Objectives- Internal Medicine
Define diastolic and systolic heart failure
Heart failure is present when cardiacoutputfails...
List the main risk factors for heart failure.
The 5 most common causes of CHF are: CAD (and other cariac risk factors),HTN...
effusion)
RIGHT-SIDED
 Peripheral edema (especially calves to feet),
 weight gain (from fluid),
 abdominal discomfort(l...
B Abnormal LV systolicfunction,MI,
valvular heartdiseasebutno HF
symptoms
1) Lifestyle modifications
2) ß-blockers (Bisopr...
List the valvular heart diseases associated with syncope
Aortic stenosis:calcification of aortic cusps (resultingfromconge...
RHYTHM: a normal sinus rhythmmust have
a) HR between 60-100
b) P before every QRS and QRS after every P
c) PositiveP wave in either leads 2, 3, avf (inferior leads)
d) PR of less tha...
mm deep) – best visualized in V1
VENTRICULAR HYPERTROPHY
RVH R>S in V1 + right axis deviation (lead I –ve, II positive)
LV...
3rd degree AV block
- Variable PR intervals
- Narrow or wide QRS
- Variable PPandPR intervals
- No relationshipbetween P
a...
patient’s typical chestdiscomfortis reproduced or if the ECG abnormalitiesconsistentwith ischemia develop (i.e.
>1mm horiz...
List the most common causes of AF
 association with age (sharp increasein incidenceafter 70 yrs of age)
 idiopathic
 mo...
- Scars
- Palpation
- Heaves/thrills
- Apex (location,diameter, force of impulse)…pt. in left lateral decubitus if difficu...
Sotalo - ↑ phase3 repolarization →↑ refractory
period
- Photosensitivity
- Pulmonary toxicity
- Hepatotoxicity
- Thyroid d...
o Wide pulsepressure:suspectaortic insufficiency,which could bea complication of proximal
aortic dissection
o Pulsus parad...
- history is essential:assessriwk factors,attempt to ruleout potentially lifethreateningconditions (PE, tension
pneumothor...
ECG No changes ST-segment elevations,Q waves, bundle
branch block,T wave inversions
Normal/unchanged does not ruleout acut...
4) Firbinolyticdrugor Primary PCI
6) GP IIb/IIIa inhibitors
Recognize the complications of acute coronary syndrome
(taken ...
a) Papillary Muscle Rupture – ischemic necrosisand ruptureof an LV papillary musclemay be rapidly fatal
because of acute s...
o infiltrativedisease(sarcoidosis)
Diagnostic triad:
1) pleuritic chestpain (may be sharp,dull,aching,burningor pressing) ...
Age: develops before 20 or after 50
Severity: dramatic risein BP
Onset: abrupt
Family hx: not present
Associated signs and...
- Syndrome characterized by truncal obesity,HTN, fatigability and weakness,amenorrhea, hirsutism,
purplish abdominal stria...
pacemaker to stimulatethe diaphragmor mechanical ventilation,either invasivevia a tracheostomy tube or
noninvasivevia face...
ii. Osmotic dieresis:eg. mannitol
iii. Hypoaldosteronism:causes saltwasting
Note: aldosterone ↓ Na concentration in sweat
...
Perte estimative de liquide et de sang
(pour une personne de 70 kg)
selon les premières manifestations
Catégorie I Catégor...
CO/CI = cardiac output,cardiac index
Pathophysiology and hemodynamic profileof shock states
Physiologic
variable
Preload P...
Peripheral lymphatic system:provides drainage of surplus tissuefluid and leaked plasma proteins to the
bloodstream, as wel...
LOCAL EDEMA (unilateral or localized) GENERALIZED EDEMA
- Inflammation / infection
o Vasculitis,cellulitis,etc.
- Venous o...
- Cool, paleextremities ± cyanosis
(only if severe)
- Swelling,heaviness and achingin
legs (usually medial lower 1/3)
- Ar...
 Lymphoscintigraphy – used to define anatomy and patency, evaluatedynamics of flow and reversal of
flow, and determine th...
Different Tests:
1) Total Lung Capacity (TLC)- volume of air in lungs after max inspiratory effort
2) Vital Capacity (VC)-...
Interpret a plain film chest x-ray
1) Clichés:patientupright (PA et lateral) or patientsupine/sitting (portable;AP – heart...
 Pa02 < 95 mmHg which may not improve by giving100% O2
Discuss the criteria for qualification of home oxygen
AUTOMATIC QU...
Examination of the chest discloses an increased anteroposterior diameter as a resultof hyperinflation of lungs.
Patients m...
Spirometry (routine pulmonary function tests) Decreased Forced Expiratory Volume in 1 sec (FEV1),
hyperinflation,improveme...
Severe
persistent
 Continual symptoms
 Extremely limited w
normal activity
 Frequent exacerbations
 Often
nightly
 FE...
Long-acting inhaled ßagonists (LABA)
Formoterol (Oxeze, Serevent), Salmeterol/Fluticasone(Advair),Budenoside/Formeterol (S...
- fatigue (lack of restful sleep and persistenthypoxia (later stage of pulmonary hypertension)
- daytime hypersomnolence (...
Influenza virus -- 8%
Hantavirus -- rare
Recognize pneumonia on a chest x-ray
Lobular consolidation
 Suggests bacterial p...
** mortality < 0.5% if none of the above criteria
** use Pneumonia Severity Index Calculator or seePneumonia severity asse...
- Congestive heart failure +10
- Cerebrovascular disease +10
- Renal disease +10
Physical exam findings:
- Altered mental ...
-listed in the tableare the etiologic agents for adults – Strep, Mycoplasma pneumonia,and Haemophilus influenza
are the 3 ...
because of conditions associated with agingthat alter consciousness,such as sedativeuseand medical
conditions (eg, neurolo...
o Lung abcess:predisposingfactorsto this includealcoholism,seizures,poor oral hygieneand previous
aspiration,chestCT most ...
 Resp:
o Inspection:chest deformities (barrel chest),signs trauma,clubbing,capillary refill
o Palpation:areas of tenderne...
Propose an effective investigation plan to establish a diagnosis of chronic cough
Investigate each of the possiblecauses
O...
3. Trauma (especially fractures of the spine, pelvis,femur)
4. Neoplasms (especially lung,pancreas,colon,rectum, kidney an...
 Venous valvular insufficiency
 Ruptured popliteal cyst
 Cellulitis
 Arterial occlusivedisease
PE
 Cardiac:ACS, aorti...
o Frequently normal and often nonspecific (e.g. areas of atelectasis,elevation of a hemidiaphragm,
pleural effusion)
6) V/...
o ↑ in: polycythemia vera, vigorous exercise,high altitude
o ↓: anemia
- Hg: male 135-175;female 120-155
o ↑: polycythemia...
Demonstrate a detailed history focused on anemia
 Obtain details of previous blood tests to establish duration of problem...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
Objectives - Internal Medicine Define diastolic and systolic heart ...
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Objectives - Internal Medicine Define diastolic and systolic heart ...

  1. 1. Objectives- Internal Medicine Define diastolic and systolic heart failure Heart failure is present when cardiacoutputfails to meet the metabolic demands of the body or meets those demands only if the cardiac fillingpressures areabnormally high. Systolic Heart Failure: In systolic dysfunction,theaffected ventriclehas a diminished capacity to eject blood because of impaired myocardial contractility or pressureoverload (i.e. excessiveafterload). Loss of contractility may resultfrom destruction of myocytes, abnormal myocyte function, or fibrosis. Pressureoverload impairsventricular ejection by significantly increasingtheresistanceto flow. In impaired contractility,the end systolic pressure-volume relationship (ESPVR) is shifted downward such that systolic emptyingceases at a higher-than-normal end-systolic volume. When normal pulmonary venous return is added to the increased end-systolic volumethat has remained in the ventriclebecause of incomplete emptying, the diastolic chamber vol umeincreases,resultingin a higher- than-normal end-diastolicvolumeand pressure. Whilethat increases in preload induces a compensatory risein stroke volume (via the Frank-Starlingmechanism),impaired contractility and the reduced ejection fraction cause the end-systolic volumeto remain elevated. Duringdiastole,the persistently elevated LV pressureis transmitted to the left atrium(through the open mitral valve) and to the pulmonary veins and capillaries. An elevated pulmonary capillary pressure(>20mm Hg) results in the transudation of fluid onto the pulmonary intersititumand symptoms of pulmonary congestion. Diastolic Heart Failure: Abnormalities of impaired diastolic function includeeither impaired early diastolic relaxation (an active,energy- dependent process),increasingstiffnessof the ventricular wall ( a passiveproperty), or both. Acute myocardial ischemia is an exampleof a condition that transiently inhibitsenergy delivery and diastolicrelaxation. Conversely, left ventricular hypertrophy, fibrosis,or restrictivecardiomyopathy causes theLB walls to become chronically stiffened. In diastole,fillingof the ventricleoccurs athigher-than-normal pressures becauseof reduced complianceof the ventricle. Patients with diastolicdysfunction often present with signs of vascular congestion because the elevated diastolic pressureis transmitted retrograde to the pulmonary and systemic veins. Discuss the underlying pathophysiology of heart failure Heart may not provide tissues wadequate blood for metabolic needs Systolic or diastolicfunction abnormalities → ↑ pulmonary or systemic pressures → organ congestion - Systolic dysfunction:ventriclecontracts poorly,and doesn’t empty fully → ↑ diastolic volumeand pressure,↓ EF - Diastolicdysfunction:difficulty fillingventricle→ ↓ end-diastolic volume,↑ end-diastolic P (EF normal) - LV failure:LV dysfunction → ↓ CO and ↑ pulmonary vein P → extravasation fromcapillaries into interstitial spaceand alveoli =↑ work of breathing - RV failure:↑ BP → extravasation into periphery = edema, liver highly affected (↑ conjugated and unconjugated bilirubin,PT,ALP, AST, ALT)
  2. 2. List the main risk factors for heart failure. The 5 most common causes of CHF are: CAD (and other cariac risk factors),HTN, idiopathic,Valvularheartdisease (AS, AR, MR) and alcohol (which may causedilated cardiomyopathy). Patients areoften asymptomactic for long periods of time becauseof mild impairement or because compensatory mechanisms are present (adrenergic nervous system, RAAS) to balancethe dysfunction. Manifestations of HF occur when factors increasecardiac workload or tip the state of balance= decompensation. Think in terms of preload,afterload,cardiac output, contractility. Think of HEART FAILED (risk factors and precipitants of heartfailure) o Hypertension (increased afterload) o Environment/endocarditis o Anemia (cardiacoutput) o Rheumatic heart diseaseand other valvediseases o Thyrotoxicosis (increased metabolic demand with insufficientCO) o Failureto take medications o Arrhythmia (with tacchy,decreased diastolicfillingtimeand increased heart O2 demand) o Infection, Ischemia or Infection o Lung problems (PE (hypoxemia because of decrease O2 supply to heart), pneumonia, COPD- emphysema is associated with right-sided failure) o Endocrine (pheo, hyperaldosteronism=increased metabolic demand) o Dietary indiscretions (too much salt=increased preload = congestion) Also:  age (over 65)  gender (male)  ethnicity (higher rate in African american)  genetics, family history  chronic alcohol abuse(thiamineinsufficiency) =impaired contractility  CAD (associated with smoking, obesity) Demonstrate an appropriate physical examination for heart failure Symptoms Signs (Physical Findings) LEFT-SIDED  Dyspnea,  orthopnea,  paroxysmal nocturnal dyspnea,  fatigue, dulled mental status (from decreased perfusion),  decreased urineoutput in daytime (decreased renal perfusion),nocturia LEFT-SIDED  Cachexia,diaphoresis (increased SNS activity), cool extremities,  sinus tachycardia,  tachypnea (+/- Cheyne Stokes breathing),  pulmonary rales,  loud P2,  S3 gallop +/- S4,  mitral regurgitation,  pulsus alternans(alternatingstrongand weak contractions in peripheral pulse),  dullness in baseof lungs on percussion (pleural
  3. 3. effusion) RIGHT-SIDED  Peripheral edema (especially calves to feet),  weight gain (from fluid),  abdominal discomfort(liver becomes engorged),  anorexia and nausea (edema of GI tract)  Jugular venous distention,  hepatomegaly,  peripheral edema (ankles and presacral regions),  right-sided S3 or S4,  tricuspid regurgitation,  dullness in baseof lungs on percussion (pleural effusion) Implement emergency management for heart failure  Removal/correction of precipitatingcause o Infection/arrhythmia/valvular disease/MI/PE…  Prevention of deterioration of cardiac function o ACE inhibitors o ß-blockers o Digitalisglycosides  Control of congestive HF state o Diuretic (+ weigh daily and adjustdose) o Liquid and saltrestriction Tx. of acute pulmonary edema  LMNOP o Lasix o Morphine o Nitrates o Oxygen o Position (situpright) Write a series of appropriate ordersto treat heart failure Acute CHF (presenting with pulmonary edema) 1. O2 and intubation 2. Nitroglycerin 0.4 mg sublingiual (may be repeated every 1-5 min) 3. Potent IVdiuretic.E.g. Furosemide 40-80 mg IV a. Monitor electrolytes, especially K+ 4. Morphine 2-5 mg IV PRN ** Dopamine 5-10 µ/kg/min should be started for hypotensive pt or pt in need of additional inotropic support Long term tmt of CHF (accordingto ACC/AHA HF classification) Stage Description Tmt A No structural heartdiseaseand no symptoms but risk factors:CAD, HTN, DM, cardio toxins,familial cardimyopathy 1) Lifestyle modification (diet,exercise,smoking cessation) 2) Treat hyperlipidemia (Lipitor,Crestor) 3) ACE inhibitor for HTN (Ramipril,Enalapril)
  4. 4. B Abnormal LV systolicfunction,MI, valvular heartdiseasebutno HF symptoms 1) Lifestyle modifications 2) ß-blockers (Bisoprolol,Carveditol,Metoprolol) C Structural heart diseaseand HF symptoms 1) Lifestyle modifications 2) ACE inhibitors 3) ß-blockers 4) Diuretics (HCTZ, Bumetamide, Furosemide) 5) Digoxin D Refractory HF symptoms to maximal medical management 1) Therapy under A, B, and C 2) Mechanical assisted device 3) Heart transplantation 4) Continuous IV inotropic infusion 5) Hospicecarein selected pt Identify the pharmacological agents likely to increase survival with heart failure Long Term Management of Heart Failure Pharmacological Therapy:  Vasodilators: o ACEis: standard of care– slowprogression and improvesurvival  All symptomatic patients functional classII-IV(gradeA)  All asymptomatic patients with LVEF <40% (grade A)  Post-MI  Target dose as used in mortality trials,or maximumtolerated dose o Angiotensin II receptor blockers  Second lineto ACEi if not tolerated (grade B), or as adjunctto ACEi if β-blockers not tolerated (grade A) o Hydralazine and nitrates  Second lineto ACEi, decreasein mortality not as great as with ACE-i  β-blockers: standard of care– slowprogression and improvesurvival  should be used cautiously,titrateslowly becausemay actually worsen CHF  class I-IIIwith with LVEF <40% (grade A)  stableclassIVpatients (grade A)  Aldosterone Antagonists: mortality benefit in severe CHF  Spironolactonefor classIIIb and IVCHF already on ACEi and loop diuretic (gradeA)  Hyperkalemia!! Monitor K+ after initiation and avoid if Cr>220 or K>5.2mmol/L  Diuretics: symptom control management for fluid overload  Furosemide for potent dieresis  Metolazone may be used with furosemide to increasedieresis
  5. 5. List the valvular heart diseases associated with syncope Aortic stenosis:calcification of aortic cusps (resultingfromcongenital abnormality or rheumatic inflammation or age-related degenerative calcific) - Symptoms: asymp until <1cm o Exertional dyspnea o Angina pectoris o Exertional syncopemay resultfrom ↓ in arterial pressurecaused by vasodilatation in exercising muscles and inadequate vasoconstriction in nonexercisingmuscles in theface of a fixed cardiac output or from sudden ↓ in cardiac outputby an arrhythmia - If aortic stenosis and mitral stenosiscoexist,↓ in CO induced by MS lowers pressuregradient across aortic valveand masks many clinical findings produced by AS Use a systematic approach to interpret an ECG, including determining rate, rhythm and axis. - Firstthingrequired is to check the calibration =1mm = 0.1 mV RATE:
  6. 6. RHYTHM: a normal sinus rhythmmust have a) HR between 60-100
  7. 7. b) P before every QRS and QRS after every P c) PositiveP wave in either leads 2, 3, avf (inferior leads) d) PR of less than 0.12 sec AXIS:  Look at leads I and avF: if both arepositive,axis mustliebetween -30 and +90 degrees  If they arenot both positive,look for the isoelectic lead  Look for the most isoelectric lead  The net QRS axis isperpendicularto the most isoelectric lead (ex: assumelead avl is the most isoelectric then the net QRS axis isperpendicularto avl,either 60 degrees or – 120 degrees)  Axis implies the net vector of depolarization of the ventricles  LAD: causes includeLVH, LBBB, left anterior hemiblock, inferior MI,elevated diaphragm,WPW  RAD: causes includeRVH, left posterior hemiblock, PE, COPD, septal defects, lateral MI,WPW INTERVALS: - PR: normal is 0.12 – 0.2 sec - QRS: normal is approximately lessthan 0.12 sec - QTc: normal is approximately lessthan 0.44 sec Apply ECG criteria for diagnosing chamber enlargement ATRIAL HYPERTROPHY LEAD II LEAD V1 RA enlargement P wave taller than 2.5mm – best visualized in lead II LA enlargement Greater than normal negative deflection (at least1mm wide and 1
  8. 8. mm deep) – best visualized in V1 VENTRICULAR HYPERTROPHY RVH R>S in V1 + right axis deviation (lead I –ve, II positive) LVH S in V1 + R in V5 or V6 > 35mm + left axis deviation (lead I +ve, II –ve) Interpret an ECG with atrial fibrillation (AF) - atrial rate350-600 discharges/minute(cannotsee distinctp waves) - ventricular rate140-160 bpm - ventricular (QRS) rhythm is irregularly irregular Recognize the various forms of heart block on an ECG AV CONDUCTION BLOCKS 1st degree AV block - ↑ PR interval - Found in otherwise healthy aduls - No tmt required 2nd degree AV block - TYPE I - Gradual ↑ PR interval preceeding QRSdrop - Due to failure of conduction of a Pwave - Frequentlybenign - TYPE II - Constant PR interval - Abrupt QRS drop - Block is usuallydistal to AV node - ↑ risk ofhighgrade 3rd degree AV block
  9. 9. 3rd degree AV block - Variable PR intervals - Narrow or wide QRS - Variable PPandPR intervals - No relationshipbetween P and QRS - Management – electrical pacing BUNDLE BRANCH BLOCKS LBBB - Wide QRS - InitialR wave absent in V1 - Absent small Q wave in V6 RBBB - Wide QRS - R’ in V1 - Terminal deepS inV6 LAFB - Left axis deviation - Small Q in aVL andI - Small R ininferior leads (II, III, aVF) LPFB - Right axisdeviation - Small R inaVL and I - Small Q in inferior leads (II, III, aVF) Bifascicular block - RBBB plus either LAFB (common) orLPFB (uncommon) - Featuresof RBBB plus frontalplane features ofthe fascicular block (axisdeviation, etc.) Interpret an ECG consistent with ischemia One of the most useful tools for diagnosingischemia isobtainingan ECG duringan ischemic episode. During myocardial ischemia,STsegment and T wave changes often appear. Acute ischemia usually resultsin transient horizontal or downslopingST segment depressions and Twave flatteningor inversions. Occasionally,STsegment elevations areseen, suggesting more severe transmural myocardial ischemia,and can also beobtained duringthe intense vasospasmof variantangina. In contrastto the ECG of a patient with an acute MI, the ST deviations seen in patients with stableangina quickly normalizewith resolution of the patient’s symptoms. In fact, ECGs obtained duringperiods free of ischemia arecompeletely normal in approximately half of oatients with stableangina. In others, chronic “non-diagnostic”ST and T wave deviations may be present. Evidence of a previous MI (pathologic Q waves) on the ECG also points to the presence of underlyingcoronary disease. Standard Exercise Testing: The test is continued until angina develops,signs of myocardial ischemiaappear on ECG, a target HR is achieved (85% of max predicted HR) or the patient becomes too fatigued to continue. The test is considered positiveif the
  10. 10. patient’s typical chestdiscomfortis reproduced or if the ECG abnormalitiesconsistentwith ischemia develop (i.e. >1mm horizonatal or downslopingSTsegment depressions). The stress test is considered markedly positive if one or more of the followingsigns of severe ischemic heartdiseaseoccur: 1. Ischemic ECG changes develop in first3 minutes of exercise or persist5 minutes after exercisehas ceased. 2. The magnitude of the ST segment depressions is >2mm 3. Systolic blood pressuredecreases duringexercise(i.e. resultingfrom ischemic induced i mpairmentof contractilefunction) 4. High-grade ventricular arrhythmiasdevelop 5. The patient cannot exercisefor at least2 minutes because of cardiopulmonary limitations Recognize the ECG abnormalities associated with electrolyte abnormalities - Hyperkalemia:“tenting” of T waves, wider QRS with ↑ K concentration,P waves ↓ in amplitudeand may disappear,sinewavepattern → asystoleif severe hyperK - Hypokalemia,IA antiarrhythmics (quinidine,procainamide,TCA), III (amiodarone,sotalol,ibutilide):QT prolongation or prominent U waves, and ↑ susceptibility to Torsades - Hypothermia: prolonged repol,QRS “hump” atJ-point = Osborn wave - Hypocalcemia:prolonged QT - Hypercalcemia:shortened QT - Digitalis:shortened QT, “scooping”of ST-T wave Interpret an ECG consistent with pericarditis o CharacteristicECGchanges are1) diffuseST elevation initially thatresolves to flattened and inverted T waves over days and 2) PR depression in several leads,3) +/- T wave inversions
  11. 11. List the most common causes of AF  association with age (sharp increasein incidenceafter 70 yrs of age)  idiopathic  most frequent predisposingcondition:hypertension  underlyingcardiac abnormality:valvular heartdisease(especially rheumatic),heartfailureand ischemic heart disease  Other precipitants:pericarditis,thyrotoxicosis,pulmonary emboli,pneumonia,acute alcohol ingestion, post-op for 1/3 of patients who undergo cardiac surgery Demonstrate the ability to perform an appropriate cardiac physical examination General observation - Pale/diaphoretic/cyanotic/SOB/extremities (temperature, cap refill)/etc Vital signs (TA, HR, RR, SatO2,Temp) - Bed at 30° Observation - JVP (whileat the neck, auscultateand palpatecarotids)
  12. 12. - Scars - Palpation - Heaves/thrills - Apex (location,diameter, force of impulse)…pt. in left lateral decubitus if difficultto find Auscultation - Aortic, Pulmonary,Tricuspid and Mitral areas - Diaphragmand bell - B1B2 (B3B4 and murmur/regurg.) o Emphasize mitral regurg by pt. in left lateral decubitus o Emphasize aortic regurg by pt. sittingup and leaningforward Periphery - Peripheral pulses - Pittingoedema Resp exam must also bedone (ex. Pulmonary oedema caused by CHF – crepitus in lungbases) Abdo exam may also reveal findings (ex.Hepatomegaly in right-sided CHF) Discuss the various anti-arrhythmia medications available to treat AF Tmt focuses on 3 aspects of the arrhythmia: 1) Ventricular ratecontrol = agents that ↑ conduction through AV node a. ß-blockers or CCB (diltiazemor veramapil) b. Digitalis(Digoxin) less effectivebut may be useful if impaired ventricular contractilefonction 2) Rhythm control = drugs that modify impulseformation/propagation to prevent initiation of AF a. Pharmacologic cardioversion = Class III b. Maintenance of sinus rhythm = Class I,II,III,IV c. Electric cardioversion d. Catheter ablation 3) Prevention of thromboembolitic events a. For AF that persists >48 hr b. Anticoagulation tmt ≥ 3 weeks c. Consider chronic warfarin anticoagulation (superiorto ASA and clopidogrel) ANTI-ARRHYTHMIA MEDICATIONS Class Agent Mechanism of action Side effects IA Quinidine Pracainamide Disopyramide - Moderate Na channel blockade - ↓ phase0 upstroke - ↑ repolarization → ↓ conduction - Torsadede pointe - Diarrhea - Lupus-likesyndrome - Anti-cholinergic sideeffects (↓ memory, confusion, lightheadedness, constipation, blurred vision, dry mouth) II Propanol Metoprolol - ß-blocker - ↓ phase4 depolarization - Bronchospasm - Negative inotropy - Bradycardia - AV block - Impotence - Fatigue III Amiodarone - Blocks K channel - Same as II +
  13. 13. Sotalo - ↑ phase3 repolarization →↑ refractory period - Photosensitivity - Pulmonary toxicity - Hepatotoxicity - Thyroid disease - ↑ INR - Torsadepointe - Bradycardia - Heart block IV Verapamil Diltiazem - CCB - ↓ phase4 spontaneous depolarization → ↓ AV node conduction - Bradycardia - AV block - Hypotension - Do not always maintain sinusrhythmduringlongterm follow-up but ↓ # of AF episodes - Usually notused in asymptomatic pt because of the severity of their sideeffects (↓ efficacy,↑ toxicity so limited use) ** Class IC can also beused in pt with structurally normal heart(only) IC Propafenone Flecainide Encainide - Marked Na channel block - Markedly slows phase0 upstroke - Exhacerbation of VT and heart failure - Negative inotropy - Bradycardia and Heartblock Prescribe appropriate medications for anticoagulation in a patient with AF. The decision to anticoagulatepatients with a fib involves weighingthe risks of an embolic event without therapy vs the risk of hemorrhage event on therapy. Improved methods of monitoring anticoagulation with the International Normalized Ratio (INR), and recent evidence of the efficacy and safety of low-dosewarfarin (INRrange 2.0 to 3.0) have clarified the roleof anticoagulation in AF.  Initiate therapy with the estimated daily maintenance dose (2-5 mg.).  Elderly or debilitated patients often require low daily doses of warfarin (2-4 mg.).  Patients are confused by alternating daily doses (e.g. 7.5 and 5.0 mg).  Significant changes in INR can usually be achieved by small changes in dose (15% or less).  4-5 days are required after any dose change or any new diet or drug interaction to reach the new antithrombotic steady state. Demonstrate an appropriate approach in performing a history and physical examination for a patient with chest pain Quick look test: - Patients with MI look paleand anxious - Pts with pericarditis,pneumothorax or PE involvingpleural surfacelook apprehensiveand breathe with shallow/painful breaths - Pts with esophagitis or MSK problems look well Airway and vitals: - BP: most pts with chest pain havenormal BP o Hypotension may be seen with MI, massivePE, aortic dissection → cardiac tamponadeor tension pneumothorax
  14. 14. o Wide pulsepressure:suspectaortic insufficiency,which could bea complication of proximal aortic dissection o Pulsus paradoxus:pericardial effusion with aortic dissection or pericarditis - HR: o Tachy: severe chest pain,>100BPM could possibly mean a-fib,supraventriculartachys or ventricular tachy o Brady: sinus or AV node ischemia,beta blockadeor calciumchannel blockadedueto drugs - ECG analysis Selective Hx and chartreview: - How does pt describepain? - Is pain sameas usual angina - Pain worsewith deep breathingor coughing? Pleuritic chestpain suggests pleuritis,pneumothoriax,rib fracture, pericarditis,PE,pneumonia, costochondritis - Does pain radiate? - Associated nausea,vomiting,diaphoresis,lightheadedness? - Chest pain worse with swallowing? Suggests esophageal disorder or pericarditis Selective physical: - Vitals - HEENT: white exudates in oral cavity or pharynx → thrush with possibleconcomitantesophageal candidiasis - Resp: o Asymmetrical expansion of chest → pneumothorax o Deviation of trachea to one side→ large pneumothorax on sideopposite of deviation o Hyperresonance to percussion → on sideof pneumothorax o ↓ breath sounds → on sideof pneumothorax o Crackles → CHF secondary to acute MI, pneumonia o Consolidation → pulmonary infarction,pneumonia o Pleural rub → PE, pneumonia o Pleural effusion → PE, pneumonia, ruptured aortic dissection o Chest wall:check for fractures,sensitiveareas - CVS: o Unequal carotid pulses → aortic dissection o Unequal upper limb BP or ↓ femoral pulses → aortic dissection o ↑ JVP → rightventricular failuresecondary to MI or PE; tension pneumothorax o Right ventricular heave→ acute rightventricular failuresecondary to PE o Left ventricular heave→ CHF o Displaced apical impulse→ away from sideof pneumothorax o Loud P2 → acute cor pulmonale,S3 → CHF o Mitral insufficiency murmur → proximal aortic dissection o Pericardial rub (scratchy sounds thatvary with position) → pericarditis - Abdomen: o Guarding,rebound tenderness → perforated ulcer o Epigastric tenderness → peptic ulcer disease o Generalized abdo pain → mesenteric infarction fromaortic dissection - CNS: o Hemiplegia → aortic dissection involvingcarotid artery Distinguish between coronary versus non-coronary causes of chest pain
  15. 15. - history is essential:assessriwk factors,attempt to ruleout potentially lifethreateningconditions (PE, tension pneumothorax, MI (HTN, hyperlipidemia,DM,smoking, genetics, race, age, gender), aortic dissection,etc.) - investigations:Troponin-t,CK-MB, EKG, CXR, CT, echo, CBC + diff Angina/MI - retrosternal pain radiatingto shoulder/jaw,dyspnea,diaphoresis,N/V, exertion or not, relieved by NTG Pericarditis - sharp pain radiatingto trapezius,aggravated by breathing and relieved by sitting forward Aortic dissection - sudden onset of pain,tearing,knife like,anterior or posterior,mid-scapular Pneumothorax - unilateral,sharp,pleuritic,sudden onset PE - pleuritic,sudden onset, tachypnea, tachycardia,hypoxemia…may also havecalf pain, erythema, swelling,also think of Virchow’s triad (alteration in blood flow,damage to endothelium, hypercoagulability) Esophageal reflux - retrosternal burning,acid taste in mouth, worse with eating (especially caffeine, chocolate,EtOH), better with antacids and PPI MSK - localized pain,may radiate,tender to palpation (costochondritis,broken ribs,muscle tear) - other causes of non-coronary pain include:pneumonia,pancreatitis,psychogenic,PUD Describe the differences in the acute coronary syndromes: Unstable angina, non ST elevation MI and ST elevation MI FEATURE UNSTABLE ANGINA NSTEMI STEMI Typical symptoms Crescendo (increasing), rest, or new onset severe angina Prolonged crushingchestpain,more severe and wider radiation than usual angina Serum biomarkers (i.e. Troponin T, CK) None Yes Yes ECG initial findings ST depression and/or T wave inversion ST depression and/or T wave inversion ST elevation and later on, Q waves (ST depression in reciprocal leads) Describe the difference between stable angina and ACS Stable angina ACS Anatomy Lumen narrowed by more than 70% by atherosclerotic plaque Inappropriatevasoconstriction Rupture of an unstableatherosclerotic plaqueand plateletaggregation and thrombosis Unopposed vasoconstriction Symptoms Aching/pressurechest pain that may radiate to neck, jawand arm Lasts 5-15 minutes Is relieved by rest or nitroglycerin Chest pain arises upon predicted level of exertion Character of each attack varies littlewith recurrent episodes Aching/pressurechest pain that may radiate to neck, jawand arm Lasts more than 15 minutes Is not relieved by rest or nitroglycerin Chest pain arises with increasingfrequency, severity or at rest
  16. 16. ECG No changes ST-segment elevations,Q waves, bundle branch block,T wave inversions Normal/unchanged does not ruleout acute MI Serum markers Negative Serial enzyme evaluation is needed for appropriateassessment PositiveCK-MB and TnT May be negative Serial enzyme evaluation is needed for appropriateassessment Echocardiography Regional wall motion abnormalities may represent previous myocardial injury therefore a previous echo would be useful Regional wall motion abnormalities Regional wall motion abnormalities may represent previous myocardial injury therefore a previous echo would be useful Treatment Nitro Rest ASA LMWH Clopidogrel ß-blocker nitrates oxygen pain control (morphine) ACE inhibitor Statin If STEMI, reperfusion is required  Fibrinolytic Or  Primary PCI Implement emergency treatment for acute coronary syndromes Genertal (all pt) 1) General measures a. O2 b. Pain control (morphine) 2) Anti-ischemic medications a. ß-blocker b. Nitrate c. +/- CCB 3) Additional therapy a. ACE inhibitors b. Statins Antithrombic approach (UA and NSTEMI) 1) ASA 2) Heparin (UFH or LMWH) 3) Clopidogrel ** For high risk pt: 4) GP IIb/IIIa inhibitors 5) Cardiac cath Reperfusion approach (STEMI) 1) ASA 2) Heparin (UFH or LMWH) 3) Clopidogrel
  17. 17. 4) Firbinolyticdrugor Primary PCI 6) GP IIb/IIIa inhibitors Recognize the complications of acute coronary syndrome (taken from Lilly) Complications: In unstableangina,the potential complicationsincludedeath (5-10%) or progression to infarction (10-20%) over the ensuingdays or weeks. Once infarction has transpired,especially STEMI,complicationscan resultfromthe inflammatory,mechanical or electrical abnormalities induced by regions of necrosingmyocardium. Early complicationsresultfrommyocardial necrosisitself. Thosethat develop several days to weeks later reflect the inflammation and healingof necrotic tissue. 1. Recurrent Ischemia: -Postinfarction anginahas been reported to occur in 20-30% of patients followingan MI. 2. Arrythmias: -These occur frequently duringacute MI and are a major sourceof mortality prior to hospital arrival. Mechanisms that contribute to arrhythmogensis after MI include: a) Anatomic interruption of perfusion to structures of the conduction pathway. b) Accumulation of toxic metabolic products (e.g. cellularacidosis) and abnormal transcellular ion concentrations owingto membrane leaks. c) Autonomic stimulation (SNS and PSNS) d) Administration of potentially arrhythmogenic drugs (e.g. dopamine)  Ventricular Fibrillation: Largely responsiblefor episodes of sudden cardiac death duringthe course of an acute MI. Episodes of v fib that occur duringthe first48 hours of MI areoften related to transientelectrical instability ,and the long-term prognosis of survivorsof such events is not affected. However, v fib occurringlater than 48 hours after acute MI usually reflects severeLV dysfunction and is associated with high subsequent mortality rates.  Ventricular ectopic beats, ventricular tachycardia,and v fib duringan acute MI arisefrom either reentrant circuits or enhanced automaticity of ventricular cells.  SVTs – sinus brady results fromeither excessivevagal stimulation or sinoatrial nodal ischemia usually in the setting of an inferior wall MI. Sinus tachy occurs frequently and may resultfrom pain and anxiety, heart failure,drugadministration (dopamine,etc), or intravascular volumedepletion. Becausesinus tachy increases myocardial oxygen demand and could exacerbate ischemia,treat its causes!!  Conduction blocks:resultfrom ischemia or necrosisof conduction tracts or in caseof atrioventricular blocks,may develop transiently as a resultof increased vagal tone. 3. Myocardial Dysfunction: a) CHF: -Acute cardiacischemia resultsin impaired ventricular contractility (systolicdysfunction) and increased myocardial stiffness(diastolicdysfunction),both of which may lead to symptoms of HF. b) Cardiogenic Shock: - Condition of severely decreased cardiac outputand hypotension with inadequateperfusion of peripheral tissues thatdevelops when more than 40% of the LV mass has infracted. 4. Right Ventricular Infarction: 1/3 of patients with infarction of the LV inferior wall also develop necrosis of portions of the right ventricle, becausethe same coronary artery (usually RCA) perfuses both regions. 5. Mechanical Complications
  18. 18. a) Papillary Muscle Rupture – ischemic necrosisand ruptureof an LV papillary musclemay be rapidly fatal because of acute severe mitral regurgitation,which causes the valveleaflets to losetheir anchoring attachments. b) Ventricular free wall rupture – an infrequent but deadly complication,ruptureof the free LV wall through a tear in the necrotic myocardiummay occur within the first2 weeks followingan MI. Hemorrhage into the pericardial spaceowingto LV free wall rupture results in rapid cardiac tamponade,in which blood fills the pericardial spaceand severely restricts ventricular filling. -on occasion a pseudoaneurysm results if rupture of the free wall is incompleteand held in check by thrombus formation that plugs the holein myocardium. c) Ventricular Septal Rupture - blood is shunted across the ventricular septumfrom the LV to RV, usually precipitatingCHF because of subsequent volume overload of pulmonary capillaries. d) True ventricular aneurysm – a late complication of MI,a true ventricular aneurysmoccurs weeks to months after acute event. It develops as the ventricular wall isweakened, but not perforated by the phagocytic clearanceof necrotic tissueand it results in a localized outward bulge (dyskinesia) when the residual viableheartmuscle contracts. Complication of LV aneurysm include(1) thrombus formation within this regions of stagnantblood flow; (2) ventricular arrhythmiasassociated with the stretched myofibers; and (3) heart failureresultingfromreduced forward cardio output. 6. Pericarditis: -may occur in the early post-MI period as necrosis and neutrophilicinfiltrates extend from the myocardiumto the adjacentpericardium. *Dressler syndrome: uncommon form of pericarditis –immune process directed againstdamaged myocardial tissueis suspected to play a role. The syndrome is heralded by fever, malaise,and sharp,pleuritic chestpain typically accompanied by leukocytosis,an elevated ESR, and a pericardial effusion. 6. Thromboembolism: Stasis of blood flow in regions of impaired LV contraction after an MI may inciteintracavity thrombus formation. Subsequent thromboemboli can resultin devastatinginfarction of peripheral organs (e.g. stroke). Choose appropriate long-term therapy post-acute coronary syndrome - Beta blocker:metoprolol 25-50mg BID or atenolol 50-100mgDIE - Statin: atorvastatin 80mgDIE - Ca channel blockers:for pts w ongoing/recurrent symp of ischemia despitegood beta blocker tmt OR a-fib - Blood transfusion if Hg<11g/dL - Antiarrhythmic drugs if needed - Venous thromboembolism prophylaxis(LMWH) if immobilized - Proton pump inhibitor:prophylaxisof GI bleed - ACE-I: especially for STEMI, consider for NSTEMI, no evidence for unstableangina Recognize pericarditis as a cause of chest pain Pericarditis is an inflammation of the pericardium(sac around heart).Causes include: o idiopathic which ismostcommon o infection (Coxsackievirus,echovirus,S.Penumoniae, S. aureus,TB, histoplasmosis,blastomycosis) o post-MI (Dressler`s syndromeif 2-8 weeks, directextension if earlier) o metabolic (uremia, hypothyroidism) o neoplastic (hodkin`s disease,breast,lung, renal cell,melanoma) o collagen vascular disease(SLE, scleroderma,RA) o meds (hydralazine) o radiation
  19. 19. o infiltrativedisease(sarcoidosis) Diagnostic triad: 1) pleuritic chestpain (may be sharp,dull,aching,burningor pressing) –often alleviated by leaningforward, aggravated by respiration,can radiated to trapezius 2) pericardial friction rub (in atrial/ventricular systoleor rapid ventricular fillingphase) 3) characteristic ECGchanges (diffuseST elevation initially thatresolves to flattened and inverted T waves over days,PR depression) Define, and describe the treatment for, the following: severe hypertension, hypertensive crisis and malignant hypertension Severe Hypertension (hypertensive urgency): - Severely elevated blood pressure(usually DBP >115) with no evidence of end-organ damage - Most commonly due to non-compliancewith anti-hypertensivemeds - Treatment: gradually reduceBP over 24-48 hours to a level appropriatefor patient MalignantHypertension (hypertensive crisis): - Acute elevation of SBP and DBP (SBP > 200-220mmHg, DBP >120mmHg) associated with end-organ damage (CNS, eyes, heart, kidney) Common S&S: angina,dyspnea, neuro deficits - cardiac:angina,MI,pulmonary edema, orthostasis - neuro: occipital headache,cerebral infarctor hemorrhage, visual disturbance,encephalopathy (nausea, vomiting, etc.) - renal:oliguria,or any sign of renal disease - GI: nausea and vomiting Causes: 1) Meds: cocaine, MAOIs,OCPs, withdrawal of beta-blockers,clonidineor alcohol 2) idiopathic 3) renal artery stenosis 4) pheochromocytoma 5) aortic coarctation 6) hyperaldosteronism 7) hyper and hypothyroidism Treatment: - BP should not be lowered to normal levels;rapid reduction in BP results in decreased perfusion to cerebral,renal and coronary systems; MAP (mean arterial pressure) should never be lowered more than 20% in the firsthour. - If patient is stable,BP can be lowered to 160 systolic and 100-110 diastolic;requires continuous infusion of shortactingparenteral (IV) antihypertensiveagent with constantintensivemonitoring (ex. Labetolol: 20mg IV over 2 min; up to 40-80mg at 10 min intervals) - Most common drugs used to treat: Labetolol (B-blocker) and Sodium nitroprusside(vasodilator – vascularsmooth muscle) - Other drugs used: o Vasodilators:nicardipine(CCB),enalapril (ACE-I),nitroglycerin IV;Adrenergic inhibitors: esmolol (B-blocker) Recognize the clinical presentation of secondary hypertension
  20. 20. Age: develops before 20 or after 50 Severity: dramatic risein BP Onset: abrupt Family hx: not present Associated signs and symptoms: depend on causeof secondary hypertension Type Clinical clues Chronic renal disease Increased creatinine Abnormal urinalysis Primary aldosteronism Decreased serum potassium Renovascular Abdominal bruit Sudden onset Decreased serum potassium Pheochromocytoma Paroxysms of palpitation,diaphoresis and anxiety Episodic hypertension Coarctation of the aorta BP in right arm> left arm CXR: aortic indentation Cushingsyndrome Central obesity, hirsutism Define hyperaldosteronism, renovascular hypertension, pheochromocytoma and Cushing’s disease ** All 4 causesecondary HTN. Hyperaldosteronism (primary and secondary) - Conditions in which the adrenal gland releases too much of the hormone aldosterone o Primary aldosteonism= dysfunction of the gland itself.Rare. Usually caused by a adrenal adenoma/hyperplasia  ↑ aldosteronesecretion↑ → Na+ retention → arterial pressure  Hypokalemia is also a prominentfeature (from Na+/K+ tubular exchange) o Secondary aldosteronism= something outside of the adrenal gland mimics theprimary condition.Generally related to high blood pressure.Also related to: cirrhosis of the liver,HF, and nephritic syndrome. - S&S: fatigue, headache, high blood pressure, intermittent paralysis,muscleweakness,numbness Renovascular hypertension: - Decreased perfusion of renal tissuedue to stenosis of main or branch of renal artery activites the rennin- angiontensin system. o ↑ circulatingangiotensin II→ vasoconstriction +↑ aldosteronesecretion↑ → Na+ retention + stimulation of adrenergic NS → ↑ arterial pressure Pheochromocytoma: - Rare catecholamine-secreting tumor derived from chromaffin cells - Hypertension is the most common sign o Often severe o Sustained or only duringcrises o Hypertensive paroxysms or crises,often spectacular and alarming,occur in > 50% of cases Cushing’s disease:
  21. 21. - Syndrome characterized by truncal obesity,HTN, fatigability and weakness,amenorrhea, hirsutism, purplish abdominal striae,edema, glucosuria,osteoporosis,and a basophilic tumor of the pituitary - Due to increased production of cortisol by the adrenal gland - HTN: o Not necessarily volumedependant o May be secondary to glucocorticoid-induced production of rennin-substrate(angiotensin- mediated hypertension) Recognize sleep apnea and describe its main features, diagnosis and management. Sleep apnea is a syndrome in which people have repetitive periods of apnea that occur duringsleep. A period of more than 10 seconds without airflowis generally considered to constitute an apneic episode,and patients with OSA often have hundreds of such episodes duringthe courseof a night’s sleep. Clinical Features:  Markedly deranged sleep pattern – loud snoringis particular prominent  Patients may have snortingand agitation as a resultof tryingto breathe againstobstructed airway (may also haveviolentmovements duringobstruction)  Complaints fromsleep partner of being hit or injured  Complaints of headache on waking – relatingto cerebral vasodilatation associated with derangements in gas exchange that occur duringapneic episodes.  Sleep deprivation – so overly somnolent duringthe normal wakinghours – can be debilitating  Intellectual impairment(reduced attention and cognitiveability),memory loss,personality disturbances (as a resultof chronic hypoxia and extreme fatigue)  Polycythemia  Secondary cardiovascular complicationsof OSA are believed to be mediated in partby increased sympathetic nervous system activity. Duringthe episodes of apnea, patients may have a variety of cardiac arrhythmias or conduction disturbances.  As a resultof prolonged hypoxemia at night, pulmonary hypertension can result,and unexplained cor pulmonalemay be presenting clinical problem.Thus peripheral edema may result.  Systemic hypertensions associated with OSA Diagnosis: Doctors diagnosesleep apnea based on medical and family histories,a physical exam,and results from sleep studies. Normal Sleep Apnea Apneic Events few Many Periods of Deep Sleep (S4) 2-3 of typically >15 mins duration Few to many, but of barely measurableduration Periods of Re-awakening Few, 2-3 many O2 saturation level Erratic and long-lastingfluctuations with density of apneic episodes Heart rate Constant with minor short-lasting fluctuations Erratic and fluctuatingwith density of apneic events Snoring Intermittent, sparse Excessive,persistent Management: In patients with central apnea (no drive to breathe duringthe apneic period – no signal for respiratory center to initiaterespiration),treatment consists of the use of respiratory stimulants,an electrical,implanted phrenic nerve
  22. 22. pacemaker to stimulatethe diaphragmor mechanical ventilation,either invasivevia a tracheostomy tube or noninvasivevia facemask. In obstructive apnea (drive to breathe still presentduringapneic episode,but transientobstruction of the upper airway prevents inspiratory airflow–so inspiratory muscles areactivebut attempts to initiateairfloware unsuccessful),treatment includes weightloss in obesepatients, elimination of respiratory depressants (alcohol and sedative-hypnotic drugs). First-linetherapy used in most patients with OSA is nasal CPAP. A mask connected to an air compressor is placed over the nose at bedtime. The compressor maintains positivepressurein the upper airway throughout the respiratory cycle,thus providinga pneumatic splintto keep the airway open. A modification to this treatment is Bilevel Airway Pressure(BiPAP) which provides a lower pressureduringexpiration and greatly increases the comfort of the patient. CPAP can be used in conjunction with oxygen in extreme cases of chronic hypoxia in severe sleep apnea. Oral/dental appliances: to trap the tongue forward and/or to pull the jawforward to keep the airway open. Surgical modes of therapy may be beneficial in selected patients. Uvulopalatopharyngoplasty is sometimes used but has many complications. Demonstrate an appropriate approach in performing a history and physical examination for the hypotensive patient (including listing potential causes and treatment) Hx: - Fatigue, weakness, muscle cramps,thirst,postural dizziness - More severe: oliguria,cyanosis,abdo and chestpain,confusion,obtundation Physical:assessvolumelevel (only cardiogenic has volumeoverload) - Sunken eyes, furrowed tongue, dry mucous membranes, extremity weakness - Assess hypovolemia:BP (↓ systolic,↑ diastolic),reflex tachycardia,dry mucous membranes, skin tenting/↓ cap refill - ↓ intravascular volume:↓ JVP, postural hypotension,postural tachycardia - Larger/acute fluid loss:hypovolemic shock → hypotension, tachycardia,peripheral vasoconstriction, hypoperfusion (cyanosis,cold/clammy extremities, oliguria,altered mental status) - Labs: itseems like this might be too much detail, but I’ve been quizzed on it twice… o ↑ BUN, plasma creatinine(because↓ GFR) Normally BUN:creatinine ratio 10:1  Prerenal azotemia: hypovol → ↑ urea reabsorption =↑ BUN → 20:1 or higher  Ratio can ↑ with ↑ urea production from hyperalimentation (high protein), glucocorticoid therapy, GI bleeding o Urine: normally hypovolemia → ↑ Na reabsorption => Na <20mmol/L Urine osmolality and specific gravity in hypovol >450mosmol/kgand 1.015 - ↑ AVP secretion  Acute tubular necrosis:↓ Na reabsorption  Hypovol from vomiting: metabolic alkalosis =>more HCO3 secreted => less Na reabsorbed; However Cl is low(<20mmol/L)  Diabetes insipidus:urineosmolality and specific gravity indicateinappropriateurinedilution Diff dx: 1) ECF volume contracted a. Extrarenal Na loss: i. GI: vomiting, NG suction,drainage,fistula,diarrhea ii. Skin/respiratory:fluid lostto thermoregulation – sweat, Na/H2O loss fromskin iii. Hemorrhage iv. Burns,pancreatitis,peritonitis b. Renal Na and water loss i. Diuretics
  23. 23. ii. Osmotic dieresis:eg. mannitol iii. Hypoaldosteronism:causes saltwasting Note: aldosterone ↓ Na concentration in sweat iv. Salt-wastingnephropathies c. Renal water loss i. Diabetes insipidus:central or nephrogenic 2) ECF volume normal or expanded a. ↓ CO i. Myocardial,valvular,pericardial disease b. Redistribution i. Hypoalbuminemia:hepatic cirrhosis,nephritic syndrome ii. Capillary leak:acutepancreatitis,ischemic bowel,rhabdomyolysis c. ↑ venous capacitance i. sepsis Discuss the types of shock and clinical markers thereof Le choc est un état pathologiquerésultantde troublecirculatoireet/ou métabolique majeur, TOUT choc a une hypotension artérielle(tension artérielle=débit cardiaqueX résistancevasculairepériphérique) et une hypoxie tissulairegénérale,aussi étatmental diminuéou altéré, pâleur et cyanose,peau froideet moite, mauvais remplissagecapillaire,RR plus de 32/min,PA systoliquemoins de80, débit urinairemoins de 0.5 ml/kg/h, lactate sanguin plus de5 mmol/L - penser au corps comme une plomberie - cardiogénique = problème de pompe, diminution de débit cardiaque,perfusion et TA, compensation = vasoconstriction,tachy,augmentation extraction O2 par les tissus périphériques - diminution de contractilité:ischémie, IM, arythmie, cardiomyopathie - trouble de remplissage:tamponage, péricarditeconstrictive,Tension penumothorax - obstruction du débit : EP, coarctation,sténose valvulaire - hypovolémique : penser à une fuite dans lesystème = sang(trauma ou chirurgie),plasma ou eau (deshydratation,brulures,obstruction intestinale,pertes rénales anormales),donc diminution volume circulantou précharge, diminution du débit cardiaque,compensation = vasoconstriction,tachy,augmentation extraction O2 par les tissus périphériques - choc septique : penser dilatation des tuyaux,syndrome infectieux avec 2 signes de SIRS (T plus de 38C, p plus de 90/min, RR plus de 32 /min, leucocytoseou leucopénie), hypoperfusion et dysfonction d’au moins un organe vital, DONC diminution de RVP, vasodilatation,hypotention, augmentation du shunt artério-veineux, diminution extraction O2 par les tissus périphériques, compensation =tachy, augmentation débit cardiaque - anaphylaxie : penser tuyaux perforés, libération desubstances vasoactives,extravasation du volumecirculatoire, bronchospasme,mixte de hypovolémie et distributive,fuite capillaire,diminution débit cardiaqueet RVP, vasodilatation,hypotension,compensation = tachy
  24. 24. Perte estimative de liquide et de sang (pour une personne de 70 kg) selon les premières manifestations Catégorie I Catégorie II Catégorie III Catégorie IV Perte de sang (ml) jusqu’à 750 750 à 1 500 1 500 à 2 000 > 2 000 Perte de sang (% volume sanguin) jusqu’à 15 % 15 à 30 % 30 à 40 % > 40 % Pouls < 100 > 100 > 120 > 140 TA normale normale à la baisse à la baisse Tension différentielle normaleou à la hausse à la baisse à la baisse à la baisse Fréquence respiratoire 14 à 20 20 à 30 30 à 40 > 35 Diurèse (ml/h) > 30 20 à 30 5 à 15 Nulle État du SNC légère anxiété légère anxiété anxiété / confusion confusion / léthargie Remplacement liquidien (règle du 3:1) solutécristalloïde soluté cristalloïde solutécristalloïdeet sang solutécristalloïdeet sang Le rapport3:1 constitueune lignedirectricefondée sur lefaitque la plupartdes patients ont besoin de 300 cc de solution d’électrolytes pour chaque100 cc de sangperdu. (Extrait adaptédu manuel ATLS, 1997). CVP PAOP SVR/SCRI CO/CI Hypovolenic ↓ ↕ ↓ ↑ ↓ Cardiogenic ↑ ↑ ↑ ↓ Distributive - Sepsis - anaphylaxis ↔ ↓ ↔ ↓ ↔ ↓ ↔ ↓ ↓ ↓ ↕ ↑ Neurogenic ↔ ↔ ↓ ↔ ↑ Obstructive - tamponade - tension ptx - massive PE ↑ ↕ ↑ ↑ ↕ ↕ ↑ ↑ ↑ ↓ ↓ ↓ CVP = central venous pressure PAOP = pulmonary artery occlusion pressure SVR = systemic vascular resistance SVRI = systemic vascularresistanceindex
  25. 25. CO/CI = cardiac output,cardiac index Pathophysiology and hemodynamic profileof shock states Physiologic variable Preload Pump function Afterload Tissue perfusion Clinical measurement Pulmonary capillary wedge pressure Cardiac output Systemic vascular resistance Mixed venous oxygen saturation Hypovolemic ↓ ↓ ↑ ↓ Cardiogenic ↑ ↓ ↑ ↓ Distributive ↓ or ↔ ↑ ↓ ↑ Demonstrate an appropriate approach in performing a history and physical examination in the care of a patient in shock -shock: systemic organ hypoperfusion,usually associated with hypotension. -strategy: gain vascular access quickly & aggressively replacevolume  Monitor BP and organ perfusion (ex. Cerebral, cardiacand renal function)  Central venous linefor fluids  Arterial line:measurement of oxygen exchange -History & Physical Examarespecific to 4 classifications of shock  In General: tachycardia(weak pulse),hypotension, +/- fever, +/- O2 Sat changes, +/- rapid,shallow breathing, shiftinglevel of consciousness 1) CARDIOGENIC SHOCK (decreased cardiac outputas a resultof cardiac dysfunction) a. Hx: pain? MI symptoms: sweating, palpitations,etc., symptoms of CHF (edema, orthopnea, PND), antecedents: cardiac,other? b. P/E: sweating, MI signs (incl.ECG), cardiac exam:B1, B2, B3 (surchargevolumique),B4 (ventricules moins complaints),creps in baseof lungs,edema (lower limbs) 2) HYPOVOLEMIC SHOCK (decreased intravascular volume) a. Hx: diarrhea? Vomiting? dehydration? Heat exhaustion? Hemorrhage/bleeding? b. P/E: muqueuses sèches,dry skin;improvement with normal salineinfusion? 3) SEPTIC OR REDISTRIBUTIVE SHOCK (decreased systemic vascular resistance a. Hx: cuts,sites of infection? Bleeding site? Recent injury/trauma,surgery? Recent infection? Timeline important b. P/E: likehypovolemic, although may have fever, palpitations and tachycardia 4) OBSTRUCTIVE SHOCK (decreased cardiac outputas a resultof obstruction or anaphylaxis) a. Hx: allergies? Recent exposures? 5) P/E: stridor,laryngeal swelling,sweating,tachycardia,tacchypnea Describe the anatomy and physiology of the peripheral vascular and lymphatic systems Peripheral vascularsystem:blood caries nutrients,oxygen and waste products to and from the cells,exchangeis done in the capillary bed.
  26. 26. Peripheral lymphatic system:provides drainage of surplus tissuefluid and leaked plasma proteins to the bloodstream, as well for removal of debris from cellulardecomposition and infection .  Lymph nodes: small masses of lymphatic tissuethrough which lymph from the lymphatic vessels mustbe filtered.  Lymphoid tissue: in the walls of the digestive tract, in the spleen, thymus, lymph nodes List the main causes of both unilateral and bilateral edema Demonstrate an ability to elicit the various clinical signs and symptoms of edema in order to establish the etiological diagnosis
  27. 27. LOCAL EDEMA (unilateral or localized) GENERALIZED EDEMA - Inflammation / infection o Vasculitis,cellulitis,etc. - Venous or lymphatic obstruction/stasis o Crhonic venous insufficiency/phebitis o DVT o Chronic lymphangitis o Filariasis - Arterial insufficiency - Trauma/injury - Increased hydrostatic pressure o Increased fluid retention  Cardiac cause(e.g. CHF)  Hepatic causes (e.g. cirrhosis)  Renal causes (e.g. acute and chronic renal failure) o Vasodilators(especially CCB) o Refeeding edema - Decreased oncotic pressure o Hypoalbuminemia - Hormonal o Hypothyroidism o Exogenous steroids o Pregnancy o Estrogens Clinical signsand sx 1) Hx o Atherosclerotic RF : smoking, HTN, DM, FHx, Lifestyle (diet, exercise), hyperlipidemia o CHF: peripheral edema, pulmonary congestion, exerciseintolerance o Precipitants of venous thrombosis  Recent prolonged immobilization (DVT)  Post-operatively (especially ortho,thoracic,GI,GU)  Trauma (fractureof femur, pelvis,spine,tibia)  Post-MI/CHF  Long travel  Hormone-related: pregnancy, oral contraceptivepill,hormonereplacement therapy  Inheritablehypercoaguability (APLA syndrome, Factor V Leiden, Prothrombin G20210A, etc.)  Underlyingmalignancy o Risk factor for thromboembolitic events  A fib,post MI <3 months, valvular disease,prosthetic valves,endocarditis,cardiomyopathy o Vasculitis  Skin changes, mucosal ulceration,jointpain,changes in vision and/or eye pain o Symptoms of ischemia (6 Ps)  Polar (cold) – comes first  Pain – absent in 20 %  Pallor  Paresthesia –lighttouch lostfirst(small fibers) followed by other sensory modalities  Paralysis/Power loss –further progression of ischemia  Pulselessness o Critical ischemia  Acute = look for 6Ps + neuromotor dysfunction  Chronic = night pain,rest pain,tissueloss (ulceration/gangrene) 2) PE o Check for pitting edema  Suggestive of orthostasis,chronic venous insufficiency or CHF o Firm, non pittingedema suggests lymphatic obstruction o Note prominent veins Arterial insufficiency Venous statis Vasculitis
  28. 28. - Cool, paleextremities ± cyanosis (only if severe) - Swelling,heaviness and achingin legs (usually medial lower 1/3) - Arterial bruitmay be present - ↓BP in the affected limb (and pulse) - Loss of hair on the legs or feet - Painful,non-bleedingulcers on the feet or toes (usually black) that are slowto heal (severe) - Shiny, tight skin (severe) - Thick toenails (severe) - Warm, thinkening and erythema over ankle and lower leg - Stasis ulceration of ankleor above medial malleolus o Painless o Develop slowly o No distinctborders - Varicosities/prominentveins CHRONIC VENOUS INSUFFICIENCY - Warm, erythematous, thickened skin,↑ pigmentation, ± brown ulcers around ankles SUPERFICIAL PHELBITIS - Warm, painfull,erythema secondary to inflammation around vein ACUTE DVT - Pain secondary to inflammation in absence of superficial ∆, swellingof distal partof extremities - Livedo reticularisrash (bluish- red discolouration,network pattern) - Malar or discoid rash on facein SLE - Raynaud’s phenomenon: episodes of sharply demarcated pallor and/or cyanosis,then erythema of digot - Purpura - Look for activeswollen joints - Inflammation of eye chambers - Venous/arterial thrombosis/ulcers,ulcers, gangrene 3) Special tests Arterial insufficiency Venous insufficiency ALLEN TEST - Test of good collateral flowthrough ulnar artery before doingpuncture of radial artery ofr arterial blood-gad STRAIGHT LEG RAISE (Pallor on elevation) - Raison leg40-60 degree for 30 sec., or until pallor of the feet develops - Normal = mild pallor on elevation - Abnormal = marked pallor on elevation (suggestive) RUBOR ON DEPENDENCY - After straightlegraise - Ask pt to situp and dangle both legs over the side of the bed - Normal = Return to normal colour within 10-15 sec. - Abnormal = persistent pallor of the feet > 10 sec. followed by rubor (marked redness) on dependency (after 1-2 min) ** seen in pt with critical ischemia INCOMPETENT SAPHENOUS VEIN - Ask pt to stand and compress the vein proximally with one hand and placethe other hand 15-20 cm distally - Briskly compresse/decompress the distal site - Normal = hand on proximal siteshould feel no impulse - Abnormal = any impulsetransmitted to proximal site BRODIE-TRENDELENBURG MANEUVER - Ask pt to liein supineposition and raiselegto 90 degree x15 sec (to empty vein) - Placetourniquet around pt upper thigh, ask pt to stand and watch for venous fillingwith tourniquet still x60 sec - Normal = superficial saphenousshould fill slowly below tourniquet within 35 sec - Abnormal = early fillingindicates incompetence of deep and perforator veins. Fillingof vein from above (retrograde flow) suggests superficial bvenous incompetence (after tourniquet has been removed) Outline a useful investigation plan for the diagnosis of edema Lymphedema:
  29. 29.  Lymphoscintigraphy – used to define anatomy and patency, evaluatedynamics of flow and reversal of flow, and determine the severity of obstruction  CT and MRI – delineate nodal architectureatincreased costbut limited advantage over scintig.  Doppler – presence of DVT is in the differential of unilateral swelling,and itmay also occur concomitantly with lymphedema – cost-effective test in appropriatesituation. Cardiogenic Pulmonary Edema:  CBC – asses for severe anemia and may suggest sepsis or infection if markedly increased WBC  Lytes – People with CHF often use diuretics so would be predisposed to lyte abnormalities  Patients with CKD areat risk for hyperkalemia  BUN and Cr – help to assessrenal failure  CXR – distinguish CPEfrom other pulmonary causes of severe dyspnea  An enlarged heart, Kerley B lines,absenceof air bronchograms and presence of pleural effusion suggest CPE  Arterial blood gases  Oxygen sats  ECG – LVH Ankle edema in general:  Pregnancy  Meds – CCBs, NSAIds, estrogens  LFTs, albumin,  Cr, BUN, CK  D-Dimer and ultrasound of calvesc to R/O DVT Propose a treatment plan for edema Conditions associated with development of edema: heart failure,cirrhosis,nephritic syndrome,venous/lymphatic disease Pulmonary edema = lifethreatening - Loop diuretic (furosemide10-40mg): monitor degree of dieresis,fluid and electrolytecomplications (hypokalemia,metabl alkalosis,hyponatremia,hyperuricemia,hypoperfusion - ↑ serum creat) - Cirrhosis:spironolactone+ furosemide, proceed slowly in absenceof edema - Tense ascites:total paracentesis - Heart failure:monitor hypoperfusion (↑ serum creat) - Nephritic syndrome: may need higher than normal doses of loop diuretic bc bindingof diuretic by albumin in tubular lumen → inactive+ ↓ total functioningnephrons - Idiopathic edema already on diuretics:discontdiuretic 2-3 wks (could be diuretic induced) - Resistantedema from any cause:high-dose IV loop diuretic + thiazide(metolazone, hydrochlorothiazide) Interpret a pulmonary function test
  30. 30. Different Tests: 1) Total Lung Capacity (TLC)- volume of air in lungs after max inspiratory effort 2) Vital Capacity (VC)- max volume of air thatcan be expelled from the lungs followingmax inspiration 3) Residual Volume (RV)- volume of air remainingin lungs after a maximal expiratory effort 4) FEV1 – forced expiratory volume in one second, commonly used to screen for airway disease,a measure of flow rate 5) Diffusion capacity (DLCO)- evaluation of the diffusingcapacity for carbon monoxideindicates the adequacy of alveolar-capillary gas exchange.Common causes of  DLCO are emphysema, interstitial lungdisease,and pulmonary vasculardisease Obstructive Restrictive - obstructiveairflow,decreased flow rates (most marked duringexpiration),air trapping(increased RV/TLC) and hyperinflation (increased FRC,TLC) - decreased lungcomplianceand lung volumes  asthma  COPD  Cystic fibrosis  bronchiectasis  interstitial lungdisease  neuromuscular disease  chest wall disease  pleural disease  parenchymal disease(penumonia) FEV1(%) = FEV1/FVC. FEV1(%) is the percent of the forced vital capacity expelled in one second. Approach: 1. Look at the FEV1 first: -if the FEV1(%) is normal or high, may be restrictive disease -if the FEV1(%) is decreased (<80%), then the patient has airflowlimitation suggestiveof obstructive disease ->if the FEV1 does not improve after bronchodilator administration,the patient has fixed airway obstruction (COPD) 2. Look at the lungvolumes: - TLC, RV: suggests hyperinflation and gas trapping,consistentwith obstructive disease - TLC, RV: suggests restriction and is diagnosticof restrictive lungdisease 3. Look at the DLCO; -DLCO should be corrected for hemoglobin (DLCO-C) and alveolar volume(DLCO/VA) -if patient has restrictivedisease,a lowDLCO/VA implies interstitial lungdisease -if DLCO is lowbut DLCO/VA is normal,restrictivediseasedueto low lungvolumes (obesity, skeletal deformities) -if patient has obstructivedisease,lowDLCO-C suggests presence of emphysema
  31. 31. Interpret a plain film chest x-ray 1) Clichés:patientupright (PA et lateral) or patientsupine/sitting (portable;AP – heart appears more magnified) 2) Pulmonary volumes: in a normal CXR, you can see 8-10 posterior ribs 3) Heart size: in a normal CXR, the heart width is ½ the width of the total lungspace 4) Mediastinal or pulmonary hilarabnormalities? a. Ex. Mediastinumtoo large: mass or vascularabnormlity (i.e.aneurysm) b. Hilar ‘swelling’:lymph nodes or dilated pulmonary arteries (NB: each hilumshould be concave!) c. Cardiomegaly (i.e. in heart failureor congenital problem) 5) Look at each lung individually and comparethe 2 sides a. Lungs too white: alveolar consolidation - pneumonia, atelectasia,interstitial disease,mass, pleural effusion (épanchement – look for signedu ménisque when patient is standing) i. NB: bronchogramme aérique: vessels become more black againstinterstitial consolidation –pneumonia ii. Signe de silhouette: the contours of 2 adjacentstructures with similar densities arenot well-defined b. Lungs too black:pneumothorax or emphysema (hyperinflation) 6) Are the diaphragmatic curves (both sides) well-defined? 7) Examine the ribs,clavicles,shouldersand vertebrae a. Fracture? Mass? 8) Examine the soft tissue a. Mass? 9) Look under the diaphragmfor abnormalities 10) Rule of thumb: if you find one abnormality,keep lookingfor others Interpret arterial blood gases in the context of pneumonia  ABG is not commonly done in the context of pneumonia, unless very diffuseor with severe underlying COPD  Assesses adequacy of gas exchange and ventilator insufficiency  Respiratory acidosismay be present (due to parenchymal infiltration resultingin hypoventilation) or respiratory alkalosis (due to hypoxemia causinghyperventilation)  Increased A-a gradient
  32. 32.  Pa02 < 95 mmHg which may not improve by giving100% O2 Discuss the criteria for qualification of home oxygen AUTOMATIC QUALIFICATION for the followingconditions: o Pulmonary fibrosis o Cor pulmonale o Pulmonary hypertension GERENAL CRITERIA 1) The condition must be stabilized and treatment regimen optimized before long-term oxygen therapy is considered.Optimum treatment includes smokingcessation. 2) Pt must have chronic hypoxemia on room air atrest  Pa02 ≤ 55mmHg, OR  Sa02 ≤ 88% 3) Pt with persistent Pa02 in the range of 56 to 60 mmHg may be considered candidates for long-term oxygen therapy if any of the followingmedical conditionsarepresent:  cor pulmonale  pulmonary hypertension  persistenterythrocytosis 4) Also,some pt with a persistentPa02 in the range of 56 to 60mmHg may be candidates for long-term oxygen therapy if the followingoccurs:  exerciselimited hypoxemia and  documented to improve with supplemental oxygen  nocturnal hypoxemia HYPOXEMIA ON EXERTION = Pt who exhibitexertional hypoxemia only 1) Pt must exhibithypoxemia on exertion (exertional saturation ≤88%) on room air and improve exercise tolerance with O2  Desaturation < 80% on walking,regardless of dyspnea or distancewalk  If pt ableto walk > 5 min, must demonstrate an objective measured improvement in walking performance on O2 so that the distancewalked increaseby 25% + one unitin the BORG scoreat the end-exercise point of the shortest test  If pt ableto walk < 5 min, must demonstrate an objective measured improvement in walking performance so that the time walked increases ≥2 min + one unitin the BORG scoreat the near end-exercise pointof the shortesttest Demonstrate an ability to perform an appropriate physical examination of a patient with COPD On physical examination,patients with emphysema often appear thin (cachectic),and they frequently lean forward and rest on extended arms (tripod position). This position allows fixation of one end of the shoulder and neck muscles,allowingthem to function more effectively as muscles of respiration. Thesepatients arenot cyanotic and do not demonstrate peripheral edema characteristic of RV failure. In contrast,patients with chronic bronchitis often are obese and sometimes cyanotic butgenerally appear to be in less respiratory distressthan those with emphysema.
  33. 33. Examination of the chest discloses an increased anteroposterior diameter as a resultof hyperinflation of lungs. Patients may be usingaccessory musclesof respiration,such as sternocleidomastoid and trapezius,and there may be retraction of intercoastal muscles with inspiration. When diaphragmatic excursion is assessed by percussion of the lung bases duringinspiration and expiration,diminished movement is noted. Breath sounds aregenerally decreased in intensity,and expiration is prolonged. Wheezing may be heard or it may be brought out with forced exhalation. In patients with chronic bronchitisand profuseairway secretions,coarsegurglingsounds labeled as rhonchi arefrequently appreciated.  Blue Bloaters  patients often present with a hx of recurrent infection,chronic cough and abundant purulent sputum; patients can show signs of hypercapnia and severe hypoxemia resultingin cyanosis; patients may have peripheral edema due to RV failure; pulmonary hypertension and cor pulmonale (overload on RV) are complicationsof chronic bronchitis  Pink Puffers  severe dyspnea; barrel chest; px may sitfwd in hunched-over position,with a pinched face and pursed lips; patients may overventilate and remain well oxygenated Establish an appropriate treatment plan for exacerbations of COPD, taking into account the latest Canadian consensus guidelines 1) Oxygen: Sat 90-94% 2) Short actingBeta Agonist: nebulized albuterol 2.5mg q1-4h PRN or 4-8 puffs (90mcg/puff) w spacer → NOTE: ↑ dose does not affect outcome 3) Short actinganti-cholinergic:500mcgnebulized ipratropriumq4h 4) Systemic corticosteroid:prednisone – 2 week therapy w taper atend - First24 hours: 80-125mg - If symptoms ↓: 40-60 mg/day 5) Ab: only treat severe exacerbation requiringmechanical ventilation,or exacerbation w↑ sputum purulence + ↑ dyspnea OR ↑ sputum volume – see Ab choicefor pneumonia Describe the mechanism of action of the main pharmacological agents available to treat COPD B2-agonsists Act on B2 receptors resultingin bronchodilation,improvelungfunction and symptoms (salbutamol for short-acting,salmeterol for long-acting) Anticholinergics Block acetylcholineresultingin bronchodilation (synergistic with b- agonists),ipatropiumfor short acting,tiotripiumfor longacting Glucocorticoids Systemic steroids work by decreasingthe inflammatory immune response, used for exacerbations and NOT longterm management Methylxananthines Weak bronchodilator and offer modest improvement in pulmonary function, not used acutely (Theophylline) - use a combination of shortand longactingtreatments Discuss the various diagnostic tests for asthma -requires documentation of 1) hyperactive airways,and 2) reversibleobstruction to flow *sinceasthma attacks/symptoms come and go, you may need a bronchoprovocation test/challenge;NB: history maybe enough in most cases Test Description and Expected Results, If Asthmatic
  34. 34. Spirometry (routine pulmonary function tests) Decreased Forced Expiratory Volume in 1 sec (FEV1), hyperinflation,improvement with bronchodilator Provocation with bronchoconstrictor (histamine, metacholine, cold air,exercise);methacholine is a synthetic acetylcholinethatis preferred becauseit has fewer systemic effects Diagnosisdepends on amount of stimulus to produce an effect: the concentration of methacholinerequired to produce a 20% reduction in baselineFEV1 is reported; NB: not alonediagnostic,butcan help rule out asthma. Lung volume measurements May show hyperinflation duringactivediseasebutit’s typically normal becauseasthma alonedoes not destroy acini Arterial blood gas May be useful duringacute exacerbations for determining gas-exchange status Chest radiograph Usually only doneif concern for infection;fleeting infiltrates and central bronchiectasuscommon in allergic bronchopulmonary aspergillosis Blood tests May show eosinophiliaand increased IgE(increased in atopy) Skin prick Allergy tests for household items and antigens that might precipitate attacks  Asthmatics will show REVERSIBILITY of airway obstruction o FEV1 with increase≥12% (>180 ml) 15-20 minutes after inhalation of B2-agonist o FEV1 decreases >10% after 6 minutes of exercise o Methacholinechallenge: FEV1 will decrease 20% with <8mg/ml methacholine compared to control subjects List the criteria for adequate control of the asthmatic patient Classification of asthma by severity : clinical aspects and treatment Asthma severity Clinical features before tx Nighttime symptoms Lung function Treatment Mild intermittent  Symptoms < 3x/week  Capableof normal activity  Exacerbations brief  <3x/mont h  FEV1 > 80% predicted  FEV1/FVC normal  Short actingß2 agonistprn Mild persistent  Symptoms 3x/week, but < 1x/day  Minor limitation w normal activity  3- 4x/month  FEV1 > 80% predicted  FEV1/FVC normal  Short actingß2 agonistprn  Inhaled corticosteroid or sustained release theophylline, leukotriene modifier or cromoglycate Moderate persistent  Daily symptoms  Daily useSA ß2 agonist  Limitation w normal activity  Exacerbations >2x/week; may lastdays  >1x/week but not nightly  FEV1 60- 80% predicted  FEV1/FVC reduced 5%  Low-dose inhaled corticosteroid +long actingß2 agonist OR  Medium-dose inhaled corticosteroid
  35. 35. Severe persistent  Continual symptoms  Extremely limited w normal activity  Frequent exacerbations  Often nightly  FEV1 <60% predicted  FEV1/FVC reduced 5%  Medium or high-dose inhaled corticosteroid +long actingß2 agonist  Consider short courseoral corticosteroid Discuss the various treatmentsavailable to control asthma 1) Lifestyle/risk modification 2) Medication 3) Desensitisation Medication Management algorithmbased on level of control If well-controlled for ≥ 3 mo, step down ↔ If not well-controlled,step up after addressing: - Avoidance - Adherence - Comorbities - Triggers Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Rapid medication As-needed SABA Preferred controller medication - Low-dose ICS Low-dose ICS + LABA Or Medium-dose ICS Medium-dose ICS + LABA High-dose ICS + LABA + Evaluation for omalizumab Add OCS to Step 5 medication Alternate controller medication - LTRA or Cromolyn Or Sustained release theophylline Low-dose ICS + LTM Or Sustained release theophylline Consider addingLTM And/or Sustained release theophylline 1st line Short-acting ß2 (bronchodilators) MDI or Inhaler prn Salbutamol (ventolin) - 1st linetmt for LT management of all severities of asthma + rapid tmt of exacerbations Inhaled corticosteroids DPI, MDI or nebulized Budenoside (pulmicort),Fluticasone (Flovent),Beclomethasone (Qvar) - For persistentasthma - Dosingdepends on assessmentof severity and control - Attemps should be made to ↓ doseof ICS every 2-3 mo to the lowest possibledoseto maintain control
  36. 36. Long-acting inhaled ßagonists (LABA) Formoterol (Oxeze, Serevent), Salmeterol/Fluticasone(Advair),Budenoside/Formeterol (Symbicort) - Recommended for moderate and severe persistentasthma, in pt not adequately controlled with ICS - Should be used in combination with ICS: Salmeterol/Fluticasone,Budenoside/Formeterol) - Salmeterol and Formoterol, added to ICS have been shown to ↑ lungfunction , both day and nighttime, ↓ exacerbations,and minimizethe required dose of ICS Systemic corticosteroids - May be necessary to gain control of diseasequickly via either oral or IVroute - If chronic sx aresevere, accompanied by nighttime awakening,or PEF < 70 % of predictive values,a short courseof systemic corticosteroids (prednisone40-60 mg/d q 5-7 days) might be necessary - Should be administered to all ptduringan exacerbation o Speed the resolution of exacerbation o Ideal doseto speed recovery and limitsx not well defined. Various options. 2nd line Leukotrienes modifiers - Leukotriene-receptor tantagonists =Montelukast (10 mg PO qd) and Zafirlukast(20 mg PO bid) o Recommended as alternativemedication for mild persistent asthma - 5-lipoxygenaseinhibitor =Zileuton (extended release1200 mg bid) o Recommended as an add-on to ICS for more severe forms of asthma - Improve lung function,quality of lifeand lead to fewer exacerbations butnot as effective as ICS + LABA in improvingasthma outcomes Discuss the treatment options for OSA 1) Modifiablefactors:weight loss,↓ alcohol/sedativeuse(↓ sleep quality),nasal decongestion,underlying medical condition 2) Postural therapy: for pts with positional sleep apnea (ie. Sleep apnea only when lyingon back). Suggest “tennis ball technique”: put tennis ball in sock,and sew to pyjamas → prevents pt from rollingonto back 3) Mild apnea: dental appliance(expensive) 4) CPAP: in some pts, if CPAP is too high,central sleep apnea can be induced – therefore we want the lowest pressurepossiblethatgets the AHI <5/hr, without causingCSA 5) Peds: uvulopalatopharyngoplasty,tonsillectomy → not proven effective in adults 6) Tracheostomy: used as lastresort Describe the signs and symptoms of Obstructive Sleep Apnea (OSA) - Frequent arousals and fragmented sleep cause: daytime somnolence, personality/cognitivechanges, snoring – most obvious symptom - Hypoxemia, hypercapnia cause:headacheupon waking, polycythemia,pulmonary/systemic HTN, cor pulmonale/CHF, nocturnal angina,arrhythmias - Leg movements can be related to apneic events … also… - habitual snoring - witnessed apneas - nocturnal gaspingor choking
  37. 37. - fatigue (lack of restful sleep and persistenthypoxia (later stage of pulmonary hypertension) - daytime hypersomnolence (excessivedaytime sleepiness) - intellectual impairment(reduced attention and cognitiveability),memory loss,personality disturbances - swollen ankles / peripheral edema (cor-pulmonale– rightheart failureresultingfrom pulmonary hypertension as a resultof chronic hypoxia duringthe apneic events) - obesity (presumably from reduced daytime physical activity - fatigue) - pulmonary hypertension (resultingfrom chronic hypoxia in pulmonary vasculature) - systemic hypertension (chronic sympathetic stimulation after the apneic events) - chronic hypoventilation/CO2 retention (reset central respiratory control level) Discuss the complications of OSA - Depression,weight gain (due to hormonal changes with ↓ sleep, AND ↓ energy because of less sleep),↓ energy, ↓ quality of life,motor vehicleaccidents risk x6,cardiac complications(HTN, CHF, cor pulmonale, nocturnal angina,arrhythmias),↓ social function,complicationsduringand post-surgery Describe the underlying pathophysiology of pneumonia -Most common routes of entry: aspiration of oropharyngeal secretions Ex. Legionelle, mycobateria,endemic fungi, mycoplasma pneumonia,Chlamydia pneumonia,most virus’ -Less common route: hematogenous or embolic spread from infection heart valves or venous clot(often multifocal with peripheral lesionssusceptibleto cavitation) COMMUNITY-ACQUIRED PNEUMONIA  Streptococcus pneumonia - most common (an encapsulated gramp +ve diplococcal bacteria)  Mycoplasma pneumonia (facultativeanaerobic organism) NOSOCOMIAL PNEUMONIA  3 types: 1) hospital-acquired,2) ventilator-associated,3) health care –association (contactwith health careworker)  Based on colonization of oropharynx and stomach with virulentpathogens and subsequent aspiration into lower respiratory tract  Gastric colonization by gram–ve organisms increased by neutralization of gastric acidity  Within 1st 5 days: H. influenza,Strep. pneumonia, S. Aureus  More than 5 days: P. aeruginosa,S.Aureus, anaerobics,acinobacter PATHOGEN COMMUNITY-ACQUIRED NOSOCOMIAL BACTERIAL 70-80% 90% S. pneumonia 60-75% 3-9% H Influenza 4-5% Up to 25% Legionella 2-5% 10-20% S Aureus 1-5% 10-20% Gram –ve bacilli Rare 50% ATYPICAL 10-20% Rare M pneumonia 5-18% -- Clam. Psittaci 2-3% -- CloxiellaBurnetti 1% -- VIRUS --
  38. 38. Influenza virus -- 8% Hantavirus -- rare Recognize pneumonia on a chest x-ray Lobular consolidation  Suggests bacterial pneumonia Interstitial infiltrates  Suggest non-bacterial pneumonia (but may be seen in early staphylococcal pneumonia Inlarged hilar lymph nodes  Concomitant lungtumor  Primary tuberculosis,viral or fungal pneumonias Large pleural effusions  Streptococcal pneumonia or tuberculosis Negative CXR  Cannot ruleout pneumonia Identify the severity criteria associated with pneumonia Factors increasing severity of pneumonia: 1) age < 50 years 2) neoplastic disease 3) heart failure 4) cerebrovascular disease,renal diseaseor liver disease 5) altered mental status 6) pulse> 125 beats/minute 7) respiratory rate> 30 breaths/minute 8) systolic blood pressure< 90 mm Hg 9) temperature > 40 degrees C (104 degrees F) or < 35 degrees C (95 degrees F) 10) Hx of cancer, CHF, CRF, chronic liver disease
  39. 39. ** mortality < 0.5% if none of the above criteria ** use Pneumonia Severity Index Calculator or seePneumonia severity assessmentto predict mortality if risk factors (see below) Mortality/severity varies by etiology - Mortality ranges from < 2% for certain pathogens to > 30% for gram-negative bacteria - Legionella pneumonia also associated with ↑ severity Prognostic factors associated with mortality are: - Male gender - Pleuritic chestpain - Hypothermia - Systolic hypertension - Tachypnea, diabetes mellitus - Neoplastic disease - Neurologic disease - Leukopenia, bacteremia - Multilobar infiltrateon x-ray Pneumonia Severity Index/Assessment STEP 1 Presence of: - Over 50 years of age Yes/No - Altered mental status Yes/No - Pulse≥125/minute Yes/No - Respiratory rate >30/minute Yes/No - Systolic blood pressure<90 mm Hg Yes/No - Temperature <35°C or ≥40°C Yes/No History of: - Neoplastic disease Yes/No - Congestive heart failure Yes/No - Cerebrovascular disease Yes/No - Renal disease Yes/No - Liver disease Yes/No If any yes, proceed to step 2. If all no,assign Risk Class I STEP 2 Demographics: - If Male +Age (yr) - If Female +Age (yr) - 10 - Nursinghome resident +10 Comorbidity: - Neoplastic disease +30 - Liver disease +20
  40. 40. - Congestive heart failure +10 - Cerebrovascular disease +10 - Renal disease +10 Physical exam findings: - Altered mental status +20 - Pulse≥125/minute +20 - Respiratory rate >30/minute +20 - Systolic blood pressure<90 mm Hg +15 - Temperature <35°C or ≥40°C +10 Lab and radiographic findings: - Arterial pH <7.35 +30 - Blood urea nitrogen ≥30 mg/dl (9 mmol/liter) +20 - Sodium <130 mmol/liter +20 - Glucose≥250 mg/dl (14 mmol/liter) +10 - Hematocrit <30% +10 - Partial pressureof arterial O2 <60mmHg +10 - Pleural effusion +10 Interpretation of Pneumonia Severity Index Class Description of severity Class I Exhibitno severe clinical signs and aged less than 50 yrs old. This classhas a 30-day mortality rateof 0.1%, however, it is not relevantto residents of RACFs. Class II PSI score 1-70 This classhas a 30-day mortality rateof 0.6% and are usually treated in the RACF home. Class III PSI score 71-90. This classhas a 30-day mortality rateof 0.9% and should be assessed for appropriateness of IV treatment in the facility or hospital. Class IV PSI score 91-130. This classhas a 30-day mortality rateof 9.3% and is usually treated in hospital. Class V PSI score >130. This classhas a 30-day mortality rateof 29.2% and should be treated in hospital. List the main pathogens by age group for pneumonia
  41. 41. -listed in the tableare the etiologic agents for adults – Strep, Mycoplasma pneumonia,and Haemophilus influenza are the 3 most common etiologic agents Newborns (age 0-30days) -infections with Strep group B, listeriamonocytogenes or gram-negative rods (e.g. E. coli,Klebsiellapneumonia) are a common causeof bacterial pneumonia. These pathogens can be acquired in utero, via aspiration of organisms presentin the birth canal,or by postnatal contactwith other people or contaminated equipment. -some organisms acquired perinatally may not causeillnessuntil later in infancy –Chlamydia pneumonia, CMV, etc. - Community-acquired viral infectionsoccur in newborns,although less commonly than in older infants –RSV is most common Infants and Toddlers: - Viruses arethe most common causeof pneumonia, accountingfor approximately 90% of all lower respiratory infections. RSV is the most common viral pathogen, followed by parainfluenza types 1, 2, and 3 and influenza A or B. RSV infection occurs in the winter and early spring.Parainfluenza type3 infection occurs in the spring,and types 1 and 2 occur in the fall.Influenza occurs in thewinter. Other viruses thatcausepneumonia less frequently in infants includeadenovirus,enterovirus,rhinovirus,coronavirus,herpesvirus,and cytomegalovirus.Arecent addition to this listishuman metapneumovirus, which causes an illnesssimilar to RSV and may be responsiblefor one third to one half of non-RSV bronchiolitis. -Bacterial infections in this agegroup are uncommon and are attributableto Streptococcus pneumoniae, H influenzae type B (less common in immunized children2 ),or Staphylococcus aureus. Children aged 5 - Mycoplasma pneumoniae is the most common causeof community-acquired pneumonia and accounts for 20% of pneumonia cases in the general population,9-16%of cases in early-school–aged children,16-21%of cases in older children,and 30-50% of cases in collegestudents and military recruits.C pneumoniae is also fairly common in this age group and presents in a similarfashion. School-aged children and adolescents: - Bacterial pneumonia (10%) is common, and these children areoften febrileand appear ill. **In immunosuppressed individuals,opportunistic infectionswith organisms such as Aspergillus species,Candida species,Pneumocystis species,and cytomegalovirus can occur. Elderly: (in 30-50%, no specific pathogen is found) Colonization of the respiratory tractwith potentially pathogenic gram-neg and gram-pos bacteria occurs more often in the elderly, owing in partto such factors as repeated antibiotic therapy,endotracheal intubation,smoking, malnutrition,surgery,and therapy that lowers gastric acidity,thereby raisingpH.  S pneumonia (causingpneumococcal pneumonia – most common bacterial causeof community-acquired pneumonia in the elderly (15-50%).  Gram-negative bacilli (Klebsiella,Pseudomonas, enterobacter sp, proteus sp, E. coli.  Anaerobic bacteria - cause20% of community-acquired and 31% of nosocomial cases of pneumonia in the elderly.Pneumonia caused by anaerobes usually resultsfromaspiration.Elderly patients tend to aspirate
  42. 42. because of conditions associated with agingthat alter consciousness,such as sedativeuseand medical conditions (eg, neurologic disorders,weakness).  Haemophilus Influenza  Legionella – increases with age  Viruses - influenza and parainfluenza viruses,respiratory syncytial virus,and possibly adenoviruses. Influenza is the most important causeof pneumonia in the elderly. Its incidencein persons >= 70 is about 4 times that in persons < 40. About 90% of influenza-associated deaths in the USA occur in persons >= 65. Secondary bacterial pneumonia may complicatea courseof influenza. Select the antibiotic treatment of choice for pneumonia Tmt for pneumonia depends on infection conditions: - Outpatient: o 1stchoice: macrolides (erythromycin,azithromycin,clarithromycin) 250-500mgQID o 2nd choice:doxycyclin - COPD: o No antibiotic tmtor steroid use in past3 months:  § 1stchoice: new macrolides (azithro,clarithro)  § 2nd choice: doxycyclin o Recent (within 3 months) Ab/steroid use:  § 1st: levofloxacin,gatifloxacin  § 2nd: amoxi-clavulanate+ macrolide,OR2nd generation cephalosporin +macrolide o Microaspiration:  § 1st: amoxi-clavulinate+/- macrolide;OR moxifloxacin  § 2nd: levofloxacin +clindamycin ORmetronidazole - Nursinghome pt: o 1st: levofloxacin/amoxi-clavulinate+macrolide o 2nd: 2nd generation cephalo + macrolide - Pt on ward: o 1st: levo, gatifloxacin,moxifloxacin o 2nd: cefuroxime/cefepime/cefotaxime/ceftriazone + macrolide - Pt in ICU: o 1st: IV levofloxacin +cefotaxime/ceftriaxone/beta lactamaseinhibitor o 2nd: IV macrolide+ cefotaxime/ceftriaxone/beta lactamaseinhibitor o P. aeruginosa:  § 1st: cipro + ceftazidime/carbapenem/pip-tazo OR gentamycin/tobramycin/amikacin  § 2nd: tripletherapy w antipsudomonal beta lactamaseinhibitor +aminoglycoside+ macrolide Describe the complications of pneumonia o Pleural effusion:an excess amount of fluid in the pleural space o Hypoxia:missingoxygen o Empyema: rare complication (person more likely to be younger of drug user), pus in the pleural spaceor an effusion with organisms seen on a gram stain or culture – for example when pleural fluid isgrossly purulent– positivecultureNOT required for diagnosis,resultsfromcontiguous spread from lunginfection (eg anaerobes) or infection through chest wall (eg trauma or surgery)
  43. 43. o Lung abcess:predisposingfactorsto this includealcoholism,seizures,poor oral hygieneand previous aspiration,chestCT most sensitivetest to detect, increased mortaility with largecavity size,longer duration of symptoms, lower lobelocation,association with malignantdisease o ARDS: respiratory failure o Sepsis and toxic shock:bacteremia and septicaemia,systemic infection spreadingfromthe lungs o Bacterial resistance:prolonged bacterial infection with resistanceto antibiotics o Pneumothorax: collection of gas in the pleural spaceresultingin thecollapseof the lungon the affected side, especially associated post-penumonia with Staph, klebsielle,Pseudomonas and Pneumocystis o Hemoptysis: coughing up blood Interpret the results of a thoracocentesis for pleural effusion -Thoracocentesis:fluid aspirated from pleural space;2 types: exudate and transudate TRANSUDATES -due to changes in osmotic and hydrostatic forces;usually small,may not require drainage -Ex. CHF, hypoalbuminemia,nephrotic syndrome, malnutrition,cirrhosis,intra-abdominal fluid,ascites, peritoneal dialysis EXUDATES -due to alterations in vascular permeability;can be observed in inflammatory states, infection,or cancer -Ex. Infection,empyema, primary lungcancer,llymphoma,metastatic camcer, pulmonary embolismor infarct, lupus,rheumatoid arthritis,trauma,hemothorax, myexedema, uremia,asbestosis,lymphedema, drug-induced lupus Exudate Transudate Protein More than 3g/dl Less than 3g/dl Pleural:serumprotein ratio More than 0.5 Less than 0.5 Lactate dehydrogenase (LDH) Two thirds the upper limitof normal Pleural:serumratio of LDH More than 0.6 Less than 0.6 Establish an appropriate history and physical examination for a patient with hypoxemia History  Symptoms: o Cough (+ character),dyspnea, SOBOE, sputum production and colour,hemoptysis, fever, chills, infectious contacts,travel,chest trauma o Orthopnea, PND, leg swelling,exercisetolerance  Pastmedical history o COPD, asthma, lungcancer, other cancers,CHF, hypertension, neuromuscular disease  Medication (+ compliance) includinghome oxygen  Systems review Physical examination  General appearance:level of consciousness,respiratory distress(tachypneic,gasping),useof accessory respiratory muscles,colour (cyanosis),diaphoresis,pain,oxygen need  Vital signs  Head and neck: peripheral and central cyanosis,mucous membranes, lymph nodes
  44. 44.  Resp: o Inspection:chest deformities (barrel chest),signs trauma,clubbing,capillary refill o Palpation:areas of tenderness, tactilefremitus, o Percussion:areas of hyperresonance,or matte areas o Auscultation:air entry, breath sounds,wheezing, crackles,rhonchis,pectoriloquy, bronchophony, egophony  Cardiovascular: o Inspection:JVP, peripheral oedema, o Palpation:apical impulse,fremitus o Auscultation:S1, S2, extra heart sounds (S3, S4), murmurs Discuss the differential diagnosis of chronic cough Common causes: - Upper airway cough syndrome (postnasal drip) - Asthma - GERD Other causes: - ACE inhibitors - Aspiration - Bronchiectasis - Cystic fibrosis - Chronic interstitial lungdisease - Lung/laryngeal cancer - Pertussis - Psychogenic - Restrictivelung disease - TB, atypical mycobacterium,and other chronic lunginfections Will diagnoseetiology in most patients: 1) Directed history and physical 2) Pulmonary function testing 3) Sinus radiographs 4) Bariumesophagography,or 24 hour esophageal pH monitoring Signs and symptoms of postnasal drip havelowpredictivevaluedue to poor specificity.Not clinically possibleto distinguish simplepostnasal drip frompostnasal drip dueto chronic sinusitis When consideringonly patients with cough at least3 weeks, who are non-smokers and not on ACE inhibitors,with normal or nearly normal and stablechestradiographs: - 99.4% will haveGERD, postnasal drip syndrome and/or asthma Consider pertussis in: - Infants with apnea or severe coughingof any duration - Children or adults with prolonged cough (> 2 weeks), especially if o Inspiratory whoop o Household exposure to prolonged cough illness
  45. 45. Propose an effective investigation plan to establish a diagnosis of chronic cough Investigate each of the possiblecauses Outline the various treatmentsavailable to control chronic cough Non-specific therapy: Cough supressors  Centrally acting:supress central cough centre o Codeine or other opioids (morphinecommon) o Dextromethorphan  Peripherally acting:benzonatate - anesthesizes stretch receptors in lung  Inhaled Glucocorticoids:reduces inflammation;?results in non-asthmatic/non-eosinophilicpatients  Ipratropiumbromide: anticholinergic,blocksefferent limb of cough reflex and decreases stimulation of cough receptors Condition specific: - Post nasal drip:oral antihistamine-decongestant,avoid allergicstimulus - Asthma: inhaled glucocorticoid +SABA - GERD: PPI + lifestyle - ACE-I: change tmt plan - Chronic bronchitis:stop smoking - Eosinophilic bronchitis:inhaled glucocorticoids List the main risk factors for venothromboembolic disease The main risk factors for venous thrombosis arepartof Virchow’s Triad:  Endothelial damage (leads to decreased inhibition of coagulation and local fibrinolysis,trauma,surgery, prior DVT)  Venous stasis (immobilization,egpost MI, CHF, stroke, post-op, which inhibits clearanceand dilution of coagulation factors)  Hypercoagulability (acquired or inherited) 1. Increases with age 2. Surgery (especially ortho)
  46. 46. 3. Trauma (especially fractures of the spine, pelvis,femur) 4. Neoplasms (especially lung,pancreas,colon,rectum, kidney and prostate cancer) 5. Blood dyscrasias(myeloproliferativedisorders) 6. Prolonged immobilization (CHF,stroke, MI, leg injury) 7. Hormone related (preggers, OCP, HRT, SERMs) 8. Antiphospholipid antibody syndrome(APLAS) 9. Hyperhomocystenemia 10. Heart failure  Idiopathic  Malignancies  Previous DVT Describe the usual signs and symptoms of venothromboembolic disease Venothromboembolic diseaseencompasses both deep vein thrombosis (DVT) and pulmonary embolism(PE) DVT: -Symptoms:  Lower extremity: pain and swelling,but may be asymptomatic if restricted to calf  Upper extremity: superior vena caval syndrome(facial swelling,blurred vision,dyspnea);thoracic outlet obstruction can compress brachial plexus and causeunilateral pain and hand weakness -Signs:  Lower extremity: tenderness, erythema, warmth, swellingbelowsite of thrombosis,+/- Homan sign (pain with dorsiflexion),dilated superficial veins,lowgradefever  Upper extremity: brachial plexus tenderness in supraclavicular fossa,atrophichand muscles PE: -Symptoms (acute):  Sudden onset dyspnea and pleuritic chestpain (sharp pain,worsewith breathing and movement)  Angina chest pain possiblefromrightventricular ischemia  Hemoptysis from pulmonary infarction  Syncope/presyncope from acute right-ventricular failure(cor pulmonale) -Signs:  Tachynpnea  Tachycardia  Inspiratory crackles  Loud P2  Expiratory wheezing  Pleural friction rub on auscultation  Signs of DVT present in 10-20% of patients  Arterial blood gas:+/- hypoxemia, respiratory alkalosis Discuss the differential diagnosis of venothromboembolic disease DVT  Musclestrain/tear  Lymphangitis / lymph obstruction
  47. 47.  Venous valvular insufficiency  Ruptured popliteal cyst  Cellulitis  Arterial occlusivedisease PE  Cardiac:ACS, aortic stenosis,atrial fibrillation,CHF,MI, pericarditis,  Resp: ARDS, asthma, COPD, pneumonia, pneumothorax, TB  Other: MSK, acute anemia, shock Order appropriate investigations for a patient with suspected venothromboembolic disease 1) ECG and CXR useful to look for other causes 2) D-dimer o Only useful if negative in lowrisk pt 3) Duplex scan o High sensitivity and specificity for proximal clotbutonly 73% sensitivity for calf DVT 4) CT angiography: high sensitivity and specificity for PE 5) V/Q scan: useful when Ct angio not available 6) Pulmonary angiography: gold standard but more invasive Specific investigationsfor DVT 1) D-dimer test only useful to ruleout DVT if negative and low clinical suspicion of disease 2) Doppler US o Most useful dx test o Sensitivity and specificity:proximal DVT= 95%, calf DVT = 70% 3) MRI 4) Plethysmography 5) Venography o Gold standard,but expensive, invasiveand higher risk Specific investigation for PE(if highly suspicious,go straightto spiral CT) 1) D-dimers (products of thrombotic/fibrinolytic process) o D-dimer results alonedo not rule in or out DVT/PE o Need to use in conjunction with leg dopplers, other investigations 2) Spiral CTscan with contrast o Sensitiveand specific for PE 3) Venous duplex ultrasound or doppler (high specificity) o With leg symptoms: (+) test can rulein a proximal or distal DVT, (-) test can only rule out a proximal DVT o Without leg symptoms: (+) test rules in proximal DVT, (-) test does not ruleout a DVT (a possible non-occlusiveDVT?) 4) ECG (not sensitiveor specific) o sinus tachycardiamostcommon, may see non-specific STand T waves changes o RV strain,RAD, RBBB S1 Q 3 T3 with largeembolus 5) CXR
  48. 48. o Frequently normal and often nonspecific (e.g. areas of atelectasis,elevation of a hemidiaphragm, pleural effusion) 6) V/Q scan (very sensitivebut low specificity) o Order scan if:CXR normal/mild abnormalites,no COPD o Avoid if: CXR abnormal or COPD, inpatient, suspectmassivePE o If normal, excludes dx of PE, although 60% arenondiagnostic Establish an appropriate treatment plan for venothromboembolic disease Treatment of DVT:  Goal is to prevent extension of thrombus and PE  Initial tx involves therapeutic doses of either unfractionned heparin or LMW heparin. Initial treatment with an oral anticoagulantaloneis unacceptable.  Doppler Legs to evaluate extent of thrombus and have a baseline  Long-term treatment – oral therapy with vitamin K antagonists (e.g. warfarin) is very effective for long- term prevention of thrombosis.If firstproximal DVT occurs in the context of a transientfactor (e.g. surgery, trauma), the risk of recurrence is very low and a limited duration of therapy (3 months) is required. If firstDVT occurs in the context of activemalignantdisease,which is an ongoingrisk factor, longterm anticoagulation with LMW heparin has been shown to be more effective than warfarin. See http://www.cmaj.ca/cgi/reprint/175/9/1087 for extensive details on time of anticoagulation required post DVT event – if thrombophilic cause,lifelonganticoagulation recommended.  Addition of systemic thrombolysis leadsto earlier patency of the occluded vein; however, itdoes not affect the rate of PE. There is a definite increasein the risk of hemorrhage so not recommended.  Placement of an inferior vena cava filter in addition to anticoagulation therapy has notbeen found to prolongsurvival amongpatients with DVT. Whilepreventing PE, insertion of a filter increases therisk of recurrent DVT (and is only recommended when anticoagulation iscontraindicated). Treatment of PE:  ED: heparin (either unfractionated or LMWH) reduces risk of mortality of PE becauseit slows or prevents clotprogression and reduces the risk of further embolism. Heparin does nothing to dissolveclotthathas developed already,but it is still thesinglemost importanttreatment that can be provided, becausethe greatest contribution to the mortality rate is the ongoing embolization of new thrombi. Treatment of DVT and PE: 1 mg/kg SC q12h or 1.5 mg/kg SC qd for 5 d; overlap w/warfarin until INR 2-3  Oxygen should be administered to every patient with suspected PE, even when the arterial PO2 is perfectly normal,because increased alveolaroxygen may help to promote pulmonary vasculardilatation.  IV fluids may help or may hurt the patient who is hypotensivefrom PE depending on which point on the Starlingcurvedescribes the patient's condition Fibrinolytictherapy has been the standard of carefor patients with massiveor unstablepulmonary embolism(PE) sincethe 1970s.Unless overwhelming contraindicationsareevident, a rapidly actingfibrinolyticagentshoul d be administered immediately to every patient who has suffered hypotension (even if resolved) or is significantly hypoxemic from PE. Fibrinolysis isindicated for any patient with a PE large enough to causehypotension, even if the hypotension is transientor correctable.As noted above, early fibrinolysis may reducethe mortality rate by 50% for patients who have rightventricular dysfunction dueto PE, even if they are hemodynamically stable Interpret a complete blood count Normal CBC: - RBC: male 4.32-5.72; female 3.9-5.03
  49. 49. o ↑ in: polycythemia vera, vigorous exercise,high altitude o ↓: anemia - Hg: male 135-175;female 120-155 o ↑: polycythemia vera, tobacco abuse, high altitude,stress,renal cell CA, cardiovascular disease, dehydration, thalassemia trait o ↓: anemia,hemolytic anemia,acute hemorrhage, marrow failure,CRF - Hematocrit: male 38.8-50%; female 34.9-44.5% o ↑: dehydration,profound diuresis,hemoconcentration (burn, trauma, shock),polycythemia vera, high altitude o ↓: anemia,pregnancy - WBC: 3.5-10.5 o ↑:  Neutrophilia:stress,acute infection,tissueinjury/inflam,metabolic condition (ARF, eclampsia,ketoacidosis),acutehemorrhage, steroids,lithium,beta agonists  Lymphocytosis,monocytosis  Acute leukemia: thrombocytopenia, peripheral smear w immature cells (blasts), hyperuricemia  Chronic leukemia: normal plateletand Hg o ↓: neutropenia, lymphocytopenia,monocytopenia, eosinopenia - Platelet: 150-450 o ↑: thrombocytosis – CML, polycythemia vera, myelofibrosis,essential thrombocythemia o ↓: thrombocytopenia  Platelet destruction:immune, prosthetic heart valve, TTP, sepsis,DIC,hemorrhage w extensive transfusion  ↓ production: hereditary,infiltrative(leukemia,myelofibrosis,neuroblastoma…), suppression of megakaryocytes (alcoholism,radiation,infection by TORCH, meds, aplastic anemia) Demonstrate an approach to the differential diagnosis of anemia - In general, hemoglobin must be <135 Microcytic (MCV <80) Normocytic (MCV 80-100) Macrocytic (MCV >100) Lead poisoning Fe deficiency (Increased loss, decreased intake) Thalassemia Sideroblastic Chronic disease Acute blood loss Hemolysis Anemia of chronic disease (cancer,thyroid, infection, inflammation) Aplastic anemia MDS Renal/kidney failure Drugs B12 Folate EtOH abuse Hypothyroid Drugs (methotrexate, chemotherapy) Pregnancy - Also look at RDW for different populations of RBC and reticulocyte count - B12 and folate are megalobastic - CBC + differential - Personal medical history and presentingsymptoms!!!
  50. 50. Demonstrate a detailed history focused on anemia  Obtain details of previous blood tests to establish duration of problem  Family history:anemia,jaundice,cholestasis,splenectomy,bleeding disorders and abnormal hemoglobins  Blood loss:pregnancies,abortions,menstrual losses  Changes in bowel habits (red streaks,tarry stools,etc.)  GI history:hemorrhoids,gastritis,peptic ulcers,hiatal hernia (and potential symptoms of these conditions)  Abnormal urinecolour (can be present in renal,hepatic and hemolytic disorders)  Thorough dietary history (foods patients eats and those patient avoids) o Meal-by-meal description o Consumption of clay or laundry starch (makes iron less absorbable)  Changes in body weight: may suggest malabsorption or infectious,metabolic or neoplastic disease  Unusual symptoms associated with nutritional deficiencies o Iron: suck or chew ice(pagophagia),dysphagia,brittlefingernails,impotence, fatigue, cramps in calves with exercise/effort o B-12: early grayingof hair,burningsensation of the tongue, decreased proprioception o Pernicious anemia:paresthesia,unusual sensationsdescribed as pain o Folate: sore tongue, cheilosis,symptoms associated with steatorrhea o Stools: color,bulk,frequency, odor, oily(?),whether stools sink or float(malabsoption)  Fever (infections, neoplasms,collagen vascular disease)  Purpura,ecchymoses, petechia (thrombocytopenia, bleeding disorders)  Dark urine associated with physical activity or particular timeof day (march hemoglobinuria,paroxysmal nocturnal hemoglobinuria)  Other symptoms that might suggest underlyingdisease(cardiac,hepatic,renal,chronic infection, endocrinopathy,malignancy) Demonstrate the ability to perform a physical examination focused on anemia VS: BP, HR, RR, Temperature, SatO2 General: cachexia,jaundice Skin: pallor (lips,buccal mucosa,conjunctiva,palmar creases),koilonychias(brittle,ridged or spoon nails) HEENT: Glossitis,angularcheilosis,abnormal facies Lymphatic system: lymph nodes in head and neck, axilla and groin (size,shape,mobility,consistency, tenderness, warmth, number of enlarged nodes) CVS: signs of cardiac compromise(displaced apex,hyperdynamic precordium,bounding pulses Abdomen: examine for hepatosplenomegaly, DRE Discuss the use of appropriate investigations for anemia Basic investigations: 1) Rule out dilutional anemia (lowHb due to ↑ effective circulatingvolume) 2) CBC with differential (pay special attention to MCV and RDW) 3) Reticulocyte count

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