26 September 2009

Abnormalities In Dermal Connective Tissue



Abnormalities In Dermal Connective Tissue
By: Erik Austin, D.O., M.P.H.

Elastosis perforans serpiginosa – Serpiginous arrangement of confluent, keratotic papules on the arms, face/neck, legs

Keratotic papules of EPS
Typical site affected = neck
Elastosis perforans serpiginosa
EPS
* MC in young adults with a M:F ratio of 4:1
* Runs a variable course of 6 mos to 5 years with spontaneous resolution
* Associated with: Down Syndrome, Ehlers-Danlos, osteogenesis imperfecta, Marfan’s, Rothmund-Thomson, acrogeria, systemic sclerosis
* Tx = LN2, Penicillamine
* Annular plaques of EPS
* Atrophic scars often form
* Hyperelastic epidermis that clutches the increased dermal elastic fibers like a claw
* Transepidermal elimination of neutrophils and elastic fibers from the dermis through a channel in the epidermis

Reactive perforating collagenosis (RPC)
Keratotic papules on upper extremity, face or buttocks

Reactive perforating collagenosis
RPC
* Rare, familial, non-pruritic skin disorder
* Lesions begin in 2nd decade
* Involution occurs after 6-8 weeks, with new crops appearing for years
* May be a reaction to trauma
* Acquired form may be assoc. w/systemic dz
* TX = treat underlying disease

Pseudoxanthoma elasticum (PXE)
* Yellow papules, calcified plaques, sagging skin; chicken skin
* Inherited disorder of the skin, eyes, and cardiovascular system
* Has recessive and dominant inheritance
* Exaggerated nasolabial folds is characteristic
* Involvement of the cardiovascular system occurs with a propensity to hemorrhage

Mucosal lesions
* Retinal change = Angioid streaks; in up to 85%
* Mitral valve prolapse, 71% of 14 pts
* Young pt w/hypertension = r/o PXE
* Histo: mid-dermis w/elastic fibers that are swollen and granular - “raveled wool”
* No distinctive therapy
* Limit dietary calcium and phosphorus

Histopathology of PXE
* A. calcium deposits on elastic fibers in advanced PXE
* B. irregularly clumped elastic fibers, Verhoeff van Giesson

Perforating calcific elastosis
* Acquired, localized disorder
* Frequently found in obese, multiparous, middle-aged women
* Yellowish, lax, well circumscribed, reticulated or cobblestones plaques occur in the periumbilical region with keratotic papules
* Shares features with PXE, without systemic features
* Trauma of pregnancy, obesity or surgery promote elastic fiber degeneration
* No effective therapy

Ehlers-Danlos syndromes
* A group of genetically distinct disorders characterized by excessive stretchability and fragility of the skin
* Tendency toward easy scar formation, calcification of the skin to produce, pseudotumors, and hyperextensibility of the joints

Clinical features of Ehlers-Danlos syndrome
* Two types of growths seen with EDS
* Molluscum pseudotumor = a soft fleshy nodule seen in areas of trauma
* Spheroids = hard subcutaneous nodules that become calcified, ?Result of fat necrosis
* Types I, II, III and one subtype each of types of IV, VII and possibly VIII = AD
* One subtype of IV, VI, VII, and X = AR
* Type V = X-linked inheritance
* Treatment is supportive
* Avoidance of trauma

Marfan syndrome
* AD
* Skeletal, cardiovascular, and ocular involvement
* Important abnormalities include: tallness, loose-joints, a dolichocephalic skull, high arched palate, arachnodactyly, pigeon breast, pes planus, poor muscular tone, large deformed ears
* Ascending aortic aneurysm and mitral valve prolapse are commonly seen
* Ectopic lentis and striae
* Gene defect = chromosome 15
* Abnormal elastic tissue in fibrillin 1 and fibrillin 2

Cutis Laxa – loose, hanging skin – usually entire integument is involved
Cutis laxa (generalized elastosis)
* AD = primarily cutaneous, good prognosis
* AR = significant internal involvement, die young
* X-linked recessive = occipital horn syndrome
* Nonfamilial forms have been described
* May be associated with an underlying disease or inflammatory skin process
* Mid-dermal elastosis is an acquired, nonfamilial condition affecting primarily young women, cause unknown
* Tx = disappointing; surgery is unsuccessful

Cutis laxa (generalized elastosis)
* Premature aging, severe pulmonary emphysema, and fragmentation of dermal elastic fibers

Blepharochalasis
* Lax eyelid skin due to swelling of lids
* Uncommon
* AD
* Lack of elastic fibers, and abundant IgA deposits have been demonstrated
* Ascher Syndrome = progressive enlargement of the upper lip and blepharochalasis / treatment is surgical

Anetoderma (macular atrophy)
* A group of disorders characterized by looseness of the skin due to loss of elastic tissue
Anetoderma – macular atrophy and atrophic plaques – buttonhole sign. Typical location: trunk, arms, shoulders, thighs
* Anetoderma: decreased elastic fibers in the papillary and reticular dermis
Striae rubra, striae alba: depressed lines or bands

Striae distensae
* Can occur secondary to pregnancy or after sudden weight gain or muscle mass
* Associated with Cushing’s syndrome and
* Prolonged application of topical steroids
* Overtime striae become less noticeable
* Tx = topical tretinoin; vascular lasers

Linear focal elastosis (elastotic striae)
* Asymptomatic, palpable, striaelike yellow line of the middle and lower back
* Distinguished from striae in that there is no depression

Acrodermatitis chronica atrophicans
* Acquired diffuse thinning of the skin
* Reddish appearance on extensor surfaces
* Progresses to smooth , soft, atrophic skin
* Results from infection with Borrelia

Osteogenesis imperfecta
* Affects: bones, joints, eyes, ears, and skin
* types I-IV, I and IV = AD
* II and III = AD/AR
* 50% are type I
* type II is lethal within 1st week of life
* Brittle bones, fractures occur early in life, sometimes in utero
* Loose-jointedness and dislocations
* Blue sclera
* Deafness
* Thin skin; atrophic scars
* EPS has associated
* Defect is abnormal collagen synthesis, resulting in type I collagen of abnormal structure
* Major causes of death = respiratory failure and head trauma
* Type I and IV have a normal life span
* TX = Pamidronate

Homocystinuria
Inborn error in the metabolism if methionine
* Homocystine in the urine and CT abnormalities
* cystathionine synthetase deficient
* Genu valgum, kyphoscoliosis, pigeon breast, frequent fractures
* Facial skin has a characteristic flush
* Other skin is blotchy red
* Hair is fine, sparse and blonde
* Teeth are irregularly aligned
* Downward dislocations of lens
* TX = hydroxocobalamin and cyanocobalamin – variable results

ERRORS IN METABOLISM
SYSTEMIC AMYLOIDOSIS primary systemic amyloidosis
* Involves mesenchymal tissue, the tongue, heart, gastrointestinal, and skin
* Cutaneous manifestations in 40%
* Amyloid fibril proteins are composed of AL
* Derived from immunoglobulin light chains
* 90% will have fragment in urine and serum
* Waxy, firm, flat-topped or spherical papules
* Coalesce to form nodules and plaques
* Eyes, nose, mouth, and mucocutaneous junctions are commonly involved
* Purpuric lesions and ecchymosis (15%)
* Results from amyloid infiltration of vessels
* Glossitis with macroglossia (20%)
* May cause dysphagia
* Bullous disease is rare and scarring
* Subepidermal: DDx PCT and EBA
* Systemic findings: peripheral neuropathies, arthropathy, GI bleeding, cardiac disease
* Prognosis is poor, median survival 13 mos, 5 mos in myeloma associated cases
* Treatment is difficult = melphalen, prednisone, hematopoietic stem cell transplantation
* Macroglossia with dental impression of the tongue
* Periorbital ecchymosis, “raccoon sign”
Secondary systemic amyloidosis
* Amyloid involvement of adrenals, liver spleen, and kidney as a result of some chronic disease (TB, leprosy, etc.)
* Skin is not involved
* Amyloid fibrils are designated AA, protein component is unrelated to immunoglobulin
* Treat the underlying condition

CUTANEOUS AMYLOIDOSIS primary cutaneous amyloidosis
* Divided into macular and lichen amyloid
* Asian , Hispanic, and Middle Eastern
* Amyloid deposition contains keratin
* Histologic picture is similar for both
* Differ only in size of amyloid deposits
* Absence of amyloid deposits around blood vessels excludes systemic involvement
* Macular Amyloidosis: pruritic, brown macules with a rippled pattern

Lichen amyloidosis
* Pruritic, keratotic, hyperigmented plaques on the legs
* Tx = high potency corticosteroids, oral retinoids, cyclophosphamide, dermabrasion and occlusion
Extremities, trunk, genitals and face with localized nodules

* Lesions contain numerous plasma cells, amyloid is immunoglobulin-derived AL
* TX = physical removal or destruction

Secondary cutaneous amyloidosis
* Following PUVA therapy and in benign and malignant cutaneous neoplasms, deposits of amyloid may be found
* Most frequently associated neoplasms are NMSC and SKs
* In all cases, this is keratin-derived amyloid

Familial syndromes associated with amyloidosis (heredofamilial amyloidosis)
* Muckle-Wells syndrome
* MEN IIA
* Most present with neurologic disease and are now designated familial amyloidotic polyneuropathy
* Four types identified FAP I through IV
* AD inherited

PORPHYRIAS
* Porphyrinogens are the building blocks of hemoproteins
* Produced primarily in the liver, bone marrow and erythrocytes
* Each form is associated with a deficiency in the metabolic pathway of heme synthesis
* Absorption of UV radiation in the Soret band (400-410 nm) by the increased porphyrins leads to photosensitivity
* Activated porphyrins form reactive oxygen species that causes tissue damage

Current grouping of the porphyrias is based on the primary site of increased porphyrin production
* Erythropoietic forms
o Congenital erythropoietic porphyria (CEP)
o Erythropoietic protoporphyria (EPP)
o Erythropoietic coproporphyria ECP
* Hepatic forms
o Acute intermittent porphyria (AIP)
o ALA dehydrogenase deficiency
o Hereditary coproporphyria (HCP)
o Variegate porphyria (VP)
o Porphyria cutanea tarda

Porphyria cutanea tarda
* Most common porphyria
* Photosensitivity leads to bullae, which leads to ulcers, scarring, milia and dyspigmentation
* Hypertrichosis, fragility and skin thickening
* Alcoholism is common; Hep C in 94%
* Associated with DM, LE, HIV, and

estrogen therapy
* Multiple erosions with hemorrhagic crusts, as well as an intact blister on the lateral fourth finger

PCT in chronic renal failure
* Deficiency = uroporphyrinogen decarboxylase
* Most common = sporadic nonfamilial form, (80%), abnormal enzyme activity
* Presents in midlife
* Familial type = AD; deficiency in liver and RBCs
* Nonfamilial = acquired toxic; associated with exposure to hepatotoxins
* Diagnosis = suspected on clinical grounds
* Coral red fluorescence of urine
* 24 hour urine
* Uroporphyrins to coproporphyrins 3:1 to 5:1
* DIF shows IgG and C3 at the DEJ, and in the vessel walls in a linear pattern

Histologic features of PCT
* Subepidermal blister with minimal dermal inflammatory infiltrate. Festooning of dermal papillae.

treatment
* Remove environmental exposures
* Sunscreens
* Phlebotomy / uroporphyrinogen decarboxylase is inhibited by iron
o 500 ml at 2 week intervals, hemoglobin 10 g/dL
o Several months, 6-10 phlebotomies
* Antimalarials / full doses may produce severe hepatotoxic reaction
* Remission may last for years
* Iron chelation
* May respond to transplant in renal failure
* May improve with treatment if assoc. with Hep C

pseudoporphyria
* Skin and Histo similar to PCT
* Normal urine and serum porphyrins
* No hypertrichosis, dyspigmentation or cutaneous sclerosis
* Commonly caused by NSAIDs, naproxen, sunbed use, hemodialysis

treatment
* Sun protection
* Discontinue inciting medication
o May resolve over several months

Hepatoerythropoietic porphyria
* Very rare form / AR
* Deficiency of uroporphyrinogen decarboxylase, 10% of normal in both the liver and erythrocytes
* Dark urine at birth
* Vesicles, scarring, hypertrichosis, pigmentation, red fluorescence of teeth
* Abnormal urinary porphyrins as in PCT
* Elevated erythrocyte protoporphyrins
* Increased coproporphyrins

Hepatoerythropoietic porphyria
Acute intermittent porphyria
* Second most common form
* Characterized by periodic attacks of abdominal colic, gastrointestinal disturbances, paralyses, and psychiatric disorders
* No skin lesions are seen
* AD / deficiency in porphobilinogen deaminase
* Only 10 % develop disease, all are at risk for primary liver cancer
* Severe abdominal colic +/- NVDC
* Elevated urinary porphobilinogen
* Increased dALA in plasma and urine
* No specific treatment
* Avoid precipitating factors
* Glucose loading
* Hematin infusions
* Pain management
* Oral contraceptives may prevent attacks in women with premenstrual symptoms

Hereditary coproporphyria HCP
* Rare, AD
* Deficiency of coproporphyrinogen oxidase
* One third are photosensitive
* Prone to GI attacks
* Fecal coproporphyrin is always increased
* Urinary coproporphyrin, ALA, and PBG are only increased during attacks

Variegate porphyria VP
* AD
* Decreased activity of protoporphyrinogen oxidase
* Majority of relatives have silent VP
* Characterized by skin lesions of PCT and the GI and neurologic disease of AIP
* Suspect VP when finding indicate both PCT and AIP, esp. with history of South African ancestry
* Fecal coproporphyrins and protoporphyrins are always elevated
* During attacks, urine porphobilinogen and ALA are elevated
* Urinary coproporphyrins are increased over uroporphyrins
* A finding in the plasma of “X porphyrin,” fluorescence at 626 nm is characteristic and distinguishes this form from others
* Symptomatic treatment as for PCT and AIP

Erythropoietic protoporphyria EEP
* AD and AR forms
* Ferochelatase activity is 10 to 25% of normal in affected persons
* Typically presents in childhood, 2-5 years
* Burning of the skin upon sun exposure
* Elevated protoporphyrin IX absorbs both the Soret band and also at 500-600 nm
* Severe liver disease in 10%
* Excessive porphyrins are deposited in liver
* Diagnosis on clinical grounds
* Urine porphyrin levels are normal
* Erythrocyte protoporphyrin is elevated
* Erythrocyte, plasma, and fecal protoporphyrin can be assayed to confirm the diagnosis
* Skin biopsy confirms diagnosis
* Tx = sun protection
* Beta carotene, phototherapy, cysteine
* Transfusions for anemia

Erythropoietic protoporphyria
* Subtle scarring
Erythropoietic protoporphyria
* Erythema and hemorrhagic crusts
Congenital erythropoietic porphyria, CEP
* Gunther’s disease
* AR; defect of uroporphyrinogen III synthase
* Presents after birth with red urine
* Severe photosensitivity
* Blistering, scarring, ectropion and corneal damage
* Mutilating scars, hypertrichosis, profuse eyebrows, long eyelashes, “monkey face”
* Growth retardation, hemolytic anemia, thrombocytopenia, porphyrin gallstones, osteopenia
* Suspect in an infant with dark urine and photosensitivity

Congenital erythropoietic porphyria
* Erythrodontia
* Severe mutilation
* Fluorescence of circulating red blood cells, CEP with UVA
* Vs. transient fluorescence in EPP
* High amounts of uroporphyrin I and coproporphyrin I are found in the urine, stool and red cells
* Treatment – strict avoidance of sunlight and sometimes splenectomy for the hemolytic anemia
* Oral activated charcoal
* Repeated transfusions to maintain hematocrit level at 33% - turns off demand for heme
* Bone marrow transplantation
Transient erythroporphyria of infancy (purpuric phototherapy-induced eruption)

* Report of seven infants exposed to 380 to 700 nm blue lights, for the treatment of indirect hyperbilirubinemia, who developed marked purpura on the exposed skin
* All infants had received transfusions
* Elevated plasma coproporphyrins and protoporphyrins were found in 4
* Pathogenesis is unknown

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25 September 2009

Cardiac Assist Devices



Cardiac Assist Devices
By: Wayne E. Ellis, Ph.D., CRNA

Types
Pacemakers
AICDs
VADs

History
* First pacemaker implanted in 1958
* First ICD implanted in 1980
* Greater than 500,000 patients in the US population have pacemakers
* 115,000 implanted each year

Pacemakers Today
* Single or dual chamber
* Multiple programmable features
* Adaptive rate pacing
* Programmable lead configuration

Internal Cardiac Defibrillators (ICD)
* Transvenous leads
* Multiprogrammable
* Incorporate all capabilities of contemporary pacemakers
* Storage capacity

Temporary Pacing Indications
* Routes = Transvenous, transcutaneous, esophageal
* Unstable bradydysrhythmias
* Atrioventricular heart block
* Unstable tachydysrhythmias
* *Endpoint reached after resolution of the problem or permanent pacemaker implantation

Permanent Pacing Indications
* Chronic AVHB
* Chronic Bifascicular and Trifascicular Block
* AVHB after Acute MI
* Sinus Node Dysfunction
* Hypersensitive Carotid Sinus and Neurally Mediated Syndromes
* Miscellaneous Pacing Indications

Chronic AVHB
* Especially if symptomatic

Pacemaker most commonly indicated for:
* Type 2 2º
o Block occurs within or below the Bundle of His
* 3º Heart Block
o No communication between atria and ventricles

Chronic Bifascicular and Trifascicular Block
* Differentiation between uni, bi, and trifascicular block
* Syncope common in patients with bifascicular block
* Intermittent 3º heart block common

AVHB after Acute MI
* Incidence of high grade AVHB higher
* Indications for pacemaker related to intraventricular conduction defects rather than symptoms
* Prognosis related to extent of heart damage

Sinus Node Dysfunction
* Sinus bradycardia, sinus pause or arrest, or sinoatrial block, chronotropic incompetence
* Often associated with paroxysmal SVTs (bradycardia-tachycardia syndrome)
* May result from drug therapy
* Symptomatic?
* Often the primary indication for a pacemaker

Hypersensitive Carotid Sinus Syndrome
• Syncope or presyncope due to an exaggerated response to carotid sinus stimulation
• Defined as asystole greater than 3 sec due to sinus arrest or AVHB, an abrupt reduction of BP, or both

Neurally Mediated Syncope
* 10-40% of patients with syncope
* Triggering of a neural reflex
* Use of pacemakers is controversial since often bradycardia occurs after hypotension

Miscellaneous
* Hypertrophic Obstructive Cardiomyopathy
* Dilated cardiomyopathy
* Cardiac transplantation
* Termination and prevention of tachydysrhythmias
* Pacing in children and adolescents

Indications for ICDs
* Cardiac arrest due to VT/VF not due to a transient or reversible cause
* Spontaneous sustained VT
* Syncope with hemodynamically significant sustained VT or VF
* NSVT with CAD, previous MI, LV dysfunction and inducible VF or VT not suppressed by a class 1 antidysrhythmic

Device Selection
* Temporary pacing (invasive vs. noninvasive)
* Permanent pacemaker
* ICD

Pacemaker Characteristics
• Adaptive-rate pacemakers
•Single-pass lead Systems
• Programmable lead configuration
• Automatic Mode-Switching
• Unipolar vs. Bipolar electrode configuration

ICD selection
* Antibradycardia pacing
* Antitachycardia pacing
* Synchronized or nonsynchronized shocks for dysrhythmias
* Many of the other options incorporated into pacemakers

Approaches to Insertion
Mechanics
Unipolar Pacemaker
Bipolar Pacemaker
Indications
1. Sick sinus syndrome (Tachy-brady syndrome)
2. Symptomatic bradycardia
3. Atrial fibrillation
4. Hypersensitive carotid sinus syndrome
* Second-degree heart block/Mobitz II


Complete heart block
* Sinus arrest/block
* Tachyarrhythmias
Supraventricular, ventricular
To overdrive the arrhythmia
Atrial Fibrillation
1. Asynchronous/Fixed Rate
2. Synchronous/Demand
3. Single/Dual Chamber
4. Programmable/nonprogrammable
Synchronous/Demand
Examples of Demand Pacemakers
DDI
VVI/VVT
AAI/AAT
Disadvantage: Pacemaker may be fooled by interference and may not fire

Dual Chamber: A-V Sequential
Facilitates a normal sequence between atrial and ventricular contraction
Provides atrial kick + ventricular pacing
Atrial contraction assures more complete ventricular filling than the ventricular demand pacing unit
A-V Sequential
Disadvantage: More difficult to place
More expensive
Contraindication: Atrial fibrillation, SVT
Developed due to inadequacy of “pure atrial pacing”
Single Chamber
Atrial
Ventricular
“Pure Atrial Pacing”
Problems with Atrial Pacing
Electrode difficult to secure in atrium
Tends to float

Ventricular
Programmability
Table of Pacer Codes
Types of Pulse Generators
Examples
Other Information
Undersensing: Failure to sense ... much more in 105 slides

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Arrhythmia



ARRHYTHMIA
Edited by Yingmin Chen

* Definition of Arrhythmia:
The Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation are abnormally.

Anatomy of the conducting system
Pathogenesis and Inducement of Arrhythmia
* Some physical condition
* Pathological heart disease
* Other system disease
* Electrolyte disturbance and acid-base imbalance
* Physical and chemical factors or toxicosis


Mechanism of Arrhythmia
* Abnormal heart pulse formation
* Sinus pulse
* Ectopic pulse
* Triggered activity
* Abnormal heart pulse conduction
* Reentry
* Conduct block

Classification of Arrhythmia
* Abnormal heart pulse formation
* Sinus arrhythmia
* Atrial arrhythmia
* Atrioventricular junctional arrhythmia
* Ventricular arrhythmia
* Abnormal heart pulse conduction
* Sinus-atrial block
* Intra-atrial block
* Atrio-ventricular block
* Intra-ventricular block
* Abnormal heart pulse formation and conduction

Diagnosis of Arrhythmia
* Medical history
* Physical examination
* Laboratory test

Therapy Principal
* Pathogenesis therapy
* Stop the arrhythmia immediately if the hemodynamic was unstable
* Individual therapy

Anti-arrhythmia Agents
* Anti-tachycardia agents
* Anti-bradycardia agents
Anti-tachycardia agents
* Modified Vaugham Williams classification
* I class: Natrium channel blocker
* II class: ß-receptor blocker
* III class: Potassium channel blocker
* IV class: Calcium channel blocker
* Others: Adenosine, Digital

Anti-bradycardia agents
* ß-adrenic receptor activator
* M-cholinergic receptor blocker
* Non-specific activator

Clinical usage
Anti-tachycardia agents:
* Ia class: Less use in clinic
* Guinidine
* Procainamide
* Disopyramide: Side effect: like M-cholinergic receptor blocker

Anti-tachycardia agents:
* Ib class: Perfect to ventricular tachyarrhythmia
1. Lidocaine
2. Mexiletine
Anti-tachycardia agents:
* Ic class: Can be used in ventricular and/or supra-ventricular tachycardia and extrasystole.

1. Moricizine
2. Propafenone

Anti-tachycardia agents:
* II class: ß-receptor blocker
* Propranolol: Non-selective
* Metoprolol: Selective ß1-receptor blocker, Perfect to hypertension and coronary artery disease patients associated with tachyarrhythmia.
* III class: Potassium channel blocker, extend-spectrum anti-arrhythmia agent.
* Amioarone: Perfect to coronary artery disease and heart failure patients
* Sotalol: Has ß-blocker effect
* Bretylium
* IV class: be used in supraventricular tachycardia
* Verapamil
* Diltiazem
* Others:
Adenosine: be used in supraventricular tachycardia

Anti-bradycardia agents
* Isoprenaline
* Epinephrine
* Atropine
* Aminophylline
Proarrhythmia effect of antiarrhythmia agents
* Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery disease and heart failure patients
* III class: Like Ia, Ic class agents
* II, IV class: Bradycardia

Non-drug therapy
* Cardioversion: For tachycardia especially hemodynamic unstable patient
* Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, AF, AFL)
* Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular arrhythmia patients.

Sinus Arrhythmia

Sinus tachycardia
* Sinus rate > 100 beats/min (100-180)
* Causes:
* Some physical condition: exercise, anxiety, exciting, alcohol, coffee
* Some disease: fever, hyperthyroidism, anemia, myocarditis
* Some drugs: Atropine, Isoprenaline
* Needn’t therapy
Sinus Bradycardia
* Sinus rate < 60 beats/min
* Normal variant in many normal and older people
* Causes: Trained athletes, during sleep, drugs (ß-blocker) , Hypothyriodism, CAD or SSS
* Symptoms:
* Most patients have no symptoms.
* Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope.
* Needn’t specific therapy, If the patient has severe symptoms, planted an pacemaker may be needed.
Sinus Arrest or Sinus Standstill
* Sinus arrest or standstill is recognized by a pause in the sinus rhythm.
* Causes: myocardial ischemia, hypoxia, hyperkalemia, higher intracranial pressure, sinus node degeneration and some drugs (digitalis, ß-blocks).
* Symptoms: dizziness, amaurosis, syncope
* Therapy is same to SSS
Sinoatrial exit block (SAB)
* SAB: Sinus pulse was blocked so it couldn’t active the atrium.
* Causes: CAD, Myopathy, Myocarditis, digitalis toxicity, et al.
* Symptoms: dizziness, fatigue, syncope
* Therapy is same to SSS

Sinoatrial exit block (SAB)
* Divided into three types: Type I, II, III
* Only type II SAB can be recognized by EKG.

Sick Sinus Syndrome (SSS)
* SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node automaticity and SA conduction.
* Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor, trauma and congenital disease.
* With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms
* Bradycardia-tachycardia syndrome

Sick Sinus Syndrome (SSS)
* EKG Recognition:
* Sinus bradycardia, ≤40 bpm;
* Sinus arrest > 3s
* Type II SAB
* Nonsinus tachyarrhythmia ( SVT, AF or Af).
* SNRT > 1530ms, SNRTc > 525ms
* Instinct heart rate < 80bmp

Sick Sinus Syndrome (SSS)
* Therapy:
* Treat the etiology
* Treat with drugs: anti-bradycardia agents, the effect of drug therapy is not good.
* Artificial cardiac pacing.

Atrial arrhythmia
Premature contractions
* The term “premature contractions” are used to describe non sinus beats.
* Common arrhythmia
* The morbidity rate is 3-5%
Atrial premature contractions (APCs)
* APCs arising from somewhere in either the left or the right atrium.
* Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemia
* Symptoms: many patients have no symptom, some have palpitation, chest incomfortable.
* Therapy: Needn’t therapy in the patients without heart disease. Can be treated with ß-blocker, propafenone, moricizine or verapamil.

Atrial tachycardia
* Classify by automatic atrial tachycardia (AAT); intra-atrial reentrant atrial tachycardia (IART); chaotic atrial tachycardia (CAT).
* Etiology: atrial enlargement, MI; chronic obstructive pulmonary disease; drinking; metabolic disturbance; digitalis toxicity; electrolytic disturbance.........

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