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 ❑ Uncommon causes of syncope especially in younger patients ❑ In syncope related to SVT , vasovagal syncope or ventricular arrhythmia should be investigated ❑ In syncope related to rapid atrail fibrillation without preexcitation, vasovagal syncope and sinus node dysfunction in the presence of long pause should be considered

Ventriculat arrhythmia : (Class I, Level of Evidence C)

❑ Treatment of underlying cardiac causes of ventricular arrhythmia ❑ Making decision for ICD implantation related to the recurrence of tachyarrhythmia In ventricular tachycardia with the rate>200 min, the incidence of syncope and near syncope is 65%

Ischemic and non ischemic cardiomyopathy:(Class I, Level of Evidence C)

❑ Treatment of underlying causes of cardiomyopathy ❑ ICD implantation in the presence of ventricular arrhythmia during electrophysiological study

Valvular heart disease : (Class I, Level of Evidence C)

❑ In severe AS and syncope the mechanism of syncope is low cardiac out put ❑Aortic valve replacement should be considered in patients with severe AS and exersional syncope

Hypertrophic cardiomyopathy (Class I , Level of Evidence C):

❑ Inadequate data about the relation between unexplained syncope as the predictor of SCD ❑ ICD implantation indicated only in patients with recent history of more than one episode of syncope suspected to be ventricular tachyarrhythmia

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 ❑ Mechanism of [[ventricular tachycardia] is macroreentry around granulomas and triggered activity and automaticity due to myocardial inflammation ❑ The role of immunosuppression therapy in decreasing ventricular arrhythmia is controversial ❑ In patients with AV block , immunosuppression therapy and in irreversible AV block permanent pacemaker is recommended

Brugada : (Class IIa, Level of Evidence B)

❑ ICD implantation in suspected arrhythmia leading syncope

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 Short QT syndrome definition: QTc interval≤340 ms Syncope is not the risk factor of SCD in the absent of documented VT or VF

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 definition: QTc interval ≥ 500 ms

Long QT syndrome : (Class IIa, Level of Evidence B)

❑ICD implantation in syncope related arrhythmia in patients are on betablocker or intolerant to betablocker ❑ Left cardiac sympathectomy in frequent episodes of syncope arrhythmia in patients are on betablocker or intolerant to betablocker (LOR=C)

CPVT : (Class I, Level of Evidence C)

❑ Exercise restriction in patients suspected arrhythmia leading syncope ❑ Betablocker therapy for reduction of sympathetic activity in stress-induced tachyarrhythmia CPVT definition: catecholamine-induced (often exertional) bidirectional VT or polymorphic VT in the setting of a structurally normal heart and normal resting ECG

CPVT : (Class IIa, Level of Evidence C)

❑ Flecainide in patients with arrhythmia leading syncope in spite of betablocker therapy ❑ICD implantation in patients with arrhythmia leading syncope in spite of optimal medical therapy ([[LOR=B)

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 ❑ Physical counter maneuvers (leg crossing, limbs or abdominal contraction, sqqadding in long prodrome phase ❑ Midodrine in recurrent vasovagal syncope without history of hypertension, heart failure, urinary retension

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 ❑Flodrocortisone in patients with inadequate response to salt, fluide intake ❑ Betablocker in patients with recurrent vasovagal syncope ,older than 42 years ❑ Elimination or reduction the medications causing hypotension and syncope ❑ Selective serotonin reuptake inhibitors such as fluoxetine ,paroxetine for prevention of recurrent vasovagal syncope ❑ Dual chamber pacing in patients older than 40 years and recurrent syncope with pause > 3 seconds related with syncope or asymptomatic pause >6 seconds

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

Uncommon conditions associated with syncope	Clinical aspect	Cause of syncope
Cardiac tamponade	Hypotension, tachycardia, cardiogenic shock	Tachycardia, hypotension, abrupt bradycardia
Constrictive pericarditis	heart failure symptoms, exertional dyspnea, orthopnea, edema	Cough syncope
Left ventricular non compaction	Trabeculation and recess in left ventricle	Tachyarrhythmia
Takotsubo cardiomyopathy	Apical ballooning , basal hyperkinesia , following stressful event, chest pain and ECG change mimicking ischemia	Uncommon cause of syncope, multifactorial
Pulmonary embolus	Cardiac arrest and pulseless electrical activity following hypoxia, tachycardia, hypotension and shock	Bradycardia, hypotension
Pulmonary arterial hypertension	Exertional syncope, specially in younger patients	Peripheral vasodilation following exercise, low cardiac output state
Amyloidosis	Amyloid deposition in heat, kidney, peripheral and autonomic nervous system	AV block, arrhythmia, low cardiac output due to restrictive cardiomyopathy
Hemochromatosis	[[Dilated cardiomyopathy] due to Iron deposition	Myocardial involvement, sick sinuse syndrome, AV block
Myocarditis	Chest pain, arrhythmia, left ventricular systolic dysfunction, hemodynamic collapse	Ventricular tachycardia, AV block, transient hemodynamic collapse
Lyme disease	Myocarditis accompanied by erythma migrant, neurologic involvement	AV block, syncope
disease	Cardiomyopathy caused by trypanosomiasis	Ventricular tachycardia, AV block
Friedreich ataxia	Hypertrophic Cardiomyopathy (HCM), gait ataxia, bladder dysfunction	Tachycardia, bradycardia, SCD is common
Cardiac tumors	Triad of valve obstruction , emboli, systemic signs and symptoms	Obstruction to blood flow
Prosthetic valve thrombosis	Asymptomatic or symptomatic heart failure	Embolic event, valve obstruction
Anomalous coronary artery	Common cause of exertional syncope and SCD specially in young athletes]]	Bezold jarisch reflex,[[hypotension], [[VT], AV block
Subclavian steal syndrome	Significant stenosis in subclavian artery leading flow reversal in vertebral artery and vertebrobasilar ischemia and syncope	Syncope following upper extremities activity
Aortic dissection	Neurologic symptoms, heart failure symptoms, myocardial infarction	Increased risk of inhospital death, tamponade, neurologic deficit in patients with syncope
COA	heart failure symptoms, dissection of aorta	Associated with bicuspid aortic valve stenosis
Rheumatoid arthritis	Systemic inflammatory disorder	Complete heart block
Carcinoid syndrome, Pheochromocytoma, Mastocytosis,  Vasoactive intestinal peptide tumor	Vasodilation, flushing, pruritus, gastrointestinal symptoms	Transient hypotension
Beta thalassemia major	Dilated cardiomyopathy , severe anemia, multiple organ failure	Arrhythmia
Migraine	Association between headache and syncope	Vasovagal syncope, orthostase intolerance
Seizure-induced bradycardia, hypotension	Temporal lobe epilepsy	Postictal [[bradyarrhythmia] due to temporal lobe or limbic system

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 ❑ High proportion in apex of the lung due to higher ventilation compared with perfusion ❑ Easily corrected by supplemental oxygen therapy ❑ widened (A-a )oxygen gradient ❑ High V/Q mismatch such as pulmonary embolism that ventilation is higher than perfusion ❑ Asthma ❑ COPD ❑ Bronchectasia ❑ Cystic fibrosis ❑ Interstitial lung disease (ILD) ❑ Pulmonary hypertension due to lung disease Diffusion limitation: ❑ Normal PCO2 level ❑ Good response to oxygen therapy ❑ widened P(A-a)O2 level ❑ Alveolocapillary impairment ❑ ILD ❑ Emphysemia

Right to left shunt: ❑ Poor response to oxygen therapy ❑ Normal PCO2 level ❑ Widened P(A-a) O2 gradient ❑ Presence of Small physiologic pulmonary shunt about 2-3% of cardiac output due to deraining of bronchial veins into pulmonary veins and deraining coronary veins into left ventricle ❑ If the shunt fraction reaches 50%, hypercapnia may be present ❑ Shunt fraction<20% if PaO2/FIO2>200 ❑ Shunt fraction>20% if PaO2/FIO2<200 ❑ Cyanotic congenital heart disease with right to left shunt ❑ Pneumonia ❑ Pulmonary edema ❑ Acute respiratory distress syndrome(ARDS) ❑ Alveolar collapse ❑ Pulmonar arterionenous connection

Hypoventilation: ❑ High PCO2 level ❑ Low ventilation leading to Low PAO2, PaO2 level ❑ Normal P(A-a)O2 gradient due to normal alveolar capillary memberane ❑ longstanding hypoventilation leading to atelectasia and widened P(A-a)O2 gradient ❑ Corrected by supplemental oxygen therapy ❑ One Cause of respiratory failure in COPD, Asthma,ILD ❑ Disorders leading to hypoventilation include: ❑ Impaired central drive: ❑ Opiom overdose, benzodiazepine, alcohol ❑ Brain stem infarct, hemorrhage ❑ Primary alveolar hyperventilation ❑ Spinal cord level: ❑Amiotrophic lateral sclerosis ❑Cervical spinal cord injury ❑nerve supplying respiratory muscle: ❑Guillain-Barre syndrome ❑ Neuromascular junction: ❑Myasteni-Graves ❑Lambert-eaton syndrome ❑Respiratory muscle: ❑Myotony ❑ Defect in chest wall: ❑Kyphoscoliosis ❑Thoracoplasty ❑Fibrothorax

Management of cyanotic congenital heart disease: ❑ Measurement of oxygen saturation at rest( about 5 min) rather than after walking ❑ Using air filter for all venous access ❑ Cerebral imaging in the presence of new headache or any neurologic signs for evaluation of brain abcesss,hemorrhage, stroke ❑ Checking serum uric acid in patients with history of gout ❑ Supplement oxygen ❑ Avoidance of excess oxygen supplement or narcotic due to reduction hypoxia-mediated derived to ventilation ❑ Adequate hydration and movement during the long flight, NO need for checking oxygen saturation before flight ❑ Measurement of coagulation parameters(Activated partial thromboplastin time,international normalized ratio,thrombin time) in hematocrite>55%

CYANOSIS.https://doi.org/10.1016/j.chest.2017.11.003 PMID: 19561940 PMID: 16764526 PMID: 15545679

Important points in treatment of eisenmenger disease: ❑ Bosentan for treatment of symptomatic VSD, ASD, PDA,Aortopulmonary window,Complex congenital heart disease,Down syndrome(CLASS 1 Recommendation) ❑ Phosphodiesterase-5 inhibitor( Tadalafil,sildenafil) for treatment of Symptomatic ASD, VSD, Great artries shunt(CLASS 2a Recommendation)

{{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]| }}

Eisenmenger disease

Increased pulmonary vascular resistant leading to right to left shunt, systemic arterial desaturation, central cyanosis

Tamponad

low cardiac output, low stroke volume, elevated cardiac filling pressures, increased sympathetic tone( tachycardia, peripheral vasoconstriction, peripheral cyanosis)

Diagnosis of peripheral and central cyanosis

Pulmonary thromboembolism

Pulmonary artery vasoconstriction, hypoxia, right ventricle pressure overload, right to left shunt via patent foramen ovale,central cyanosis

Cardiogenic shock

Decreased myocardial perfusion, muscle hypoxia,necrosis, impaired myocardial contraction., decreased cardiac out put, Increased vasoconstrictor,peripheral cyanosis

Methemoglubinemia

Increased level of reduced hemoglobin,normal oxygen saturation, congenital or due to medication, central cyanosis

Chronic obstructive pulmonary disease

Central cyanosis, respiratory failure, PO2<60 mmHg, PCO2>45mmHg while breathing at sea level, prepheral edema due to right heart failure

Pulmonary edema

Decreased arterial oxygen saturation, central cyanosis

High altitude

Hypoxia, peripheral cyanosis due to ischemia and occlusion small peripheral vessels, central cyanosis due to pulmonary edema in acute mountain sickness, pulmonary hypertension in chronic mountain sickness

Pneumonia

Central cyanosis due to impaired gas exchange and intrapulmonary shunt

ARDS

Acute pulmonary parenchimal disease other than cardiac origin or volume overload, alveolar filling with exudates or alveolar collapse, central cyanosis due to decreased oxygen saturation and intrapulmonary shunting

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 ❑ Total anomalous pulmonary venous connection(TAPVR),connection between pulmonary veins and right system and mixing the oxygenated and deoxygenated blood ❑ Truncus arteriosus, one great vessel arise from both ventricle then the gives rise to the aorta and pulmonary artery

Cyanosis +shock and collapse within hours or days after birth:

❑ Tetralogy of fallot: pulmonary stenosis (valvular, subvalvular) with ventricular septum defect and overridding aorta ❑ Severe pulmonary stenosis with intact ventricular septum ❑ Ebstein anomaly: small functional right ventricle, huge right atrium, severe tricuspid regurgitation, right to left shunt from ASD or PFO

Cyanosis +shock and collapse in the first week of birth:

❑ Hypoplastic left heart syndrome ❑ Severe coarctation of aorta ❑ Severe aortic stenosis ❑ Tachycardia induced cardiomyopathy due to atrial flutter or PSVT ❑ Dilated cardiomyopathy Other differential diagnosis: neonate sepsis, menangitis or hypoglycemia

Differencial cyanosis ( upper limbs O2 saturation > lower limbs O2 saturation):

❑ Severe pulmonary hypertension with PDA ❑ Severe aortic coactation or interruption

Differencial cyanosis ( lower limbs O2 saturation> upper limbs O2 saturation):

❑ TGA + severe pulmonary hypertension + PDA ❑ TGA + severe aortic arch interruption + PDA ❑ Connection right subclavian artery to right pulmonary artery Right upper limb oxygen saturation is lower than left upper and left lower limbs oxygen saturation

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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

Cardiac cause: ❑ Cardiomegaly in CXR ❑ Relatively comfortable at rest ❑Cyanosis may worsen with crying ❑ Cardiac murmur ❑ Abnormal rhythm or axis in ECG ❑ Normal Pco2 level ❑ NO response to O2 therapy

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: ❑ Complete blood count ❑ Urinalysis ❑ Blood sugar ❑ Creatinine ❑ Thyroid-stimulating hormone ❑ Serum Albumin ❑ D-dimer ❑ B-type-natriuretic peptides ❑ Aspartate aminotransferase ❑ Alanine aminotransferase ❑ Total Bilirubin ❑ Prothrombin time ❑ Alkaline phosphatase

Medications Associated With Edema: ❑ Monoamine oxidase inhibitors, trazodone ❑ Beta-adrenergic blockers, dihydropyridine calcium channel blockers,clonidine , hydralazine, methyldopa, minoxidil ❑ Acyclovir ❑Cyclophosphamide, cyclosporine (Sandimmune), cytosine arabinoside,mithramycin ❑ Androgen, corticosteroids, estrogen, progesterone,testosterone ❑ Celecoxib, ibuprofen ❑ Pioglitazone,rosiglitazone ❑ Levofloxacin ❑ Citalopram

References

Template:WikiDoc Sources

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Diagnostic tools: ❑ Duplex sonography in patients with unilateral lower limb swelling and positive D-dimer, or high clinical suspicion of thrombosis ❑ Abdominal or pelvic CT scan in patients with lower limb swelling and evidence of malygnancy ❑ Magnetic resonance venography of the lower leg in patients with unilateral leg swelling with out evidence of thrombosis on duplex ultrasonography if there is high clinical suspicion for deep venous thrombosis ❑ Echocardiography in patients with obesity, obstructive sleep apnea, and edema for evaluation of pulmonary arterial pressures and also in patients with evidence ofheart failure for assessment ofejection fraction and pulmonary artery pressure and structural heart disease. ❑Ankle-brachial index in patients with chronic venous insufficiency and cardiovascular risk factors before compression therapy, which is contraindicated in peripheral arterial disease

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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

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Laboratory test:<be>

❑ Complete blood count

❑ Urinalysis

❑ Blood sugar

❑ Creatinine

❑ Thyroid-stimulating hormone

❑ Serum Albumin

❑ D-dimer

❑ BNP

❑ AST

❑ ALT

❑ Total Bilirubin

❑ Prothrombin time

❑ Alkaline phosphatase

Overview

❑Pioglitazone,roziglotazone

❑ Levofeloxain

Medications associated with edema:<be> ❑ Monoamine oxidase inhibitors, trazodone ❑ Beta-adrenergic blockers, calcium channel blockers, clonidine , hydralazine, methyldopa, minoxidil ❑ Acyclovir ❑ Cyclophosphamide, cyclosporine (Sandimmune), cytosine arabinoside, mithramycin ❑ Androgen, corticosteroids, estrogen, progesterone, testosterone ❑ Celecoxib, ibuprofen

{{familytree | | | | | B01 | | | | | B01=

mechanisms of edema :

---

❑ 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: ❑ Magnetic resonance venography of the lower extremity and pelvis should be obtained in patients with unilateral left leg swelling and negative results on duplex ultrasonography if there is high clinical suspicion for deep venous thrombosis ❑ Echocardiography should be performed in patients with obesity, obstructive sleep apnea, and edema to evaluate pulmonary arterial pressures. ❑ Ankle-brachial index should be measured in patients with chronic venous insufficiency and cardiovascular risk factors before initiation of compression therapy, which is contraindicated in peripheral arterial disease/div>

Treatment: ❑ Compression stockings should be used in patients following deep venous thrombosis to prevent postthrombotic syndrome ❑ Pneumatic compression devices should be used in conjunction with standard therapy in patients with lymphedema ❑ Daily hydration with emollients and short courses of topical steroid creams for severely inflamed skin should be used to treat eczematous (stasis) dermatitis associated with chronic venous insufficiency> ❑ Anticoagulation therapy in deep vein thrombosis/div

Inherited causes of cardiac arrest and malignant arrhythmia associated covid-19	long QT syndrome	Brugada syndrome	Short QT syndrome	Cathecolaminergic polymorphic ventricular tachaycardia
Gene mutation	KCNQ1(LQT1), KCNH2(LQT2), SCN5A(LQT3)	loss of function in SCN5A in %30 of patients	KCNH2(SQT1), KCNQ1(SQT2) KCNJ2(SQT3)	RYR2(CPVT1) CASQ2(CPVT2) KCNJ2(CPVT3)
EKG finding	QTc>450ms in men QTc>470ms in women T waves alternance	Coved-type ST-segment elevation T-wave inversion in lead V1 and/or V2	QTc<330 msec	Normal EKG Bradycardia mild u waves
Specific considerations in COVID19 patients	causion in administration of QT prolongation drugs(hydroxychloroquine, azithromycin lupinavir/ritonavir) Controlling the fever for prevention of QT prolongation Avoidance of using≥ one drugs inducing QT prolongation	Controlling the fever as the main cause of cardiac arrest in brugada syndrome, especially in children less than 5 year old	Safety of hydroxychloquine due to prolongation of QT interval in short QT syndrom type 1 (KCNH2 related) and type3(KCNJ2)	Avoidance of administration of epinephrine, isoproterenol, and dobutamine, all α and/or B1 receptor agonists inducing ventricular arrhythmia Controlling the sress related to COVID-19 Safety of flecainide without any interaction with lopinavir, ritonavir and chloroquine.
fatal arrhythmia	Torsade de pointes Ventricular fibrillation	Ventricular fibrillation, Polymorphic VT	Ventricular fibrillation	Bidirectional VT

• 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