... Let it
be something good" -Unknown