October 5, 2000

Heart Failure definition: Inability of the heart to maintain adequate output to meet metabolic demands of the body


Pathophysiology: Decrease organ perfusion (due to arteriosclerosis, vasospasm, shock, etc.) causes inadequate tissue OXYGEN delivery



  1. Coronary artery DZ
  2. Hypertensive Heart DZ
    1. Diastolic dysfunction floppy heart due to volume overload
    2. Systolic dysfunction concentric thickened ventricle due to pressure overload
  3. Dilated cardiomyopathy
    1. Idiopathic
    2. Toxic (chronic alcoholic, doxorubicin)
    3. Infection (viral, parasite)
    4. Collagen vascular DZ
  4. Valvular Heart DZ (stenosis, Insufficiency)
  5. Hypertrophic cardiomyopathy (similar to systolic dysfunction)
  6. Restrictive cardiomyopathy
    1. Amyloidosis
    2. Sarcoidosis
    3. Hemachromatosis (most common)
  7. Constrictive pericarditis (heart cant expand)
    1. Cardiac tamponade
    2. TB
  8. High output heart failure
    1. Chronic anemia
    2. Atrioventricular shunt increase output
    3. Thyrotoxicosis
    4. Beriberi (B12 deficiency)


Left sided CHF pulmonary congestion

Right sided CHF systemic congestion

You needed to know what are the differences between systolic vs. diastolic heart failure because your treatment is based on this.


Chronic heart failure myocytes changed to adapt to failure (you should see hypertrophy of myocytes)

Acute heart failure abrupt disturbance so the body cant adapt to the change (call 911)


Strategies to treat Heart Failure

  1. correction of precipitating cause
  2. control of fluid and Na++ retention.
  3. optimization myocardial contractile function
  4. minimization cardiac workload
  5. decrease pulmonary/ systemic venous congestion


Monitor wt, vital signs, fluid intake/output

Non pharmacologic Rx

1.     bed rest decrease myocardial workload and myocardial OXYGEN consumption

2.     wt. Loss decrease systemic vascular resistance (SVR)

3.     dietary Na++ restriction < 2 grams a day

4.     fluid restriction

5.     discontinue negative inotropic medicine

a.      Beta-blockers

b.     Calcium channel blockers

c.      Disopyramide (Class IA antiarrhytmia)

d.     Flecainide (Class IC antiarrhythmia)

e.      ASA/NSAIDS decrease efficacy of treatment, also increase renal toxicity. Why?

6.     increase oxygen (stop smoking) decrease pulmonary constriction

7.     dialysis/ultrafiltration (renal dysfunction)

a.      phlebotomy

b.     rotating tourniquets

c.      paracentesis

d.     thoracocentesis


Pharmacological Rx


Venodilators decrease preload decrease ventricular filling pressures

Arterial dilators decrease afterload increase CO (be careful in fixed cardiac output such as aortic stenosis, diastolic dysfunction, idiopathic hypertrophic subaortic stenosis)


  1. Vasodilator: ACE inhibitors decrease ventricular filling and decrease SVR and will increase CO with change in BP/HR. All these ACE inhibitors will decrease ventricular hypertrophy. Contraindicated in renal insufficiency with bilateral renal arterial stenosis
    1. Captopril
    2. Enalapril
    3. Lisinopril
    4. Quinapril
  2. Venodilator: Nitrate decrease ventricular filling pressure and dilate coronary arteries. Decrease mortality.
  3. Vasodilator: hydralazine decrease after load; works directly on arterial smooth muscle; can get reflex tachycardia which consumes tremendous amounts of oxygen.
    1. Good in regurgitant valvular lesions
    2. Side effect is SLE like syndrome (positive FANA or fluorescent antinuclear antibody); remove the drug immediately if this occurred.
  4. Alpha-adrenergic receptor antagonists block nor epinephrine decrease vasoconstriction, decrease SVR, and decrease afterload
    1. Prazosin, tolazosin, doxasin
    2. Side effect is reflex tachycardia
  5. Beta-adrenergic receptor antagonists decrease chronic adrenergic stimulation decrease myocytes toxicity and decrease Beta receptors.
    1. Good for diastolic dysfunction, outflow obstruction, hypertrophic cardiomyopathy.
    2. Carbedilol has both alpha and beta blocker and also is an antioxidant so decrease mortality by 65%
  6. Calcium channel blockers inhibits Ca++ entry into myocytes diastolic relaxation; be careful because it is a negative inotropic agent.
    1. Verapamil, diltiazam. they work mostly on the heart
    2. Nicardopine, amlodipine and telodopine. They work on the vasculature.
    3. digoxin, diuretic, and ACE inhibitor work better.
  7. Parenteral vasodilators:
    1. Nitroglycerine

                                                    i.     Venous with some arterial vasodilator

                                                  ii.     Half life is about 1-3 minutes

                                                iii.     Tolerance develops after 12 hours

    1. Sodium nitroprusside

                                                    i.     Direct arterial vasodilator with some venodilation

                                                  ii.     Coronary steal

                                                iii.     Half life is 1-3 minutes

                                                iv.     Metabolize to cyanide and thiocyanate which is very toxic so NO chronic use because the toxic will build up and kill you.

                                                  v.     FOR ACUTE USE ONLY

                                                vi.     Signs of toxicity: mental status changes, abdominal pain, nausea, seizures, metabolic acidosis

    1. Enalaprilat acute metabolite of enalapril
  1. Digitalis inhibits sarcolemal Na+/K+ ATPase increase myocardial contractility and blocks AV node conduction
    1. IV- begins 15-30 min
    2. PO- begins 2 hrs.
    3. Contraindicated in

                                                    i.     High output failure

                                                  ii.     MI

                                                iii.     AV conduction blocks

                                                iv.     Aberrant pathways (increase conduction accessory pathway)

                                                  v.     Cardioversion with digoxin toxicity is fatal ventricular arrhythmias

    1. Drug interactions

                                                    i.     Decrease digoxin absorption if taken with cholestyramine, kaolin-pectin, antacids

                                                  ii.     Increase digoxin levels with erythromycin, tetracycline, verapamil, flecainide, amiodarone, quinidine (increase twofold)


October 11, 2000

Thiazide Diuretics goal is to increase urinary output U/O to 0.5-1.0 kg/day

1.     Thiazides- used in heart failure for out patient; also used in hypertension;

2.     Metolzone- works on proximal/distal tubules; administered with loop diuretics to increase U/O

3.     indapamide- has less effect on lipids

Loop diuretics

1.     Furosemide venodilation within minutes of IV decreases preload

a.      If allergic to sulfa cant use furosemide or bumetamide

b.     With heart failure use multiple amounts in a day

K+ sparing- use more for hypertension

1.     spirolactone, amiloride,

2.     use with ACE inhibitor is better than ACE inhibitor alone. the theory is to prevent aldosterone escape with chronic administration of ACE inhibitor

3.     low dose of spirolactone will decrease mortality by 30%;

Positive Inotropic

1.     Dopamine (sympathomimetics)

a.      Different effects at different dosages. (DA>B1>B2)

b.     1-3 microgram/kg/min will stimulate dopanergic receptors selective renal/mesenteric vasodilatation

c.      2-5 microgram/kg/min will stimulate Beta-adrenergic receptors positive inotropic

d.     5-10 microgram/kg/min will stimulate alpha-adrenoreceptors increase SVR, increase BP

e.      hypotensive of early acute renal failure

2.     Dobutamine selective Beta-one-adrenergic receptor stimulation (Beta-two is much less)

a.      Direct inotrope stimulation with reflex arterial vasodilation

b.     Not effective for diastolic dysfunction increase output heart failure

3.     Phosphodiesterase inhibitors increase cAMP

a.      Increase cAMP will cause increase in myocardial contractility and vasodilation

b.     Amirone, milrinone, vesnanone (PO)

c.      Vesnanone will increase mortality

4.     Intra aortic balloon pump (bypass surgery gives time until medicine kick in)

a.      Placid percutaneously via femoral artery then to the distal aorta then to the Left subclavian artery then synchronize-inflate-diastole. This will decrease afterload by decrease PVR and decrease myocardial oxygen consumption and increase coronary blood flow)




90% of hypertension is essential while only 10% is either due to the following conditions:

a.      renal parenchymal DZ

b.     pheochromocytoma

c.      cushings syndrome

d.     primary hypertension

e.      coarctation of the aorta


Target organ damage:

a.      arteriosclerosis heart DZ

b.     CHF

c.      Renal insufficiency

DX: multiple readings unless > 210/120 mmHg

Urine analysis; CBC; glucose; K+; Ca++; creatine; uric acid;; cholesterol;

triglyceride; HDL; ECG; CXR


Consider secondary HTN in people if

1.     <30 or > 60 y/o

2.     difficult to control BP

3.     stable difficult to control

4.     accelerated or malignant HTN

5.     signs/symptoms of secondary cause

Classification > 18 years old



Normal level



High Normal



Stage 1 HTN



Stage 2 HTN



Stage 3 HTN



Stage 4 HTN




Stage 1-2 and if NO target organ damage; no other cardiovascular risk factor and Diastolic is in the range of 90-94 mmHg, begin with NON-pharmaco RX by lifestyle modification.

1.     decrease salt uptake <6 gm/day

2.     decrease EtOH

3.     decrease Wt.

4.     increase exercise

5.     stop smoking


Stage 3 and 4 if <180/110 still do life style modification as above; however, if diastolic >120 then immediate treatment with the following drugs:


A. Beta-blocker is a good drug to block catechoamines release so you will get the following results:

a.      Decrease HR and CO

b.     Decrease plasma

c.      Increase vasodilating prostaglandins

d.     Decrease plasma volume


1.       Here is a list of beta-one selective blockers:

a.      sotolol

b.     esmolol

c.      betaxolol

d.     atenolol

e.      bisoprolol

f.       metoprolol

2. Here is a list of beta non-selective (beat-one and beta-two blockers)

a.      timolol

b.     propanolol

c.      penbutolol

d.     nadolol


3. Here is another list of beta-blockers with Intrinsic Sympathomimetic Activity (ISA). These drugs have less bradycardia and will increase HDL and decrease Triglyceride.

a.      careolol

b.     acebutolol

c.      pindolol


4. Here is a list of alpha and beta blockers

a.      carnedilol 10 times more selective for beta than for alpha

b.     labetolol 4 times more selective for beta than for alpha; and no effects on lipid

6.     Side Effects of the above drugs

a.      Bronchospasm

b.     Negative inotropic CHF

c.      Hypotension

d.     Conduction disturbances

e.      Increase triglyceride and decrease HDL; look at the exception.

B. Alpha adrenergic antagonists; block alpha receptor will cause atrial and venous dilator.

1. Here is a list of alpha blockers

a.      prazosin

b.     terazosin

c.      doxazosin

2.       Side effects

a.      First dose effect

b.     Orthostatic hypotension

c.      Decrease cholesterol and triglyceride and increase in HDL (this is good)

d.     Decrease smooth muscle tone in prostate and bladder neck


C. Centrally acting adrenergic agents stimulate alpha-adrenergic receptor in CNS decrease peripheral tone decease HR and CO

1. here is a list of centrally acting drugs

a.      Clonidine side FX: fluid retention

b.     Guanfacine side FX: bradycardia

c.      Guanabenz orthostatic hypotension

d.     methyldopa CHF

2.     The main side FX of all these drugs are abrupt withdrawal syndrome (increase BP, tachycardia, diaphoresis)



OCTOBER 19, 2000

Other adrenergic antagonists that inhibits the release of nor epinephrine from peripheral nerve terminals.

Reserpine side FX is depression and sedation

Guanthidine orthostasis



Diuretics: natriuresis increases PVR (peripheral vascular resistance) decreases CO return to normal after chronic administration.

Thiazides (for chronic hypertension; use at home)

1. work on the distal convoluted tubule to cause increase sodium/water excretion; good for menopausal women; can use acutely in Diabetes Mellitus.

a.      Hydrochlorothiazide

b.     Chlorothalidone

c.      Indapamide

d.     Metalazone

2. side effects

a.      Hypokalemia

b.     Hypomagnesemia

c.      Hypercalcemia

d.     Hypercholesteremia

e.      Hyperglycemia

f.       hyperuricemia

Loop diuretics (use for hypocalcemic emergency usually for acute HTN)

1.     work on the thick ascending loop of Henle

                                                              i.     bumetamid

                                                            ii.     ethacrynic acid

                                                          iii.     furosemid

                                                          iv.     torsemide

2.     side effects

                                                              i.     hypomagnesemia

                                                            ii.     hypokalemia

                                                          iii.     hypocalcemia


K+ sparing agents (usually combo with other diuretics so wont lose K+)

1.     work on the distal convoluted tubule and collecting tube by inhibiting K+ excretion

                                                                   i.     Amiloride

                                                                 ii.     Triamterene

                                                               iii.     Spironolactone side effect = gynecomastia

2.     side effects

                                                                   i.     spironolactone causes gynecomastia

                                                                 ii.     caution in using with ACE inhibitors

                                                               iii.     used in small dosages for heart failure


Calcium channel antagonists (best for blacks)

1.     decrease Ca++ influx in vascular smooth muscles arteriolar vasodilation. Can be used for angina, hypertension, or antiarrhythmia. First generation Ca++ channel antagonists:

                                                              i.     Verapamil most negative inotrope strongest for AV node cuasing bradycardia

                                                            ii.     Diltiazam in between negative inotrope

                                                          iii.     Nifedipine least negative inotrope; doesnt block AV node; causes tachycardia

2.     second generation Ca++ channel antagonists; more vasoselective less negative inotropoe and decrease work on AV node; longer half life.

                                                              i.     Felodopine

                                                            ii.     Nicardipine

                                                          iii.     Isradapine

                                                          iv.     Amlodipine

3.     side effects of all Ca++ channel antagonists

                                                              i.     constipation; orhtostatic hypotension; edema (nifedipine); flushing; NO impotence; NO lipid effects

                                                            ii.     increase mortality post MI or mild CHF

                                                          iii.     increase mortality with short acting (nifidipine)


ACE inhibitors (good for diabetic neuropathy; decrease protein loss and slow failure of any kidney DZ.


1.     competitively inhibit ACE resulted in decrease production of Angiotensin II which causes arterial and venous dilation; causes decrease stimulation and release of aldosterone. Increase bradykinin (vasodilation)

                                                              i.     Benazapril

                                                            ii.     Capropril

                                                          iii.     Enalapril

                                                          iv.     Fosinopril

                                                            v.     Lisinopril

                                                          vi.     Quinapril

                                                        vii.     Ramipril

2.     side effects

                                                              i.     cough, angioedema, NO impotence

                                                            ii.     hyperkalemia

                                                          iii.     decrease renal perfusion in severe renal insufficiency or bilateral renal artery stenosis (decrease blood flow secondary to vasodilation of efferent arteriole in the kidneys)


Angiotensin II receptor antagonists

1.     selectively blocks binding of angiotensin II to AT1 receptor blocks vasoconstriction effect aldosterone secretion arterial and venous dilation.

a.      Losartan

b.     Valsartan

c.      Candesartan

d.     Irbesartan

e.      Telmisartan

2.     side effects: NO cough; and expensive


Direct Acting Vasodilations (reserve for refractory HTN/pregnancy when nothing else is working.

1.     Direct arterial vasodilation reflex Na+ and fluid retention; tachycardia so add diuretic or beta blocker

a.      Minoxidil

b.     Hydrazaline used in pregnancy

2.     side effects

a.      hydralazine causes nausea and vomiting; tachycardia; orhtostais; SLE like.

b.     Minoxidil causes weight gain and trichosis


First line drugs recommended according to effectiveness and cost. Now used as combo drug of short doses and decrease side effects

1.     Beta blockers

2.     Ca++ blockers

3.     Ace inhibitors


Nitroprusside direct arterial > venous dilator;

1.     Parenteral Agents used for

a.      intracranial hemorrhage

b.     aortic dissection

c.      rapidly progressive renal failure

d.     eclampsia

e.      accelearated malignant HTN (papilledema, hematuria, retinal hemorrhages, azotemia, pulmonary edema, mental status changes, seizures, coma)

2.     Side effects

a.      Cyanide poisoning (to prevent this you need to add thiosulfate drip

b.     Increase toxicity in chronic renal insufficient


Nitroglycerin venous > arterial vasodilators

1.     good at dilating the coronary arteries

2.     good to treat

a.      HTN and coronary DZ

b.     HTN and renal/hepatic DZ

c.      HTN and post coronary arterial bypass graft (CABG)


Labetolol 4 times more selective for beta than for alpha; and no effects on lipid

1.     Good for states of adrenergic crisis (hypothyroidism, pheochromocytoma with alpha blocker phentolamine)

2.     side effects and contraindicated

a.      MAO inhibitor toxicity

b.     Clonidine withrawal

c.      Cocaine intoxication

d.     Post CABG


Esmolol cardio selective beta blocker; short acting (10 minutes) therefore put as drip for 24 hours. Used to treat

1.     Aortic dissection

2.     malignant HTN need to add to Nipride or other drug


Nicardipine Ca++ blocker; used in postop HTN


Enalaprilat precursor of ACE inhibitor (drip); used to treat:

1.     increase rennin states

a.      renovascular HTN

b.     scleroderma renal crisis

c.      concomitant use of vasodilation



October 25, 2000


Angina Pectoris: chest discomfort associated with myocardial ischemia when myocardial Oxygen demand is greater than supply. Most common cause is atherosclerosis. It is a retrosternal pain, discomfort, pressure heaviness radiate to neck, jaw, shoulders, arms last about 2-5 min. precipated with exertion; relieved with rest;

How to Dx angina:

1. Signs and symptoms: dyspnea, diaphoresis, N/V, palpitations, lightheadedness. Typical story and heart risk factors = 90% probability

2.     ECG

a.      Q wave is greater thatn 40 sec = old MI

b.     ST segment elevated of depressed = ischemia

c.      T wave inversion

3.     Stress test

a.      Plain

b.     With thallium

c.      With echocardiography

d.     If unable to exercise, use pharmacologic test (Dipyridamole, adenosine, dobutamine)

e.      Echo or multigated acquisition (MUGA) scan

4.     Coronary anigography > 70% narrowing

Treatment: first behavior change then use nitroglycerin

1. Nitroglycerine increase venous capacitance; decrease ventricular volume or pressure; improve subendocardial perfusion and coronary vasodilation; increase collateral flow; decrease afterload.

a.      Side effects: headache and hypotension; if needs 3 within 15 minutes then go to the E.R


2. Long acting nitrate (12 hrs nitrate free period to prevent tolerance; take off at night and put back in the morning.

e.      Isosorbide dinitrate

f.       Isosorbide mononitrate

3.     Beta adrenergic antagonists

a.      Decrease frequency of episodes

b.     Increase exercise threshold for angina

c.      Decrease mortality after MI statistically pre-MI


4.     Beta-one selective (matoprolol/atenolol/andolol) Aim for HR between 50-60/min at rest and 90-100/min during exercise

a.      Decrease bronchospasm

b.     Decrease exacerbation peripheral vascular DZ

c.      Atenolol and nadolol are water soluble so they cant penetrate to CNS; less CNS side effects

d.     Contraindications:

a.      Active CHF

b.     AV nodal block

c.      Severe PVD (peripheral vascular DZ(

d.     Resting bradycardia

e.      Taper over 2 wks when stopping

f.       Side effects

a.      Bronchospasm, hypotension, claudication;

b.     Impotence; nightmare; hallucination

c.      Masking of hypoglycemia so be careful in diabetes


5.     Calcium channels antagonists (good for coronary vasospasm)

a.      Treat Prinzmetals angina

b.     Intolerance to Beta-blockers; nitrates (if not working)

c.      Negative inotropic

a.      Papveine: Verapamil (very powerful negative inotropic)

1.     arterio vasodilator

2.     decrease AV node conduction

3.     treat supraventricular tachyarrythmia

4.     Side effects

a.      Bradycardia

b.     Advanced AV block

c.      Increase digoxin levels

d.     Might increase mortality

b.     Benzothiazine: Diltiazem (intermediate)

1.     arteriolar vasodilation

2.     decrease AV nodular conduction

3.     increase mortality with left ventricular dysfunction and reentry M.I

c.      Dihydropyridines: nifedepine, amlodipine, felodopine, isradapine, nisardipine (least powerful)

1.     potent coronary and peripheral vasodilator hypotension and increase HR

6.     Aspirin

a.      Decrease mortality secondary to platelet inhibition

b.     Decrease thromboxane A2 (vasoconstriction)

c.      Ticlodipine, clopidogril, abcoximab are better than ASA but more costly


7.     CABG (coronary artery bypass graft)

p    Shown to be better than medical therapy if you have triple vessel DZ particularly if LV dysfunction or easily inducible ischemia.

p    Use internal mammary artery for bypass 90% patency of 10 years

p    Saphenous vein 40% patency in 10 years

p    Operative mortality 1-3%

p    Perioperative mortality MI 5-10%


8.     PTCA (percutaneous transthoracic coronary angioplasty)

p    90% successful dilation

p    30-50% restenosis in 1st 3-6 months

p    Mortality <1%

p    Nonfatal MI <5%

p    Emergency CABG 3-5%

p    Needs ASA pre procedure; heparin post procedure; Ca++ channel blockers decreases vasospasm


9.     Stents decrease restenosis; decrease arterial rupture


UNSTABLE ANGINA emergency, this is the preinfarction syndrome; if dont do anything then will infarct

p    Defined as: new onset; at rest; with minimal exertion; crescendo pattern

p    Caused by secondary to rupture or fissuring of atherosclerotic plaque thrombosis formationplatelet aggregation increase vasomotor tone

p    Rx: hospitalization; bed rest; sedation; correct precipitating conditions (HTN, anemia, hypoxemia)

p    Pharmaco Rx:

o      IV nitroglycerine

o      Beta blocker or Ca++ blocker (verapamil or diltiazem)

o      Morphine sulfate if pain continues (need to get rid of pain)

o      IV heparin decrease MI

o      ASA 325 QD will decrease mortality and decrease non fatal MI; if allergic to ASA then use ticlodipine

o      Intro aortic balloon counterpulsation if refractory to Rx CABG/PTCA



p    Chest pain at rest with ST segment elevation on EKG secondary to coronary vasospasm after evolution to MI with fixed atherosclerotic lesion or normal coronary artery; rarely progresses to MI; thought to cause MI with cocaine/amphetamines

p    Dx is transient ST segment elevation on EKG = coronary vasospasm

p    Rx: nitroglycerine S/L; nifedipine



p    Transmural MI = occlusive thrombosis nidus = ruptured atherosclerotic plaque which had undergone liquefactive necrosis erodes rupture into blood stream clot

p    Mortality greatest in the first 2 hours

p    Prognosis at least 2

o      History prolonged chest pain (20-30minutes)

o      EKG changes (ischemic or necrosis)

       Convex ST segment elevation with peaked increase or decrease T wave = myocardial injury (tombstone MI)

       ST segment depression = non Q wave MI = increase risk recurrent MI

       Q waves = MI; prolonged ischemia; myocarditis

o      Increase cardiac enzymes

       CPK-MB increases with in 4-6 hours then peaked at 12-20 hours; comes to baseline in 36-48 hours (admission)

       Increase CPK = myocardial cell death almost always

       Increase CPK with no heart attack can be found in CRF, hypothyroidism, polymyositis, deamatomyositis

       LDH detectable in 12 hours; peak 24-48 hours; elevated 10 to 14 days; good if presenting after 24 hours

       Toponin-1 -- increases within 3 hours and perists 5 days

o      Non invasive cardiac imaging

       Technetiumgood to detect once cardiac enzymes disappear; optimal 2-3 days after MI; 90% sensitive for large transmural infart (increase uptake in area of infarct)

       Radioactive ventriculographyassess cardiac output and regional wall motion abnormalities

       EchocardiogramDoppler flow images cardiac structure; pericardium and ascending aorta

p    Rx: since MI evolves over several hours, early restoration of perfusion (thrombolysis or PTCA) will decrease infarct size and preserve LV function.





Goal to treat MI

       Relieve ischemic pain

       Control of pain decrease O2 consumption and decrease catecholamines

       Give nitroglycerine; if pain persists give morphine

       If nitroglycerine cause hypotension, put them in Trendelenberg position or/and IV saline

       If bradycardia give atropine to increase the heart rate

       Morphine sulfate induces venodilation therefore decrease pre-load this will decrease preload

       Morphine also causes modest arteriolar vasodilation and bradycardia

       If bradycardia use meperidine or give atropine

       Recognize and treat life-threatening complication (hypotension, pulmonary edema, ventricular arrythmia)

       Give supplemental O2

       The theory is to increase arterial oxygen so that the heart get more

       If respiratory distress use face mask

       If severe respiratory distress intubation respiratory

       Try to maintain HBO2 saturation by 90%

       Thrombosis if no contraindication

       The earlier the better because it increases survival

       Streptokinase or anistrplasesystemicly converts plasminogen to plasmin then plasmin will breakdown fibrin

       Tissue plaminogen activator (TPA)locally binds to fibrinogen in clot therefore converting plasminogen to plasmin

       No allergic reaction

       More expensive, but save more lives

       Complication of thrombosis


       Hematoma at vascular access

       Need to do transfusion of frozen plasma to reverse the bleeding

       If bleeding times increases, do platelets transfusion

       Adjuvant therapy

       IV heparin- started with thrombolysis and continue until 3-5 days

       ASA (decrease mortality with streptokinase)

       Beta-blocker decrease nonfatal reinfarction and decrease recurrent ischemia with and without TPA

       Lidocaine for life-threatening arrythmias (class II and class III anti-arrythmias will increase MI mortality); amiodarones decrease mortality


MI with ischemia

       Need coronary angiogram to decrease infarct size

       Beta blocker to decrease myocardial Oxygen consumption by decrease HR and decrease contractility and decrease blood pressure

       Metoprolol, propanolol, esmolol, atenolol, timolol, etc.


       HR is less than 60/min

       Sytolic BP < 90mmHg

       AV block

       1st >0.24 sec; second or third degree block



       CHF on CxR

       Nitroglycerine IV

       Give if CHF or recurrent ischemia with MI; did not decrease mortality

       Ca++ channel blockers

       Little indicative for use during MI

       Nifedipine increase mortality and reinfarction

       Verapamil no benefit during MI; decrease mortality and reinfarction if start 1 week after MI

       Diltiazem no benefit during MI; increase mortality with ejection fraction less than 40% or CHF; however, with Q wave infarction you will decrease recurrent infarction

       Anticoagulants /antiplatelets treatment

       Heparin IV or high dose subcutaneous will decrease mortality with or without thrombolysis will decrease mural thrombi

       Increase risk of bleeding so becareful; risk of recurrent MI

       Warfarin mural thrombus or extensive anterior MI with apical involvement use 3-6 months

       ASA if no contraindications

       Additional Rx:

       No prophylactic lidocaine

       IV magnesium

       Dilates coronary artery

       Decrease platelet aggregation

       Decrease arrhythmias

       Protects against re-perfusion injury by blocking intra-cellular Ca++ accumulation; no decrease in mortality

       Use when you have hypokalemia, hypocalcemia, arrhythmia, patients on diuretics without Mg++ supplements


       AV block


       Severe heart failure

       ACE ihibitors

       Decrease mortality if used in the first 24 hours

       Have the greastest benefits in patients with


       Ant. MI

       Previous MI


       Decrease cholinergic, decrease salt, no caffeine or very hot/cold foods after first day; liquid or soft food first day

       Stool softeners/laxatives

       Complication of MI


       Pump failure



       Look for precipitating causes (drugs, hypoxemia, acidosis, electrolyte abnormality (K+, Ca++, Mg++)

       Recurrent ischemia


       Any sustained arrhythmias causing compromise: hypotension, angina, CHF Tx by synchronized electrical cardioversion

       Ventricular arrhythmias

       PVC (premature ventricular contraction)

       Multifocal treat with lidocaine if ineffective then use procaimide

       Ventricular fibrillation

       Immediate cardioversion or defibrillation

       Accelerated idioventricular rhythm (AIVR) = wide complex escape

       Rhythm (10-110/min)

       Frequent in patients with coronary reperfusion

       Usually benign lasts < 48 hours therefore close observation

       If associated with hemodynamic deterioration or pecipitates VT or VF treat them with atropine or overdrive pacing

       Supraventricular tachycardias or sinus tachycardia very common

       Look for and treat the cause (pain, anxiety, fever, hypovolemia, side effects of drugs, hypoxiemia)

       Paroxysmal supraventricular tachycardia (PSVT)

       If stable vacotonic maneuvers, carotid massage, valsava maneuver;

       If no response then give adenosine, diltiazem, verapamil, digoxin

       If compromise then give synchronized cardioversion (hypotension, angina, CHF)

       Atrial flutter (regular saw tooth pattern; atrial rate 280-350/min; decrease ventricular response may convert to atrial fibrillation)

       If compromised- synchromized cardioversion

       If digoxin intoxication --> rapid pacing

       If stable use diltiazem, verapamil, propanolol, digoxin

       If no response --> cardioversion

       Atrial fibrillation

       If hemodynamic compromise then do cardioversion

       If < 100 beats/min (with drugs that decrease AV node conduction) then treat with a pacemaker and cardioversion

       If stable then give them the same treatment as trial flutter





       Accelerated junctional rhythm

       Usually benign escape rhythm secondary bradycardia

       No treatment necessary

       If cardiogenic shock or digitalis toxicity or non paroxysmal junctional then treat the cause


       Sinus bradycardia (<60/min)

       Usually with MI

       If hypotension and decrease cardiac output then treat them with temporary transvenous pacing or atropine

       AV conduction disturbances

       First, second, or third degree blocks

       First degree heart block

       PR interval is greater than 20 seconds

       Dont use verapamil, diltiazem, beta blockers nor digoxin

       If symptomatic just decrease the electrolytes and withdraw drugs

       Second degree heart block

       Morbitz type I (gradual prolongation of PR interval with narrow QRS complex before nonconducted P wave)

       If asymptomatic then no treatment

       If symptomatic bradycardia then temporary transvenous pacing or atropine

       Mobitz type II (dropped beats with wide QRS

       Pacemaker insertion even if asymptomatic

       May progress to complete heart block (third degree heart block)

       Third degree heart block (complete heart block)

       AV dissociation (slow ventricular response)

       Usually associated with large anterior MI and increase mortality or inferior MI with RV infarction\

       May develop abruptly- preceded by any blocks including first degree block

       Treatment: Emergency tranvenous pacing to prevent progression to asystole




o      Sinus bradycardia

       Increase vagal tone

       Anti-arrhythmia drugs

       Myocardial ischemia

       Primary sinus node DZ (sick sinus syndrome)

       If asymptomatic then no treatment

       If symptomatic then treat with

       IV atropine

       Transcutaneous pacemaker




o      First degree AV blocks

       Delay of impulse in AV node

       PR interval is greater than 20 sec

       Increase vagal tone

       Anti-arrhythmic drugs

       Electrolyte abnormality (increase Ca++, K+, Mg++)

       If asymptomatic then no treatment

       If symptomatic then correct the causes and treat them the same as sinus bradycardia

o      Second degree block same atrial beats but not conducted to the ventricle

       Mobitz type I (Wenckebach)

       Progressive prolonged of PR interval till dropped beat

       Causes same as first degree block and inferior wall MI

       If symptomatic then treat them the same as sinus bradycardia

       Mobitz type II

       2:1 , 3:1

       site of block = bundle of His

       causes: conduction systemic DZ, anti-arrhythmics drugs, increase vagal tone, anterior wall MI

       often precedes transient complete heart block



o      Supraventricular (long QRS complex)

o      Ventricular



November 1, 2000


Third degree block (complete)

p    Dissociated atrial P-wave and ventricular QRS contractions

p    Can be acquired by

o      Drug toxicity

o      MI and scarring

o      Degeneration process

o      Infiltrative diseases: amyloidosis, sarcoidosis

o      Infective causes: lymes disease and chagas disease

p    Symptomatica bradycardia; some as sinus bradycardia


Premature contraction

p    After no structural change

p    Can be caused by increased catecholamines

o      Excessive EtOH, caffeine, cigarettes (Saturday night heart syndrome)

o      Electrolytes imbalance

o      Ischemic

p    Generally they are benign lesions

p    Treat the cause and if they are still bothered by it then give BETA-BLOCKERS or Ca++ channel blockers


Premature junctional complexes

p    Usually benign

p    Usually absence of structural heart DZ

p    No treatment


Premature ventricular contractive (PVC)

p    Most often no structural heart DZ

p    Bizarre morphorlogy (contraction origninated in ventricles; larger QRS; wider QRS)

p    QRS is usually prolonged (greater than 20 msec)

p    T wave will go in opposite direction and polarity

p    Treat the causes

p    Sometimes you have different forms of bizarre QRS

p    If premature complex comes from T wave, it is more dangerous

p    Treat the symptomatic: lidocaine is the drug of choice; mexilatine, amirodorone, sotalol are also good. Remember these drugs can cause arrhythmia.



p    Sinus tachycardia coming from normal sinus node (100-160/min)

p    Anything that decrease vagal tone can cause it

o      Pain

o      Hypovolemia

o      Pulmonary embolism

o      Fever

o      Heart failure

p    Treat the causes first then treat with drugs

o      If ischemic give beta blockers

o      If dehydrated give fluid

p    Usually normal QRS complex

p    Could look like an abnormal QRS complex


Atrial tachycardia

p    If second degree block with it then suspect digitalis toxicity

p    Multifocal atrial tachycardia

o      Usually 130-200/min

o      Usually see P wave

o      Remember if P wave look the same it is from a single focus, if not it is multiple focuses

o      QRS could be normal or aberrant

o      Usually seen in patient with COPD (theophylline potentiate this) or HF

o      Treatment:

       Oxygen, agonist, steroids

       If they have digitalis toxicity then decrease the digitalis

       Make sure K+ is normal; maintain K+ level

       If refractory and symptomatic use:

       Beta blockers

       Ca+ channel blockers

       Digitalis (if not caused by digitalis)

       Oblation (surgical or radiofrequency)


AV junctional tachycardia

p    60-130/min

p    because from junction it is slower

p    caused by

o      MI

o      Myocarditis

o      Decrease catecolamine

o      Digitalis toxicity

p    Treatment:

o      Always find out what is the cause and treat it

o      Usually goes away by itself

o      Can use propanol or lidocaine

o      If not getting better can use an atrial overdrive (pacemaker)


AV nodal reentrent tachycardia

p    Also called PSVT (paroxysmal supraventricular tachycardia)

p    Born with accessory pathway

p    2 pathways (fast and slow)

p    Woffian Parkinson Syndrome can cause this

p    Typically 150-250/min and the onset is abrupt

p    Triggered by premature atrial contraction

p    P wave is hard to see

p    Atypical (inverted P wave in T wave)

p    It comes down the accessory pathway

p    Initiated by a PVC that has a long RP interval

p    Usually narrow complex tachycardia

p    Atrial, ventricular activation syndromes

p    Treatment

o      Try to break them by vagal maneuver (carotid massage, valsva maneuver

o      If vagal maneuver does not work then use adenosine IV, or verapamil, or diltiazem

o      Chronic treatment: use Ca++ channel blockers, or beta blockers, or digitoxin, or radiofrequency to delete the slow pathway


Wolf-Parkinson White Syndrome

p    Short PR interval and delta wave (QRS goes up very early)

p    If used accessory as retrograde pathway (QRS during tachycardia is normal)

p    Treatment:

o      Class IA

p    Quinidine

p    Procainimide

p    Disopyramide

o      Class IC

p    Flecanide

o      Class II

p    Propanolol

o      Class III

p    Aminodone

p    Soltalol

p    Bretyllium

o      Do not give them drugs that block AV node (beta blockers, Ca++ channel blockers, digitalis) because if you block the AV node it will force the conduction down the accessory pathway and it can cause ventricular fibrillation or ventricular tachycardia.


Atrial Fibrillation QRS irregularly irregular

p    No P waves

p    Anything that increase atrial size (atrial hypertrophy) will cause atrial fibrillation; i.e pulmonary embolism; heart failure; hypertension, acute alcohol ingestion; theophylline or stimulants; hyperthyroidism or hypothyroidism; pheochromocytoma (increase catecolamine); MI; pericarditis.

p    Treatment

       Cardioversion for any responses such as increase CHF, decrease BP; ischemia

       Beta blockers; Ca++ channel blockers; digoxin; dofelidede if the patient is stable and you want to prevent conduction from the atrial to the ventricle which can cause ventricular tachycardia.

       They need to be on anticoagulant if they have chronic atrial fibrillation. (this prevents embolisms and strokes)

o      Heparin or warfarin

o      Aspirin if they cant handle heparin or warfarin


Atrial flutter

p    Causes of atrial flutter:

       Sometimes patient come in with atrial fibrillation and it can turn into atrial flutter;

       Drug therapy for atrial fibrillation

       Prior atrial surgery

       Prior atrial fibrillation

p    Dx :

       Regular undulation (saw tooth pattern)

       250 350/ min

p    Rx:

       Same as atrial fibrillation

       Debated if we should give anticoagulants

       The goal is to restore back to regular sinus rhythm


Ventricular tachycardia

p    Dx:

       100-250 /min

       usually have abnormal heart such as

o      coronary artery disease (most common) with infarcts

o      cardiomyopathy

o      infiltrative diseases (sarcoidosis, amyloidosis)

o      infections

       Greater than 3 beats in a row = ventricular tachycardia originating in the ventricle

       Wide QRS and bizarre morphology

       T wave plarity (opposite direction) and QRS deflection

p    Rx:

       If unstable then do cardioversion

       If stable then give lidocaine, procainamide, or berytellium


Ventricular fibrillation

p    250-400 per minutes

p    Ventricular fibrillation is an emergency and must do cardiovesion immediately. If unsuccessful, give epinephrine and lidocaine.

p    If someone has primary deep fibrillation and dont have MI then these patient will have recurrences so you need to give amiradarone or automatic defibrillator

p    If in first 72 hours after MI then there is no recurrence



























p    Recurrent episodes of circulatary inflammation (edema and mucous production)

p    Increase responsiveness of bronchioles constriction

p    No or only mild progression to chronic obstructive disease

p    Symptoms: dyspnea, wheezing, cough usually dry or small amounts of sputum unless bacterial; chest tightness

p    Dx:

       PFT (pulmonary function test): decrease FEV (forced expiratory volume); decrease FVC (forced vital capacity)

       Methacoline challenge will produce bronchospasm then will bronchodilate with brochodilators (terbutaline, acebuterol..)

       If the patient has asthma then ask:

o      How long or how much corticorsteroid have they been taken.

o      Frequent of hospitalization

o      Intubation previously

o      Frequent of thinitis

       Assess severity (in emergency situations)

o      Respiratory distress

o      Difficulty of speaking sentences

o      Diaphoresis

o      Using accessory muscles

o      Respiratory rate: the higher the more severe (greater than 22/min is severe)

o      HR greater than 120/min is severe

o      Pulsus paradoxicus is severe (greater than 12 mmHg)

o      Patient can usually recognize severity

o      If you gave them medicine for their asthma in the ER but they come back again then admit them.

o      Spirometry (done in ER) if FEV is less than 30% of predicted or less than 40% of predicted then treat them vigorously for 1 hour and admit them.

o      Peak flow less than 10 liters/min or less than 50% improvement after treating them for 1 hour then admit them

o      ABG (arterial blood gases): Oxygen of less than 60 mmHg or PaCO2 normal or increase impending respiratory failure (should be intubated)

p    Rx:

       Acute attacks:

o      Epinephrine (sub Q) quick response

o      Rebulizer with beta agonist (albuterol and meproterol)

o      IV fluids

o      IV steroids (methylpredisone for 36-48 hours)

o      Put them on oxygen

o      Amirophylline IV

       Improves mucocillary clearance


       Increase ventillatory drive

       Increase diaphragmatic constraction

o      If refractory use

       ipratropium (inhaled)

       IV Mg++ and bronchodilators (acebulterols, terbutaline)

       Leukotrienes inhibitors (drug of choice for exercise/allergy induced asthma



       Chronic attacks:

o      Step I: mild asthma (2 attacks or less per week)

       use bronchodilators (albuterols)

       If precipated by exercise use terbulterol, or liloterol, pirobutol, cromolyn Na+, or leukotriene inhaler.

o      Step II: mild persistence asthma (attack 3-6 attacks per week during day time or 3-4 attacks per month at night)

       Use low dose inhaled steroids, or inhaled cromolyn Na+, or theophylline or leukotiene inhibitors.

o      Step III: moderate persistence (have attacks everyday or more than 5 attacks per month at night, or peak expiratory flow 60-80%)

       Use medium dose inhaled steroids

       Salneterol (long acting beta 2 agonist) and theophylline use for acute attack.

o      Step IV: severe persistence (frequent at night)

       Use high dose of inhaled steroids and salneterol, theophylline and beta two agonist.

       Steroids: methotrexone



November 2, 2000


COPD (chronic dyspnea with respiratory air flow obstruction; exacerbation by increase airway inflammation, bronchospasm, mucus plugging, fibrosis of small airways)

p    Emphysema

       Alpha one antitrypsin deficiency in patient younger than 50 yrs/old and/or nonsmoker; worse in lower lobes bullae and blebs in lung

p    Chronic bronchitis

       Chronic productive cough for 3 months in 2 consecutive years.

p    Dx:

       Chest X-Ray low flat diaphragm; hyperlucent lung field with decrease vascular markings worse in upper lobes.

       P.E: tachypnea; pursed lip breathing (trying to get air out); use of accessory muscles; barrel chest (hyperresonant to percussion); decrease breath sounds and sometimes wheezing; mid inspiratory crackles.

       PFT decrease respiratory airflow (decrease FEV1; decrease FEV; decrease FVC)

       Increase total lung capacity (TLC) and residual volume (RV) and functional residual capacity (FRC)

       Decrease diffusion capacity of CO (DLCO)

       Arterial blood gases (ABG) increase P(A-a) (oxygen gradient ) because secondary perfusion to poorly ventilated areas of lung decrease PaO2 . (arterial oxygen pressure)

       Increase in PaCO2 will cause an increase in serum bicarbonate to compensate for the respiratory acidosis so the arterial pH is near normal.

p    Complications:

       Cor pulmonale

o      Parasternal heave (feeling heart beat)

o      Increase P2 (pulmonary valves closing = S2)

o      Pasrsternal s4 s3

o      Murmur of tricuspid regurgitation

o      Pulsative liver

o      Peripheral edema

o      CXR: low flat diaphragms

p    Rx:

       Acute exacerbation vs. long term management

       Look for cause and remove it:

o      Infection (most common)

o      Pulmonary embolism

o      Pulmonary edema

o      Pneumothorax


o      Maintain PaO2 at least 55-60 (88-90% oxyhemoglobin staturation)

1.     Low flow O2 (nasal cannula) 1-3L/min or 24-33% O2 via ventricular mask. Remember to intubate to prevent acute respiratory failure

2.     Inhaled beta-two agonist = mainstay of treatment: albulterol, metaproterenol; terbutaline; bitolterol

3.     Anticholinergic agents = ipatropium bromide inhaler = efficacious with bronchodilation. Benefit with combining the 2 longer duration of action and less toxicity.

4.     Glucocorticoids = methylprednisolone IV prednisone

a.      You must taper off to prevent cushing syndrome

5.     theophylline individualize because of the narrow therapeutic index which can cause big time toxicity

6.     antimicrobial therapy TMS/Sulfametroxazole; amoxicillin, doxycillin

7.     Chest physiotherapy if increase secretions (chest percussion, postural drainage)


1.     Stop smoking smoking cessation program; nicotine patch/gum

2.     Bronchodilators inhaled

a.      Anticholinergic ipatropium is the first line of drug for most stable patients or

b.     Beta agonist (terbutaline, acebuterol..)

                                                                                                         i.     May cause rebound bronchoconstriction and decrease pulmonary function

                                                                                                       ii.     Tachyphylaxis (tolerance to the drug so it stops working)

c.      Oral theophylline may help those with increase symptoms and decrease pulmonary function at night and early morning

3.     Glucocorticcoids - minority respond; follow PFT if improved in 2-3 weeks then continue

4.     Oxygen - improve survival and quality of life if PaO2 is less than 55 mmHg or saturation is less than 88%

a.      PaO2 is between 55 and 59 mmHg and cor pulmonale or secondary polycythemia then can get O2 at home

b.     If cor pulmonale then optimize bronchodilators, O2 and digoxin with LV-HF; if hematocrit is greater than 50% then do phlebotomy

5.     Pulmonary rehab exercise, training, proper nutritional

6.     Flu and pneumoccocal vaccines

7.     Psychoactive drugs with decrease respiratory drive use buspirone for anxiety; doxepin for depression (mild broncho dilator)

8.     lung transplant if remove everything is more functional





Hypercapnea (increase CO2)



PaCO2 is greater than 45-55 mmHg and respiratory acidosis

PaCO2 is less than 60 mmHg or SaO2 is less than 90%


1.     Increase CO2 production

2.     Increase dead space

3.     Decrease minute ventilation

4.     Increase CO2 production

-        Fever

-        Sepsis

-        Seizures

5.     Increase dead space areas of lung are ventilated but NOT perfused (i.e intrinsic lung DZ, scoliosis)

6.     Decrease minute ventilation (i.e CNS disorders such as ALS, Guillain Barre, muscular dystrophy, drug OD, metabolic disorders)

7.     Normal gradient

1.     Shunt

2.     V/Q (ventilation/perfusion) mismatch

-        Airflow obstruction (COPD)

-        Interstitial inflammatory pneumonia

-        Vascular obstruction

3.     Decrease inspired O2

4.     Hypoventilation

5.     Diffusion impairment

6.     Decrease mixed-venous oxygenation

7.     Shunt fraction of mixed venous blood

8.     Systemic arterial circulation, bypassing functioning gas exchange lung units

9.     Increase P(A-a) O2 gradient

10.  Hypoventilation (increase PCO2 decrease O2)

11.  Diffusion impairrment responds to O2

12.  Low mixed venous oxygenation



Treat the cause

O2 respiratory as a last resort

Treat the cause

O2 respiratory as a last resort





1.     Majority secondary to DVT in ileofemoral veins pelvic venous plexus (after surgical or gynecologic complications)

2.     Signs and Symptoms

a.      Dyspnea, tachypnea

b.     Pleuritic chest pain (deep breath it hurts)

c.      Increase anxiety

d.     Cough

e.      Hemoptysis

f.       Tachycardia decrease BP death

g.      Increase P2 (S2) of second heart sound

h.      Inspiration crackles

3.     Diagnosis

a.      ABG (PaO2 < 80 mmHg; P(A-a)O2 gradient

b.     ECG serious tachycardia (atrial fibrillation; atrial flutter)

c.      Chest X-Ray: subsegmental atelectasis, small pleural effusion area of hyperlucency in lung fields

d.     V/Q scan (ventilation/perfusion) mismatch

e.      Doppler blood flow imaging

f.       MRA (magnetic resonance angiogram)

g.      Spiral (T scan)

h.      Pulmonary angiogram for equivocal or contradictory results

4.     Treatment

a.      IV heparin or low molecular weight with warfarin

b.     Saline norepinephrine/dapamine for decrease BP

c.      Thrombolysis or surgical intervention unstable patients

d.     Inferior vena caval interruptions (umbrella)

                                             i.     When anticoagulants are contraindicated when active bleeding; post op, neurosurgical patient; severe diastolic HTN

                                           ii.     Recurrent emboli on adequate anticoagulation

                                         iii.     Massive P.E with hemodynamic compromise

                                          iv.     Cardial pulmonary diseases (decrease survival with recurrent event)

                                            v.     Pulmonary embolectomy

                                          vi.     Paradoxical emboli with PFO (patent foramen ovale)

                                        vii.     Septic P.E from legs/pelvis veins

e.      Pulmonary embolectomy

                                             i.     If patient remains in shock after thrombolytic treatment and supportive care

                                           ii.     If thrombolysis are contraindicated

                                         iii.     Complications post phlebitis syndrome (has swollen leg) and pulmonary HTN




1.     Decrease level of consciousness (coma, seizures, intubation)

2.     Impaired pharyngeal/laryngeal function (myopathy, after intubation)

3.     Increase gastric pressure/volume (N/V, ileus, tube feeding)

4.     Esophageal disorders reflux


Aspiration of gastric contents

1.     Aspiration of inert liquids or foreign body acute respiratory distress, hypoxia

a.      Examples: pulmonary infiltrate; atelectasis; lobar collapse

b.     RX: early bronchospasm to remove foreign body

2.     Chemical pmeumonitis

a.      pH < 2.5 or increase volume of gastric fluid

b.     cough, dyspnea, wheezing, tachypnea, decrease BP, fever, rales

c.      increase P(A-a)O2 gradient

d.     pulmonary infiltrates

e.      RX: antibiotics only if evidence of bacterial infection or intestinal obstruction, immunocompromised, severe gingival/periodontal DZ.

3.     Aspiration pneumonia 2-5 days after event with anaerobes and aerobes

a.      RX: penicillin or clindamycin; if hospitalized then give piperacillin/tazobactam

                                             i.     Gram negative and staph use ampicillin/sulfbactam


November 8, 2000



1.     Aspiration (most common cause is anarobes)

a.      Extensive gingival/dental disease)

b.     Symptoms insidious fever, weight loss, foul smelling sputums

c.      Need to rule out

                                             i.     Chronic bronchitis

                                           ii.     Fungus

                                         iii.     Carcinoid

                                          iv.     Vasculitis

                                            v.     Septic emboli

                                          vi.     Pulmonary emboli and infection

d.     Diagnosis

                                             i.     Sputum cultures

                                           ii.     CT scan

                                         iii.     Bronchoscopy definite disease

e.      Treatment

                                             i.     Postural drainage

                                           ii.     Pipercarcilline/tazobactam or ampicilline/sulfbactam until culture return

                                         iii.     Surgical resection percutaneus

1.     Drainage if not resolving

2.     Persistent fevers, increase WBC, emphysema; persistent hemoptysis; increase cavity

3.     Ventilation depression




Peptic ulcer disease

1.     Ulceration is in gastroduodenal mucosa extending via the muscularis mucosa

2.     Common 5-10% of the population

3.     Helicobacter pylori causes 90% of duodenal ulcer

4.     NSAIDS causes 70-80% of gastric ulcer

Gastric ulcers

1.     5% malignant gastroscopy with biopsy to diagnose

2.     repeat gastroscopy of upper GI after 6-8 weeks after treatment

3.     if no change in size rebiopsy

4.     if smaller then continue treatment for 6 more weeks repeat test

5.     if not healing then do surgery


Duodenal ulcer

1.     Almost never malignant

2.     Helicobacter pylori serologic testing

3.     Rapid urease test (H. pylori produces ureases); culture or histological analysis after endoscopy

4.     Treatment: decrease acid secretion and eradicate H. pylori

a.      To eradicate H. pylori use multiple regime

                                             i.     TCN with metronizadole and peptolormol

                                           ii.     Omeprazole with amoxicillin, and clarithmycin

                                         iii.     Ranitidine with metronizadole and amoxicillin

b.     H2 histamine blockers

                                             i.     Ranitidine

                                           ii.     Famotidine

                                         iii.     Nazitadine

                                          iv.     Cimetidine

1.     Do not give cimetidine concomittenly with digoxin, fluroquinolone, phenytoin nor TCN because these drugs cause increase absorption of cimetidine

c.      Proton pump inhibitors

                                             i.     Omeprazole

                                           ii.     Louzaprazole (more powerful)

d.     Sucrafate

                                             i.     Works locally with mucosal surface

                                           ii.     Must have acidic stomach for it to work

e.      Antacids

                                             i.     Aluminum hydroxide cause constipation also binds to phosphate in the intestine thus causes hypophosphatemia because of decrease absorption of phosphate

1.     Cause decrease absorption of TCN, thyroxine, chloropromazine

                                           ii.     Aluminum hydroxide and Magnesium hydroxide causes diarrhea

                                         iii.     Calcium carbonate constipation CaCO3

                                          iv.     Aluminum hydroxide and Magnesium hydroxide and calcium carbonate

                                            v.     Avoid food that causes symptoms

1.     Avoid late evening snacks to avoid acid production at night

2.     Decrease cigarette smoking

3.     Decrease EtOH because EtOH damages gastric mucosa

f.       X-ray abdominal

                                             i.     Dilated stomach with circular fluid level nasogastric tube suction

                                           ii.     Free air under diaphragm then do surgery

                                         iii.     Intractibility surgery; be sure all reversible causes have been eliminated

g.      Complications

                                             i.     GI bleeding

1.     Upper GI bleeding you will see hematemesis, melena

2.     Lower GI bleeding you will see hematochezia

                                           ii.     Gastric outlet obstruction


Upper GI bleeding you will see hematemesis, melena

       Peptic ulcers bleeding are the most common cause of UGI bleeding


o      H2 blockers or proton pump inhibitors

o      When to do surgery:

       If severe bleeding (>5 units /day) or unstable

       If arterial bleeding

       If recurrent bleeding

       If inability to obtain blood

o      Arterial angiography can be used to control massive bleeding in those patients who are considered to be at high surgical risk

o      Arterial vasopressin

o      Arterial embolization

o      Esophageal variceal hemorrhage is a medical emergency associated with 33% mortality

o      Endoscopic therapy (treatment of choice for acute variceal bleeding)

o      Sclerotherapy

o      Pharmacologic therapy

       IV vasopressin with nitroglycerin if there is also coronary artery disease

       IV osteopeptide

       Propanolol and nadolol reduces portal hypertension

o      Balloon tamponade

       Sengstaken Blakemore tube

       Minnesota tube

       Linton tube

o      Endotracheal intubation to prevent asphyxiation

o      Transjugular intrahepatic portosystemic shunt stent placed between hepatico portal veins

o      Liver transplantation is selected in patient with severe portal hypertension and esophageal and gastric variceal hemorrhage

       Mallory-Weiss tear

o      Normal vomitus followed by hematemesis

o      Mucosal tear of gastroesophageal junction

o      Heals spontateously or catherize endoscopically if its still bleeding

       Aortic enteric fistula

o      History of prior aortic graft surgery

o      Consider fistula until proven otherwise

o      Usually aorta duodenal fistula excessive bleeding so neeed immediate endoscopy and surgery to prevent death

       Stress ulcers

o      ICU patients with head injuries, burns, shock, sepsis, respiratory failure, coagulophaty , CNS disease

o      Should give prophylaxic H2 blockers

o      Rx with H2 blockers, proton pump inhibitors, sucrafate, and antacids


o      Recurrent episodes, elderly

o      Renal failure is a predisposing factor

o      Diagnose and treated by endoscopy

o      Rx: Progesterone and estrogen, catherize


Lower GI bleeding you will see hematochezia


o      Recurrent; most common cause of lower GI bleeding

o      Rx: arterial vasopressin; if severe or do not respond to arterial vasopressing then do surgery


o      Occur at the cecum and colon

o      Rx: arterial vasopressin, heater probe, laser therapy or surgical resection


       Inflammatory bowel disease

       Ischemic colitis

       Infectious colitis

o      Diagnosis:

       Rectal exam

       Bleeding scan C technetium 99m-labeled RBC scan; if the scan is negative then the patient should undergo colonoscopy


o      Initial treatment is to maintain adequate circulatory volume

o      Signs of distress



       Clammy or mottled skin


o      Assesses intraventricular volume

       Heart rate

       Blood pressure

       Decrease blood pressure of greater than 10 mmHg and HR of greater than 20 beat / minute moderate blood loss (10-20% of circulatory volumes)

       Severe blood loss (greater than 20% of circulatory volume)

o      Labs:

       CBC, PT, PTT, chemistries

o      RX:

       2 large bags IV of Normal Saline (NS) or Ringers lactate

       Transfusion packed RBCs (increase Hb by 1 gram and increase hematocrit by 3) until hematocrit is equal to or greater than 25%

       If coagulopathy then use fresh frozen plasma (FFP)

       If decrease mental status then intubation, O2



Gastritis (erosion limited to mucosal)

1.     Acute

a.      Critically ill hospitalized patients

                                             i.     Severe trauma

                                           ii.     Hepatic renal failure

                                         iii.     Respiratory failure

                                          iv.     Shock

                                            v.     Massive burns

                                          vi.     Septicemic

b.     Drug induced gastritis

                                             i.     ASA

                                           ii.     NSAIDS

                                         iii.     Ethanol

                                          iv.     Bile acids

                                            v.     Pancreatic enzymes

c.      Prophylactics and treatment with H2 blockers with or without antacids, sucrafates, or proton pump inhibitors.

d.     Remove offending agents and treat them with H2 blockers, antacids, sucrafate or poton pump inhibitors.

e.      If life threatening blood loss

                                             i.     Gastric artery embolization

                                           ii.     Vasopressin

                                         iii.     Vasotomy or pylorotomy

f.       Helicobacter pylori (active chronic gastritis)

                                             i.     Rx: Choose any of the following cocktails

1.     amoxicillin and clarithromycin and lonsaoprazole or ameprazole for 14 days

2.     clarithromycin and metronizadole and lanzoprazole or omeprazole

3.     peptobismol and metronizadole and TCN and lonsaprazole or omeprazole (you can replace the proton pump inhibitors with ranitidine, nizatidine, or famotidine)

2.     Chronic gastritis

a.      Type A is autoimmune (make Ab against parietal cells or intrinsic factor)

b.     Type B is H. pylori and more common than type A

c.      Menetriers disease

                                             i.     Large tortuous gastric mucosal folds can develop ulcers and can turn into carcinoma

                                           ii.     Protein losing gastropathy hypoalbumenic and edema

                                         iii.     Rx:

1.     increase protein diet

2.     H2 blockers

3.     anticholinergics

4.     if severe and persistent total gastroectomy

d.     Gastritis due to corrosive agents

                                             i.     Strong acids (hydrochloric acid , sulfuric acid)

                                           ii.     Strong alkali (sodium hydroxide)

                                         iii.     Rx: dilution with water; if acids then antacids; if alkaline then frequent and early endoscopy and dilute strictures

e.      Prior gastric surgery = alkaline gastritis or bile reflux gastritis

                                             i.     Reflux secondary to Bill Roth II

                                           ii.     Ranges from asymtomatic to severe epigastric distress

                                         iii.     Rx: difficult to treat

1.     cholestyramine

2.     H2 blockers

3.     sucrafate

4.     antacids

5.     pancreatic enzyme replacements


November 9, 2000


Abdominal cramps, N/V, diarrhea, paresthesias, nerve palsies, decrease blood pressure

10% death due to secondary respiratory paralysis

Rx: induce vomiting (IPECAC)

       Gastric lauage



       Cooking does not destroy neurotoxin


Salmonella (chicken, egg) 3 syndromes

1.     Gastroenteritis- incubation period is 8-48 hours

a.      Abdominal pain, N/V, watery diarrhea, fever (100-102 Fahrenheit)

b.     Symptoms subside spontaneously in 2-5 days

c.      Rx: supportive

2.     Enteric fever

a.      Fever, HA, abdominal tenderness, 50% get diarrhea some even get constipation

b.     Rx: antibiotics or can get septic

                                             i.     Ceftriaxone/cefotaxime

                                           ii.     TMP/Sulfa

                                         iii.     Fluroquinolones

                                          iv.     Ampicillin (if sensitive)

3.     Metastatic infection

a.      Osteomyelitis (common in sickle cell dz)

b.     Meningitis

c.      Arterial intravascular plaques

d.     Aneurysm

e.      Rx: same as enteric fever but prolonged for endocarditis/osteomyelitis (6 weeks) and surgery for arterial tension


Vibrio parahemolyticus (raw or improperly cooked shellfish)

       Incubation is 3-76 hours

       N/V, diarrhea, cramps, weakness, HA, fever duration up to 3 days

       Rx: supportive, TCN or TMP/SMX


Viral 30 to 40% of infectious diarrhea in the US

       Rotavirus severe watery diarrhea in kids

       Enteric adenovirus in children less than 1 year old

       Norwalk virus cramps, cruises, schools, nursing homes, hospital wards

       Rx: supportive




Nephrolithiasis (stones)


       Flank pain (groin)

       Oliguria/ARF if both collecting systems blocked

       Dx: U/A blood/crystals;

       abdominal flat plate (uric acid lucent cystine; all other stones are opaque)

       urine culture

       strain urine send stone for analysis

       24 hours urine Ca++, PO4, urate, Na+, cystine, urea, creatinine, oxylate, citrate

       Rx: icrease IV fluids

       Demoral (meperidine) for pain

       Lithotripsy fragment stone with radio waves

       Removal (basket) or surgery

       Specific treatments depending on type of stone

       Ca++ stones (compose 80% of all stones)


       Increase calciuria greater than 4 mg/Kg/day on normal diet (800-1000 mg/day Ca++)

       Increase GI absorption of Ca++

       Decrease renal tubular Ca++ reabsorption

       Increase skeletal resorption (increase PTH)

       Treatments: D

       Decrease Ca++ intake 800mg/day

       Decrease protein 1g/kg/day (protein increase Ca++ in uric acid and increase oxalate excretion and decrease pH)

       Increase fluid intake

       Decrease Na++ < 6g/day (Na++ inhibits reasbsorption of Ca++)

       Hydrochlorothiazide (increase Ca++ reabsorption) rebound after 2 yrs

       If hyperparathyroidism surgery

       If hyperoxaluria (inflammatory bowel DZ, distal RTA (renal tubular acidosis), medullary sponge kidney, sarcoidosis) >0.7 mg/kg/day

       Decrease oxalate

       Give Calcium phosphate


       If hypocitraturia K+ citrate

       Uric Acid stones: greater than 11 mg/kg/day

       Maintain U/O greater tha 2L/day

       Alkalinize urine pH 6.5-7 with Shohls solution (citric acid and crystalline sodium citrate)


       Cystine stone: inborn error of amino acid transport

       Maintain U/O of greater than 32/day

       Alkalinize the urine pH to greater than 7 with Shohls solution


       Struvite stones staghorn calculi (caused by chronic inflammation)

       Cause by urea splitting organisms (Proteus mirabalis)

       Rx: treat the infection and remove stones


Acute Renal Failure (ARF) sudden decline in ability of the kidney to maintain homeostasis --> failure to clear waste and electrolytes, acid/base and volume disturbances


o      Functional oliguric (U/O < 500 cc/day); nonloguric (U/O > 500 cc/day therefore easier to take care of)

o      Ethiological





o      P.E distended bladder foley catheter

o      Ultra sound dilated kidneys, ureters

o      Renal scan

o      Urine and serum of creatinin/Na+

o      Urine osmolatity

o      Electrolytes, BUN, creatinine



U/A creatinine

Urine Na+

FE Na+

Urine osmolality


> 40




Oliguric ATN






Prerenal azotemia decrease effective blood volume such as dehydration, CHF

       If poor cardiac function CVP or swan gang catheter

       Fluid challenge 500-1000 cc over 30-60 minutes

o      If no response IV lasix (to force urine down) with metalazone or 20% mannitol 10-29ml/hr

       If you still have no response in 6-12 hours (no urine) then use dopamine (<3 microgram/kg/min)

       If still no response --> D/C


Obstructive nephropathy

       Upper or lower obstruction

       Lower bladder catherization --> diagnosis and treatment after relief of obstruction --> increase diuresis

       If increase U/O then replace fluids/electrolytes (usually 0.45% IV fluid)

       Mesure daily weights, U/O, serum/urine electrolytes


Intrinsic Renal Failure injuries to renal blood vessels, glomeruli, tubules, or interstitium

       Radiocontrast nephropathy

o      Risk factors:

       Diabetes mellitus

       Chronic renal insufficiency (CRI)

       Multiple myeloma


       Older than 65 y/o

o      Usually oliguric, serum creatinine peaks 72 hours rsolves 7-14 days

o      Prevention volume expansion for 24 hours post study

       If normal heart function mannitol 25 gram in 1 Liter of 0.45% saline

       Replace U/O for 24 hours

       Aminoglycoside nephrotoxicity

o      Directly toxic to tubules --> non oliguric

o      Prediposing factors

       Large doses

       Prolonged exposure

       Advanced age

       Volume depletion

       Liver disease

       CRI (chronic renal insufficiency)

o      Give QD dosing (5/mg/kg)

       If TID measure trough levels (1-1.5 mg/kg)

       Pigment-induced nephrotoxicity

o      From hemolysis and rhabdomyolysis

o      Aggressive volume expansion

o      Treatments:

       Mannitol --> 25 gram IV --> decrease tubular pigment reabsorption

       Bicarbonate 2-3 ampules in IV in DSW maintain urine pH> 6.5 (present dissociateion of myoglobin and hemoglobin)

       Acute uric acid nephropathy

o      Increase cell lysis --> increase uricemia secondary cytotoxic treatment of hematologic malignancy (i.e- chemoRx for leukemia)

o      Intratubular precipitation of uric acid

o      Preventions:

       Allopurinol 600mg before starting chemoRx

       Forced alkaline diuresis and maintain pH 6.5-7.0

       Acetazolamide 250 mg PO Q1D

       NaHCO3 2-3 amps in D5W

November 15, 2000

       Allergic interstitial nephritis (secondary to drugs)

o      Signs and symptoms



       Renal dysfunction

o      Diagnosis:

       Increase in serum eosinophils

       Increase in urine eosinophils

o      Causes:

       Drugs such as PCN, sulfamide, NSAIDS

o      Treatments:

       D/C drugs

       If severe or prolonged give predinisone

       Glomerular DZ (glomerulonephritis)

o      Biopsy extensive crescent formation

o      Increase proteinuria

o      Membranoproliferativa no treatments helps

o      Idiopathic rapidly progressive --> hemauria, RBC casts

o      Good Pasteur disease

       Antibodies against glomerular basement membrane (GBM) of renal and pulmonary

       Rx: plamaphoresis (remove antibodies)

       Cyclophosphamide and prednisone

o      SLE treat with steroid

o      Vasculitis treat with cyclophosphamide and presdinone

o      Post-streptococcal supportive treatment

o      General management

       Daily weights

       Mesure water in and outs

       Serum electrolytes at least 3 times a week





       Fluid replacement = U/O any other loss (vomiting, diarrhea, drains) and insensible loss (around 500 cc if afebrile, icrease by 100-150cc for each degree over 37)

       If hyponatremic usually overaggressive diuresis with decrease oral intake

       Diet protein 0.5 grams/kg/day

       Total calories 35-50 kcal/kg/day

       Na+ 2-4 g/day NaCl

       K+ 40 nEq/day

       Phosphate 800mg/day

       Avoid Mg++ (antacids)

       If hypotensive then give fluid and vasopressors

       If hypertensive due to volume overload then give loop diuretics

       If there is no decrease in renal blood flow then give Ca++ blockers, clonidine, prazosin

       If there is decrease in blood flow then DO NOT give ACE inhibitors instead give:

o      Larsotan (angiotensin receptor antagonist)

o      Hydralazine

o      Minoxidil

o      Hydralazine and minoxidil increase Na+ and fluid retention

       If hypertensive crisis then give nitroprusside IV

o      Follow thiocyanate levels --> signs of toxicity include: delirium, tinnitus, blurred vision


o      If phosphate is increased aluminum hydroxide antacids (decrease intestinal absorption)

o      If calcium is decreased then give calcium carbonate only if phosphate level is well controlled because if the product of calcium times phosphate is greater than certain value you will have metastasis calcification

o      Decrease in Ca++ will cause tetany

o      Increase uric acid but not toxic to kidney unless in rhabomysis treat with allopurinol

o      Hyperkalemia

       If less than 6 mg then treat with sodium

       If greater than 6 mg or ECG changes or neuromuscular changes (flaccid paralysis) then treat with 1 amp of D10 with 10 units of regular insulin and 1 amp of Ca++

       If no response dialysis


       Metabolic Acidosis

o      Mild serum HCO3 is greater than or equal to 16mEq/L no treatment

o      Moderate serum HCO3 is less than or equal to 16 give PO of 325-650 mg of Na HCO3

o      Severe serum pH < 7.2 give IV NaHCO3

o      NEVER BOLUS 1-2 amps in 16 D5 or 0.45% saline


       All drugs excreted by kidney need to decrease the dosing

       Infection treat the infection


GI bleeding mucosal changes and decrease platelet function secondary to anemia

Anemia decrease RBC prodution, increase blood loss

       Transfusions Hematocrit < 30%, active bleeding or symptoms



o      Severe hyperkalemia

o      Severe acidosis

o      Severe volume overload

       Decrease heparin in the present of:

o      Uremic pericarditis

o      Encephalopathic

o      Nutritional regugitants

       Maintain BUN < 100 mg/dl because if BUN > 100 mg/dl you will have neurological manifestation such as lethargy, seizures, myoclonic (jerky movement in seizure), polyneuropathy

       Recovery often have polyuria therefore monitor and replace electrolyte/volume loss

       Recovery may continue for weeks to months




Asymptomic til late


o      Usually started once GFR < 10 ml/min

o      Can plot loss vs time to see a sudden decrease in GFR then look for the causes:

Prevent complications by:

Hypertension --> decline in GFR therefore treat them rapidly

o      loop diuretics continue to work up to GFR of 25 cc/min

If serum HCO3 < 16 mEq/L --> give NaHCO3 360-600 mg

Anemia give recombinant human erythropoietin

Renal osteodystrophy 3 types

1.     secondary hyperparathyroidism

2.     decrease bone turnover

3.     mixed November 29, 2000


!          Secondary hyperparathyroidism

o      Increase PTH secondary to resistance in skeleton to PTH causes decrease in Ca++ and increase in phosphate osteitis fibrosa increase bone turnover

o      Symptoms:

       Pruritis, periarticular calcifications, mucho increase in PTH


!          Osteomalasia and aplastic bone DZ

o      Secondary aluminum retention

o      Increase PTH and mild increase in Ca++

o      Symptoms:

       Spontateous fractures

       Needs bone biopsy for diagnosis

o      Treatments:

       Decrease phosphate (0.6-0.9 g/day)

       Increase dose of Calcium Bicarbonate

       Maintain predialysis phosphorous between 4.5-6 mg-dl

       Calcitriol (the active form of Vit D) 0.25-1 mg PO QD

       Maintain Ca++ between 10.5 11 mg/dl

       Parathyroidectomy if there is no response

       Aluminum toxicity avoid alumninum antacids

       If bone biopsy is positive have increase aluminum retention give deforoxamine 1-3 grams IV over 2 hours per week increase removal with dialysis


Anemia decrease circulating RBC mass

!          Hb < 12 g/dl or HCT < 36% in female

!          Hb < 14 g/dl or HCT < 41% in male

!          Symptoms depends upon degree rapidity and etiology

o      Hb < 7 tissue hypoxia fatigue and headache, dyspnea, pallor, angina, lighthead

!          Anemia and hypovolemic the treatment is emergency

o      Tachycardia

o      Syncope

o      Blurred vision

!          Reticulocyte index should be > 2-3% increase RBC production (responding to anemia






!          MCV classifies anemias

o      Macrocytic decrease vit B12; folate

o      Normocytic blood loss, acute

o      Microcytic decrease Fe++


Do any test before transfusion


Anemia secondary to decrease RBC production

!     Aplastic anemia usually leukopenia and thrombocytopenia

o      Causes:

       Idiopathic more common

       20% drugs gold, penicillamine, chloranfenicol, sulfonamides

       10% by viruses EBV, CMV, Hepatitis

o      Diagnosis: need bone marrow biopsy to rule out leukemia, tumor, granuloma

o      Treatments:

       Withdrawing the offending drugs

       RBC transfusion if needed keep to minimum

       Platelet transfusion if < 10,000 or active bleeding

       Bone marrow transplant

       Avoid transfusion from family members because of increase rejection rate

!     Iron deficiency

o      In U.S.A majority menstrual blood loss increase requirement of pregnancy

o      Other causes:

       Decrease Fe++ absorption, cliac DZ, after gastrectomy

       Increase requirements lactation, infancy

       Usually GI bleed if no menstrual bleeding

       Pica syndrome where they eat clay, ice, starch, hair, or computers will cause severe Fe++

o      Signs and symptoms

       10-15% splenomegaly

       koilonychias (spoon nail) rare

       Plummer-Vinson syndrome glossitis, dysphagia, subcricoid esophageal web get better when treat the Fe++ deficiency

o      Labs:

       Early MCV-within normal --> HCT <30% --> angiocytosis, hypochromia, microcytosis --> decrease MCV

       Peripheral smear pencil cells, occasional target cells, increase platelet count, increase soluble transferring receptors

       Decrease Fe++ < 60 mg/dl

       Increase TIBC > 360 mg/dl

       Decrease Ferretin < 12 mg/L --> acute phase reactant --> can increase in inflammation, malignancy, liver disease but usually < 200mg/L

o      Diagnosis bone marrow biopsy if not confirmed with serum ferritin

o      Treatments:

       FeSO4 325mg PO T/D (65 mg elemental Fe++)

       Takes 6 months to deplete iron store

       Reticulocyte count peaks 5-10 days

       Hb/Hct increase over 1-2 months

       Parenteral Fe++ for:

       Poor absorption

       Increase requirements

       Intolerance of oral

       Amounts of Fe++ needed to restore Hb to normal and replenish Fe++ stores:

       Iron (mg) = 0.3 x wt (lbs.) x [(100-pt.Hb in g/dl)/4.8 x100]

       IM or IV 2 ml (1 ml in each buttock) or total dose in 250-500ml NS at 6 mg/min in blood loss

       1 ml normochromic, normocytic RBC = 1 mg Fe++ therefore replacement Fe++ in mg = blood loss in ml x Hct

       Always give test dose (0.5 mg) with first dose because of the possibility of anaphylaxis

       Give 0.5 ml epinephrine 1:1000 SQ or IM if anaphylaxis

       Side effects delayed flu-like syndrome 24-48 hrs later subsides within 3-7 days


!     Magaloblastic anemia = abnormal in DNA synthesis

1.     Decrease folic acid develops within a few months

a.      Decrease intake

b.     Malabsorption

c.      Increase utilization (pregnancy, hemolytic anemia)

d.     Drugs (EtOH, anticonvulsants, oral contraceptives, methotrexate, trimethoprim, sulfasalazine, pyrimethamine)

e.      Signs and symptoms

                                                              i.     Jaundice

                                                            ii.     splenomegaly

2.     Decrease vit B12 5 years of storage

a.      Pernicious anemia

b.     Gastrectomy

c.      Pancreatic insufficiency

d.     GI bacterial overgrowth

e.      Ileitis or ileal resection

f.       Intestinal parasitis diphyllobathrium latum, a fish tape worm

g.      Signs and symptoms:

                                                              i.     Jaundice

                                                            ii.     Splenomegaly

                                                          iii.     Decrease vibratory/positional sense

                                                          iv.     Ataxia

                                                            v.     Paresthesias

h.      Confusion/elementia

3.     Labs:

a.      Increase MCV

b.     Leukopenia

c.      Thrombocytopenia

d.     Decrease folic acid (RBC folic acid more accurate indicator of body folate levels

e.      Decrease Vit B12 increase methyl malonic acid

f.       Decrease hold transcobolamine II

g.      Increase homocystein in both vit B12 and folic acid deficiency

h.      Schilling test give radioactive then oral vit B12 check urine if no intrinsic factor add it with treatment

4.     Peripheral smear

a.      Ansiocytosis

b.     Poikilocytosis

c.      Macro ovalocytes

d.     Hypersegmented neutrophils > 5 nuclear lobes

e.      Increase LDL, and increase in indirect bilirubin

5.     Diagnosis

a.      Bone marrow biopsy rule out myelodysplastic syndrome, malignancy

6.     Treatments:

a.      Folic acid 1 mg QD (5 mg QD with malabsorption)

b.     Vit. B12 1mg 1 MX x 7 days

c.      Increse reticulocytes in 1 week --> increase Hb over 6-8 weeks

d.     1/3 have decrease Fe++ --> therefore incomplete response --> give FeSO4


!     Anemia of chronic disease

o      Long standing inflammatory DZ (> 1 mon.)

o      Malignancy

o      Collagen vascular disease

o      Chronic infection

o      Normochromic-normocytic

o      Fe++ and TIBC are both decreased

o      Ferretin normal or increase

o      Transferring saturation > 1%

o      Treatments:

       Treat underlying DZ

       Rheumatoid arthritis --> erythropoietic 12.5 25.0 mg SQ


!     Anemia with increase RBC destruction = hemolysis = reticulocyte index increase

o      Symptoms of intravascular hemolysis

       Fever, chills, tachycardia, backache

       Decrease haptoglobin (binds and removes Hb)

       Hemosiderin in urine 7 days later --> reliable indicator of chronic intravascular hemolysis

o      Symptoms of extravascular hemolysis in reticuloendothelial system (spleen)



       Haptoglobin normal or slightly decrease

       Direct antiglobulin test (direct COOMBS) measures IgG and C3 on RBC = autoimmune anemia

o      Sickle cell Disease

!     Sickle cell Disease any sickle cell disorder in which significant morbidity occurs from sickling example:organ failure

o      Vaso-occulusive pain crisis

o      Sickle cell anemia = homozygous HbS

o      Several genotypes produce crisis



       S-thalassemia alpha or beta



o      Sickle cell trait BetaA-BetaB mostly asymptomatic except occasionally hematuria, isothenuria, VPC and extreme hypoxia in highaltitude or submarine

o      Decrease life expectancy by at least 20 years

       HbSC- live to 7-8th decade

       HbF diminish sickle cell DZ

       Glutamine residue at 87 prevent cross-binding of Hb beta chins

o      Labs:

       Hb 5-10 g/dl

       MCV slightly increase (increase reticulocyte)

       RBC lifespan = 10-12 days

       Chronic neutropenia 10-20,000

       Increase platelet count

       Peripheral smear sickles, target cells

       Howell-Jolly bodies (asplenic)


       Nucleated erythrocytes

       Reticulocyte count decrease in anaplastic crisis

o      Diagnosis Hb electrophoresis or isoelectric focusing

       Sickle cell prep- adds metabisulfite to sample --> sickling will not distinguish trait from DZ

o      Treatments:

       Prevention health maintenance

       Avoid dehydration and hypoxia

       Avoid cold weather

       Take folic acid 1 mg QD

       Prompt Rx of infections (prophylaxis for pneumococcus)

       Oral PCN 125 mg

       Immunization usual 2 year old pneumococcal vaccine

       Hepatitis B

       Yearly influenza

       Yearly ophthalmologic exam to rule out retinopathy

       Surgery increase fluids

       Avoid hypoxia and hypernatremia

       Partial exchange transfusions decrease HbS <50%

       For major or ophthalmologic surgery

       Acute pain relief:

       Nonopioids acetaminophen, NSAIDS

       Opioids out patient

o      Oxycodone with aceteminophen

o      Codein

o      Becareful with side effects


       antihistamine pruritics

       nausea antiemetics

       N/V, rash, pruritis if taken meperidine

o      Active metabolite normeperididne t1/2 is 18 hours so accumulate and cause seizre, anxiety, tremor

o      Active metabolite of morphine will acculmulate with renal insufficiency --> increase sedation, decrease respiratory

o      Hydromorphone does not accumulate with renal insufficiency DOC for renal compromise

       Clotrimazole prevents erythrocyte dehydration --> decrease sichling

       Mg++ decrease K+ efflux in RBC --> decrease dehydration --> decrease sickling

       IV fluids 0.45% NaCl or D5W maintain Na+ 130-135 mg/L --> increase RBC H2O uptake

       O2 only helps if hypoxic 9acute chest syndrome, pneumonia..)

       Incentive spirometry 10 max breaths every 2 hours while awake

       Hydroxyurea significantly decrease VPC, acute chest syndrome, transfusions

       Potential risk of increase neoplasms therefore CBC every 2 wks for myelotoxicity

       Bone marrow transplant November 30, 2000

       Short term mortality 5-10% therefore use only when benefit outweights risk i.e recurrent CUA

       Priapism give Ca++ channel blockers

       Spinal anesthesia


       Exchange transfusion

       Transfusions - aplastic crisis (from virus)

       Sequestration of slpleen and liver

       Acute chest crisis

       Aplastic crisis usually secondary to viral illness parvovirus B19; revover in 10-14 days

       Colelithiasis > 50% adults

       Choecystitis --> cholecystectomy once attack subsides

       Complications vaso-occlusisve episodes

       VPC- pain bilateral symmetrical

       Pain in back, ribs, limbs last 5-7 days

       Pain usually consitant in same place in each crisis; if NOT look for another cause

       Transfusion does not change course of crisis

       Acute chest syndrome

       Chest pain, leukocytosis, hypoxia, pulmonary infiltrate often distinguishable from pneumonia

       Transfusion if multiple lobes, worsening DZ, PaO2<60mmHg

       Sequestration crisis occurs in patients with intact spleen, hypotentsion shock (organ rupture), sudden splenomegaly, decrease in kids with HbSS or adults with HbSC or HbS-beta-thalassema.

       Splenic Involvement

       5-6 months splenomegaly

       9 months 4 years sequestration crisis

       5-8 years splenic involution to resolution


       Children encapsulated organisms

o      Streptococcus pneumonia

o      H. influenza

o      K. pneumonia

o      Meningococcus

o      Emperical treatment for the above infections with ceftriaxone

       Adults- in tissues susceptible to vasoocclusive such as bone, kidney, lungs

o      S. aureus

o      Salmonella

o      Enteric organisms (E. Coli, Klebsiella, Proteus)

o      Pneumoniae most likely

o      Mycoplasma, H. influenza

o      Emperical treatments for the adults are ceftriaxone and macrolides

       Chronic organ damage

       Osteonecrosis femoral/humeral heads with 10% of the patients

o      Treatment is local heat, analgesics, non weight bearing

       CVA- most commonly occur less than 10 y/o and recurrent in 2/3 within 3 years

o      Median age of occurrence is 6 y/o

o      By 14 y/o 8% has CVA

o      80% - major artery therefore hemiplesia

o      treatment is transfusion to maintain HbS < 50% of 5 years

Leg Ulcers lower lateral shin

a.      2 to major trauma

b.     Stasis

c.      Pressure

d.     Sickling in small skin vessels

!     Treatments:

o      Rest

o      Elevation

o      Wet-dry dressing q2h (debride)

o      Topical antimicrobials

o      If non-healing Unna boots (zinc oxide impregnated bandage) changed wkly X 3-4wks

o      Transfusion

o      Split thickness grafts

o      Priapsm permanent impotence


Renal Tubular defects - 2 sickling in pos AR,

!     Causes:

o      Anoxic environment

o      Isothenuria increase risk dehydration

o      Hematuria

o      Pregnancy increase incidence premature delivery and fetal death

o      If crisis --- transfusion ---decrease incidence of occlusive episodes


Autoimmune Hemolytic Anemia (AIHA)


1.)Warm antibodies extravascular hemorrhage; IgG RBC best test @37

!     Causes:

o      Idiopathic

o      malignancy (lymphoma, CLL)

o      CVD (collagen vascular disease)

o      Drugs

!     Signs and symtomps

o      weakness, jaundice, splenomegaly

o      if severe hemolysis -- fever, chest pain, syncope

o      hemoglobinuria - renal failure

!     Labs

o      Decrease haptoglobin

o      So herocytes??

o      Direct antiglobulin test (DAT)

!     Rx -

o      Treat underlying disease

o      Folic acid 1mgQD

o      Glucosteroids

o      Splenectomy

o      Transfusions (if needed)


2.)Cold Antibody (AIHA) extravascular hemolysis

!     Common in nose, finger, toes cyanotic

!     Causes:

o      cold agglutinin disease

o      chronic - 2 to paraprotein

o      lymphoma, waldenstroms macroglobinemia

o      acute - 2 to infection

o      mycoplasma pneumoniae

o      mononucleosis

o      DAT + C3

!     Rx

o      Underlying cause

o      Supportive keep warm, transfusion 37

!     Paroxysmal cold hemoglobinuria (rare)

o      Intravascular hemolysis decrease haptoglobin

o      Causes:



       Acute viral infection mumps, measles, 3 syphyllis

o      Rx

       Avoid cold

       Transfusions heated to 37 ↓

       Prevent exacerbation of hemolysis



Drug Induced Hemolytic Anemia


3 Mechanisms


1)     Immune IgG

a.      Classic methyldopa

b.     20% + DAT

c.      1% hemolytic anemia


2)     Haptens coats RBC antigen

a.      Classic PCN

b.     +DAT

c.      hemolytic anemia


3)     immune complexes IgM

a.      (occasionally IgG)


!     Drug Ab complex +DAT for C3

o      Causes

       Classic whine



o      Rx

       Remove offending drug


!     Microangiopathic Hemolytic Anemia --- traumatic


!     Intravascular hemolysis

o      Causes

       2 to deposition of fibrin in the lumen of small blood vessels

       DIC disseminated intravascular coagulation

       TTP- thrombocytic thrombocytopenia purpura

       HUS- hemolytic anemia syndrome

       Severe HTN



       Disseminated malignancy

o      Dx

       Peripheral smear -- schistocytes are fragmented RBCs , thrombocytopenia

o      Rx

       1) DIC

       Rx disease ie sepsis, acute leukemia, CVD (activation of coagulation & fibrinolytic systems)

       if bleeding transfusions platelets

       FFP or cryoprecipitate

       Decrease dose heparin

       Follow bleeding, increase in fibrinogen & platelets

       Decrease FSP (Fibrin Split Products)

       D-Dimers (Fibrin Cross Links)


       2)TTP (decrease platelets, microangiopathic hemolysis anemia, neurologic abnormalities +/- fever, renal dysfunction), shicstocytes, increase reticuloctye counts, increase LDH

       (-)FSPs or D-dimers =medical emergency radioneurologic detenoration - death

       AVOID platelet Txs -- increase thrombosis

       Daily total plasma exchange (plasmapharesis) or FFP Until platelets nil

       Prednisone 1mg/Kg PO QD or methylprednisone 1mg/Kg IV

       ASA 325mg PO QD + Dipyridamole 75 mg PO q6h

       If refractory plasmapharesis with onyopoor = plasma replacement

       Vincristine 1-2 mg IV qwh or Immune globulin 0-4 g/Kg V QD X 5 days


       3)HUS closely related to TTP but renal failure = predominant manifestation

       Rx same as for TTP

       *** Neurological

       cerebrovascular disease

       stroke 80% ischemic

       thrombolytic 60% vs Embolic 20%

       15% Hemorrhage

       10% intracerebral vs 5% subarachnoid (AV malformation) ischemic

!     TIA (transient) symptoms resolve within 24 hr (no infarction)

o      History abrupt onset fucal deficit without change in level of consciousness (reticular activating system in brainstem CVA in cortex) - ischemia (tumor, migraine, hemorrhage) loss of consciousness

o      Look for embolic causes (etiology in 20%)

o      Atrial fibrillation

o      Rheumatic valvular disease

o      Recent anteroseptal MI or aneurysm

o      DVT with patent foramen ovale (paradoxal cerebral embolism)

o      Aphasia Left cerebral hemisphere = dominant hemisphere for speech in 50% (left MCA)

o      Receptive = difficulty understanding verbal remarks

o      Expressive = difficulty understanding verbal expressions

o      Global = both

o      weakness in contralateral limbs also seen in sepsis, uremia, post ictal state

o      seizures 1st 24 hours more frequent with hemorrhage

o      Neuro Exam


Carotid circulation

!     Hemiparesis

!     Hemisensory loss

!     Homonymous hemianopsia

!     Ipsilateral monocular visual loss (amarosis fugaz)

!     Aphasia/dysarthria


Vertebro-basilar circulation

!     Unilateral or bilateral weakness

!     Sensory loss

!     Diplopia

!     Ataxia

!     Nystagmus

!     Dysarthria

!     Hoarseness

!     Dysphagia

!     Hearing loss

!     Vertigo

!     Diagnosis

o      Routine labs

o      Electrolytes, sed rate

o      BUN/creatinine

o      Glucose, PT, PTT

o      ECG

o      Chest X-ray, CBC< VDRL

o      Carotid ultrasound

o      CT scan without contrast or MRI

o      Repeat in 36 hr if (-) & presenting as ischemic CVA

o      LP (lumbar puncture) if suspecting infarction ie endocarditis, abscess, meningitis, bacterial, fungal, spirochetes

o      Suspecting hemorrhagic stroke

o      CT scan miss posterior fossa CVA but MRI will pick them up

o      If suspecting intracranial vasculitis - angiogram (ischemia)

o      Hemorrhagic -- angiogram R/O AV malformation

o      Rx

       Cardiogenic embolus heparin prolong PTT 1.5-2Xnormal

       INR (internation normalized ratio) 2-3 -- warfarin

       If prostethic heart valve --> Dipyridamole and warfarin

       -TIA or Rind

       ASA 325 mg QID

       Ticlodipine or clopidogrel (alternative or add on if ASA fails)

       Carotid Endarterextomy >70% -99%

       Stroke in Evolution --> heparin

       thrombolysis if <3hrs


Ischemic CVA

!     Treatments

o      Prevent aspiration pneumoniae

o      Prevent DVT

o      Physical therapy

o      Speech therapy

o      If (hypertensive)

       HTA only Rx if severe or end organ damage (CHF, proteinuria, hematuria, papilledema) >220/130mmHg cerebral autoregulation is lost - need higher pressures to perfuse that area, if low BP worsening of neurological defecit

       Nicardipine (preserves cerebral blood flow)

       Ace inihibitors (little effect on cerebral vessels)

       AVOID nitrprusside and NTG (cerebral vasculitis & increase intracranial pressure)

       ASA + Ticlodipine , Clopidogrel - decrease subsequent CVAs

       Endarterectomy if further brain tissue is at risk


Cerebral edema maximal 24-72 hrs

In cerebellar infarct increase edema - brainstem compression - surgical decompression

!     Thrombolysis if <3hr


Intracranial Hemorrhages

Acute onset


1)     sudden increase in intracranial pressure

a.      decrease mental status

b.     headache

c.      vomiting

2)     focal deficit

3)     if massive herniation


Midline bilateral herniation

!     Drowsy

!     Bilateral miosis

!     Defective upward gaze

!     Preserved papillary response


Unilateral depressed unconsciousness

!     Contralateral hemiparesis

!     Ipsilateral myoriasis

!     Rx

o      Decrease intracranial pressure

o      Keep bed at 30

o      No endotracheal suctioning

o      Hyperventilation

o      Mannitol IV over 20 min (increase permeability of blood-brain barrier increase movement into brain increase edema no repeat doses)


most common cause of intracerebral bleed = HTN


!     Trauma

!     anticoagulant therapy

!     sacular aneurysm

!     AV malformation

!     Tumor

!     Blood dyscrasia

!     Ancropathy (amyloid)

!     Vasculitis

!     Rx

o      Supportive

o      Slowly decrease BP over drugs

o      If cerebellar brainstem compression or obstructive hydrocephalus - surgery


Subarachnoid hemorrhage

!     Most common cause ruptured berryaneurysm

!     Others

o      Intracranial bleed

o      Blood dyscrasia

o      Head trauma

o      Cocaine/amphetamine abuse

o      Tumor

o      Ruptured fusiform aneurysm (atherosclerosis)

o      Ruptured mycotic aneurysm (septic embolism)

!     Symptoms: Suden onset: severe headache (sentinel HA: Severe but self limited)

o      Altered mental status

o      Fever

o      Vomitting

o      Nuchal Rigidity

o      Low back pain

o      Focal neurological deficits

o      Seizures

o      Retinal hemorrhaages (subhyaaaloid)

!     Morbidity/Mortality

o      Recurrence- 20% in 2wks

o      Vasospasm- ischemia (4-14 days)

!     Dx: CT scan without contrast in 90% with contrast or mRI, may show etiology

o      (AV malformation)- enlarged drainage vein = focal hypodensity +/- speckled calcification.

o      (CT misses SAH (subarachnoid hemorhage) in post fossa (brainstem/cerebellum)MRI +

o      Lumbar puncture: if not Diagnostic

!     Hemorrhagic_ centrifuge immediately, if supernatant is xantachromic(yellow)= SAH

!     If not: Traumatic tap (xanchromia= lysis of RBC- takes several hours...

!     for every 700 RBCs-1WBC

!     for every 1000 RBCs-1mg/dl protein

!     Rx:

o      Embolization (polyvinyl alcohol paarticles...)

!     Goals:

       To take smaller size preop> decrease blood loss and simplify surgery.

       Allows brain to adjust to new flow dynamics(restore autoregulation)

       Decrease size- preradiation.

       Palliation if otherwise untreatable

o      Surgery-microscopic using sensory and motor evoked potentials.

o      Radiosurgery (gamma knife, Linal)

!     If nidus <3-4 cm after embolization used if AVM(ateriovenous malformation) is Dep. or in eloquent aarea(high risk)

!     Cause endotelial proliferation- thickening of vessel wall bliteration

!     Continued risk of bleeding for 1-2 years

!     New neurological deficits can be edema-steroids-improve infarct- 12-18 months later-permenant

!     If comatose- subtotal removal of clot- decreased intracraneal pressure-which will allow traumatized brain to recover

!     8-12 weeks later- definitive Rx:

o      Supportive care

o      Bed rest

o      Sedation

o      Analgesia

o      Laxatives

o      Bp.220/130- Nimodipine(prevents vasospasm) 60 mg po q4h

!     If neurolical deterioration? Seconary vasospasm-volume expansion and induced hypertensin


Seizures- Acute

W       Status epilepticus (prolonged generalized seizures or recurrent seizures without recovery of conciousness >30min..) Life threatening

W       nonconvulsive status epilepticus not life threatening (absence, simple, or complex partial seizures.

o      Simple- no loss of consciousness

o      Complex loss of consciousness

W       Brief seizures supportive care only

o      Goal of treatments

       Support vital functions

       Stop seizures

       Identify and treat precipitating causes

       Antilipate and treat complications

       Prevent further seizures

o      Treatments:

       Use nasal or oral airway maximal O2 with mask or intubate 2-IV lines; 1 without glucose

       Draw blood- glucose, electrolytes, Ca++, Mg++, BUN, CBC, toxicology screen (blood and urin), antivonvulsant blood levels

       Padding around bed to prevent them hurting themselves

       NG tube- remove gastric contents so wont aspirate

       IV- diazepam 5-10mg or lorazepam 2-4 mg at 1-2mg/min (works immediately to stop seizures)

       Phenytoin loading 20mg/kg in glucose free IV

       Has ethylene glycol as solvent therefore if rapid injection can cause hypotension and arrythmias (heart block)

       Takes effect in 20 mins

       Fosphenytoin Na+

       Prodrug conversion to phenytoin in blood (take 15 min)

       Max IV levels = end of infusion

       Max IM levels = 30 mins

       H2O soluble (NO ethylene glycol) therefore same dose as phenytoin

       Phenobarbital if above doesnt stop seizure

       Peak plasma levels in 1 hour

       20mg/Kg IV < 50 mg/min

       Valproate Na+

       10-15 mg/kg/day over 60 min

       same dose as oral not yet approved for status epilepsy

       Barbituate coma and/or general anesthesia if seizures continue

       Diazepam rectal gel for break through seizures at home 90% bioavailability of IV dose

       Look for etiology CT scan/MRI to rule out tumor, bleed, LP-CNS infection, CBC, electrolytes, BS, Ca++, BUN, ABG, ESR, drugs (theophylline, amphetamines, cocaine, isoniazid), EtOH, sedative withdrawal, fever, etc.

       To prevent subsequent seizures give them:

       Phenytoin 4-7 mg/kg/day

       Phenobarbital 1-5 mg/kg/day

       Valproic acid

o      Complications aspiration,

       Rhabdomyolysis, myoblobinuria with renal failure