Cardio-Respiratory Flashcards
Pulmonary Hypertension: Causes
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
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.
PDA signs: Continuous machinery murmur (systolic) along 2nd ICS, left parasternal, below Left clavicle & posteriorly, Thrusting apex, displaced to AA line, with collapsing nature of pulse if large PDA, Toe clubbing
and
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
Causes of continuous MURMUR
Continuous Murmur + collapsing pulse
= MR + AR
= VSD + AR
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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)
Mitral Regurgitation
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
Skin Petechiae Causes
Petechiae can be seen with:
= Severe thrombocytopenia
= Infective endocarditis
= Scurvy
= Renal Failure
= Bacteremia without IE (meningococcemia)
= Fat embolism in Cardiopulmonary bypass
Duke’s Criteria for Infective endocarditis
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
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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
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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
Duckett- Jones Criteria for Acute Rheumatic Fever
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
Eisenmenger Syndrome
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
Eisenmenger Syndrome, causes
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
Co-arctation of Aorta, signs
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
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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
Associations of Co-arctation
= 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
Causes of rib notching
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
Cannon JVP waves:
are giant a waves & occur whenever a right atrium contracts against closed TV
Causes of Regular pattern cannon waves:
= nodal rhythm (AV nodal)
= Paroxysmal nodal tachycardia
= Partial Heart block with very long PR
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Causes of Irregular Cannon waves:
= CHB
= Multiple ectopic beats
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p wave in ECG will fall between QRS/T or at end of T wave.
Tetrology of Fallot
- ventricular septal defect,
- overriding aorta,
- pulmonary stenosis and
- ## 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
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Most patients will present in the neonatal period with mild-to-moderate cyanosis, but typically without respiratory distress.
What is Blalock Shunt
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.
Dextrocardia, apex to right
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
Kartagener syndrome
a primary ciliary dyskinesia + Situs
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
HOCM,
Autosomal dominant
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
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All first degree relatives- screen by echo
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Fainting attacks at end of exercise in HOCM as opposed to fainting during exercise in Aortic stenosis.
HOCM Diagnosis
= 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
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Rx options:
= Beta blockers
= Calcium channel blockers
= Septal ablation or Myomectomy
= implantable cardiac defibrillators
JVP Waves and meanings
a-x-c-x1-v-y
A= Rt atrial contraction pushes some blood into IJV (upright wave)
x-descent = RA relaxes dropping pressure
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C= TV closes and RV contract so bulges into right atrium (upright)
X1-descent=end of RA contraction creates space when RA starts filling
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V =RA filling against closed TV pushes some blood into IJV (upright)
y-descent = opening of TV so blood goes into ventricles
High JVP Causes
= Heart failure
= Tricuspid stenosis
= Pulmonary stenosis
= Cor pulmonale, PAH
= PAH 2ry to Mitral disease
= Constrictive pericarditis
= Large pericardial effusion
= SVC obstruction, flushed face
Ebstein’s anomaly
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
Ebstein’s associations
It is - tricuspid valve in the wrong position and the valve’s flaps (leaflets) are malformed.
= 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
Pulmonary stenosis
1 mmHg = 1.35951 cm H2O
congenital or Post TOF repair
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.
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Repair if gradient across PV> 50 mmHg
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
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Maladie de Roger - loud VSD murmur due to small hole, low gradient, more sound.
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Eisenmenger syndrome can develop
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Mitral mid-diastolic flow murmur if VSD large - left sided - reduces with inspiration - LA flow crashes with VSD flow.
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.
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
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.
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
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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
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
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
MVP - Manoeuvre effects on murmur
- Manoeuvres reducing cardiac venous return - such as -
Standing/ Valsalva = increases prolapse
Click and murmur occurs early
Murmur gets prolonged in duration
——————- - ## Manoeuvres increasing venous return such as - squatting, Hand squeeze, raising legs = delayes click. murmur which shortens duration of murmurOther causes of Short systolic murmurs
= Early minor Mitral regurg
= Aortic stenosis or sclerosis
= HOCM
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
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
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Surgery required when LV End Diastolic dimension is more than 45 mm
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
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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.
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
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.
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
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.
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.”
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.
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.
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.
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.
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
Aortic stenosis Causes
= Degenerative calcification in elderly
= Rheumatic HD: calcification/ scarring Streptococcal
= Bicuspid Aortic valve (congenital)
= Congenital
= Paget’s, IE, Hyperuricemia
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Rx Options:
= Valvotomy
= TAVI: Transcatheter Aortic Valve implantation
= Open surgery with CABG
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
Indications for intervention in MS
when to correct mitral stenosis
- an episode of pulmonary edema
- MS in pregnancy
- Significant symptoms, SOB
- Recurrent embolic phenomenon
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S2 to Opening snap interval > 0.07 sec with heart rate < 100 means MS is significant.
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Anti-coagulation is recommended in all with MS even if mild and in sinus.
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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
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)
Cardiomyopathy causes
- Toxic: = Alcohol, Adriamycin, Cyclophosphamide, Emetine, Steroids, Lithium, Phenothiazines
- Metabolic: = Thiamine deficiency, Kwashiorkar, Pellagra (niacin), Obesity, Prophyria, Uremia, Electrolyte imbalanc
- Endocrine: = DM, Thyrotoxicosis, Acromegaly, myxoedema, Cushing’s
- Collagen: SLE, PAN
- Infiltration: Amyloidosis, Hemochromatosis, Wilsons, Sarcoid, GSD, MPS, Gaucher’s, Whipples
- Infections: viral, Rickettsial, TB
- Genetical: HOCM, Muscular dystrophies
- Fibroplastic: Loeffler endocarditis, Endomyocardial fibrosis, Carcinoid
- Miscellaneous: Postpartum, persistent atrial tachycardia
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
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.
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
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
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Lung diseases Occasionally causing Cor pulmonale:
= Progressive Massive fibrosis in coal workers
= Bronchiectasis
= Cryptogenic fibrosis alveolitis
= Systemic sclerosis with PAH
= Sarcoidosis
= Asthma, Severe, Chronic
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
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
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.
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.
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.
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.
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
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.
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.
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
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
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
Permanent Pacemaker
third degree CHB
Symptomatic 2nd degree CHB
Asymptomatic Mobitz 2 CHB
Sinus pauses > 3 seconds (15 big squares)
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
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
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
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)
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
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
Mid Diastolic Murmurs
Left atrial myxoma
Mitral Stenosis-best at Apex which is not displaced, Pulse and pulse pressures are normal., AFib may be present.
#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)
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
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.
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
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.
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.
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
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 ++
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
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
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.
Secondary Pulmonary Hypertension
Cause of secondary PAH:
01. High pulmonary venous pressures: AV/MV/LV diseases
Venous occlusions,
in Autoimmunes
- Poor-reduced Pulmonary vascular Bed: ILD, PE, COPD, CTD’s
- Chronic Hypoxia conditions:
ILD, COPD, OSA, High altitude, Obesity-Hypoventilation, Kyphoscoliosis, NMJ (GBS, MG, Polio) - Left to Right shunts: ASD, VSD
Primary PAH: Familial or with CTD’s or HIV or Fenfluramine induced
Types of VSD (PSPM)
- Perimembranous VSD:
infra-cristal, 80%, most common, just below aorta origin. Can have a RA to LV connection called Gerbode defect
——————— - ## Supra-cristal: infundibular, below Pulmonary valve, communicates with RV outflow tract to lungs
- ## Muscular VSD: trabecular, in muscular inter ventricular septum
- Posterior Endocardial Cushion Type:
Posterior to septal leaflet of Tricuspid valve
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.
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
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
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
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.
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
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
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
Malar Flush Causes
- Mitral stenosis
- SLE
- Hypothyroidism
- Cold weather
- Carcinoid syndrome
- Systemic sclerosis
- Irradiation to face/ head
- Polycythemia
Erysipelas.
Cellulitis.
Rosacea.
Pellagra.
Dermatomyositis.
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
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.
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
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.
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.
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%
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
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.
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.
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
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
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
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
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
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
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
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
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
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
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.
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
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
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
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
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.
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
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
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
Clues to cause of Aortic Regurg
Bicuspid AV: young patient with AR, ejection click in systole
Marfan Syndrome: Tall, spidery long fingers, High arch palate, Arm span > Leg span, Pectus anomaly
Syphilitic Aortitis: Argyl Robertson pupils, Sensory ataxia, Neurotrophic foot ulcers
# Other Cause: Hypertension, Rheumatic Fever, Perimembranous VSD
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
Loud ESM in Expiration
seen with:
- Aortic stenosis
- HOCM
- Supra valvular AS (William’s Syn)
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)
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
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
Collapsing pulse
Aortic regurgitation
Pregnancy, Hyperdynamic status
PDA
Paget’s disease, Hyperdynamic
Anemia, long standing
Thyrotoxicosis
Moderate Mitral regurg
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
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
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
Idiopathic Pulmonary Fibrosis classification (ATS-ERS)
- Acute interstitial pneumonia (Hamman Rich syndrome)
- Usual interstitial pneumonia
- Non specific interstitial pneumonia
- Desquamative interstitial pneumonia
- Lymphoid interstitial pneumonia
- Cryptogenic organising pneumonia
- Respiratory bronchiolitis (ILD)
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
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
Eosinophillic Lung diseases
- Atopic, Asthma, ABPA - High IgE, skin test to Aspergillus fumigatus
- Associated with Helminth, parasitic infestation
- Drug induced eosinophilia - NSAIDs, nitrofurantoin, Methotrexate
- 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
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
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.
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
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
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
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
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
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
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.
SVC Obstruction
Pancoast tumor (Lung)
Thymoma
Goiter
Teratoma
Lymphoma
Lymphadenitis
Aortic aneurysm
Mediastinal mass
Mediastinal fibrosis
Do pemberton maneuver
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
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
DPLD secondary to Drugs
Methotrexate
Cyclophosphamide
Amiodarone
Sulfasalazine
Gold injections
Nitrofurantoin
Sulfonamides
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
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
DPLD XRay Mimics
Pneumonias
Miliary TB
Bronchiectasis
LVF - Pulmonary edema
Lymphagitis carcinomatosis
Bronchoalveolar cell carcinoma
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
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
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
Light’s criteria for pleural Effusion
- Pleural protein: Sr protein > 0.5
- Pleural LDH: Serum LDH > 0.6
- 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
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
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
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
Chylothorax
Trauma
Lymphoma
Congenital absence of thoracic duct
Filariasis
TB Lymphadenitis
Lymphangioleiomyomatosis
Yellow Nail Syndrome
Left subclavian venous thrombsosi
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
Pleurodesis
permanent scarring of pleura done for recurrent malignant effusions or recurrent pneumothoracec
Agents used are:
- Talc
- Doxycycline
- Belomycin
- Zinc sulfate
- Quinacrine
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
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
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
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
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
Lung cancers: Histology Type
- Non small cell Ca Lung: 80%
= Squamose > Adenocarcinoma > Alveolar cell > Large cell in frequency
staging: Ia, Ib, IIa, IIb, IIIa, IIIb, IV (TNM based) - Small cell Lung cancer: 20%
aggressive
Limited or diffuse
Risk Factors: Smoking, ILD, Radon exposure, Asbestos, Arsenic, Chromium, Iron oxide, Coal Tar, Radiation
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
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
Clubbing: Respiratory Causes
A - Abscess, Asbestosis
B - Bronchiectasis
C - Cystic fibrosis
D - Dirty tumors Mesothelioma, Ca bronchus
E - Empyema
F - Fibrosing alveolitis
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
Bronchiectasis Complications
Pulmonary:
= Recurrent infections
= Haemoptysis
= Pulmonary HTN
= Cor pulmonale, Right CHF
= Empyema, Lung abscess
Extra Pulmonary:
Anemia
Metastatic infections
Secondary amyloidosis
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
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
TB pleural effusions
Diagnosed with combination of: Fluid culture + Gram/AFB stain + Biopsy
Also:
Adenosine deaminase levels > 43
IFN Gamma release assay > 140pg/ml
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
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
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
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
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
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
Non Atherosclerotic Angina
= Thyrotoxicosis
= Aortic Regurgitation
= Aortic stenosis
= HOCM
= Anaemia
Phlegmasia cerulea dolones
venous gangrene, a severe form of iliofemoral thrombosis by massive venous occlusion. Diffuse limb swelling upto groin.
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
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
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
Oliver’s Sign
Feeling a downward tracheal pulsation coincident with pulse and not associated with inspiration suggests thoracic outlet aneurysm
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.
Takayasu Arteritis
affects major big vessels as ascending and arch of aorta causing fibrotic occlusion, upper limb claudication, cerebral ischemia, syncope, poor prognosis
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.
Malignant Hypertension
Progressive retinopathy, papilloedema
Worsening renal function
Proteinuria
Microangiopathic Hemolytic anemia
Encephalopathy
Prinzmetal variant angina
Angina at rest but not during exertion or exercise, due to focal spasm of an epicardiac coronary artery
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
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.
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.
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..
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
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
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.
Clinical predictors of raised LVEDP
- Tachycardia
- Bibasilar crackles
- Distended neck veins
- Low systolic BP
- CXR - cardiomegaly, pulmonary vascular redistribution
- Third heart sound
- Lower leg see
Fractional LV shortening
FS is calculated by formula:
FS = (LVEDD - LVESD)/ LVEDD x 100
It’s normally 30-40%
Reduced with systolic dysfunction
LV volume by Teicholz Equation
V = (7/ 2.4 + D) D3
D - diameter of LV
D3 - cube of D
Another way, V = D3
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
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
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.
