Cardio-Respiratory Flashcards

1
Q

Pulmonary Hypertension: Causes

A

Causes of Pulmonary Hypertension:
1. Primary: Rare
2. Secondary: mostly
= Pulmonary stenosis
= Pulmonary regurgitation
= Lung disease: CF, Bronchiectasis
= Schistosomiasis
= Vasculitis
= ASD, VSD, PDA
= High altitude
= Thromboembolism, PE
= Valve destruction due to IE
= PR caused by carcinoid effects

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2
Q

Patent Ductus Arteriosus
It occurs because a normal fetal connection between the aorta and the pulmonary artery does not close as it should after birth. PDA happens most often in premature infants. It often occurs with other congenital heart defects. A small PDA may close on its own as your child grows.

A

PDA signs:
1. Continuous machinery murmur (systolic) along 2nd ICS, left parasternal, below Left clavicle & posteriorly, 2. Thrusting apex, displaced to AA line, with collapsing nature of pulse if large PDA,
3. Toe clubbing
and
4. signs of PAH if long standing as:
= Palpable P2
= TR murmur with RV heave
= Eisenmenger syndrome & cyanosis as R-L shunt develops
= moratility 20% after 20 years

complications: Endocarditis, Ductal rupture, PAH, aneurysm, calcification

Rx: IV Indomethacin, percutaneous closure, Surgical closure

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3
Q

Causes of continuous MURMUR

A

Continuous Murmur + collapsing pulse
= MR + AR
= VSD + AR
——————————–
C-Murmur without Collapsing pulse:
= Venous hum in children - disappears on lying flat or on compressing Rt Jugular vein
= Pulmonary AV fistal or shunt (Blalock)

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4
Q

Mitral Regurgitation

A

Signs of MR
= Volume overload, displaced apex
= Thrusting apex, RV Lift(heave)
= Pallor, Inner conjunctival petechie
= Systolic murmur, radiates to axilla
= Peripheral signs of IE:
= Splinter haemorrhages@ nailbeds
= Janeway lesion, flat-macular,
= Osler nodes, tender,finger/toe pulps
= Roth’s spot in Retina
= Skin necrosis
= Spleenomegaly

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5
Q

Skin Petechiae Causes

A

Petechiae can be seen with:
= Severe thrombocytopenia
= Infective endocarditis
= Scurvy
= Renal Failure
= Bacteremia without IE (meningococcemia)
= Fat embolism in Cardiopulmonary bypass

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6
Q

Duke’s Criteria for Infective endocarditis

A

Duke’s Criteria for IE
1. Pathological Criteria
= Micro-organisms in a vegetation - demostrated by blood cultures, Histological examination of a vegetation or in intra-thoracic abscess specimen
= Pathological lesions - vegetation or intra-cardiac abscess confirmed by histologic exanination showing active endocarditis
———————————–
2. Major Clinical Criteria:
= Blood cultures positive, 2 bottles
= Single Blood cultures + for Coxiella
= Antiphase I anti-IgG antibody titre>1:800
= Evidence of Endocardial involvement: ECHO+, abscess, new partial dehiscence of Prosthetic valve, new regurgitation
————————–
3. Minor Clinical Criteria:
= Predisposing heart condition/IV DU
= Fever
= Vascular phenomenon: Major arterial emboli, stroke, septic PE, Mycotic aneurysms, ICH, Conjunctival petechiae, Janeway lesions
= Immunological phenomenon: Acute GN, Osler nodes, Roth spots, RA Factor
= Micro-biological evidence but doesnt meet as in major criteria

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7
Q

Duckett- Jones Criteria for Acute Rheumatic Fever

A

Jones Criteria for ARF
1. Evidence of preceding Group A strep infection:
= Rising or high ASO titre
= ++ Group A strep CHO antigen test
= Positive Throat culture
= History of ARF or established Rheumatic heart disease
2. Population at risk
= Low Risk < 2 cases per 100k children
= High Risk
3. Major Criteria:
= Carditis
= Arthritis
= Chorea
= Erythema marginatum
= Subcutaneous nodules
4. Minor Criteria:
= Prolonged PR interval
= Monoarthralgia
= Fever > 38c/ 100.4F
= ESR > 30 CRP > 3 or more than upper level of normal for your Lab

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8
Q

Eisenmenger Syndrome

A

It is development of right to left shunt in congenital cardiac anomalies with development of cyanosis and usually irreversible with high mortality.
Signs:
= Central cyanosis
= Clubbing of fingers, or toes in PDA
= Large a wave in JVP
= RV heave along parasternal
= Palpable P2 heart sound
= Pulmonary Regurg with murmur
= Single Loud S2
= Pansystolic murmur of TR with PAH

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9
Q

Eisenmenger Syndrome, causes

A

Causes of ES:
= Large VSD
= Primary PAH
= ASD with severe RVH
= PDA with Leg cyanosis, Toe clubbing
= Fallot’s Tetrology
= no PS systolic murmur or thrill

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10
Q

Co-arctation of Aorta, signs

A

Signs of Co-Arctation, unrepaired
= Radio-femoral delay
= Weak Leg pulses, strong radials
= BP higher in UL > LL
= Aortic, Supra sternal systolic murmur + thrill
= Heaving apex beat but undisplaced
= Posteriorly left 4th ICS loud systolic murmur
= Right arm BP > Left arm
——————————–
Repaired co-arctation signs:
= no radio-femoral delay
= Left sided thoracotomy scar
= Ejection click with SSM in Aortic area
= Normal undisplaced apex
= Absent/Reduced Left radial pulse
= AR some times

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11
Q

Associations of Co-arctation

A

= Bicuspid Aortic valve lead to AR
= Rib notching
= Post Stenotic dilatation in CXR
= Berry aneurysm in Brain, (SAH risk)
= PDA (machinery murmur, toe clubbing)
= Turner syn: Web neck, short, carrying angle is more,
= Marfan syn: Tall, Arachnodactyly, High arch palate, Lens dislocation, AR
= Hypertension, resistant
= Early High mortality after 40s

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12
Q

Causes of rib notching

A

Causes of rib notching
= Co-arctation of aorta
= Neurofibromas of Intercostal nerves
= Nerve enlargement in amyloidosis, cong. Hypertrophic polyneuropathy
= IVC obstruction
= Blalock shunt operation
= congenital anomaly

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13
Q

Cannon JVP waves:
are giant a waves & occur whenever a right atrium contracts against closed TV

A

Causes of Regular pattern cannon waves:
= nodal rhythm (AV nodal)
= Paroxysmal nodal tachycardia
= Partial Heart block with very long PR
——————-
Causes of Irregular Cannon waves:
= CHB
= Multiple ectopic beats
————–
p wave in ECG will fall between QRS/T or at end of T wave.

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14
Q

Tetrology of Fallot

A
  1. ventricular septal defect,
  2. overriding aorta,
  3. pulmonary stenosis and
  4. ## right ventricular hypertrophy.Signs of TOF:
    = VSD murmur
    = PS murmur, systolic with thrill
    = RV Heave parasternal
    = Central cyanosis + clubbing
    = Rt pulse weak than left or vice versa
    = ? early diastolic murmur of AR
    = Large VSD has no murmur =equal pressure between RV/LV
    —————————
    Most patients will present in the neonatal period with mild-to-moderate cyanosis, but typically without respiratory distress.
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15
Q

What is Blalock Shunt

A

A Blalock-Taussig (BT) shunt is a small tube that connects the arterial circulation to the pulmonary circulation in order to get more blood to the lungs. This is the first in a series of operations required to correct complex congenital heart defects.
A modified BT shunt, a Gore-Tex tube graft is placed between the subclavian artery and the ipsilateral pulmonary artery, and in the central shunt a Gore-Tex tube of a known diameter is placed between the ascending aorta and the pulmonary artery.

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16
Q

Dextrocardia, apex to right

A

About 1 in 4 people with dextrocardia also have primary ciliary dyskinesia such as Kartagener’s syndrome
= Dextrocardia with situs inversus is usually normal, alone it has cardiac anomalies.
= Turner syndrome may have it
= Listen to Lung fields to bronchiectasis associated with Kartagener

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17
Q

Kartagener syndrome
a primary ciliary dyskinesia + Situs

A

rare, autosomal recessive genetic ciliopathy, that causes defects in the action of cilia lining the upper and lower respiratory tract, sinuses, Eustachian tube, middle ear, Fallopian tube, and flagella of sperm cells. Within the first few months of life, most develop a chronic mucus-producing cough and runny nose.
= Dextrocardia
= Bronchiectasis
= Situs inversus
= Infertility
= Frontal sinus dysplasia
= Sinusitis
= Otitis media

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18
Q

HOCM,
Autosomal dominant

A

Clinical features of HOCM:
= mildly displaced forceful apex
= Double apical impulse due to atrial systole
= ESM, 4th Heart Sound
= Associated MR with radiating murmur
= Carotid pulse jerky when severe
= Atrial fibrillation possible
———————-
All first degree relatives- screen by echo
————————
Fainting attacks at end of exercise in HOCM as opposed to fainting during exercise in Aortic stenosis.

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19
Q

HOCM Diagnosis

A

= Genetic studies
= echo, gradient > 40 mmHg
= Echo septal thickness > 18 mm, asym
= LVH, V3V4 tall QRS, LAD in ECG
= H/o Syncope after exercise
= Family H/o Sudden deaths
————————————
Rx options:
= Beta blockers
= Calcium channel blockers
= Septal ablation or Myomectomy
= implantable cardiac defibrillators

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20
Q

JVP Waves and meanings
a-x-c-x1-v-y

A

A= Rt atrial contraction pushes some blood into IJV (upright wave)
x-descent = RA relaxes dropping pressure
——————–
C= TV closes and RV contract so bulges into right atrium (upright)
X1-descent=end of RA contraction creates space when RA starts filling
—————————
V =RA filling against closed TV pushes some blood into IJV (upright)
y-descent = opening of TV so blood goes into ventricles

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21
Q

High JVP Causes

A

= Heart failure
= Tricuspid stenosis
= Pulmonary stenosis
= Cor pulmonale, PAH
= PAH 2ry to Mitral disease
= Constrictive pericarditis
= Large pericardial effusion
= SVC obstruction, flushed face

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22
Q

Ebstein’s anomaly

A

The annulus of the T valve is still in the normal position. The valve leaflets, however, are to a varying degree, attached to the walls & septum of the right ventricle. A subsequent “atrialization” of a portion of the morphologic right ventricle (which is then contiguous with the right atrium) is seen. This causes the right atrium to be large and the anatomic right ventricle to be small in size.
= S3 heart sound
= S4 heart sound
Triple or quadruple gallop due to widely split S1 and S2 sounds plus a loud S3 and/or S4
Systolic murmur of tricuspid regurgitation = Holosystolic or early systolic murmur along the lower left sternal border depending on the severity of the regurgitation
= Right atrial hypertrophy
= Right ventricular conduction defects
= Wolff-Parkinson-White syndrome often accompanies

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23
Q

Ebstein’s associations
It is - tricuspid valve in the wrong position and the valve’s flaps (leaflets) are malformed.

A

= PFO/ ASD >50%
= VSD/PS < 5%
= Rt to Lt shunt, Cyanosis, Clubbing
= Arrhythmias: Afib, Aflut,
= Congestive hepatomegaly
= Maternal exposure to Lithium carbonate in 1st TM is risk
= ECG tall P waves,
WPW (short PR +delta waves) + LBBB - right sided accessory pathway
RBBB without accessory pathway
= TR severity decides decompensation

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24
Q

Pulmonary stenosis
1 mmHg = 1.35951 cm H2O
congenital or Post TOF repair

A

Signs:
= ESM across PV, Thrill if severe
= RVH and left parasternal heave
= TR with systolic murmur
= Signs of RT CHF, congestive
= Post stenotic PA dilatation in CXR
= Split S2
= Pulmonary murmur increases on deep inspiration as right sided valve.
—————————–
Repair if gradient across PV> 50 mmHg

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25
VSD
= Left lower parasternal Pansystolic murmur also heard at apex = Left parasternal heave + thrill = Signs of PAH: Loud P2, PR murmur, TR murmur, RVH, CHF, neck veins, Hepatomegaly etc = displaced apex towards anterior axillary line as volume overload ----------------------------- Maladie de Roger - loud VSD murmur due to small hole, low gradient, more sound. ------------------------ Eisenmenger syndrome can develop ================ Mitral mid-diastolic flow murmur if VSD large - left sided - reduces with inspiration - LA flow crashes with VSD flow.
26
VSD, congenital
An infant with a large VSD may be asymptomatic in the first few days/weeks of life until the pulmonary vascular resistance drops. As the pulmonary resistance decreases, the left-to-right shunt increases. The right ventricle is thus subjected to high pressure and becomes hypertrophied while the left atrium and left ventricle receive more volume and become dilated. The right atrium is not usually affected. Congestive heart failure (CHF) may develop and presents as tachycardia, tachypnea, exertional dyspnea, breathlessness and sweating during feeding. The child's growth is also often delayed because of poor caloric intake. In some infants, especially those with Down's syndrome, the pulmonary vascular resistance may not significantly drop. These infants may not develop CHF but are at increased risk of developing pulmonary hypertension. They may need earlier surgical intervention to prevent worsening of pulmonary hypertension and the early development of Eisenmenger syndrome.
27
VSD associations
= congenital = Down's syndrome somt times = Turner's syndrome, some times = Post MI with septal rupture = Aortic Regurg < 5% = High Risk of SABE = Risk of PAH, Eisenmenger, CHF
28
Carvallo's Sign
Increase in murmur intensity on deep inspiration on right sided heart valves such as in Tricuspid regurgitation as blood flow/ venous return increases to heart = augmented by MULLER maneuver as inspiring against closed glottis.
29
Tricuspid Regurgitation
Signs of TR = raised JVP = Pan-Systolic murmur left para sternal = RV Heave = signs of PAH may be: Loud palpableP2 = Forceful epigastric pulsations with tender pulsatile hepatomegaly = Congestive Heart Failure ------------------------------------- Causes of TR: usually secondary = Mitral valve disease (MS, MR) = PAH, primary or secondary = dilated RV, any cause = Infective endocarditis, IVDU = RV infarction = cor pulmonale = Eisenmenger syndrome
30
Mitral Valve Prolapse
Signs: Early systolic ejection click followed by late systolic murmur. Can progress to full MR with pansystolic murmur. = Atypical chest pain = Cardiac neurosis, once diagnosed = progression to MR IF CHORDAE ruptures = risk of infective endocarditis = Palpitations, Arrhythmia's = Risk of sudden death or family history = Embolic phenomenon: Stroke, TIA = Mitral valve rupture ECHO is diagnostic Can be familial
31
MVP - Causes & Associations
= Marfan's syndrome = Polycystic kidney disease = Congenital Heart diseases = Congestive cardiomyopathy = Myocarditis = Mitral Valve surgery = Hypertrophic cardiomyopathy = SLE after Libman sack endocarditis = Ehler Danlos syndrome = Turner syndrome = Muscular dystrophy = Fabry's disease
32
MVP - Manoeuvre effects on murmur
1. Manoeuvres reducing cardiac venous return - such as - Standing/ Valsalva = increases prolapse Click and murmur occurs early Murmur gets prolonged in duration ------------------- 2. Manoeuvres increasing venous return such as - squatting, Hand squeeze, raising legs = delayes click. murmur which shortens duration of murmur -------------------- Other causes of Short systolic murmurs = Early minor Mitral regurg = Aortic stenosis or sclerosis = HOCM
33
Mitral Regurgitation, Signs
= Pansystolic murmur = Apex displaced as volume overload = Increases in expiration as Left sided = Radiates to axilla = left para sternal heave = signs of PAH may be if long standing = Systolic thrill = Atrial fibrillation may be there = MID DIASTOLIC MUMUR IF WITH AS
34
Mitral Regurgitation, Causes and Associations
= Acute infective endocarditis, IVDU = Post MI Chordae tendinae rupture = Mitral Annular calcification = HOCM cardiomyopathy (AS murmur) = with Marfans, EDS, Pseudoxanthoma elasticum or Osteogenesis inperfecta = Osteum primum ASD = Endomyocardial fibrosis (Cause unknown) = With CTD’s as SLE, RA, Ankylosing spondylitis ================ Surgery required when LV End Diastolic dimension is more than 45 mm
35
Aortic Regurgitation, signs Austin Flint murmur
= Large volume collapsing pulse = Dancing carotids, Corrigan's sign = early Diastolic murmur loudest at Aortic - not referred to carotids, louder in expiration as left sided & in sitting forward. = displaces apex to AA-line as volume++ = Visible Nailbed pulsations (Quincke) = Wide pulse pressure in BP = Uvular pulsations = Head nodding, beat to beat (deMussets sign) = Pistol shot femoral pulses -------------------------------------- The Austin Flint murmur is a rumbling diastolic murmur best heard at the apex of the heart that is associated with severe aortic regurgitation and is usually heard best in the fifth intercostal space at the midclavicular line.
36
Aortic Regurgitation, Causes Severe AR means: End Diastolic LV-Dimension > 70 mm End Systolic LV-Dimension > 50 mm
= Rheumatic fever (history) = Infective endocarditis, IVDU, History = Ankylosing spondylitis-Back pain, uveitis, sacro-ileitis, diagnosed case, Q-mark posture with fixed neck = Syphillis- Argyl Robertson pupils, Rhomberg sign+ sensory ataxia, = Marfan's syndrome - spidery hands, high arch palate, lens dislocation = Long standing HTN with aortic root dilatation
37
Austin Flint murmur of AR (mimics MDM of MS)
The Austin Flint murmur is a rumbling diastolic murmur best heard at the apex of the heart that is associated with severe aortic regurgitation and is usually heard best in the fifth intercostal space at the midclavicular line. its not palpable means no tapping apex as in MS. AR murmur is diastolic at AV but the regurgitant flow crashes with normal diastolic filling of LV through MV and this gives MDM which mimics MS but is not referred to axilla.
38
Radiation of Cardiac murmurs
MR= to axilla MS = MDM at apex, not to axilla AS = to carotids AR = Erb's point, 3rd ICS on left PDA = to back TR = right lower sternal border
39
Still's murmur, Functional
Still's murmur is a brief, vibratory quality, grade 1-3, midsystolic, and low-pitched murmur. This is best heard with the bell of a stethoscope. This murmur is heard at the left lower sternal border and occasionally radiates to the cardiac apex. Cause unknown, usually in children.
40
Gallaverdin Phenomenon
Gallavardin Phenomenon: This is the result of radiation of the murmur of aortic valve stenosis to the apex rather than coexistent mitral regurgitation. This finding is sometimes referred to as "Gallavardin dissociation."
41
Graham Steel Murmur
A Graham Steel murmur is a diastolic murmur audible along the left sternal border due to functional incompetence of the pulmonary valve in patients with pulmonary hypertension. The Graham Steel murmur is a high-pitched, decrescendo murmur, loudest during inspiration.
42
Carey Coombs Murmur
Carey Coombs murmur is short mid-diastolic murmur caused by active rheumatic carditis with mitral-valve inflammation. First described by Carey Franklin Coombs in 1907. Similar to the mid-diastolic rumble of mitral stenosis.
43
Dock's murmur
Dock's murmur occurs when there is a severe stenosis of the left anterior descending coronary artery. The murmur produced is diastolic since the coronary arteries fill in diastole. It is described as early diastolic and decrescendo sounding similar to the murmur of aortic regurgitation.
44
Seagull Cry Murmur
A “seagull's cry murmur” is defined as a murmur imitating the cooing sound of a seagull. This type of murmur is typically characterised by a musical timbre and a high frequency, and may occur as a result of various valve diseases. The cooing dove murmur is a cardiac murmur with a musical quality (high pitched). Associated with aortic valve regurgitation (or mitral regurgitation before rupture of chordae). It is a diastolic murmur heard over the mid-precordium. Patent ductus arteriosus may present as a continuous murmur radiating to the back.
45
Aortic Stenosis, Signs
= Slow rising low volume pulse = ESM radiates to carotids, after S1 = Narrow pulse pressure, = Fainting attacks on exercise = Forceful sustained heave (pressure) = No displacement of apex = Soft A2 heart sound Aortic Sclerosis: no radiation of murmur and pulse normal in character
46
Aortic stenosis Causes
= Degenerative calcification in elderly = Rheumatic HD: calcification/ scarring Streptococcal = Bicuspid Aortic valve (congenital) = Congenital = Paget's, IE, Hyperuricemia -------------------- Rx Options: = Valvotomy = TAVI: Transcatheter Aortic Valve implantation = Open surgery with CABG
47
Mitral Stenosis, usually Rheumatic
= Malar flush, cheek hyperpigmentation = Mid-diastolic murmur@apex (not axilla) + presystolic accetuation if sinus + opening snap - MDM can be increased with exercise as touching toes 10 times = slow volume pulse = Atrial fibrillation possible = Apex not displaced, tapping = Palpable Loud S1 = Left parasternal heave = Signs of PAH (palpable P2, TR murmur, left parasternal heave, pulmonary edema, hepatomegaly) = Giant v waves if TR ++, secondary = Graham Steel murmur, due to PR
48
Indications for intervention in MS
when to correct mitral stenosis - an episode of pulmonary edema - MS in pregnancy - Significant symptoms, SOB - Recurrent embolic phenomenon ------------------------------------- S2 to Opening snap interval > 0.07 sec with heart rate < 100 means MS is significant. ------------------------------------ Anti-coagulation is recommended in all with MS even if mild and in sinus. -------------------------- In moderate mitral stenosis the valve area is 1.0 to 1.5 cm² & the mean gradient is 5 to 10 mm Hg. In severe mitral stenosis the valve area is less than 1.0 cm² & the mean gradient is greater than 10 mm Hg. Gradient of 20 will cause LA pressure of about 25 mmHg
49
Atrial Fibrillation, causes
= IHD, post MI = Rheumatic heart disease = Hypertensive heart disease = Thyrotoxicosis = Cardiomyopathy = acute infections as pneumonia = Constrictive pericarditis = viral myocarditis/ idiopathic = Local malignant infiltration (lymphoma)
50
Cardiomyopathy causes
1. Toxic: = Alcohol, Adriamycin, Cyclophosphamide, Emetine, Steroids, Lithium, Phenothiazines 2. Metabolic: = Thiamine deficiency, Kwashiorkar, Pellagra (niacin), Obesity, Prophyria, Uremia, Electrolyte imbalanc 3. Endocrine: = DM, Thyrotoxicosis, Acromegaly, myxoedema, Cushing's 4. Collagen: SLE, PAN 5. Infiltration: Amyloidosis, Hemochromatosis, Wilsons, Sarcoid, GSD, MPS, Gaucher's, Whipples 6. Infections: viral, Rickettsial, TB 7. Genetical: HOCM, Muscular dystrophies 8. Fibroplastic: Loeffler endocarditis, Endomyocardial fibrosis, Carcinoid 9. Miscellaneous: Postpartum, persistent atrial tachycardia
51
Constrictive Pericarditis
Raised JVP, abrupt x, y descents Loud early S3 (pericardial knock) Paradoxical pulse - Pulsus paradoxus refers to an exaggerated fall in a patient's blood pressure during inspiration by greater than 10 mm Hg Clear lung fields
52
Parodoxical Pulse
Pulsus paradoxus is a phenomenon when your blood pressure decreases with inhalation (breathing in). More than 10 mm, It's a sign that you have a condition that affects your heart or lungs. It is seen with constrictive pericarditis.
53
Auscultatory signs of PAH
- Loud P2 component of S2 - Pulmonary early ejection systolic click - Right ventricular 4th Heart Sound - Pansystolic murmur of TR (+ giant v waves in JVP) - Early diastolic murmur or functional PR
54
Cor pulmonale Causes Cor pulmonale if heart failure secondary to Lung disease.
= COPD with emphysema = Recurrent pulmonary emboli = Primary PAH = Non Pulmonary causes of alveolar hypo-ventilation such as Kyphoscoliosis, Obesity, Neuromuscular weak ----------------------- Lung diseases Occasionally causing Cor pulmonale: = Progressive Massive fibrosis in coal workers = Bronchiectasis = Cryptogenic fibrosis alveolitis = Systemic sclerosis with PAH = Sarcoidosis = Asthma, Severe, Chronic
55
Cor Pulmonale Signs
* Signs of PAH basically - Loud palpable P2, TR murmur with parasternal heave, Graham steel murmur of PR, * Barrel Chest due to all around hyperexpansion * muffled heart sounds due to Hyper expansion * Hyper resonant chest wall all around * Tracheal tug * Accessory muscles at use * Purse lip breathing to create PEEP * Cyanotic lips, oral mucosa * Widespread expiratory rhonchi * Inspiratory crackles all over * Clubbing if also has pulmonary fibrosis * Prolonged noisy expiration * if flapping hand tremor present- examine for papilloedema
56
Pneumothorax
= usually tall thin male patient = Hyper resonant percussion chest on same side = Tracheal deviation to opposite side = REDUCED vocal resonance = Reduced tactile fremitus = REDUCED breath sounds = Already expanded chest, doesn't expand further with breath in. = Subcutaneous emphysema might be felt/ seen
57
Patent Foramen Ovale
Patent foramen ovale (PFO) is a hole between the left and right atria of the heart. This hole exists in everyone before birth, but most often closes shortly after being born. PFO is what the hole is called when it fails to close naturally after a baby is born. A foramen ovale directs the oxygen-rich blood from the umbilical cord in a fetus's right upper chamber (right atrium) to the left upper chamber (left atrium). From there, the blood goes to the left side of the fetus's heart and provides oxygen to fetus' brain. The foramen ovale normally closes after birth.
58
Thrombophillia risks
= Factor V leiden presence = Protein C deficiency = Protein S deficiency = Antithrombin III deficiency = Anti Phospholipid Antibody factor V Leiden mutation, meaning there's a change in their coagulation factor V (F5) gene. activated Protein C, turns off the clotting cascade by deactivating Factor V. Children born with Factor V Leiden produce a mutated form of Factor V that does not respond well to activated Protein C. Also protein C/S deficiencies DO NOT TURN OFF this activation. Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by lysing thrombin and factor Xa.
59
Anti-Phospholipid Antibody Syndrome
The three known APLA are: Anticardiolipin antibodies IgG or IgM (ELISA) Anti-beta-2-glycoprotein-I antibodies IgG or IgM (ELISA) Lupus anticoagulants (Functional assays). The antiphospholipid syndrome (APS) is defined by the development of vascular thrombosis, or pregnancy morbidity in the presence of persistent antiphospholipid antibodies (aPL). In contrast, when the aPTT is prolonged due to interference from antibodies to phospholipids, the patient actually has an increased risk for thrombosis. The lupus anticoagulant is one of the antibodies that binds to phospholipids in this way and frequently causes the aPTT to be prolonged. The specific antibodies in APS are called “antiphospholipids” because they attack and damage parts of cells called phospholipids. The damage increases the chance that blood clots will form in both veins and arteries. Hypercoagulable State in Patients With Antiphospholipid Syndrome Is Related to High Induced Tissue Factor Expression on Monocytes and to Low Free Protein S.
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Prothrombin and aPT time
In contrast, when the aPTT is prolonged due to interference from antibodies to phospholipids, the patient actually has an increased risk for thrombosis. The lupus anticoagulant is one of the antibodies that binds to phospholipids in this way and frequently causes the aPTT to be prolonged.
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Breast Feeding & CTPA
Need to express milk prior to CTPA or VQ scans for PE. No breast feeding for 8 hrs after CTPA No breastfeed for 12 hrs after VQ scans No breastfeed for 12 hrs after Q scan
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Aortic stenosis complications
- LV impairment, LVH, failure - cardiac arrhythmias - Sudden death risk due to VT/VF - Hemolysis - Infective endocarditis of damaged valve - Pulmonary hypertension - Heyde’s syndrome: it’s IDA due to bleeding due to acquired von willebrand factor deficiency which breaks off on damaged stenotic valve & leads to acquired vWB disease.
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Diastolic murmurs
AR, PR and MS, TS Atrial myxoma Carrey-Coomb murmur Austin Flint murmur Early Diastolic Murmur: in Aortic or pulmonary regurg Austin Flint murmur of severe AR but heard at apex as jets of blood from AR collides with LA blood flow through mitral. Mid-Diastolic: in Mitral and Tricuspid stenosis Carey-coomb murmur of acute rheumatic fever due to inflammation of mitral valve (inflammatory damage) Pre-Systolic: accentuation: MS, TS, Atrial myxoma.
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Rx Strategies for Mitral Stenosis
Medical treatment: - fluid restriction - Diuretics - Prophylaxis for Infective endocarditis - Atrial fibrillation-Rate control with digoxin, Beta blockers, CCB OR rhythm control with flecainide, Sotalol, Amiodarone Surgical options: when: PAH, Pulmonary edema, Haemorrhage, PE develops How: = Open/closed commisurotomy = MVR: Metal if young, Bioprosthetic if Old = Valvuloplasty: when: Mobile valve, Minimal calcification, No MR, NO LA thrombus = Anticoagulation assessment for AF = Anticoagulation for MVR
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Endocarditis prophylaxis
When to or for whom: = Prosthetic valves = H/o Infective endocarditis = Unrepaired Cyanotic CHD = Repaired CHD but has prosthetic valve = Cardiac transplants = All dental procedures in High risk Standard Medications = Amoxycillin 2 grams po/iv/im = Clindamycin 600 mg PO = Ceftriaxone 1 gram IV = Azithromycin 500 mg PO if allergic to above
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Implantable Cardiac Defibrillators (ICD) indications
Primary ICD indications = Post MI < 4 wks with LVEF < 35% + non sustained VTach + inducible VTach OR = MI with LVEF < 20 % + QRS duration > 0.12 seconds = Long QT syndrome = Brugada syndrome = HOCM, hereditary Secondary ICD indications: = ROSC from cardiac arrest with VF = Spontaneous sustained VTach with syncope = Sustained VTach with LVEF < 35% = Surgical repair of CHD
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Permanent Pacemaker
third degree CHB Symptomatic 2nd degree CHB Asymptomatic Mobitz 2 CHB Sinus pauses > 3 seconds (15 big squares)
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Thrombolysis in MI (TIMI) Risk score
> 3 score - High risk of death 1 point for each below: = Age > 75 = > 3 Risks for CAD: Smoking, DM, HTN, Family history = Coronary stenosis > 50% (past CAG) = ST Segment deviation = > 2 anginal episodes last 24 Hrs = Positive Troponins, rising = Aspirin Use in last 7 days
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S4 Heart Sound Explained
S4 is a low pitched pre-systolic sound before S1 - due to vigorous atrial contraction filling a stiff ventricle as mitral valve opens - atrial is looking into a half fool LV. S4 peaks in intensity at LV Apex and is heard best at APEX with the bell in left lateral position. Accentuated by isotonic and isometric exercises. May occur with HTN, AS, LVH, IHD, Restrictive cardiomyopathy Always pathological and implies failing tired heart. Cannot occur in atrial fibrillation
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Added Heart Sounds
Opening Snap: in Mitral stenosis, brief, high pitch sound in early diastole as MV is forced open by high LA pressure. S2 to opening snap interval shortened with high LA pressures. Ejection click: sharp, high pitched sound in early systole soon after S1. preceded typically Ejection systolic murmur - occurs in pliable valves in Aortic/Pulmonary stenosis Mid-systolic Click: in Mitral prolapse as one or both leaflets prolapse during systolic high pressures in LV and may have late systolic murmur of MR after that click. Prosthetic Valves: ticking audible without stethoscope as if a clock Pericardial Knock: S3 equivalent heard in diastole in constrictive pericarditis Friction Rub: scratching sound in pericarditis - can be systolic, pre systolic or diastolic
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Low Pitch vs High pitch Sounds
High–pitched sounds have short wavelengths, which means that the peaks are close together (frequency high-faster vibrations) Low–pitched sounds have longer wavelengths, so the peaks are more spread out (low frequency-slow vibrations)
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Heart Valve signs before auscultation
Mitral Stenosis: Pulse regular or irregular Pulse pressure in BP - normal Apex beat - undisplaced ----------------- Aortic regurgitation: Pulse - bounding, collapsing Pulse pressure - wide (ex 180/40) Apex beat - displaced to AAline Corrigans sign + ------------------ Aortic Stenosis: Pulse low volume Pulse pressure narrow (ex 140/100) Apex beat - not displaced ------------------- Mitral Regurgitation: Pulse normal Pulse pressure normal Apex displaced to AA line
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Pulmonary Hypertension: Treatment
treat underlying cause as MS/COPD Diuretics: Frusemide, Thiazides LTOT therapy Anticoagulation with warfarin Vasodilators: = CCBs - Nifedipine, Diltiazem = Prostacyclines: Epoprostenol (IV Infusions) Ileoprost inhaled, = Adenosine infusions = Nitrous inhalation = Tadalafil, Sildenaphil = Bosentan: Endothelin antagonist
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Mid Diastolic Murmurs
Mitral Stenosis-best at Apex which is not displaced, Pulse and pulse pressures are normal., AFib may be present. #Left atrial myxoma #Left atrial thrombus #Cor triatriatum - fibromuscular band which splits one atria #Severe Mitral regurgitation (systolic primary murmur + MDM) Normal Mitral valve area: 4-6 cm2 Mild (>1.5) -moderate (1-1.5) -Severe (<1cm2)
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Continuous Murmurs, (Systolic+Diastolic both)
Patent ductus arteriosus MR + AR together present VSD + AR Pulmonary AV fistulas Coronary AV fistulas Ruptured sinus of Valsalva Pulmonary AV shunts - Blalock Tausigg Venous HUM in children
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Sinus of Valsalva
The sinuses of Valsalva, also known as aortic sinuses, are the anatomic spaces at the aortic root bounded internally by the aortic valve leaflets and externally by outward bulges of the aortic wall. A sinus of valsalva aneurysm (SOVA) is an abnormal dilatation of the aortic root located between the aortic valve annulus and the sinotubular junction. It occurs as a consequence of weakness of the elastic lamina at the junction of the aortic media and the annulus fibrosis. Sinuses of Valsalva dilatation was associated with higher left ventricular mass and lower systolic function, which may contribute to higher cardiovascular risk in subjects with aortic root dilatation.
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Holt Oram Syndrome
Autosomal dominant, 12q2 mutations Ostium secondum ASD + Hypoplasia of the thumb/ Upper Limb Irreversible PAH is a contra indication to ASD repair, can be decided by: = PAH pressure response to vasodilators as Epoprostenol = Lung Biopsy changes
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S3 Heart Sound
in Heart under strain Fever/ Tachycardia/ Pregnancy/ children with tachycardia Low pitched after S2 (after closure of A2P2) Galloping as lub-dub-ddd. It is result of rapid LV filling in early diastole from a very full LA that blood crashes into LV with a boing. A left sided S3 is best heard with bell at apex in left lateral position in expiration. A right sided S3 is best heard at left para sternal edge in inspiration. S3 occurs NORMALLY fever/ exercise/ hyperdynamic status as anemia/ hyperthyroidism.
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Atrial Septal defect, Types
**Ostium Secundum** 70%, most common, at Site of foramen ovale in upper membranous part **Ostium primum** at antero-inferior inter-atrial septum, involved mitral and tricuspid valves (may leak) **Sinus Venosus ASD**: defect at upper inter-atrial septum just below SVCava **Coronary sinus ASD**: defect at Coronary sinus, inter-atrial shunting.
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Causes of VSD
Congenital VSD: Maternal Factors: = Maternal DM = Maternal Phenyl ketonuria = Maternal Alcohol intake VSD: Fetal Factors: Aneuploidy: = Trisomy 21: Down's syndrome = Trisomy 18: Edward syndrome = Trisomy 13: Patau syndrome = DiGeorge syn: 22q11. 2 deletion Acquired VSD: Post MI Iatrogenic rupture: RV pacing Post Alcohol Septal ablation for HOCM
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Signs of ASD
**Small ASD**: Ejection systolic murmur ESM+ Normal ECG, no cyanosis, no clubbing No systolic thrill/ tricuspid flow murmur No PAH -------------------- **Large ASD** with Lt to Rt shunt: ? Atrial fibrillation present ESM + Thrill + TV Flow murmur + PAH + No cyanosis No clubbing ---------------------- **Large ASD with Rt to Lt shunt**: Cyanosis, central Clubbing present No ESM, No thrill, no TV flow, PAH ++
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S2 heart sound - Wide Split
Left to Right Shunts: During inspiration - venous blood flow to RA delays P2 (normally). In Left to right shunts - more blood comes to RA through the ASD from LA leading to delayed RV emptying, delayed P2 closure and hence wide split Additionally, less LA blood which leaks to RA - leads to early closure of Left sided valves (MV, AV) hence early A2 sound which further widens split between A2P2. Causes: ASD, VSD, MR, PS, RBBB
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ASD Complications
Eisenmenger syndrome - development of severe PAH with shunt Right to Left Atrial fibrillation Infective endocarditis Recurrent chest infection, poor growth Paradoxical embolism through ASD causing stroke
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VSD - treatment Options
Endocarditis Prophylaxis Diuretics, Fluid optimization Treat PAH (vasodilators, LTOT) Surgical closure: indications: = LV Dilatation = LV Dysfunctions with poor LVEF = Recurrent endocarditis = Acute IVSeptum = Rising Pulmonary: Systemic Blood flow QS:QP ratio > 1 The ratio between pulmonary (Qp) and systemic flow (Qs) indicates the existence of some sort of shunt between the two circulations, either intra- or extracardiac. If the Qp/Qs ratio is >1, the shunt is from the systemic to the pulmonary circulation and if <1, from the pulmonary to the systemic circulation.
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Secondary Pulmonary Hypertension
Cause of secondary PAH: 01. High pulmonary venous pressures: AV/MV/LV diseases Venous occlusions, in Autoimmunes 02. Poor-reduced Pulmonary vascular Bed: ILD, PE, COPD, CTD's 03. Chronic Hypoxia conditions: ILD, COPD, OSA, High altitude, Obesity-Hypoventilation, Kyphoscoliosis, NMJ (GBS, MG, Polio) 04. Left to Right shunts: ASD, VSD Primary PAH: Familial or with CTD's or HIV or Fenfluramine induced
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Types of VSD (PSPM)
1. Perimembranous VSD: infra-cristal, 80%, most common, just below aorta origin. Can have a RA to LV connection called Gerbode defect --------------------- 2. Supra-cristal: infundibular, below Pulmonary valve, communicates with RV outflow tract to lungs ------------------------ 3. Muscular VSD: trabecular, in muscular inter ventricular septum ------------------- 4. Posterior Endocardial Cushion Type: Posterior to septal leaflet of Tricuspid valve
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SVC Obstruction
Small cell Lung cancer 10% Non small cell Lung cancer 1.7% Thymomas, Retro sternal Goiter Fibrosing mediastinitis Non Hodgkins Lymphoma Radiation fibrosis Thoracic aortic aneurysm Thrombosis around Central Lines Pemberton manuevre: raising arm for 1 min closes thoracic outlet causing SVC obstruction and face flushes.
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Myocarditis Causes: Troponins will be High with systemic illness
Viral infections: Coxsackie, Covid, Influenza, Rubella, Polio, EBV, HepC Radiation to chest Drugs: Clozapine, Cocaine, Alcohol, Toxic: Aresnic, Lead, Iron, CO, Mephedrine, Anthracyclines (Doxorubicin, Daunorubicin) Chagas disease (Trypanosomiasis) Autoimmunes: GCA, Lupus, Allergic to Diamox/ Amitryptiline Kawasaki disease - vasculitis Snake Venom
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Differentiating Neck Pulsations
if Arterial: Single waveform, Respiration has no effect Body position has no effect Hepato-jugular has no effect Palpable with fingers Compression - doesnot vanish ---------------------------- if Venous pulsations (JVP): Double waveform when sinus inspiration will reduce it Supine position will increase it Hepato-jugular reflex will increase it Not palpable Abolishes on pressing
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Anti-thrombotics in Afib
Age < 65, Risk factor > 1= start warfarin Age < 65, Risk factor 0 = start ASA alone Age 65-71, Risks > 1 = start Warfarin Age 65-71, Risks 0 = start warfarin Age > 75 = whatever Risk = start Warfarin Risk Factors are: Age, HTN, LVF, Mitral stenosis, Stroke past, DM, Prosthetic valves in situ
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Pericarditis information
Common causes: Viral infections as Coxsackie, TB, Autoimmune SLE, RA, Malignancy, Post MI Dressler syndrome, Uremia, Hypothyroidism, Drugs Symptoms: pleuritic chest pain, more on lying down, less on bending forward, Passive SLE unduces this pain as blood flow increases. ECG: PR depressed generally except in aVR where it goes up. ST saddle shaped elevations all leads, tachycardia, no Q waves CXR - Large globular heart with effusion and muffled heart sounds Rx - NSAID, Steroids, Stop Warfarin Beck's triad (hypotension, distended neck veins and muffled heart sounds) will be present in patients with pericardial tamponade.
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VSD Signs
small VSD: Loud murmur, Pan-systole, left sternal no cyanosis/clubbing/PAH/ Apex is not displaced, normal A2P2 ------------------------- Large VSD with Lt to Rt shunt: Less loud, pan-systole murmur@Lt sternal Clubbing present, no cyanosis, PAH signs +, Displaced apex, thrusting Low P2 sound ---------------------- Large VSD with Rt to Lt shunt: No murmur now as equalization Cyanosis ++ clubbing + PAH signs ++ Displaced apex and thrusting Single S2, no split
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Cardiac Prosthetic Valves
St Jude: Aortic, bileaflet, keep INR 2-3 c warfarin Tilting Disc: Bileaflet, mechanical, Mitral, Keep INR 3-3.5 c warfarin Caged Ball or Disc: keep INR 3.0 with Aspirin also Bio-prosthetic Valves: 5 yr life, INR 2.5 with warfarin for 3 months then Aspirin alone if no AFib
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IE: common Organisms
Native Valve IE: - Viridans streptococci - Staph aureus - Enterococci - Coxiella, Brucella, Bartonella, Chlamydiae, Candida - HACEK group (Hemophilus - Actinobacillus - Cardiobacterium hominis- Eiknella corrodens - Kingella kingae) Prosthetic Valve: - coagulase negative staphylococcus aureus and epidermidis
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Malar Flush Causes
- Mitral stenosis - SLE - Hypothyroidism - Cold weather - Carcinoid syndrome - Systemic sclerosis - Irradiation to face/ head - Polycythemia Erysipelas. Cellulitis. Rosacea. Pellagra. Dermatomyositis.
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Syncope in Aortic stenosis
Low cardiac output due to critical stenosis. Transient electro-mechanical dissociatio: LV unable to contract against stenosed valve. During exercise, heart is unable to cope against this AS and peripheral dilation during exercise adds to problem. Vasodilators like nitrates are contraindicated in AS. ECG: LVH, LV strain, LAE, LAD, LBBB/Afib or both CXR - Post stenotic aortic dilation, rib notching, AV calcification
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Cardiac maneuvres
Preload - venous return is: = increased by: Squatting, Hand squeeze, passive leg raise (reduced HOCM, MVP and increases AS, MR++) = reduced by: Valsalva (increased HOCM, MVP and reduced AS, MR) Afterload - SVR Reduced by any vasodilato as nitrates which increases HOCM, AS murmur and reduces MVP, MR murmur.
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Cavernous sinus Syndrome
Structures - Internal carotid artery, 2, 3, 4, 6 and V1 branch of 5th cranial nerves, Sympathetic plexus Clinical - a headache that feels worse when you lie down or bend over., swelling around eyes, or rash, Diplopia, Painful ophthalmoplegia, Vision loss, Lost corneal reflex (V1 branch), Facial numbness (V1) Proptosis as globe pushed forward, Pulatile exophthalmous, 3,4, 6 cranial palsies Causes: Thrombosis, Aneyrusm, PCA aneurysm, Carotid cavernous fistula = Sinusitis, Herpes zoster, Sphenoid mucormycosis, Wegner's granulomatosis, Sarcoidosis, Malignancies
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Tolosa Hunst Syndrome
Tolosa Hunt syndrome (THS), also known as painful ophthalmoplegia, recurrent ophthalmoplegia, or ophthalmoplegia syndrome, is described as severe and unilateral periorbital headaches associated with painful and restricted eye movements.
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Lung volumes
TLC: volume of air in the lungs at end of full inspiration. VC (Vital Capacity): volume of air exhaled after initial full inspiration followed by full forceful expiration TV (Tidal volume): volume of air we can inspire during normal breathing. FRC (Functional Residual capacity: volume of air in the lung after normal expiration. RV (Residual volume): volume of air in lungs after full forceful expiration.
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FEV1: FVC ratio
FEV1:FVC ratio < 75% = asthma, COPD, Emphysema (obstructive) FEV1: FVC ratio = normal but btoh los = restritive lung disease: Normal FEV1 = 80-120%, 3-4 Lit Normal FVC - Forced expiration after full total maximum inspiration, 80-120%
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Yellow Nail syndrome
rare syndrome comprising of: 1. Primary lymphedema due to underdeveloped lymphatics 2. Yellow cruved nails 3. Pleural effusions, Chylothorax 4. Bronchiectasis, Obstructive PFT 5. Chronic sinusitis, Persistent cough
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Chediak Higashi Syndrome
caused by mutations in the LYST gene. This gene provides instructions for making a protein known as the lysosomal trafficking regulator. clinical features: = partial albinism, = photosensitivity, = severe recurrent bacterial infections, = bleeding diatheses, and = late-onset neurological manifestations (central and peripheral neuropathies, sensory loss, muscle weakness, parkinsonism, cerebellar ataxia, and cognitive decline. Laboratory findings: neutropenia & hypergammaglobulinemia. Bone marrow smears reveal giant inclusion bodies in leukocyte precursor cells. The granules are peroxidase positive and contain lysosomal enzymes, suggesting that they are giant lysosomes, or in the case of melanocytes, that they are giant melanosomes.
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Chronic granulomatous disease
Chronic granulomatous disease (CGD) is a genetic disorder in which white blood cells called phagocytes are unable to kill certain types of bacteria and fungi. People with CGD are highly susceptible to frequent and sometimes life-threatening bacterial and fungal infections. mutations in any one of five different genes can cause a defect in an enzyme called phagocyte NADPH oxidase. Certain white blood cells use this enzyme to produce hydrogen peroxide, which these cells need in order to kill certain bacteria and fungi. Clinical: Fever, Chest pain when inhaling or exhaling, Swollen and sore lymph glands., An ongoing runny nose. Skin irritation that may include a rash, swelling or redness, Swelling and redness in the mouth, Gastrointestinal problems that may include: Vomiting. Diarrhea. Stomach pain. Bloody stool. Diagnosis: Diagnosis of chronic granulomatous disease is by a flow cytometric oxidative (respiratory) burst assay to detect oxygen radical production using dihydrorhodamine 123 (DHR) or nitroblue tetrazolium (NBT). This test can also identify female carriers of the X-linked form and recessive forms Daily doses of the oral antifungal drug itraconazole can reduce fungal infections in CGD. Maximum infection prophylaxis for CGD involves treatment with twice-daily oral doses of cotrimoxazole and twice-daily itraconazole, voriconazole or posaconazole, plus three times weekly injections of interferon gamma.
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Pneumonectomy vs Lobectomy
Pneumonectomy: - flattened chest same side - trachea pulled to same side - reduced or absent chest expansion1/2 - absent or reduced through out as no airflow, lung has been removed. Left Lobectomy: - ribs pulled in UL/LL side - trachea deviated to same side in UL - trachea central in Lower lobectomy - reduced expansion@ ULobectomy - reduced expansion@ LLObectomy - reduced breath sounds in both cases Right Lobectomy: - ribs pulled in as above mentioned - trachea deviated to affected side - reduced expansion and breath sounds @ removed lobe side/site
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M.E.A.T Pleural effusions
low glucose content effusions Malignancy Empyema Arthritis, RA Tuberculosis Glucose < 2 mmols Fluid PH < 7.2 if LDH > 1000 = SUSPECT: Maligancy/ empyema/ RA/ Paraproteinemic/ infectious
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BODE Index
to predict long term outcome for COPD B- Body mass index O- Obstructive features D- Dyspnea scale E - exercise tolerance FEV1 = > 65, 50-64, 36-49, < 35 6min-walk = > 350m, 250-349m, 150-249m, < 149 m Dyspnea scale score: 0-1, 2, 3, 4 BMI: = > 21, < 21, -- , -- BODE 0-2 = 80% SURVIVAL@ 4 YRS BODE 7-10 = 18% SURVIVAL @ 4 YRS
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Pleural Fluid analysis PH, Glucose, LDH, Albumin, Cell count, Adenosine deaminase, Amylase, Creatinine, cultures, Lipids
Normal Pleural Fluid: clear, PH 7.60-7.64, protein < 1-2 Good morning!/Lit, WBC < 1000/hpf, LDH < 50% of plasma, Glucose same as plasma, Albumin = Serum:Fluid < 1.2 exudate, > 1.2 transudate LDH = effusion:serum > 0.6 = exudate Glucose = low in exudates < 2 mmols Ph = < 7.2, low in exudates Adenosine deminase - increased in malignancy, empyema,, CTD's, TB Haemotocrit - Fluid: Serum > 0.5 - in hemothorax Amylase: high in pancreatitis Lipids - ruptured lymphatics, TG > 1.3 in chylothorax Other Tests to ask for: cell count, gram stain, creatinine levels, culture, TB culture
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AVR indications
Aortic stenosis: Symptomatic + AV GRADIENT>50 Asymptomatic: = moderate to severe AS + CABG = Severe AS + Gradient > 40 mmHg = abnormal BP fall on exercise, Vtach = Valve Area < 0.6 Aortic Regurgitation: Symptomatic- angina, dyspnea Asymptomatic - = AR+CABG together = LEVF < 50% = Dilated LV, LVEDD > 55 other causes: = Infective endocarditis = Aortic root > 50 mm (5 cm) = Acute severe AR
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Co-arctation of Aorta
Infantile CoA, pre LSA origin Adult CoA, Post LSA origin Bicuspid aortic valve Patent Ductus arteriosus VSD MV anomalies Tricuspid atresia Hypoplastic Left heart syndrome Aortic Arch hypoplasia - Turner's (45XO), ADPKD (+Berry aneurysm), Haemangiomas, Renal anomalies
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MVR indications
Mitral stenosis: severe MS with SOB Signs of pulmonary edema Severe PAH (TR, palpable P2, dyspnea, Parasternal heave, hepatomegaly) Haemoptysis with pulm edema Recurrent thromboembolic episodes Mitral Regurgitation: Signs of LVF Episodes of Pulmonary edema LVEF < 60% LVESD > 45 mm (4.5 cm) end-systolic
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Subclavian Steal syndrome
Subclavian steal syndrome (SSS), now termed subclavian-vertebral artery steal syndrome, refers to the diversion of blood flow away from its normal target and the arm. It is a cause of syncope or presyncope related to cerebral hypoperfusion that occurs during arm use. common symtoms: = hearing loss. = tinnitus. = blurred vision. = dizziness. = vertigo. = loss of muscle coordination, or = ataxia. =fainting. Do pemberton maneuvre, Forearm exercise test, Both arm BP check
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VFib or SVT with aberrancy
Vfib or Vtach is more likely rather than SVT with aberrancy if: - IHD known - QRS prolonged > 14 ms - Fusion beats with R on T sign - all QRS in V leads points in same directions - no Bundle branch black in previous
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Cardiac Receptors B1, b2, alfa 1 & 2 (all adrenergic)
beta 1 - present in cardiac mostly, agonist action causes tachycardia, increases stregth of heart contraction (Dobutamine) beta 2 - agonist causes smooth muscle relaxation present in smooth muscles of vessels, Bronchioles, UB and uterus. (Ipratropium) beta 3 - adipose tissue, Ubladder Alfa 1 - Vaso-constriction Alpha-1 agonists: metaraminol, methoxamine, ozymetazoline, phenylephrine. Alpha-1 antagonist: doxazosin, prazosin, tamsulosin, terazosin. Alfa 2 - inhibits Norepineprhine and inhibits Acetyl-choline release Alpha-2 agonists: brimonidine, clonidine, dexmedetomidine, guanabenz, guanfacine. Alfa for Non-Epi, Beta for Epinephrine Carvedilol - non selective, B1B2 Bisoprolol - selective B1 Metoprolol selective B2
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NYHA Heart Failure
Class I - no limitations of activity Class II - Slight limitation Class III - Marked limitation of physical activity Class IV - resting breathlessness LV Ejection fraction is determined by LV End Systolic and End Diastolic dimensions and normally around 65%. Non selective beta blocker as Carvedilol is more preferred in Heart failure as it blocks both beta 1 and beta 2 receptors.
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Digoxin
must never give in WPW arrhythmia's where PR interval is short in previous ECG's as it lowers refractory period of accessory pathway and allows rapid anterograde conduction with risk of precipitating VFib CAN INDUCE LONG pauses if used with beta blockers for Afib WPW associated very High rate > 200/min ie known short PR, delta waves in past ECG's: Do not give = Digoxin, Adenosine, Diltiazem or Verapamil Do = cardioversion or give Flecainide
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Hypertension Treatment Guidelines
Targets: BP < 130-85 mmHg Step1 - Start ACE inhibitor or ARB Step 2 - Add CCB/ Diuretic to ACEi Step 3 - Add CCB/ Diuretics (ACEi + CCB + Diuretics, 3 drugs@ step 3) Step 4 - 4 drugs - add another Diuretic or Beta Blocker or Alfa blocker as Prazocin Resistant Hypertension - uncontrolled despite 4 drugs: Add Methyl DOPA (central sympatholytic) or Direct Renin inhibitor as Aliskerin Also add statins if: TC> 4, TG>2, HDL <1
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Cardioversion for A. fibrillation
unstable patient ie - confused, altered sensorium - Systolic BP < 90 mmHg - LA thrombus in echo - Fast Ventricular rate with chest pain - Heart failure clear signs Otherwise if stable: Adenosine 1 try if SVT possible IV Flecainide IV Amiodarone Anticoagulation with UFH then warfarin
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High Risk for IE development
IV Drug user Prosthetic heart valves in situ Prosthetic material used for heart Sx Past Infective endocarditis Congenital: = Unrepaired CHD = Repaired CHD before endotheliazn = Repaired CHD but defect persists Acquired valvular stenosis or leaking HOCM Post Heart Transplant valvulopathy
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Asthma Information
Nocturnal symptoms cough, chest tightness, wheeze Triggers: Damp air, Dust, Pets, Drugs, Infections, Cold weather, Pollens, Stress, Emotion, Exercise Asthma more likely with = Atopy: Eczema, Hay fever history = Family H/o atopy = Childhood asthma + = Drugs: Aspirin, NSAIDs, B-blockers = Occupational trigger Systemic Review for associations: = Acid reflux = Churg strauss syndrome = ABPA = PAN: unexplained fever, stomach pain, kidney failure or high blood pressure. PAN spares large vessels (the aorta and its major branches), the smallest vessels (capillaries and small arterioles), and the venous system.
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Churg Strauss syndrome
There are six diagnostic criteria for CSS: Adult onset asthma, peripheral eosinophilia exceeding 10%, mono- or polyneuropathy, transitory pulmonary infiltration, abnormality of the paranasal sinuses, and histopathology revealing vessels with tissue eosinophilia. Adult onset asthma + Epistaxis = small vessel vasculitis associated with antineutrophil cytoplasmic antibodies (ANCA) and has three distinct phases – prodromal, eosinophilic and vasculitic Rx - Prednisolone
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Asthma Treatment Plan
Avoidance of triggers Weight reduction Managing GORD Stop smoking measures Occupation change Proper Inhaler technique training Maintain a peak flow diary Step 1 = short acting beta 2 agonist (ventolin) Step 2 = Add inhaled steroid 200-800 mcg/Day Step 3 = Long acting beta agonist like Formoterol. Increased inhaled steroid to 800 mcg/day Step 4 = increase inhaled steroid to 2000 mcg/day Add Montelukast/ Theophylline SR or Beta agonist tablets
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Mitral Stenosis Severity Markers
- Early opening snap lost if valve gets calcified - Increasing length of MidDiastolic murmur - Signs of PAH appears with SOB, Loud palpable P2, Liver congestion - Graham steel murmur of PR - Low pulse pressure as low LV Ejection volume - Hoarse voice due to phrenic nerve compression by enlarge LA
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Clues to cause of Aortic Regurg
#Bicuspid AV: young patient with AR, ejection click in systole #RA with AR: Hand signs, Nodules #SLE: Malar rash, Anemia, Jaccouds arthropathy Marfan Syndrome: Tall, spidery long fingers, High arch palate, Arm span > Leg span, Pectus anomaly #Ehler-Danlos Syndrome: blue sclerae, Hyperextensible joint (check thumb extension), Skin purpura, Fish mouth skin scars #PseudoXanthoma Elasticum: Loose skin at axilla and neck, Plucked skin appearance Syphilitic Aortitis: Argyl Robertson pupils, Sensory ataxia, Neurotrophic foot ulcers #Ankylosing spondylitis: Fixed stooped Question mark posture, Fixed kyphosis, Loss of Lordosis # Other Cause: Hypertension, Rheumatic Fever, Perimembranous VSD
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Gallaverdin Phenomenon
with aortic stenosis Murmur of AS at apex instead of in aortic area, loudest at Apex but other signs of AS also present: - Narrow pulse pressure (140/100) - Slow rising pulse - Systolic murmur - Low volume pulse - Murmur along carotids
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Loud ESM in Expiration
seen with: - Aortic stenosis - HOCM - Supra valvular AS (William's Syn)
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Aortic Regurgitation
Wide collapsing pulse, waterhammer Hyperkinetic displaced apex Aortic area thrill (palpable murmur) Early Diastolic murmur # Vigorous neck pulsations (corrigan) # Nailbed pulsations (Quinckes) # Head nodding with beat(DeMusset) # Diastolic murmur proximal to femoral artery (Durozie's) # Pistol shot femoral sound (Traube's)
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Signs of PAH
Loud Palpable P2 heart sound TR with systolic para sternal murmur Giant systolic V waves in JVP Pulmonary congestion, SOB, tachypnea Paraesternal heave of RVH RVH, RBBB in ECG
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Mitral Regurgitation Rx
Asymptomatic MR: annual ECHO, antibiotic prophylaxis for procedures Atrial Fibrillation: Rate control: BB, CCB,M Digoxin Rhythm control: Amiodarone, Sotalol, Flecainide Anticoagulation (CHADVASC scoring) Heart Failure Rx: Diuretics, Fluid restriction, ACEi or ARB's, Digoxin MVR: if Severe, if CHF, or if CABG required also when MR present NYHA III, IV HEART FAILURE LVEF < 60% LV end systolic diameter > 45 mm
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Collapsing pulse
Aortic regurgitation Pregnancy, Hyperdynamic status PDA Paget's disease, Hyperdynamic Anemia, long standing Thyrotoxicosis Moderate Mitral regurg
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Bioprosthetic Heart valves
When to use them: - Age> 70 yrs - Anticoagulation contraindicated - Patient not expected to live long Complications of Prosthetics: - Hemolysis - Infection - Thromboembolism - Valve dysfunction - Bleeding due to warfarin
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Prosthetic Heart Valves
Metallic click : prior to carotids= Mitral prosthetic after carotid pulse = aortic prosthetic Also look for LEG CABG scars Also look for ecchymosis s/o warfarin Flow murmur across AVR is normal Regurgitant flow across AVR is abnormal Can find Signs of Stenosis or Regurg AVR = ESM present always Long standing PAH will persists even after MVR
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Reduced Left Radial pulse
diminished left radial pulse with thoracotomy scar - repaired CoA without this scar - CoA proximal to Left subclavian artery origin (unrepaired) Absent Left radial pulse - think of CABG harvesting Other Causes: - LSA stenosis - Arterial thrombosis - Atherosclerosis - arterial embolus - Vasculitis - Post LA cannulation
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Idiopathic Pulmonary Fibrosis classification (ATS-ERS)
1. Acute interstitial pneumonia (Hamman Rich syndrome) 2. Usual interstitial pneumonia 3. Non specific interstitial pneumonia 4. Desquamative interstitial pneumonia 5. Lymphoid interstitial pneumonia 6. Cryptogenic organising pneumonia 7. Respiratory bronchiolitis (ILD)
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BREAST-CLAP or CHHHAARTS Apical Lung fibrosis
Berylliosis Radiation therapy to upper chest Extrinsic allergic alveolitis Allergic Bronchopulmonary alveolitis Sarcoidosis Tuberculosis Coal workers pneumoconiosis Langerhans cell Histiocytosis Ankylosing spondylitis Psoriasis ---------------------- Coal workers pneumoconiosis Histoplasmosis Hypersensitivity pneumonitis Histiocytosis X Ankylosing Spondylitis ABPA Radiation Tuberculosis Sarcoidosis, Silicosis
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Usual interstitial pneumonia
a type of IPF # Major diagnostic criteria: - Exclude other causes - Typical Pulmonary Function Tests - Typical HRCT findings of IPF - No alternate diagnosis on biopsy/BAL # Minor diagnostic criteria: - age > 50 yrs - insidious onset - present > 3 weeks - bibasal inspiratory crackles poor prognosis in smokers Rx: Steroids - Azathioprine - IFN - Perfinide Pulmonary rehabilitation
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Eosinophillic Lung diseases
1. Atopic, Asthma, ABPA - High IgE, skin test to Aspergillus fumigatus 2. Associated with Helminth, parasitic infestation 3. Drug induced eosinophilia - NSAIDs, nitrofurantoin, Methotrexate 4. Idiopathic Eosinophilic - Simple pulmonary eosinophilia (Loeffler syndrome) - Chronic eosinophilic pneumonia - Acute eosinophilic pneumonia - Idiopathic hyper-eosinophilic syndrome - Churg Strauss syndrome: Asthma + Eosinophilia > x 1.5, Epistaxis, pANCA+, multisystem vasculitis
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Extrinsic Allergic Alveolitis
Group of disease with hypersensitivity reactions and alveolitis - clubbing, inspiratory crackles, inspiratory squeeks in midzone 1. Maltworkers EAA -Aspergillus fum. 2. Isocyanate paint associated EAA 3. Pigeon fancier's Lung - avian proteins 4. Mushroom workers Lung - Thermoactinomyces vulgaris 5. Humidifier Lung - various organism 6. Farmers Lung - micropolyspora faeni
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Pneumoconiosis
results from accumulation of dust in the lungs. 1. Asbestosis - benign pleural disease, Asbestosis, Mesothelioma 2. Coal dust pneumoconiosis: Simple or complicated: CXR shows large round opacities - can mimic TB, Wegners granulomatosis, can lead to Progressive Massive Fibrosis 3. Silicosis: due to silicon dioxide dust can be simple, Accelerated or Acute 4. Others - Siderosis, Stanosis (Tin induced) Baritosis (Barium induced) Berylliosis Caplan syndrome also has round pulmonary nodules but is RA associated and nodules are small.
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EAA: Acute vs Chronic
Acute Extrinsic Allergic Alveolitis: - within Hrs of exposure: fever, SOB, Cough, myalgia, hypoxia - inspiratory lung crackles - Type III immune complex + T cell - alveolar inflammation - Non caseating granulomas CXR: Lower zone nodules, fibrosis PFT: restrictive, reduced volume, reduced gas transfer HRCT: nodules, ground glass opacity Chronic Extrinsic Allergic Alveolitis: - prolonged low exposure - Type IV hypersensitivity delayed cell mediated reaction - chronic inflammation - exertional SOB, Hypoxia - Inspiratory lung crackles - precipitin 90% ++ CXR: Upper zone fibrosis PFT: same as in acute HRCT: fibrosis
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Asbestosis
asbestosis can be benign/ pleural/ Asbestosis/ Mesothelioma Mesothelioma risk increases with Crocidolite (blue asbestos) > Amosite (Brown asbestos) > Chrysolite (white asbestos) Effects: Lung fibrosis, PLeural nodules, diffuse pleural thickening, Clinical: SOB, dry cough, crackles, clubbing PFT: restrictive type, FEV1/PFT ratio normal Do PFT, HRCT, Biopsies Rx: Steroids, Azathioprine, Chemoradiation, Biolgicals
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Pulmonary Embolism considerations
Chest pain, dyspnea, Hypoxia, pleural rub, Haemoptysis, syncope do not do dDimer for screening PE do not do dDimer in pregnancy (rises 3 weeks to post-partum 3 months) Lone Q scan may be safest in pregnancy for PE diagnosis LMWH for 6 months better than warfarin with PE + Malignancy Massive PE with collapse: Alteplase bolus 50 mg PE in pregnancy: LMWH use from diagnosis to 6-12 weeks postpartum
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Transudative pleural Effusions
tends to be bilateral, protein < 30 Gm LVF Nephrotic syndrome Liver failure, cirrhosis Hypothyroidism Peritoneal dialysis Constrictive pericarditis SVC obstruction Meg's syndrome with benign ovarian fibroma
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Exudative pleural effusions
tends to be unilateral, protein >30 gm Ca bronchus Mesothelioma Pneumonia, Empyema Tuberculosis Pulmonary embolism 80% Connective tissue disorders Subphrenic abscess Pancreatitis, Post CABG Benign asbestosis Yellow Nail syndrome
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Pneumothorax Causes
spontaneous in young tall smokers Marfans syndrome Asthma-COPD cases Pneumonia Cystic fibrosis HIV associated Iatrogenic: CVP Line, Ventilation Traumatic, Rib fractures Catamenial with menstruation Cystic lung disease Lung cancers Small < 2 cm at hilum level
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Pneumothorax Rx Guideline
no diving till bilateral pleurectomy no air travel for 6 weeks after Rx > 2 cm - observe, aspirate, drain Initial aspirate & repeat CXR - if persists - repeat aspirate 2.5 Lit Air - if still persistent - insert ICD in 3/4th ICS in mid axillary line and keep 24 hrs, remove if no air leak without clamping Never clamp ICD if bubbling noted Common ICD size: 14-28 ICD suction should be considered after 48 Hrs only , High volume Low pressure -10 to -20 cm of H20 Repeat CXR after 2 weeks of ICD removal.
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SVC Obstruction
Pancoast tumor (Lung) Thymoma Goiter Teratoma Lymphoma Lymphadenitis Aortic aneurysm Mediastinal mass Mediastinal fibrosis Do pemberton maneuver
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Bronchiectasis Causes
Cystic fibrosis Post TB, Pneumonia, Measles, Post Pertusis Allergic BPA Hypogammaglobulinemia Primary Ciliary dyskinesia, Kartegener Localized due to bronchial FB COPD-Emphysema associated
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Diffuse Parenchymal Lung disease secondary to Systemic disease
Sarcoidosis Systemic sclerosis SLE Rheumatoid arthritis Ankylosing spondylitis Vasculitis - churg strauss Neurofibromatosis Tuberous sclerosis Ulcerative colitis Idiopathic pulmonary fibrosis
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DPLD secondary to Drugs
Methotrexate Cyclophosphamide Amiodarone Sulfasalazine Gold injections Nitrofurantoin Sulfonamides
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Risk Factors for PE
Major Risk Factors: - Any major surgery - Lower Limb ortho surgery - Late pregnancy, LSCS - Pre eclampsia - Lower Leg fractures - Varicose veins - Previous proven PE -------------------------- Minor Risk Factors: - Cardiovascular diseases - OC Pills, HRT - COPD - Occult malignancy - Obesity Poor mobility - Thrombophillic conditions - Nephrotic syndrome - Inflammatory bowel disease - Leukemias
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PAH Work up, Rx
Work up for Pulmonary HTN: - Basic Labs - ECG: RAD, RBBB, Ppulmonale,Tachy - CXR: Cardiomegaly, Enlarged PA - CTPA, Gold standard - 2D ECHO with DLCO: HIgh PA pressures > 40 with Low DLCO -------------- Treatment for Pulmonary HTN: - CCB's - Epoprostenol infusions - Nebulized Ileoprost - Sildenaphil, Tadalafil - Bosentan (Endothelin antagonist, vasodilator) - Atrial septostomy - Lung Transplantation
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DPLD XRay Mimics
Pneumonias Miliary TB Bronchiectasis LVF - Pulmonary edema Lymphagitis carcinomatosis Bronchoalveolar cell carcinoma
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Pulmonary Hypertension Signs
Initial Loud P2 then palpable Pulmonary regurgitation with EDM (Graham steel Murmur), Loud with Inspiration as right sided RV overload signs - RV Heave, prominant a wave in JVP TR murmur@ Left sternal edge, pansystolic V wave in JVP RV Failure: Tender hepatomegaly, Mild icterus, Ascites, Leg edema
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Lung Transplant: Indications
- Cystic fibrosis - Suppurative Lung diseases - Obstructive Emphysema - Alfa 1 Antitrypsin deficiency - Restrictive Lung: IPF secondary to CTD, EAA, Sarcoidosis - Pulmonary vascular disease: PAH - CHD with PAH - Rare: Langerhans cell Histiocytosis LymphangioLeiomyomatosis in Tuberous sclerosis
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MRC Dyspnea scale
Grade 1: not troubled by SOB except on strenous exercise Grade 2: SOB when walking up a slight hill Grade 3: walks slower than contemporaries on level flat ground becauses of SOB or has to stop walking at his own pace Grade 4:Stopd for breath after walking for 100 meter or after a few minutes on level ground Grade 05: too breathable to leave house or breathless even just dressing himself
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Light's criteria for pleural Effusion
1. Pleural protein: Sr protein > 0.5 2. Pleural LDH: Serum LDH > 0.6 3. Pleural LDH more than 2/3rd of upper normal limit of Serum LDHic therapy chronic diuretic therapy increases concentration of LDH, proteins in pleural fluid
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LTOT indications
must stop smoking CO levels < 3% Indicated when: 1.ABG PaO2 < 7.3 kpa when stable OR 2. PaO2 < 8 kpa with: - secondary Polycythemia - Nocturnal hypoxia - Cor pulmonale with edema - Pulmonary HTN - SaO2 < 90% at room air Use oxygen > 15 Hrs per day, max 20
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Pulmonary Fibrosis: Lower Zone
RATIO Rheumatoid arthritis Asbestosis Tissue disorders: Scleroderma, PM+DM, SLE, Sjogrens Idiopathic: UIP, Fibrotic non specific IF Other: Bronchiectasis, Drugs, Chemical
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Pink puffer: Blue Bloaters
Pink puffers: Good respiratory drive No cyanosis Pursed Lip breathing Intense dyspnea Thin elderly patients usually Little expectoration ABG is near normal Rarely Cor pulmonale TLC increased with low transfer factor ---------------- Blue Bloaters: Poor respiratory drive Cyanosed, blue lips Mild dyspnea Large expectoration Infective exacerbation, Coma ABG hypercapneic, alkalosis Cor pulmonale common Transfer factor near normal Nocturnal Hypoxia
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Chylothorax
Trauma Lymphoma Congenital absence of thoracic duct Filariasis TB Lymphadenitis Lymphangioleiomyomatosis Yellow Nail Syndrome Left subclavian venous thrombsosi
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Reactive Airways Dysfunctional Syndrome: RADS
RADS is distinct type of occupational asthma that results from a single occupational exposure to high levels of irritant vapours, gases of fumes as chlorine, bleach or ammonia. Symptoms can persist for years even after no second exposure. + Bronchial challange test to same trigger manifested as bronchospasm
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Pleurodesis
permanent scarring of pleura done for recurrent malignant effusions or recurrent pneumothoracec Agents used are: - Talc - Doxycycline - Belomycin - Zinc sulfate - Quinacrine
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Haemoptysis differentials
Respiratory causes: = pneumonia, Lung abscess, Bronchitis, Bronchiectasis = Malignancy: Ca Lung or bronchus = kaposi's sarcoma = PE, Wegner's granulomatosis = Goodpasture's, HHT AV Malformations ------------- Cardiac causes: = Pulmonary edema = Mitral stenosis ---------- Other causes: = Bleeding dirorders = Anticoagulant use = Thoracic endometriosis, Catamenial
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TB contacts
BCG taken: = Maontoux test + = IFN gamma release test + = Clinical examination, L nodes = CXR to do BCG not taken: = Montoux test + = IFN gamma test + CXR suggestive lesion = treatt Montoux negative - vaccinate Abnormal CXR - Further investigate
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Bronchiectasis: Genetic causes
Cystic fibrosis: DeltaF-508-chr07, Autosomal recessive, CFTR gene mutations - increases Chloride in sweat and secretions, mucus precipitation and chronic blockage causing bronchiectasis, pancreatitis, malnutrition Chediak Higashi syndrome: AutoRecessive, reduced lysosomal peroxidase causing chronic granulomatous disease with recurrent infections, lung destruction Yellow Nail Syndrome: Exudative pleural effusions, sinusitis, Lymphedema, bronchiectasis William Campbell syndrome: absent bronchial cartilege causes bronchiectasis Primary Ciliary dyskinesia: Kartagener syndrome: reduced mucociliary clearance with precipitation, chronic bronchial block with recurrent infections causing bronchiectasis, Infertility, situs inversus + Dextrocardia Young syndrome: excessively thick mucus but normal cilias - causes bronchiectasis Mounier Kuhn Syndrome: multiple tracheal diverticuli with tracheal enlargement - bronchiectasis, recurrent URTI, LRTI Swyer James Syndrome: post infectious bronchiectasis after measles, RSV, Mycoplasma, Influenza, Staphylococcal or streptococcal
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Paraneoplastic Syndrome: Ca Lung
Endocrinal Paraneoplastic: = SIADH, Hyponatremia (Ectopic ADH) = Hypercalcemia (ectopic PTH) = Cushing's (ectopic ACTH) = Hyperthyroidism (ectopic TSH) = Hypoglycemia (ectopic Insulin) Neurological paraneoplastic: = Myasthenia gravis = Lambert Eaton MG = Cerebellar degeneration = Sensory neuropathy = Limbic encephalopathy Musculo-cutaneous Paraneoplastic: = Polymyositis-Dermatomyositis = Pulmonary Hypertrophic Osteoarthropathy: tender wrists, swollen PIP, DIPS, clubbing = Acanthosis nigricans = Gynecomastia = Thrombophlebitis = Thrombotic tendencies = Hypertrichosis
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Cystic Fibrosis: Complications
Auto recessive, Detak F508 mutation Excessive Chloride in sweat Bronchiectasis Pancreatic destruction - DM Distal intestinal obstruction syn Meconium ileus Malabsoprtion, Steatorrhea, Vitamin deficiencies (fat soluble) Focal biliary cirrhosis Cholelithiasis Male sub fertility - defective sperm motion Osteoporosis Sinus disease, Nasal polyps, Otitis, Asthma risk
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Lung cancers: Histology Type
1. Non small cell Ca Lung: 80% = Squamose > Adenocarcinoma > Alveolar cell > Large cell in frequency staging: Ia, Ib, IIa, IIb, IIIa, IIIb, IV (TNM based) 2. Small cell Lung cancer: 20% aggressive Limited or diffuse Risk Factors: Smoking, ILD, Radon exposure, Asbestos, Arsenic, Chromium, Iron oxide, Coal Tar, Radiation
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Ca Lung: Performance score
by WHO 0 - asymptomatic 1- symptomatic SOB but able to carry out light work 2 - in bed < 50% time of day 3 - in bed > 50% time of day 4 - Bed ridden
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Rheumatoid Lung disease
five patterns 1. Pleural effusions: RAfactor in fluid 2. Pulmonary nodules: usually upper lobes 3. Fibrotic Lung disease 4. Caplan syndrome: coal workers pneumoconiosis + RA together, lung canon balls 5. Obliterative bronchiolitis - leads to necrotising pattern, common with RA treated by Gold or penicillamine
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Clubbing: Respiratory Causes
A - Abscess, Asbestosis B - Bronchiectasis C - Cystic fibrosis D - Dirty tumors Mesothelioma, Ca bronchus E - Empyema F - Fibrosing alveolitis
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Bronchiectasis Association
Associations: - Rheumatoid arthritis - Chronic sinusitis - IBD - Marfan's syndrome Anatomic location @ causes: Lower Lobe - post infectious Rt Middle Lobe - obstructive Upper Lobe - TB, Mycosis, ABPA
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Bronchiectasis Complications
Pulmonary: = Recurrent infections = Haemoptysis = Pulmonary HTN = Cor pulmonale, Right CHF = Empyema, Lung abscess Extra Pulmonary: Anemia Metastatic infections Secondary amyloidosis
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CHAMS-PINTS: Causes of pleural Effusion
CHAM - transudates C - congestive heart H - Hypothyroid, Hypoalbumin A - All failures: Liver, Kidney, Heart M - Meig's syndrome (Benign ovarian fibroma with pleural effusions) PINTS: exudates P - Pneumonia I - Infarctions as in PE N - Neoplasms T - Tumor, TB, Trauma S - Sarcoidosis, Scleroderma, CTD's Drugs: Hydralazine, Bromocriptine, Methotrexate, Methysergide, Nitrofurantoin
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Lung Fibrosis: Iatrogenic causes
BBC sport is every MANS Gold B - BLEOMYCIN B - BUSULFAN C - CYCLOPHOSPHAMIDE M - Methotrexate A - Amiodarone N - Nitrofurantoin S - Sulfasalazine Gold therapy
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TB pleural effusions
Diagnosed with combination of: Fluid culture + Gram/AFB stain + Biopsy Also: Adenosine deaminase levels > 43 IFN Gamma release assay > 140pg/ml
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Asthma Severity Assessment
Acute Severe Asthma: PEFR 33-50% (normal 600 L/min) RR > 25/min Heart Rate > 110/min Unable to speak in sentences Life threatening Asthma: PEFR <33 % SpO2 < 92% Poor Respiratory efforts Silent Chest, may be cyanotic Arrhythmia, Hypotension Acidotic ABG, normal or High Pco2
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Evaluation: Palpitations
Cardiac causes: = SVT: atrial tachycardias, Atrial fibrillation, Flutter, AVRT, AVNRT = Ventricular tachycardia = Atrial or Ventricular ectopics = Bradycardic: Intermittent AV Blocs = SA node disease Non Cardiac disease: Anemia Thyrotoxicosis Hypothyroid bradycardia Hypoglycemia Pheochromocytoma Caffeine, Ethanol, Salbutamol, Thyroxine Anxiety attacks Exercise Pregnancy
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Lump in Neck: Causes
85% - Cx lymphadenitis Thyroid swelling: - 8% = Goiter: Grave's, Multinodular, Hashimoto's, Subacute = Solitary nodule = Adenoma = Ca thyroid, Medullary ca as in MEN2 Other causes 7% = congenital: Brachial cyst, Dermoid cyst, Thyroglossal cyst = HNF: Cancers, Carotid aneurysm, Chemoductoma, Cervical Rib = Salivary: Parotid Tumors, Duct stones, other neoplasms
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Pacemaker Devices
VVI, AAI, DDD V = 1sr Letter indicates chamber being paced (V, A) V = 2nd letter indicates chamber being sensed, V/A I = 3rd letter indicates mode of pacing, Inhibited, Triggered, Dual R = Rate responsive common Indications: - arrhythmias with pre-syncope or syncope - Long sinus pauses > 3 sec - Tri fascicular block - Complete Heart block Modes: AAI with sick sinus syndrome DDD with Heart blocks VVI with blocks with Inferior STEMI UnderDrive Pacing: = old style, risk of R on T leading to VT/VF Overdrive pacing: = Senses and paces at rest > SVT thus terminates it
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Long QT causing Drugs
Apple-Google-MAPS 1. Antiarrhythmics: = Quinidine, Amiodarone, Sotalol 2. GI Motility agents: Domperidone, Cisapride 3. Macrolides: Azithromycin, Klacid 4. Antihistamines: Terfenadine, Cetrizine, Loratadine 5. Psychotropic: Phenothiazines, SSRI, TCAs
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Well's Criteria for DVT
3-8 score - High probability, 0 - low Paralysis or recent POP casting of legs = 01 Recent bedridden > 3 Days or Major Sx < 3 wks = 01 Localized tenderness in deep vein system = 01 Swelling of entire leg = 01 Calf swelling 3 cm > other legs = 01 Pitting edema greated in leg with pain = 01 Collateral non varicose superficial veins = 01 Active cancer or cancer within last 6 mths = 01 Alternative diagnosis more likely than DVT = 02
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Non Atherosclerotic Angina
= Thyrotoxicosis = Aortic Regurgitation = Aortic stenosis = HOCM = Anaemia
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Phlegmasia cerulea dolones
venous gangrene, a severe form of iliofemoral thrombosis by massive venous occlusion. Diffuse limb swelling upto groin.
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Takutsubo cardiomyopathy
catecholamine induced cardiomyopathy, Broken Heart Syndrome. Sudden chest pain mimicking MI with increased ST segments and its signature apical ballooning on ECHO, also reduced LVEF. Occurs during catecholamine surges Cause of mI in presence of normal arteries Stress may be medical or psychological
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Classification of Aortic Dissection
DeBakey system: Type I: involves both descending & ascending aorta Type II: involves only ascending thoracic aorta Type III: involves only descending thoracic aorta Type IIIb: involves descending thoracic & abdominal aorta Stanford System: Type A: involves ascending aorta Type B: all other aorta
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Congenital Heart Disease
Acyanotic CHD: (Left to RIght shunt) = ASD, VSD = Aorto-pulmonary window = PDA = Co-arctation of Aorta = Mild Pulmonary stenosis Cyanotic CHD: (Right to Left shunt) = Fallot's tetrology = Transposition of great arteries = Tricuspid atresia = Pulmonary atresia = Total anomalous pulmonary venous return = Hypoplastic Left Heart = Truncus arteriosus
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Oliver's Sign
Feeling a downward tracheal pulsation coincident with pulse and not associated with inspiration suggests thoracic outlet aneurysm
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HTN exacerbated in Pregnancy
Autosomal dominant Severe HTN in early pregnancy due to activation of mineralocorticoid receptor by progresterone. Missence mutation with substitution of Leucine for serine at codon 810.
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Takayasu Arteritis
affects major big vessels as ascending and arch of aorta causing fibrotic occlusion, upper limb claudication, cerebral ischemia, syncope, poor prognosis
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Burger's Disease: Thromboangitis obliterans
Inflammatory occlusion vascular disorder of unknown cause affecting small and medium sized vessels. Often a triad of claudication of affected limb present. Raynaud's phenomenon and migratory superficial vein thrombophlebitis.
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Malignant Hypertension
Progressive retinopathy, papilloedema Worsening renal function Proteinuria Microangiopathic Hemolytic anemia Encephalopathy
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Prinzmetal variant angina
Angina at rest but not during exertion or exercise, due to focal spasm of an epicardiac coronary artery
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Oxygen Saturation curve
Plotted % oxygen saturation against PaO2 Left shift: Reduced 2,3 DPG More ph ie alkalosis, Low CO2 ie hypocarbia, more oxygen is taken up but not released Right shift: Low PH, High CO2, High 2,3 DPG, more oxygen is released to tissues
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2, 3 Diphosphoglyerate
d-2,3-BPG is present in human red blood cells (RBC; erythrocyte) at approximately 5 mmol/L. It binds with greater affinity to deoxygenated hemoglobin (e.g., when the red blood cell is near respiring tissue) than it does to oxygenated hemoglobin (e.g., in the lungs) due to conformational differences: 2,3-BPG (with an estimated size of about 9 Å) fits in the deoxygenated hemoglobin conformation (with an 11-Angstrom pocket), but not as well in the oxygenated conformation (5 Angstroms). It interacts with deoxygenated hemoglobin beta subunits and decreases the affinity for oxygen and allosterically promotes the release of the remaining oxygen molecules bound to the hemoglobin. Therefore, it enhances the ability of RBCs to release oxygen near tissues that need it most. 2,3-BPG is thus an allosteric effector. Its function was discovered in 1967 by Reinhold Benesch and Ruth Benesch.
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Pulmonary alveolar proteinosis
Accumulation of an amorphous periodic acid schiff stain positive lipoproteinaceous material in the distal alveoli due to defect in macrophages processing surfactant. Resembles ILD but underlying lung architecture is preserved and without any inflammation. Improves if material removed.
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Polymer fume fever
Fluoropolymers such as Teflon shows a reaction at normal temperatures but when volatilized on heating, inhalation causes a characteristic syndrome of - FEVER, chills, Malaise, and wheezing Same happens on inhalation of Zinc oxide from steel welding leading to Metal fume fever..
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Parasternal Long Axis view- Normal dimensions in 2D Echo
Wall to wall lengths: Aortic annulus - 17-25 mm Sinus of Valsalva- 22-36 mm Sino tubular junction - 18.26 mm Aortic root (tubular) - 20-37 mm Anterior aortic swing - 7-15 mm AV surface area - 2.5-3.5 cm square
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PLAX- M mode scan - measurements
**Aortic valve level:** Aortic root diameter - 20-37 mm Aortic cusp separation - 15-26 mm Left arterial diameter - 19-40 mm **Mitral valve level:** AML D-E excursion - 20-35 mm AML EF slope - 18-120 mm/second E point to septum - less than 5 mm
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How to rule out COPD in chronic cough cases
**Rules out COPD if:** 1. Match test normal - ability to noodle off a match flame from distance of 25 cm 2. ⁠maximum laryngeal height > 4 cm measured from sternal notch to cricoid cartilage in end expiration.
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Clinical predictors of raised **LVEDP**
1. Tachycardia 2. Bibasilar crackles 3. Distended neck veins 4. Low systolic BP 5. CXR - cardiomegaly, pulmonary vascular redistribution 6. Third heart sound 7. Lower leg see
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Fractional LV shortening
FS is calculated by formula: FS = (LVEDD - LVESD)/ LVEDD x 100 It’s normally 30-40% Reduced with systolic dysfunction
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LV volume by Teicholz Equation
V = (7/ 2.4 + D) D3 D - diameter of LV D3 - cube of D Another way, V = D3
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Stroke volume formulae
Stroke volume = LVEDV - LVESV Cardiac output = SV x heart rate Stroke volume = CSA x FVI CSA = pi x square of r = pi x (D/2) square = 22/7 x D2/4 =0.25 d² 0.785D2 D - aortic annulus diameter CO = 0.785D2 X FVI x Heart Rate FVI - flow velocity integral, calculated by echo machine as area under the curve of aortic outflow velocity spectral display
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**I COUGH** program for respiratory care after surgery
I - incentive spirometry C - coughing & deep breathing O - oral care measures U - Understand ie pt counselling G - Get moving, early ambulation H - Head of bed elevated
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Paget Schroeder disease
Paget–Schroetter disease (which evolved from a venous thoracic outlet syndrome) is a form of upper extremity deep vein thrombosis (DVT), a medical condition in which blood clots form in the deep veins of the arms. These DVTs typically occur in the axillary and/or subclavian veins.