OCCUPATIONAL DISORDERS

2/2/10

1) chemical hazards: excessive airborne concentrations of vapors, gases, solids, dusts

2) Physical hazards: electromagntic/ionizing radiation, noise, vibration, temp extremes

3) ergonomic hazards: improperly designed tools/work areas

4) biological hazards: insects, molds, fungi, bacteria

1) inhalation via lungs

2) ingestion (eg. eating at lab space)

3) absorption via skin

4 reasons to get occupational hx:

1) disease etiology

2) evaluate toxic materials/extenet of exposure

3) recognise unusual patterns of illness

4) evaluate new chemicals introduced into industrial setting

1) possible exposure

2) atypical disease presentation

3) disease unresponsive to tx

1) type of work

2) health problem related to work?

3) sx differ btwn work and home?

4) current and past exposure: chem, dust, metal, radiation, noise, repetitive work

5) similar sx with co-workers?

GYN: miscarriages, stillbirths, prior pregnancies, difficulty conceiving, change in libido, change in menses

ALCOHOL: confounding factor in pts with suspected toxic exposure

PULMONARY EMERGENCIES

2/4/10

1) RR

2) Accessory Muscles

3) O2 Saturation

4) Tidal volume

5) Color

6) Diaphoresis on forehead/back of neck

nml RR adult, baby

nml pulse ox - rm air, copd, if # not reliable do...

cap refill nm

P CO2 nml values,

nml RR adult 10-20 rpm, baby >60 rpm

nml pulse ox - >92% rm air, copd 90%, if # not reliable do...ABG

cap refill nml  <2 sec

ABG: PCO2 nml 35-40%, COPD 55%

Lung exam findings

1) silent chest

2) crackles

3) dullness to percussion in one area

1) silent chest: emphysema & bad in asthma

2) crackles: fluid buildup: CHF, infiltrate, tumor, blood

3) dullness to percussion in one area

management of respiratory distress?

1) What is the most important issue

2) pt position

3) use what 2 drugs?

4) what helps COPD pts

1) O2 sat, keep up with nebulizer

2) upright

3) tx steroids and IV ABX (leviquin) if fever present

4) CPAP: device to deliver continuous positive pressure to keep alveoli open.

Respiratory Failure

1) PO2 and P CO2 numbers by definition

2) numbers may not be functional in what pts?

3) what procedure must you do?

1) PO2=50-60 mmHg

PCO2=50 mmHg or greater

2) COPD

3) ET tube

5 yr old pt presents to ER on a winter night with barking cough that gets better with cold air and worse at night, low grade fever.

Dx and Tx

Dx: Croup (6ms-6yrs)

Tx: steroids: racemic epinephrine (nebulizer).

tylenol+codeine+decadron (0.5mg/kg)= cough suppresent, treats, fever, decr inflamm

Bacterial Tracheitis

1) common age affected

2) tx

1) 5-10 yrs

2) IV ABX, steroids, nebulizers, admission

Adult presents to ER with fever and hot potato voice with drooling and difficulty swallowing.  Pt resides in tripod position.

Dx and Tx

dx: epiglottitis (mostly adults b/c prevented by H influenzae vaccines in children now)

tx: IV ANX, steroids, ENT involvement, admission

retropharyngeal &

peritonsillar (young adults post GABHS)

Allergic rxn that involves face, tongue, eyes.

dx, questions that should be asked, tx

dx: angioedema

q: look for allergen: PCN, foods, environment

tx: diphenhydramine (IM), H2, blockers, steroids

more than 2 or 3 ribs on one side of chest that are broken in two places.  Causes paradoxical breathing: inhale= injured part goes IN instead of OUT.  Can restrict breathing.  Due to trauma (car accidents with banging against steering wheel).

pt presents to ER with dyspnea.  Has low O2 sats, CXR hyperaeration, cyanosis , sentence dyspnea, accessory muscle use, tachycardia, tachypnea

Dx and tx

Status Asthmaticus

OR

Severe Asthma

tx: B2 agonists, steroids, IV fluid, intubation to prevent ARDS

In a COPD exacerbation, check ABG for....

tx:? (what is last resort?)

CO2 retention

tx: steroids, b2 agonists, ABX (if infxn present), IV fluids, INTUBATION last resort

This condition has no typical presentation.

Sometimes there is unexplained tachycardia, tachypnea, pleuretic chest pain (pain on inspiration), dyspnea

dx:

labs:

tx:

dx: PE: causes: immolization, recent surgery, pregancy, malignancy, lower extremity fracture, hypercoagulopathy

labs: bilat ultrasounds, V/Q, spiral CT angiogram, D dimer*

*D dimer high in pregnancy

tx: moderate PE= LMW heparin.  large PE= thrombolysis (risky!)...but this type of PE may put pt into shock, need to treat ASAP.

Long term coumadin  post PE.

D dimer usually high in pregnant pt, don´t assume clot/PE.  Get a CT, even if in 3rd trimester.

PE most common in 2nd and 3rd trimesters.

Life threatening lung failure caused by sepsis, major trauma, or inhalation of toxic fumes.

Mech: alveoli inflammed, fill with fluid, and collapse...no gas exchange.

ABGs--severe hypoxemia

dx and tx?

dx: ARDS

tx: mechanical ventilation, tx of underlying cause

1) Monitor for progression/resolution with repeat CXRs

2) Need chest tube for gradual decompression

3) Require  immediate needle decompression followed by chest tube placement

CARDIOVASCULAR TESTING

2/9/10

2-d echo pictures are obtained using 4 standard transducer positions...

Pt positions...

1) parasternal (L sternal border)

2)apical (L, midclav line)

3)subcostal

4) suprasternal

L lat decub: for parasternal & apical views

supine: subcostal & suprasternal views

a benign cardiac tumor that is usually attached by stalk to interatrial spetum, usually moves with blood flow or might completely prolapse into LV during diastole (mimics mitral stenosis w/ diastolic rumble)

what is this and how can it be seen?

A nuclear scan that evaluates the pumping function of the ventricles. Quantitatively evaluates LV ej fraction (esp pre and post chemo tx).

Indications: LV assessment, ej frac, wall motion abnmlities, LV aneurysm detection, cardio toxicity eval

Stress Test

Contraindications:  recent signif ECG changes, unstable angina, uncontrolled arryhthmias, heart blocks, acute CHF, severe AS, suspected PE/DVT, acute infection, uncontrolled DM

sensitivity 65-75%

dx: 85% of age predicted max HR (220-age)

motion: stress echo. Do this resting and with exercise.

uptake: stress nuclear, isotope lights up in walls where it is uptaked in 1hr.  No allergic rxns to T201 isotope (attached to RBCs).  Do this resting and with exercise.

Pharmacologic Stress testing

persatine + isotope in nuclear stress test*

dobutamine in stress echo

*contraindicated in COPD, bronchospastic pts, tx with theophylline.

Cardiac Catheterization

1) catheters administered via...

2) can inject.... (what do you do if there is an allergy?)

1) R femoral artery

2) can inject dye (give steroid before if known allergy to dye)

PTCA (percut transluminal coronary angiography) is used to evaluate.....

PCI (percut intervention) is used to evaluate.....(2)

**what are these two things?

PTCA: coronary artery stenosis

PCI: renal/carotid artery stenosis

**angiography

Cardiac Enzyme:

highest levels found in skeletal muscle.  Also in myocardium and brain tissue.

elevated 2-4hrs post-MI

Peaks at 24-36 hrs

returns to nml in 3 days

what enzyme and list 3 types.

CPK mb: creatine phosphokinase

CPK nm = skeetal muscle

CPK bb = brain tissue

CPK mb= cardiac

Cardiac Enzyme:

found in cardiac and skeletal muscle, but this assay is cardiac specific.

incr levels with cardiac ischemia/MI.

rises within 3hrs of injury

continously released for 5-10 post injury

peaks @ 20x nml level

remains elevated for up to 2 wks.

What is this?  Is it more sensitive than what enzyme, in what sense?

Troponin I

More senstive than CPK-MB b/c just low levels of troponin I determine necrosis.

substance secreted from ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure develops or worsens.

the level increases when heart failure develops/worsens:

give values of

-no CHF

-Suggestive of HF

-mild, mod, & severe HF

BNB B type natriuretic peptide

BNP increases in blood when HF develops and worsens

<100 pg/mL = no CHF

100-300= suggestive

300 mild

600 mod

>900 severe

ECG Timing

large box (sec)

small box (sec)

HR (measured interval btwn adjacent complexes)

large box= 0.2 sec (200msec)

small box = 0.04 sec (40msec)

HR = 300/# large boxes =

300, 150, 100, 75, 60, 50, 43

<3 large boxes=tachycardia

>5 large boxes=bradycardia

ECG

1) SA node firing (atrial depolatization)

2) AV node firing through bundle of his and purkinje fibers (ventricular depolarization)

3) time for impulse to go from SA to AV node

4)repolarization of ventricles

5) rarely seen repolarization of atria

5) time btwn  depolarizing and repolarizing

P WAVE: SA node firing (atrial depolatization)

PR INTERVAL: time for impulse to go from SA to AV node

QRS COMPLEX: AV node firing through bundle of his and purkinje fibers (ventricular depolarization)

ST SEGMENT: time btwn  depolarizing and repolarizing

T WAVE:repolarization of ventricles

U WAVE:rarely seen, repolarization of atria

[image]

NSR: normal sinus rhythm

paced at....

conducts down....

variation with....

 (paced @ SA NODE)

60-100 bpm, regular

conducts down normal pathways

can have variation with breathing

ECG INTERPRETATION: THE BASICS

2/9/2010

1) cardiac disease pt

2) screen for occult cardiac abmlty; ensure absence of acute disease

3) baseline pic of heart

Heart electrical conduction system

(state path from SA to myocardial cell innervation)

1) pacemaker

2) electrical conducting cells

3) myocardial

Myocardial cells:

1) intracellular has incr conc of....

2) extracellular has incr conc of.....

3) where is the greater positive charge located?

4) net charge of cell @ rest, what must enter cell for contraction

1) intracellular has incr conc of K+

2) extracellular has incr conc of Na+, Ca++

3) greater positive charge is extracellular

4) net charge= negative @ rest.  Influx of Na+ begins contraction.

ECG basic components:

1) Deflection from baseline that represents a cardiac event

2) Specific portion of the complex as represented on ECG, joins 2 waves

Q wave:

1) significant Q wave is defined by (2)....indicates(1)...

2) insignificant Q wave commonly found in leads (3).....due to.....

1) significant Q wave is defined by

t ≥ 0.03 seconds

OR

Amplitude ≥ 1/3 of R wave amp.

Indicates MI over involved region.

2) insignificant Q wave commonly found in leads I, aVL, & V6, due to septal innervatio (¨septal Qs¨)

Normal time intervals:

1) PR interval

2) QRS duration

3) QT interval.  Prolonged indicates...

[image]

PR segment: what length is pathologic?

ST segment: what is representative of myocardial injury or infarction?

PR segment:   >0.8mm

ST segment:elevation

Conventional  ECG

name all the leads: limb and chest leads and what plane they are in, and location on chest (picture it, I put a picture on the other side).

Limb/extremity leads:

coronal plane - hexaxial system (leads 30º apart)

-Bipolar standard limbs: I, II, III

-unipolar limb leads: aVR (R arm), aVL (L arm), aVF (L leg)

Chest/Precordial Leads:

transverse plane - precordial system

- V1, V2, V3, V4, V5, V6

[image]

Standard format for most ECGs:

1) picture of lead order on ECG printout

2) Each lead= ? seconds

3) Full ECG is how many seconds

4) boxes and time (1 sec, big, small boxes)

5) Ht (1mV, mm, small boxes, big boxes)

Standard format for most ECGs:

1) picture

[image]

2) Each lead= 3 sec

3) Full ECG = 12 sec

4) 1 sec=5 big boxes (0.20 sec each) =25 small boxes (0.04sec each)

5) Ht (1mV=10mm=2 big boxes=10 small boxes)

Clinical ECG Lead Groups:

1) inferior wall

2) lateral wall

3) anterior wall

4) septal wall

5) odd ball

[image]

odd ball is aVR (R arm)

FYI reference for table above:

[image]

ECG: HR calculation by counting thick lines:

**how many thick lines defines tachy/bradycardia

find R wave that begins on thick line, count the thick lines up to the next R wave in this order:

HR: 300, 150, 100, 75, 60, 50

<3 big boxes=tachycardia (HR>100)

>5 big boxes=bradycardia (HR<60)

[image]

Atrial fibrillation

wandering atrial pacemaker

multifocal atrial tachycardia

P waves

1) indicate  _____ or _____ compenent

2) 2 causes of un-identical P waves (abnml)

3) # of p waves: #QRS waves >1....(abnml number suggests)...

1) indicate  atrial or supraventricular compenent

2) 2 causes of un-identical P waves (abnml):

-additional pacemaker firing

-superimposistion

3) # of p waves> #QRS waves... (this is abnml, should be =)... suggests AV nodal block

QRS complex

1) narrow indicates...

2) wide indicates...

3) un-/grouping can determine...(2)

4) dropped beats occur in ...(2)

1) narrow indicates supraventricular rhythms

2) wide indicates impulses transmitted by direct cell-cell contact

3) AV nodal block or recurrent premature complexes

4) Dropped beats: AV nodal block OR sinus arrest

CAD AND ACUTE CORONARY ARTERY SYNDROMES

2/12/10

1) MI

2) Thoracic Aortic Dissection

3) PE

4) Pneumonia

5) Pneumothorax

6) Boerhaave's Syndrome: esophageal perforation due to vomitting.

MI

1) miss rate increases with...(gender, age, pain)

2) classic HPI...unrelieved by...

3) ECG (taken within how many minutes of pain onset?, ST, Q, T, arrythmia)

4) what % of MI come with normal ECG?

1) miss rate in dx of MI associated with significant morbidity/mortalities.  Increased missed rate in women, age<50y/o, SOB complaints, no pain (50% of 80 year olds), or pain in uncommon locations (neck, throat, wrist).

2) severe squeezing >30min w/ radiation to jaw, L arm, neck, unrelevied by nitroglycerin/rest. *This is not always the case.* Assoc sx: diaphoresis, N/V, fatigue.

3) ECG:

ST elevation

Q waves= appears 12-36 hrs after damage

T waves Hyperacute or Flipped

Possible Arrythmias

4) 10% MIs have normal ECG

ACS (acute coronary syndrome) epidemiology:

1) % that have STEMI?

(STEMI= ST elevated MI)

2) % that have UA/NSTEMI?

(UA=unstable angina, NSTEMI= non-ST elevated MI)

...of these pts, what % have elevated troponin

(troponin=evidence of myocardial necrosis)

1) 25% that have STEMI

(STEMI= ST elevated MI)

2) 75% that have UA/NSTEMI?

(UA=unstable angina, NSTEMI= non-ST elevated MI)

...of these pts, 40-60% have elevated Troponin levels.

**FYI: The cardiac troponins T & I...

   - released within 4–6 hours of MI

   - remain elevated for up to 2 weeks

   - nearly complete tissue specificity

   - preferred markers for asssessing myocardial damage

Angina (definition: Angina pectoris is severe chest pain due to ischemia):

1) cardiac pain secondary to...

2) etiology

3) 3 types of angina:

a) Stable: plaque, pain location/quality/precipation/palliative factor/duration?

b) Unstable: plaque, pain onset/duration/Hx.  3 other causes with same clinical presentation.

c) Prinzmetal's Angina: cause. 

1) Angina is cardiac pain secondary to cardiac ischemia*.

2) Angina etiology is caused by atherosclerosis (atheroma (fatty plaque) formation in arterial BVs)

3a) Stable Angina (thick fibrous arterial plaque cap).  Deep/squeezing/heavy chest pain anywhere btwn mandible and umbilicus.   Precipitated by exertion/emotional upset.  Alleviated by rest within 1-2 min.  Duration= 2-30min.

3b) Unstable Angina (UA): (thin plaque cap that can rupture, causing UA/MI.  Pain not associated w/exertion.  Increasing freq/duration/severity/pattern of previous ischemic symptoms.

Other causes with same clinical presentation:

-Recurrent isch 4-6 wks post PCI**/CABG***

-recurrent pulm edema

3c) Prinzmetal's Angina: angina (cardiac chest pain) at rest that occurs in cycles. It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than by atherosclerosis

FYIs:

*Cardiac Ischemia=defieciency of blood to myocardial cells.  Supply is not equal to demand.

• Ischemia > 20min may lead to irreversible damage (MI).   
• Some diseases increase myocardial oxygen consumption (MVO2) to such a point that compensatory mechanisms fail and the heart cells become ischemic (imbalance between supply and demand).

**PCI= Percutaneous Coronary Intervention: balloons, stents, angioplasty, atheroectomy, thrombectomy, etc.

***Coronary artery bypass surgery (CABG) relieves angina and reduces the risk of death from CAD. Arteries or veins from elsewhere in the body are graftedcoronary arteries to bypass atheroscleroticnarrowings and improve the blood supply to the coronary circulation supplying the myocardium . This surgery is usually performed with the heart stopped, necessitating the usage of cardiopulmonary bypass. 

Pt presents to ER with chest pain, & you dx ACS (acute coronary syndrome).  You do the standard procedure: IV, O2 mask, Heart Monitor, CXR (unremarkable), Hx, PE with vitals/pulse Ox, and ECG...

1) if ECG shows ST elevation, what are two diagnosies?

2) if ECG shows no ST elevation, what are 2 possibilities (which is majority and which is minority, and what distinguishes the two)?

1) ST elev:

Q wave MI (QwMI)= majority

non Q wave MI (NQMI) = minority.

2) No ST elev:

NSTEMI = must have elevated blood markers (Trop, CK-mB).

UA

During myocardial necrosis (from an ostructed coronary artery), why is a

very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis?

necrosis because it can be oxygenated by diffusion from the ventricle.

What 2 cardiac blood markers are released at a similar initial release time (within 2-4 hours of chest pain onset)?

When are they tested?

Which is more sensitive/specific?

Which is best for a late diagnosis of MI?

troponin I & T 

-test usually ordered with a suspected MI at presentation to ER (only suggestive of MI)

- test repeated 6-12 hours later (for def dx).

-Troponin values can remain high for 1–2 weeks post-MI.

-Very sensitive and specific: The test is not affected by damage to other muscles.

CK-MB can usually be elevated in MI pts about 3-4 hours after onset of chest pain.

-peaks in 18-24 hours

-levels return to normal within 72 hours.

TIMI (thrombolysis in MI) RISK SCORE:

the higher the number, the greater the risk of complications/death.

1) to predict the benifit of.....

2) What TIMI score do you use PCA?  (do you even know what PCA is?)

3) TIMI SCORE of 0 to 2, what is the next test to perform?

1) to predict the benifit of early invasive strategies for UA/NSTEMI.

2) PCA (percutanous coronary intervention= angioplasty) used in management of med/high risk UA/NSTEMI (TIMI >3).  PCA includes balloon angiography (w/ or w/o stent), Atherectomy, Thromboectomy.

3) TIMI 0-2= low risk. Stress test.  If high risk stress test, do coronary arteriography.  If not high risk, tx with statins, ACEi.

Pt presents with sudden onset of sharp chest pain.  Pain is relieved by leaning forward while sitting upright.  Pt is febrile.  Rub heard on physical exam.

Dx & definition

Etiology

Dx labs

f/u test

OTC tx & tx goal

Pericarditis

definition: fluid accum btwn parietal and visceral pericardium.  Inflammation as well.

Etiology: viral, bacterial , fungal ,malignancy, drugs, uremia.

Labs:CXR

f/u: echo

tx: NSAIDS, goal: look for the cause

Who can go home with chest pain?

1) age

2) risk factors

3) enzymes

1) <35 y/o

2) minimal risk factors

3) repeat cardiac enzymes in 4-6 hrs to ensure NO elevated levels of troponin of CK-mb

DYSLIPIDEMIA

2/12/10

*FYI CARD*

*Don´'t need to memorize, just helpful for this lecture*

LIPID PROFILES: don't even try to guess, just flip

Why?

- To determine risk of CHD (coronary heart disease). 

- Good indicators of likeliness of MI or CVA.

What the lipid profile includes:

-TC         Total Chol

-HDL-C    High Density Lipoprotein Chol

-LDL-C     Low Density Lipoprotein Chol

-TG          Triglycerides

...extended profile...

-VLDL-C   very low density lipoprotein chol

-non-HDL-C

When?  *know this for test*

-Screening begins @ 20y/o q. 5yrs (possibly just chol test, not full lipid profile).

-Screening begins EARLIER with +FH, DM; HTN, obesity.

Optimal Values:

• total cholesterol: <200 mg/dL.
• HDL-C: >40 mg/dL (women) & >50 mg/dL (men).
• LDL-C: <100 mg/dL.
• TG: <150 mg/dL.

Calculated Values:

• VLDL-C = TG/5 (estimated).  High levels associated with incr risk of CHD & CVA.
• Non-HDL-C = TC - HDL-C = (calculated).  Represents atherogenic cholesterol.  Used to assess risk of CVD.

Lipoproteins:

1) Composition: core, outer layer, surface molecules

2) general role

Types (low to high density):

a) carry TGs from intestines

b)carry trialglycerol from liver to adipose tissue

c) not detectable in blood

d) carry cholesterol from liver to cells, "bad cholesterol"

e) collect chol from tissues, & return it to liver,  "good cholesterol"

1) Core: TGs and chol esters carried internally, shielded from the water by the phospholipid monolayer.

Outer layer/Surface Molecules: hydrophilic polarizedphospholipids, free chol, and apolipoproteins directed outward.

2) Role:  Transport lipids (mainly TGs and cholesterol esters) and fat-soluble vitamins to/from body tissues

Types (low to high density): *memorize those in red*

a) Chylomicrons: carry TGs from intestines

b) VLDL: carry trialglycerol from liver to adipose tissue

c) IDL: not detectable in blood

d) LDL: carry cholesterol from liver to cells, "bad cholesterol"

e) HDL: collect chol from tissues, & return it to liver,  "good cholesterol"

Atheroma ¨plaque¨formation:

a) Describe (endothelial injury) to (rapid increase of collagen, lipid/debris, & smooth muscle) in stages

b) What stage is a fatty streak (early stages of atheroma) formed?

Endothelial Injury (HTN, tobacco, ↑ homocysteine, etc.)

↓

Endothelial Dysfunction (∆ permeability to leukocytes/monocytes, lipoproteins )

↓

Smooth Muscle Emigration/Monocyte Activation

↓

“Foam Cell” Formation (Monocyte and Smooth Muscle)

↓

Proliferation of: Collagen, lipids/debris, Smooth Muscle

b) after smooth muscle emigration/monocyte activation

1) cigs

2) HTN

3) FH of CHD in 1st degree relative

4) AGE (men>45, women>55)

5) HDL-C <40mg/dL

Athersclerotic Lesions

1) Fatty streaks

-Vessel narrowing & ischemia

-Sudden vessel obstruction

-Thromboemobli formation

-Aneurysm

are clinical manifestations of...

Phenotype IIb (mutation of LDL receptor gene OR APL-B gene) and phenotype IV (mutation in LP lipase) are the most common....

which has greater atherogenic potential?

IIB has increased....

IV has increased....

familial hyperlipoproteinemias.

IIB>IV in atherogenic potential.

IIB= incr LDL, VLDL, TG, Chol

IV= incr VLDL, TG

Secondary Dyslipedemic Factors (6)

HeRe

HoMe

LiMe

HeRe

HoMe

LiMe

Hepatic

Renal

Hormonal

Metabolic

Lifestyle

Meds

Therapy for Dyslipidemia:

a) Non-Pharmacologic

1) diet

2) lifestyle

3) natural products

b) Pharmacologic

MOA: name the agent

• block rate-limiting step (mevalonic acid to cholesterol)
• decreases hepatic VLDL synthesis
• Increase LPL activity and decreases VLDL synthesis
• Increase bile acid/cholesterol excretion and LDL receptors
• Decreases intestinal cholesterol absorption
• Decreases chylomicrom/VLDL synthesis

a) Non-Pharmacologic

1) diet: ↑fiber, ↓ETOH, ↓Fat (sat), ↓CH2O (¿formaldehyde?  what the fuck is this?)

2) lifestyle: quit smoking, lose weight, exercise

3) natural products: plant sterols/stanols (psyllium, soy, chinese red yeast)

b) Pharmacologic

MOA:

NSTEMI AND STEMI

2/12/10

STEMI vs NSTEMI 

1) STEMI is due to...

tx mainstay is....

2) NSTEMI is due to...

tx is....(3)

3) what 2 drugs are given immediately to any MI pt?

1) STEMI = sudden thrombotic occlusion (complete block) of a coronary artery.

Tx: thrombolytic therapy.

2) NSTEMI = unstable plaque with aggregation of platelets (sudden narrowing).

Tx: anti platelet drugs (ASA, clopidogrel) and anticoagulants (heparin). B-blockers improve symptoms of cardiac ischemia in NSTEMI.

3) Immediately: NO and Aspirin. 

REVIEW:

NO (nitroglycerine) are nitrovasodilators

ASA & Clop are antiplatelets.

. B-blockers improve symptoms of cardiac ischemia in NSTEMI.

STEMI:

ECG ST elevations are seen on what leads for the following MI locations:

1. Septal Wall
2. Anterior Wall
3. Lateral Wall
4. Inferior Wall (*what leads are reciprocal changes in?)
5. Posterior Wall (*tricky trick, what happens to ST on anterior/posterior leads?)
6. RV Infarct

What other ECG changes are seen as you move from ischemia to infarction of myocardium?

1. Septal Wall: V1, V2
2. Anterior Wall: V3, V4
3. Lateral Wall: I, aVL, V5, V6
4. Inferior Wall: II, III, aVF
   • Reciprocal Changes: I, aVL, V leads
5. Posterior Wall:
   
   • ST depression-V1, V2, V3
   • ST elevation on posterior leads: V7, V8, V9
6. RV Infarct: V3R, V4R, V5R, V6R

Other STEMI ECG changes:

• Ischemia
  • ST depression
• Infarction
  • ST elevation
  • significant Q wave (ht > than 1/3 R Wave Ht)
  • T wave inversion

STEMI MANAGEMENT:

1) Inital Management (3)

2) Initial labs (4)

3) treat pain ASAP with...but have caution with these conditions (2)...    2nd line pain tx...but caution...

4) reprofusion therapy: goal time frame, method

5) antithrombin

 6) antiplatelet (2)

7) oral of this class drug is preferred over IV

8) these drugs lower LDL

9) AVOID!!!!

1) O2, IV access, continous cardiac monitoring

2) assess ABG, 2D echo, CXR, serial ECGs

3) Nitrates: caution in AS, RV infarction

2nd line: Morphine: possible increase in mortality

4) reperfusion within 2 hrs: PCI fibrinolysis

5) antithrombin - heparin

 6) antiplatelet (2) - ASA, clopidigrel

7) beta blockers: oral of this class drug is preferred over IV

8) Statins: lower LDL

9) AVOID: NSAIDS!!!, tobacco, hyperglycemia, CCB

Conduction Disturbances (AV block)

Pericarditis (Dressler's*)

Heart Failure/LV dysfunction

LV free wall rupture

Ventral Septal Defect

Papillary muscle dysfunction

Dysrhythmias

Recurrent Angina

LV aneurysm (+/- thrombus)

....complications of what?

STEMI complications

*FYI - Don´t memorize this.

Dressler's syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). The syndrome consists of a persistent low-grade fever, chest pain (usually pleuritic in nature), a pericardial friction rub, and /or a pericardial effusion. The symptoms tend to occur after a few weeks or even months after infarction and tend to subside in a few days. An elevated ESR is an objective laboratory finding.

Poor Prognosis factors for STEMI pts:

1) gender?

2) age?

3) PMH (3)

4) wall location of current MI

females

age>70

Hx: DM, prior angina/MI

Anterior Wall MI

PERIPHERAL ARTERIAL DISEASE

2/16/10

50% asympto

40% claudication

ABI evaluates...

(ankle brachial index)

ABI Values of....

1) an ischemic lesions unable to heal

2) ¨reasonable¨

3) healthy

**Sclerotic distal arteries give what kind ankle pressures?

ABI evaluates arterial disease.

1) an ischemic lesions unable to heal= ≤0.3

2) ≥0.6= ¨reasonable¨

3) 0.9-1.0= healthy

**Sclerotic distal arteries give false high ankle pressures

Crtical stenosis is an ___% dropoff in arterial blood flow.  This is why PAD pts develop symptoms relatively ______ in the course of their disease.

State the locaton of claudication for each level of occlusion below:

1) aorta a

2) iliac a

3) s/f femoral a

1) aorta a...buttock

2) iliac a...hip & thigh

3) s/f femoral a....calf

pulse

color

temp

trophic changes

elevation/depency changes*

(*elev legs 45 seconds, look for blanching, than quickly place legs dependent.  After blanching, a very ischemic foot develops intense reddish blue on prolonged dependency.)

Allen test

Adson maneuver*

*a test for thoracic outlet narrowing (subclav a). It is performed with the patient sitting with hands on the thighs. The examiner palpates both radial pulses as the patient takes a deep breath and holds it while extending the neck and turning the head toward the affected side. If the radial pulse on the affected side is significantly diminished or there is numbness or tingling in the hand, the result is regarded as positive.

Pulsed Doppler sound for the evaluation of....(2)

describe the quality of sound in good flow and low flow.

angle of probe

venous & arterial diseases

good= sharp, high pitch, biphasic (with respiration)

low flow (occlusion) = flat, low pitch, monophasic (with respiration)

probe @ 60º

With proximal arterial stenosis (aorta, iliac, femoral), after exercise, ankle pressure and pulse volumes will be

increased or decreased?

Meds for PAD.  State the class and therapeutic goal.

1) clopidogrel (what OTC is also in this class?)

2) cilostazol

1) antiplatelet: to reduce ischemic events:  It has no effect on the symptoms of atherosclerotic disorders but, rather, helps to prevent the acute complications associated with them.

**ASA is also good, cheap antiplatelet therapy

2) antiplatlet and vasodilator: indicated to improve PAD claudication symptoms by permitting greater blood perfusion of working muscle.

invasive management of PAD.

(invasive= PTA = percutaneous transluminal angioplasty)

saphenous vein (reversed or in situ)

Synthetics: teflon

arm veins (not as good: cephalic and basilic)

Sx include sudden onset of pain, coldness and pallor of lower extremity.  PE reveals no neuro deficit.  You fix the problem by Fogarty catheter embolectomy.

What was the dx?  and two possible causes?

Acute arterial occlusion

1) embolus from heart

2) thrombosis on top of chronic atherosclerosis

FYI***

Fogarty catheter

Introduced more than 30 years ago by Dr. Thomas J. Fogarty, these embolectomy catheters are indicated for the removal of fresh, soft emboli and thrombi from vessels in the arterial system.

Remains the leading choice for simple and rapid removal of emboli and thrombi from the arterial system.

VENOUS DISEASES

2/16/10

Veins:

Perforator (communicating veins) flow from...

Deep veins carry what % of venous return?

What is the primary deep veins of the thigh?

Perforator (communicating veins) flow from superficial to deep.

Deep veins carry what 80-85% of venous return.

Primary deep veins of the thigh: superficial femoral vein.

Virchow's triad describes the three broad categories of factors that are thought to contribute to thrombosis

what are the 2 categories?

• Hypercoagulability
• Hemodynamic changes (stasis, turbulence)
• Endothelial injury/dysfunction

venous insuff (chronic) = pitting edema

DVT = pitting edema

lymohedema

this condition is characterized by local swelling, erythema, tender/indurated cord, possible fever/tachycardia/edema, with low risk of Pulm embolism.

Dx:

tx: (3 non-pharma)

subsudes in...

superficial thrombophlebitis

head, elevation, NSAIDS

1-2 weeks it goes away

the symptoms of this condition include pitting edema, dull ache (worse on dependency), tenderness, warmth, dusky color, prominent s/f venous pattern, slight fever with tachycardia

what is this?

what non-specific test can be done in office?

what % are asymptomatic?

what is the major threat of this condition?

DVT

Homan's sign: dorsiflexion of foot with knee bent 90º induces calf pain.

50% asymptomatic

pulm embolism

Venous duplex ultrasound is used in the diagnosis of....

Treatment of DVT:

2 pharmas for the treatment of DVT

Therapy to dissolve the clot (indications?)

Invasive procedure used when anticoagultion does not work OR pt cannot be anticoagulated.

anticoagulants:

Low molecular weight heparin

warafin (COUMADIN)

Fibrinolytic therapy to dissolve the clot given directly to occluded site via catheter, indicated in moderate-severe DVT (Iliac, ilio-femoral, Mae Thurner syndrome).

IVC filters

DVT PROPHYLAXIS:

Elevation of leg, active leg exercises, compression stockings, and external pneumatic compression all help to decrease...

heparin, low dose coumadin help to...

stasis of venous blood flow.

alter hypercoagulable state (ASA doen´t really do anything for DVT).

Lymphedema

(Involves s/f tissues because 80% of lymphatics are superficial).

Lymphedema:

Primary causes are...

Secondary causes (4)

1º: congential

2º: tumor, radiation, surgery, parasites

Intermittent increased or unusual sensitivity to cold or emotional factors producing vasospasm with cold, pallor, pain in the hands and fingers.  this is exaggeration of a normal response. no arterial occlusion involved in primary type.

1º type must be present for ___ years without evidence of _______________.

Raynaud's phenomenon

1º type must be present for 2 years without evidence of underlying disease.

HYPERTENSION

2/18/10

Cardiovascular Mortality Risk ____________ With Each 20/10 mm Hg BP Increment

Cardiovascular Mortality Risk doubles With Each 20/10 mm Hg BP Increment

CV risk factors: smoking, dyslipidemia, DM, >60yrs, men, postmeno women, FH

BP measurement

1) pt position

2) pt should not smoke or ingest caffeine for ____ min before measurement

3) measurement should begin ____ min after rest

4) how many readings should be averaged?

1) pt position: seated with back and arm supported

2) pt should not smoke or ingest caffeine for 30 min before measurement

3) measurement should begin 5 min after rest

4) 2 or more readings should be averaged

Self measurement

Ambulatory measurement

F/U recommendations based on initial BP measurements

1) <130/<85

2)130-139/85-89

3)140-159/ 90-99

4)160-179/100-109

5) >180/>110

1) <130/<85................recheck 2 yrs

2)130-139/85-89..........recheck 1 yr, lifestyle edu

3)140-159/ 90-99.........confirm 2 mnths, lifestyle edu

4)160-179/100-109......eval/refer within 1 mnth

5) >180/>110..............eval/refer within 7 days

blood pressure readings (2+), verify in contrlat arm

Ht, wt, waist circum

fundoscopic exam

neck

heart

lungs

abdomen

extremities

neurological

urinalysis

CBC

blood chem

lipids

ECG

1) maintaining BP <140/<90

2) controlling other cardiovascular risk factors

exercise

low salt diet

reduce alcohol

potassium supplement

7 CLASSES OF HTN DRUGS

¨AAA C DDD¨

ACEi

Adrenergic inhibitors (includes b blockers)

Ang II Receptor Blockers (ARBs)

Ca Antagonists (CCBs)

Direct Vasodilators

Diuretics (thiazide)

Direct Renin Inhibitors

Patient Compliance...

40% of pts stop within first 3 months

70% stop within 1 year

Best drug class for treating Stg 1 HTN.

for Stg II HTN?

Stg I: Diuretics (thiazides)

Stg II: diuretic + ACEi, ARB, BB (b blocker), OR CCB

What HTN drugs are contraindicated for pregnancy?

What HTN drug is recommended for women during pregnancy?

contraindicated: ACEi, ARBs

Methydopa recommended

HTN in the elderly, is systolic or Diastolic BP a better predictor of events?

1º HTN (idiosyncratic) is the most common cause, however, what identifiable cause of HTN should be considered in the elderly?

systolic

Renovascular HTN

HTN medication to use in the following comorbid condition:

1) Cardiac Failure

2) Renal Disease

3) DM (4)

4) Chronic Airway Disease (incl Asthma): *C/I

5) Gout: don´t use...

1) Cardiac Failure: ACEi + digoxin/diuretics

2) Renal Disease: ACEi

3) DM: ACEi, a-blockers, CCB, low dose diuretics

4) Chronic Airway Disease (incl Asthma): ACEi (*NO B BLOCKERS!)

5) Gout: don´t use diuretics (hyperuricemia)

Pts undergoing surgery...

surgery should be delayed until BP is less than...

if pt not on  prior drug therapy, treat with _______ before and after surgery.

<180/110

treat with b-blockers