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 is 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 or 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
