Sandbox:Sara.Zand
Recommendations for treatment of syncope |
Bradyarrhythmia (Class I, Level of Evidence C): |
❑ Implantation of dual chamber permanent pacemaker in chronic bifascicular block but without documented high grade AV block |
Supraventricular tachycardia(Class I, Level of Evidence C) : |
❑ Treatment of arrhythmia based on guideline directed medical theray |
Ventriculat arrhythmia : (Class I, Level of Evidence C) |
❑ Treatment of underlying cardiac causes of ventricular arrhythmia |
Ischemic and non ischemic cardiomyopathy:(Class I, Level of Evidence C) |
❑ Treatment of underlying causes of cardiomyopathy |
Valvular heart disease : (Class I, Level of Evidence C) |
❑ In severe AS and syncope the mechanism of syncope is low cardiac out put |
Hypertrophic cardiomyopathy (Class I , Level of Evidence C): |
❑ Inadequate data about the relation between unexplained syncope as the predictor of SCD |
Arrhythmogenic right ventricular cardiomyopathy : (Class I , Level of Evidence B) |
❑ ICD indicates in the setting of sustain VT leading syncope |
Cardiac sarcoidosis : (Class I , Level of Evidence B) |
❑ ICD indicates in the presence of syncope due to ventricular tachycardia |
Brugada : (Class IIa, Level of Evidence B) |
Brugada : (Class IIb, Level of Evidence B) |
❑ EPS may be helpful for finding ventricular arrhythmia leading syncope |
Brugada : (Class III, Level of Evidence B) |
❑ ICD is not recommended in patients suspected reflex mediated syncope |
Short QT syndrome : (Class IIb, Level of Evidence C) |
❑ ICD implantation in the presence of documented ventricular arrhythmia and family history of SCD |
Long QT syndrome : (Class I, Level of Evidence B) |
❑ Beta-blocker therapy in patients with frequent episodes of syncope reduces risk of fatal arrhythmia specially in LQTS1 |
Long QT syndrome : (Class IIa, Level of Evidence B) |
❑ICD implantation in syncope related arrhythmia in patients are on betablocker or intolerant to betablocker |
CPVT : (Class I, Level of Evidence C) |
❑ Exercise restriction in patients suspected arrhythmia leading syncope |
CPVT : (Class IIa, Level of Evidence C) |
❑ Flecainide in patients with arrhythmia leading syncope in spite of betablocker therapy |
CPVT : (Class IIb, Level of Evidence C) |
❑ Verapamil in patients with arrhythmia leading syncope during exercise in spite of betablocker therapy |
Vasovagal syncope : (Class I, Level of Evidence C) |
❑Avoidance of triggers(prolonged standing, warm environments, coping with dental and medical setting |
Vasovagal syncope : (Class IIa, Level of Evidence B) |
❑ Supine position for prevention of faint and injury in short prodrome phase |
Vasovagal syncope : (Class IIb, Level of Evidence B) |
❑ Lacking evidence about benefit of orthostasis training such as repeating tilt table test until negative result or 30-60 minutes standing against a wall daily |
Carotide sinus syndrome : (Class IIa, Level of Evidence B) |
❑ Cardiac pacemaker implantation in recurrent cardioinhibitory or mixed syncope |
Carotide sinus syndrome : (Class IIb, Level of Evidence B) |
❑ Dual chamber pacemaker in older patients with underlying sinus node dysfunction or conduction abnormality |
Recommendation for syncope due to dehydration and medications
Class I, Level of evidence:C |
Fluid rescucitation orally or intravenous is useful for syncope related to hypotension or exercise associated hypotension due to peripheral vasodialation |
Class IIa, Level of evidence:B |
Reducing or withdrawing medications causing hypotension and syncope such as diuretics, vasodilators, venodilators, sedatives, negative chronotropes |
Class IIa, Level of evidence:C |
Salt and fluid intake in syncope due to dehydration |
TGA, TAPVR ,Truncus arteriosus | Infusion of Prostaglandin, Diuretic therapy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
TOF | Hydration, modified blalock taussing shunt, insertion stent in PDA and right ventricular outflow tract, total repair | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Treatment of Cyanosis | Ebstein anomaly | Tricuspid valve repair | |||||||||||||||||||||||||||||||||||||||||||||||||||||
Hypoplastic left heart syndrome | Infusion of Prostaglandin for keeping patency of ductus arteriosus, infusion of vasodilator for reduced systemic resistance, mechanical ventilation in shock state and imposing hypercapnia and alveolar hypoxia for increased pulmonary resistance | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Sepsis, shock, low cardiac output state, cold exposure, metabolic disorder, polycythemia | Treatment of underlying disorder | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Eisenmenger syndrome with pulmonary hypertension, | Phosphodiesterase-5 inhibitor (sildenafil, tadalafil, Endothelin receptor antagonist (bosentan,macitentan, ambrisentan) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Methemoglobinemia | Infusion of Methylenblue,dextrose,N-acetyl cystein,cimethidin,ketoconazole | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
PAO2 is the mean alveolar oxygen pressure.PH2O is the water vapor pressure (47 mmHg at 37°C).
PaCO2 is the alveolar carbon dioxide tension. It is assumed to be equal to arterial PCO2.
R is the respiratory quotient and is approximately 0.8 at steady state on standard diet.
FiO2 is the fractional concentration of inspired oxygen. It is 0.21 at room air.Normal PAO2 is:
PAO2 = FiO2× (Pb − PH2O) − (PACO2/R).
=0.21× (760 − 47) − (40/0.8).
=100 mmHg.
Mechanism of hypoxemia | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
V/Q mismatch: ❑ Common cause of hypoxemia Diffusion limitation: | Right to left shunt: ❑ Poor response to oxygen therapy | Hypoventilation: ❑ High PCO2 level
❑ Spinal cord level: ❑nerve supplying respiratory muscle: ❑ Neuromascular junction: ❑Respiratory muscle: ❑ Defect in chest wall: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Management of cyanotic congenital heart disease:
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CYANOSIS.https://doi.org/10.1016/j.chest.2017.11.003
PMID: 19561940 PMID: 16764526
PMID: 15545679
Important points in treatment of eisenmenger disease:
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{{familytree | | | | | | | | | |)|-| G01 |-| G02 | | | | |G01=Tetralogy of fallot| G02= Episods of [[Tet spell] between 2-4 months of age, aggravated with crying ,feeding, stooling, ]]dehydration]], in patients with severe pulmonary stenosis and large VSD, [[central cyanosis]| }}
Cyanosis in Congenital heart disease |
Cyanosis + pulmonary edema at the time of birth: |
❑ TGA (Transposition of great vessel) without associated PDA,VSD,ASD, two great arteries are misplaced, oxygenated pulmonary blood re-enter the pulmonary circulation via morphologic left ventricle and deoxygenated aorta blood re-enter the systemic circulation via morphologic right ventricle |
Cyanosis +shock and collapse within hours or days after birth: |
❑ Tetralogy of fallot: pulmonary stenosis (valvular, subvalvular) with ventricular septum defect and overridding aorta |
Cyanosis +shock and collapse in the first week of birth: |
❑ Hypoplastic left heart syndrome |
Differencial cyanosis ( upper limbs O2 saturation > lower limbs O2 saturation): |
❑ Severe pulmonary hypertension with PDA |
Differencial cyanosis ( lower limbs O2 saturation> upper limbs O2 saturation): |
❑ TGA + severe pulmonary hypertension + PDA |
}
Differentiating cardiac and pulmonale causes of cyanosis at birth: ❑ History and physical exam ❑ Blood pressure measurement in four limbs ❑ Oxygen saturation measurement ❑ ECG ❑ Chest-X-ray | |||||||||||||||||||||||
Pulmonary cause: ❑ Respiratory distress,tachypnea at rest ❑ Rale, crackle, wheezing in chest auscultation ❑ Normal cardiac margin in CXR ❑ Ground glass appearance, pneumonia, atelectasia,pneumothorax in CXR ❑ Normal ECG finding ❑ Elevated PCO2 level ❑ Corrected with oxygen therapy | |||||||||||||||||||||||
{{familytree | | | | | | | | | |)|-| R1 |-| R2 | | | | | | | | |R1=Lymphedema |R2=Lymphatic obstruction,lymph node dissection,[[malignancy],filariasis| }}
{{familytree | | | | | | | | | |)|-| G01 |-| G02 | | | | |G01=Cellulitis| G02=Increased [[capillary permeability]}}
Heart failure | Increased capillary permeability from Systemic venous hypertension,volume overload | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Hepatic disease | Increased capillary permeability from systemic venous hypertension, decreased oncotic pressure | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Mechanism of Edema | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Chronic venous insufficiency | venous reflux, poorly functioning venous valves, incompetent venous valves, reduced venous return, blood pooling, hypoxia, and inflammation | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Obstructive sleep apnea | Pulmonary hypertension, increased capillary hydrostatic pressure | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Renal disease | Increased plasma volume, decreased plasma oncotic pressure from protein loss | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Protein losing entropathy | Decreased plasma oncotic pressure | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Deep vein thrombosis | Increased capillary permeability | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Cellulitis | Increased capillary permeability | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Pregnancy | Increased plasma volume | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Laboratory Tests should be obtained: | |||||||||||||||||||||
Medications Associated With Edema:
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Do's
References
- ↑ AVIADO DM, DALY MD, LEE CY, SCHMIDT CF (March 1961). "The contribution of the bronchial circulation to the venous admixture in pulmonary venous blood". J. Physiol. (Lond.). 155: 602–22. doi:10.1113/jphysiol.1961.sp006650. PMC 1359878. PMID 13685279.
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Diagnostic tools:
with out evidence of thrombosis on duplex ultrasonography if there is high clinical suspicion for deep venous thrombosis
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Congestive heart failure | diuretic,sodium restriction | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Nephrotic syndrome | diuretic | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Edema treatment | Lymphedema | compression stocking, skin care,manual lymphatic derenage,bandage,exercise program with compression | |||||||||||||||||||||||||||||||||||||||||||||||||||||
Chronic venous insufficiency | compression stocking,bandage/wraps,adjunctive devices,pneumatic pumps | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Lipedema | Suction lipectomy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Congestive heart failure | loop diuretic,sodium restriction | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Nephrotic syndrome | Loop diuretic | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Edema treatment | Lymphedema | Compression stocking,skin care,manual lymphatic deraning,bandage | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Chronic venous insufficiency | Compression stocking,bandage,wraps,adjunctive devices,pneumatic pumps | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Deep vein thrombosis | Anticoagulant therapy,early walking, compression stocking | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Cellulitis | Antibiotic theraphy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Lipedema | Suction lipectomy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Pulse examination | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Ulcer | lymphadenopathy/masses | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Pitting | Physical examination | Unilateral/bilateral | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Skin condition,texture,color | Distribution | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Temperature | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Associated injury/illness | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Recent surgery/procedure | Malygnancy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Painful | History | Onset(acute,chronic) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Aggravated by activity | Underlying illness | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Change in medications | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
- ❑ Complete blood count
- ❑ Urinalysis
- ❑ Blood sugar
- ❑ Creatinine
- ❑ Thyroid-stimulating hormone
- ❑ Serum Albumin
- ❑ D-dimer
- ❑ BNP
- ❑ AST
- ❑ ALT
- ❑ Total Bilirubin
- ❑ Prothrombin time
- ❑ Alkaline phosphatase
Overview
Medications associated with edema:<be>
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- ❑ Cardiac disease: Increased capillary permeability from systemic venous hypertension; increased plasma volume
- ❑ Hepatic disease: Increased capillary permeability from systemic venous hypertension; decreasedplasma oncotic pressure from reduced protein synthesis
- ❑ Malabsorption/protein-caloriemalnutrition: Reduced protein synthesis and decreased plasma oncotic pressure
- ❑ Obstructive sleep apnea : Pulmonary hypertension, increasedcapillary hydrostatic pressure
- ❑ Pregnancy and premenstrual edema: increased plasma volume
- ❑Renal disease: Increased plasma volume, decreased plasma oncotic pressure from protein loss
- ❑ Chronic venous insufficiency: venous reflux, poorly functioning venous valves, incompetent venous valves, reduced venous return, blood pooling, hypoxia, and inflammation
- ❑Lymphedema: lymphatic obstruction in upper extremities due to breast cancer and lymph nodes dissection, rich in protein
- ❑ Cellulitis: Increased capillary permeability
- ❑ Deep vein thrombosis: Increased [[capillary permeability]/div}}
Diagnostic approach:
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Treatment:
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Inherited causes of cardiac arrest and malignant arrhythmia associated covid-19 | long QT syndrome | Brugada syndrome | Short QT syndrome | Cathecolaminergic polymorphic ventricular tachaycardia |
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Gene mutation |
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EKG finding |
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in lead V1 and/or V2 |
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Specific considerations in COVID19 patients |
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fatal arrhythmia |
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Ventricular fibrillation |
- Corrected QT(QTc)=1000(QT/1000+0.154(1-RR)
- QT, QTc are measured in milliseconds)
- RR is measured in seconds and is the interval from the onset of one QRS complex to the onset of the next QRS complex