tag:blogger.com,1999:blog-63068076745793126642024-02-20T13:26:57.814-08:00NPTEstudyOnlineUnknownnoreply@blogger.comBlogger6125tag:blogger.com,1999:blog-6306807674579312664.post-43251500534286448172008-06-28T17:36:00.000-07:002008-06-28T17:38:39.574-07:00Myelodysplasia vs. SCI<applet code="Client.class" codebase="http://client11.addonchat.com/current/" archive="scclient_en.zip" alt="Java Chat Software - AddonChat" mayscript="" height="425" width="600"></applet><applet code="Client.class" codebase="http://client11.addonchat.com/current/" archive="scclient_en.zip" alt="Java Chat Software - AddonChat" mayscript="" height="425" width="600"><br /> <param name="room" value="288530"> <br /> <a href="http://www.addonchat.com/">Java Chat Software</a><br /><br /></applet>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6306807674579312664.post-20179154001803169792008-05-21T07:41:00.000-07:002008-05-21T07:42:55.468-07:00cardiac tipsFirst you have to know the function of the heart as a<br />vital organ.Make sure you know the circulation of<br />blood.from inf and superior vena cava to aorta.The<br />heart sound will be produced on CLOSURE of valves,that<br />S1 correspond to closure of Mitral and tricuspid valve<br />and not Aortic and pulmonic valve which is ur S2.They<br />both occur during systole or ventricular contraction.<br /><br />S1 marks the begining of rapid ejection of blood so ur<br />aorta should be open!It make sense right?S3 sound is<br />associated with CHF(3 letter) and S4 for MI and<br />hypertension also known as atrial kick associated with<br />hypertropied ventricle,both occur on diastole,with S3<br />produced after S2 and S4 before S1.S1 starts while<br />blood is pump out so to prevent back flow mitral valve<br />shld be close,once blood is ejected and volume<br />decreases mitral valve should open to refill(inc.<br />PRELOAD) and to create an increase pressure inside the<br />heart for contraction to be effective (frank starling<br />law)aorta should be closed(S2).just remember its the<br />closures of the valves that creates the sound( as in<br />closing door when ur mad (BANG!!),hard to produce<br />sound when you open)).Should be remembered coz when<br />you panic or get nervous you might forget.<br /><br />Nothing much to know about coronary circulation except<br />for (R) coronary artery that supplies most(80%) of ur<br />SAnode(pace maker of the heart) and AV node as injury<br />can cause a fatal arrhytmia.Coronary arteries fills<br />during DIASTOLE contrary to other organs that fills<br />during Systole.Most posterior part of heart is left<br />atrium and enlargement can cause dysphagia.The apex<br />beat is located at 5th ICSLMCL,its the most reliable<br />way to assess heart rate when peripheral pulses are<br />absent,too weak or unaccesible. Make it a practice to<br />appreciate abnormal heart sound and for accuracy for<br />patient with very weak pulses or having<br />atrial/ventricular fib may present with normal<br />palpable pulses.Elderly have collapsable artery<br />(pulse) not good to assess if with heart<br />condition.Brachial pulse is best for assessment in<br />kids.<br /><br />You should know the formula for blood pressure to<br />understand the diseases esp CHF and effects of meds on<br />management of hypertension.Remember that BP is the<br />amount of pressure that the heart should have to pump<br />the blood and distribute it to circulation.<br /><br />BP=Cardiac output(CO) x total peripheral<br />resistances(TPR)<br />your CO=stroke volume x HR.Your Stroke volume is the<br />amt of blood inside the heart being pump per<br />contraction,Your TPR represents the resistance to<br />blood flow primarilly due to arteries/arterioles which<br />is your resistance vessels(remember how<br />atherosclerosis or hardening of ur arteries lead to<br />hypertension!).Stroke volume is primarirly dependent<br />on the amount of blood that goes in ur heart ,the<br />veins which is ur capacitance vessels,and the fluid<br />both plasma and serum component of blood.It is also<br />dependent on how strong ur heart contracts(contractile<br />property of heart loss in CHF).<br />Now, what are the common meds and how they work?<br />initial management or meds will include your diuretics<br />(what makes you pee)this should decrease the preload<br />or fluid that goes in as CO(same amt with what goes<br />in)a little of afterload(the load similar to<br />TPR).Should watch out for fainting or dizziness with<br />sudden drop of BP.Strong diuretics like<br />LASIX(furosemide) can even include deafness bec. of<br />loss of fluid in your circular canal,or loss of<br />potassium leading to arrythmia and weakness.<br /><br />2nd line is Beta blockers(those with<br />OLOL,propranolol(inderal)metoprolol,atenolol,..) will<br />decrease BP by decreasing HR and force of<br />contraction(dec. INOTROPIC property).And since its a<br />beta blocker it should be used with caution in patient<br />with asthma(treatment for asthma is beta agonist like<br />albuterol)Should know that Beta 1 is for the heart(u<br />only have 1 heart) and beta 2 for Lungs(2 lobes)<br />particularly on ur bronchus.In DM, beta blockers can<br />masked the effect of TACHYCARDIA as sign of<br />hypoglycemia,you might think that ur patient have<br />normal HR but his HR without beta blockers might be<br />already more than 100.It can also increase blood<br />glucose level.Use RPE on exercise assessment instead<br />of HR which is use on most cases.Other relative or<br />absolute CI is PVD, since it has an effect on smooth<br />ms lining ur peripheral vessels leading to compromise<br />blood flow.<br /><br />So, 3 things to remember:Asthma,DM and PVD.Learn the<br />rationale so you wont forget!<br /><br />May include CHF as CI but remember that it can be use<br />once STABLE not on ACUTE cases (previous and recent<br />studies shows that like ACEI it can decrease mortality<br />and morbidity in post MI and CHF including HTN)<br />Consistent effects of beta blockers is dec. in BP and<br />HR but for those with sudden drop in BP a compensatory<br />tachycardia may appear.FYI there are betablockers that<br />are selective and affect only B1 receptors,relatively<br />safe for those with previous condition that are CI.<br /><br />Popular drug like ACE inhibitors(CAPTOPRIL) which<br />prevent conversion of Angiotensin I to angiotensin II<br />which is a potent vasoconstrictors(inc. TPR)and<br />decrease preload like diuretics due to decrease<br />production of aldosterone(salt production<br />Na(sodium))Most common side effect is dry COUGH due to<br />persistent bradykinin production,may be present for<br />several weeks ,may or may not persist.Replace with<br />ARB(angiotensin receptor blocker)those with SARTAN ,no<br />SE of cough.Directly block receptor of Angiotensin<br />II.Both are not safe for pregnant,teratogenic effect<br />bec. the fetus need AII for renal development.Renal<br />protective and prolong life in DM and MI.May increase<br />level of potassium in combination with<br />SPIRINOLACTONE(Aldactone)a potassium sparing diuretics<br />different from other diuretics that dec.level of<br />potasium, can also lead to arrhytmia.(brady<br />arrhytmia)remember potassium equals repolarization!<br /><br />Other not so important meds : vasodilators/calcium<br />channel blockers-blocks calcium and relaxes arteries<br />leading to vasodilation,(calcium equals<br />contraction)some have effect on veins decreasing<br />preload,more blood remains on the capacitance vessels<br />not on the heart(nifedipine,hydralazine-can cause drug<br />induced SLE,verapamil-constipation).<br /><br />Alpha 1 blockers/antagonist-prevent release of<br />NE(norepinephrine)-Prazosin(MINIPRESS) known for the<br />SE of FIRST DOSE EFFECT or sudden drop of BP leading<br />to syncope.<br /><br />Alpha II AGONIST(the only adrenergic agonist)Clonidine<br />(CATAPRESS) facillitates/stimulates reuptake of NE not<br />to be release in presynaptic terminals.Decrease TPR.SE<br />includes sudden withdrawal lead to rebound<br />hypertension.<br /><br />Remember that common cough and cold preparation that<br />contains phenylephrine,phenylpropanolamine(PPA) can<br />cause hypertension due to their vasoconstrictive<br />effect in preventing congestion.TCA<br />(tricyclicantidepressant)Amitryptylin(ELAVIL),imipramine<br />(DOFRANIL)- can increase NE,serotonin and dopamine<br />which is dec. in patient with depression but they also<br />block alpha adrenergic receptors(leading to<br />HYPOTENSION) and histamine leading to SEDATION.More<br />reasons to get depress if you fail to monitor<br />vitals...<br /><br />Remember that you have Baroreceptors and<br />chemoreceptors that regulate your HR and BP.your<br />Baroreceptors includes ur carotid SINUS and aortic<br />arch.<br /><br />Carotid sinus transmits via GLOSSOPHARYNGEAL nerve to<br />medulla.Your AORTIC arch transmits via VAGUS to<br />medulla(respond only to increase in BP)vagus as<br />parasympathetic will dec.HR and BP.Carotid massage<br />thru increase pressure in carotid will stimulate vagus<br />leading to dec.HR then BP.Simply stated when you have<br />increse BP your parasympathetic response will be<br />activated(dec.BP,contraction and HR) and reverse with<br />dec.BP as you activate ur symphatetic or as you<br />decrease stimulation of parasympathetic signals coming<br />from afferent receptors (CN 9 and 10)take note that 10<br />or vagus has also an efferent signals coming from<br />medulla.<br /><br />REMEMBER that when you examine patency of carotids do<br />it one at a time not simultaneouslly or patient will<br />faint.wearing a turtle neck thats to tight may do the<br />same thing.other reason why stranguation lead to loss<br />of conciousness.<br />Remember that your medulla oblongata has<br />CARDIOINHIBITORY(parasymphatetic via vagus nerve)as<br />well as CARDIOACCELARATORY center(symphatetic or<br />adrenergic via T1-T4 releasing NE and Epinephrine).<br />Chemoreceptors from carotid and aortic BODIES which<br />responds to dec. in PO2,inc. CO2 and dec.<br />ph.(acidosis).<br /><br />In response to cerebral ischemia( more of inc. in CO2<br />than dec. in O2) ur body will inc. ICP and inc. BP and<br />HR as sympathetic response but with dec. in HR as O2<br />level increases.<br /><br />Some terms to remember:Chronotropic describes property<br />on inc.<br />HR(chrono=time)Inotropic(contractility)Dromotropic(pressure).<br /><br />source: from PTforumUnknownnoreply@blogger.com0tag:blogger.com,1999:blog-6306807674579312664.post-73247248596788303762008-05-16T21:04:00.000-07:002008-05-16T21:05:01.212-07:00Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6306807674579312664.post-63032066098984017432008-05-16T20:06:00.001-07:002008-05-16T20:06:54.658-07:00AMPUTATIONAMPUTATION<br /><br /> -absence of all part of a limb asa a result of surgery,trama,or disease<br /> -aka removal of a limb through the continuity of a bone<br />-LE-most common cause of amputation is PVD<br />-UE-most common cause of amptation is trauma<br /><br /><br /> General Classisfication of Amputation:<br /> A.CONGENITALAMPUTATION <br /> -occurs in utero<br />B.ACQUIRED AMPUTATION<br />-traumatic<br />-ischemic-due to PVD<br />-surgical-done for cosmetic purposes(amputaion secondary to polydactyly)<br /><br />*can also be classified as:<br />A.Major-amputation above MCP/MTP<br />B.Minor-amputation through distal to MCP/MTP<br /><br />Indications:<br />1. Vascular accident or disease<br />-when infection is imminent and wound healing is uncertain<br />2.Infection<br />-Most common indication for amputation (i.e.gangrene)<br /><br /> a. Acute-threatens invasion to other parts of the body;endangering life<br /> b. Chronic-source of toxic absorption (i.e. osteomyelitis)<br /> 3.Congenital anomaly<br />-amputation is due to failure of the limb to develop fully<br />-surgical amputation - is indicated to improve,to form/shape the deformed/deficient limb so that fitting of an artificial limb is possible<br />4.Trauma<br />-results in destruction of blood supply or results in extensive destruction where reconstructive is no longer feasible<br /> 5.Tumor<br /> -If benign amputationis indicated only if it will result in functional limb<br /> -If malignant,amputation is done to prevent further spread of malignancy<br /> 6.Thermal,Chemical or electrical in injury (severe burn inury)<br /> -Injuries from extreme heat /cold (frostbite) can also lead to amputation<br /><br /><br /> SITES OF AMPUTATION:<br /> A.UPPER EXTREMITIY AMPUTATION:<br /> 1.Amputation thru the fingers (ray amputation)<br /> 3 Basics functions:<br /> a. grasp<br /> b. pinch<br /> c. hook<br /> <br /> Thumb<br /> a. imporatntin grasp, vital in pinch<br /> b .40%-50% function loss when thumb is amputated<br /> Index and middle finger <br /> a. most impotant in all 3fucnctions because of their proximity o the thumb<br /> b. srtrogest and most stable<br /> c. 20% index finger and 20% middle finger<br /> Ring and little finger<br /> a. 10% each for ring finger and little finger too<br /> b. provides mobility<br /> c. aids in the combineddexterity of all fingers<br /> <br /> 2.Amputation about wrist <br /> Advantages:<br /> a. pronation are preserved<br /> b .greater stump adaptability (not as cumbersome/uncomfortable compared to above <br /> the elbow amputation)<br /> c. retains natural wrist flexion and extension if amputation is done thru the carpals<br /> <br /> Amputation thru the CARPALS ( midcarpal amputation) with palmar ski<br /> a. easil;y performed since radiocarpal joint is not invaded<br /> b .rounded to smooth contour and covered with palmar skin<br /> c .retains the wrist flexion<br /> Disarticulation of the wrist at the radiocarpal joint<br /> <br /> 3.Amputation thru the lower third of the forearm<br /> a. poor since the skin is thin and underlying soft tissue are largely tendons and fascia<br />b. poor since the circulation is not good;the stump is frequently cold,tender and cyanotic <br />c. secondary skin breakdown is common<br />d. not adaptable with use of prosthesis(poor muscular padding)<br />e. NO pronation /supination<br /> <br /> 4.Amputation at the junction of the middle and lower third of the forearm<br /> a. IDEAL TRANSRADIO-ULNAR STUMP ( functionally and cosmetically)<br /> b. Ideal length:7-8 inches from the tip of the olecranon process to the end of the stump<br /> c. circulation is good in this area<br /> d. full elbow flexion is very possible <br /> <br /> 5.Amputation above the ideal <br />a.forearm/elbow flexion may be normal but can be impaired in either its range or <br /> strength<br /> 6.Amoputation through the humerus<br /> a.Disarticulation thru the elbow joint <br /> a. at the end of the humero-ulnar and the humero-radial joint <br /> b. retains near normal of the shoulder<br /> b.Transcondylar amputation<br /> a.amputation thru epicondyles(long above the elbow stump)<br /> b. hard to fit with a prosthesis<br /> c.Through the supracondylar region<br />a.still considered a long above the elbow stump<br /> 7.Amputation above the supracondylar region <br />a. IDEAL TRANSHUMERAL STUMP <br />b. Ideal length 8 inches from the acromion process to the end of he stump <br />b. most functional stump<br /><br /><br /><br /><br />8.Amputation about the shoulder<br />a. functional prosthesis cannot be worn ( worn only for cosmesis,impractical)<br />b. 2 possible levels<br />a. thru the surgical neck of the humerus<br /> b.disarticulation at the scapulohumeral jt<br /> 9.Forequarter Amputation (shoulder girdle/interscapulothoracic amputation<br />a. At the interval between the scapula and the thoracic wall <br />b. All shoulder functions are obliterated<br /> <br /><br /> B. Lower Extremity Amputations<br /> 1.Foot amputations<br /> -balance between muscle and bony support is lost<br /> A.Toes<br /> - function in tip-toeing <br /> - amputation results in loss of push-off<br /> Big /great toe<br /> -has supporting role in stance<br /> -fulfills a vital function in gait,principlal wt bearing element in the final<br /> phase of hell-off (adds rhythm and agility)<br /> -when amputated,the loss is felt more during rapid walking and<br /> running <br /> Lesser toes<br /> -principal functions:<br />1. stabilize the foot by widening the base of support during squatting <br />and tip-toeing <br /> 2.assist the great toe in push-off and heel-off during rapid gait and running<br /> -amputation at the 2nd toe in the proximal phalanx results in hallux valgus deformity<br /> B. Metatarsals <br /> -balance and weight distribution are disturbed in the direct proportion to the extent and location of loss<br /> C. Above metatarsals <br /> -stump is worthless even as support for the prosthesis<br /> 2.Amputation thru the metatarsal and ankle joint<br />a. SYME’S AMPUTATION<br />-transmalleolar amputation<br />-designed for weight bearing at the end of the stump<br />-provides stability for prosthesis,maybe used without prosthesis<br />b. BOYD’s Amputation<br />-weight bearing over calcaneous following removal of remaining bones of the foot and <br />calcaneo-tibial arthrodesis<br />c. Vasconecelos Amputation<br />-done if use of an artificial limb is not anticipated<br />-midtarsal amutation combined with tibiotalar and subtalar arthrodesis and section of the inferior surface of the calcaneous.<br />d. Pirogoff’s Amputation<br />-principle of arthrodesis of the tibia to the calcaneous after the latter has been rotated forward and upward 90degrees (anteversion)<br /> -unsuccesful for prosthetic fiiting due to its irregular shape<br /><br /><br />e. Listfranc’s Amputation<br />-disarticulation of the foot through the tarsometatarsal joint <br />-falls into moderate equines deformity<br />-like the pirogoff’s amputation,unsuccessful for prosthetic use<br />f. Chopart’s Amputation<br />-thru the transverse tarsal joint (talonavicular/calcaneocuboid)<br />-intended for end bearing<br />-prosthetic fitting not possible<br /> 3.Amputation thru the lower leg (IDEAL SHAPE for TRANSTIBIO-FIBULAR :<br /> CYLINDRICAL)<br /> a.thru the lower 3rd of the leg<br /> - unsatisfactory adaptation of the stump to the prosthesis<br />c. amputation thru the middle third<br /> -IDEAL LENGTH FOR TRANSTIBIO-FIBULAR AMPUTATION<br /> -6 inches (5-7 inches) from the medial tibial plateau/tibial tubercle to the end of the stump <br /> -quadriceps tends to weaken (vastus medialis) since hamstrings tend to pull stump into <br /> flexion <br /> 4. Amputation thru the thigh ( IDEAL SHAPE for TRANSFEMORAL AMPUTATION:<br /> CONICAL)<br />a. Grittie-Stokes amputation<br />-Similar to syme’s amputation (provides weight bearing and can withstand excessive strain)\<br /> -Utilized sectioned patella fused to the femur at or about the level of the adductor <br />Tubercle<br />-osteoplasty which involdves disarticulation of the knee joint,then sawing off the <br /> articular surface of the patella,the patella is approximated to the end of the <br /> femur,created an end bearing stump<br />b. Ischial bearing amputation<br />-IDEAL TRANSFEMORAL AMPUTATION<br />_Ideal length:10-12 inches from the greater rochanter to the ned of the stump<br />-utilizes the power of adductur muscles<br /> -iliopsoas (hip flexors) and gluteus medius (abductors) unaffected<br />-Gluetus maximus (hip extensors) and adductor magnus reduced in volume and power<br /> 5. Amputation thru the thigh above the ideal level<br /> -the shorter the stump, the greater the difficulty in maintaining and activating the<br /> prosthesis<br /> -greater tendency for contractures<br /> -when te stump is only 3-4 below ischial tuberosity and adductor tendon insertion,it is <br /> it is impossible to retain the stump within the socket of the prosthesis<br /> 6.Amputaton about the hip<br /> -amputation thru the trochanters,femoral neck and hip disarticulation<br /> -needs to be fitted with a tilt table type of prosthesis<br /> 7.Hindquarter Amputation<br /> -done only in cases where there is a malignant tumor<br /> -removal of the pelvis by disarticulation of the symphysis pubis and section of the <br /> posterior portion of the ilium near the SI jt (together with the severance of the soft <br /> tissues connecting the trunk with the extremities)<br /> 8.Hemicorporectomy<br /> -removal of the entire lower extremity through the last 2 lumbar vertebrae (L4-L5)<br /> sacrum,coccyx,half of the pelvis<br /> -Involves the creational of an artificial bladder and rectum<br /> <br /><br /> LEVELS OF AMPUTATION:<br /> A.UE <br /> -if unilateral<br /> percentage from Normal<br /> a.Transhumeral ---------------Classification<br /> 0=shoulder disarticulation<br /> 0-30 =humeral neck <br /> 30-50 =short transhumeral stump<br /> 50-90= long transhumeral stump,<br /> elbow disarticulation<br /> b.transradio-ulnarUnknownnoreply@blogger.com0tag:blogger.com,1999:blog-6306807674579312664.post-60103202308702807792008-05-16T19:04:00.000-07:002008-05-16T19:05:25.661-07:00ECG lecture of PTMDELECTROCARDIOGRAM<br /><br /> <br /><br />Normal Sinus Rhythm<br />• Each P wave is followed by a QRS<br />• P wave rate is 60 bpm<br />Rate < 60 = sinus bradycardia<br />Rate > 60 = sinus tachycardia<br /><br />P wave – atrial depolarization<br /><br />PR segment – conduction delay through AV node<br />- normally <200 msec / 0.12 – 0.20 sec<br /><br />QRS complex – ventricular depolarization <br />- normally <120 msec / .08 - .12 sec<br /><br />QT interval – mechanical contraction of the ventricles<br /><br />T wave – ventricular repolarization<br /><br />Atrial repolarization is masked by QRS complex<br /><br />ST segment – isoelectric, ventricles depolarized<br /><br />U wave – caused by hypokalemia<br /><br /><br />ANALYZING THE ECG<br /><br />1. RATE<br /><br />The first step is to determine the RATE, which can be eyeballed by the following technique. Locate the QRS (the big spike) complex that is closest to a dark vertical line. Then count either forward or backwards to the next QRS complex. For each dark vertical line you pass, select the next number off the mnemonic "300-150-100-75-60-50" to estimate the rate in beats per minute (BPM). <br />In other words if you pass 2 lines before the next QRS, the heart rate (HR) would be less than 150. Remember that this is merely an estimate<br /><br />2. RHYTHM<br />- determine if its sinus or an ectopic rhythm<br />- If there is a P wave before each QRS and the P is in the same direction as the QRS, the rhythm can be said to be sinus.<br /><br />3. AXIS<br /> normal axis- I (+) and AVF (+) <br />- I (+) and left axis deviationAVF (-) <br /> right axis deviation- I (-) and AVF (+) <br />- extreme right axis deviationI (-) and AVF (-) <br />*LEADS (important for MI)<br />• V1 V2 -- anterior note: sometimes V1 V2 V3 V4 (anterior)<br />• V3 V4 --septal<br />• V5-V6, I, aVL -- lateral<br />• II, III, aVF – inferior<br /><br />4. HYPERTROPHY<br /><br />Right Atrial Hypertrophy<br />o P wave in lead II taller than 2.5mm (2.5 small squares)<br /><br /> <br /><br />Left Atrial Hypertrophy<br />-P wave duration > 0.12s in frontal plane (usually lead II) <br />-Notched P wave in limb leads with the inter-peak duration > 0.04s<br /><br />Right Ventricular Hypertrophy<br />-Reversal of precordial pattern <br />-Tall R in V1 and V2 <br />-Deep S in V5 and V6 <br />-Normal QRS duration<br /><br /> <br /><br />Left Ventricular Hypertrophy<br />-S in V1 or V2) + (R in V5 or V6) >35 mm (over age 35)<br /><br /> <br /><br />CONDUCTION ABNORMALITIES<br />ATRIO-VENTRICULAR (AV) BLOCKS<br /><br /> <br /><br /> <br /><br />RHYTHM ABNORMALITIES<br /><br /><br />SUPRAVENTRICULAR TACHYARRHYTHMIAS<br /><br /><br />1. Sinus Tachycardia<br />- Ventricular rate >100 bpm<br />-Normal P waves before every QRS<br /><br />2. Paroxysmal Atrial Tachycardia (PAT)<br />-Rapid ectopic pacemaker in atrium (not sinus node)<br />-Rate > 100 bpm<br />-P wave with unusual axis before each normal QRS<br /><br /> <br /><br /><br />3. Atrial Flutter<br />-A characteristic 'sawtooth' or 'picket-fence' waveform of an intra-atrial re-entry circuit usually at about 300 bpm.<br /><br />4. Atrial Fibrillation<br />- Wavy baseline without discernible P waves<br />- Variable and irregular QRS response<br />- The rhythm is irregularly irregular<br /><br />5. Premature Ventricular Contraction<br /><br />o Ectopic beats arise from ventricular foci<br />o Common and often benign<br />o It is usually asymptomatic, but may cause palpitations<br />o Causese include hypoxia, electrolyte abnormalities, hyperthyroidism<br />o ECG tracings revealed early, wide QRS complexes that are not preceded by a P wave.<br />o PVCs are followed by a compensatory pause<br />o No treatment if asymptomatic. If symptomatic, give B-Blockers or other antiarrhythmics. Treat the underlying causes<br /><br /> <br /><br /> <br /><br />6. Ventricular Tachycardia<br />o Associated with CAD and MI<br />o Three or more consecutive PVCs<br />o Wide QRS complexes in a regular and rapid rhythm<br />o AV dissociation<br /><br />7. Ventricular Fibrillation<br />o A completely erratic rhythm with no identifiable waves. <br />o Treat with immediate electrical cardioversion and ACLS protocolUnknownnoreply@blogger.com0tag:blogger.com,1999:blog-6306807674579312664.post-73770941981959294782008-05-16T06:07:00.000-07:002008-05-16T06:09:03.402-07:00CTSIBStatic balance, the Clinical Test of Sensory Interaction for Balance (CTSIB)<br /> The Clinical Test for Sensory Interaction of Balance (CTSIB) is a more complex sensory strategy balance test. It is administered by:<br />1) manipulating the support surface (ie, firm vs foam), <br />2) visual conditions (ie, eyes open, eyes closed), and <br />3) vestibular system (sway reference by using a dome or computerized sway platform ), while an individual is asked to maintain their standing balance.<br /><br />The CTSIB test helps determine which sensory system (visual, somatosensory, or vestibular) the person relies on to maintain balance.<br />The Clinical Test of Sensory Interaction and Balance is a timed test (normal is 30 seconds) that was developed for systematically testing the influence of visual, vestibular, and somatosensory input on standing balance.[2] This test is inexpensive, requires minimal equipment, and is currently in use by some clinicians. Conditions 1, 2, and 3 involve standing on the floor with eyes open, eyes closed, and wearing a visual-conflict dome. The dome provides a sensory conflict by depriving the subject of peripheral vision and introducing a sway-referenced image. Use of the conflict dome results in a discrepancy between vestibular input stimulated by postural sway and visual flow.[1] Thus, conditions 2 and 3 should examine different aspects of sensory organization of visual information that may require different postural adjustments.[3] That is, condition 2 examines how well subjects maintain balance in the absence of any vision, and condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.<br />Conditions 4, 5, and 6 involve standing on foam and repeating the visual conditions described for conditions 1 through 3. For each condition, the length of time the subject can maintain standing and the amount of body sway that occurs are assessed.<br /><br /><br />1: eyes open and firm surface, ( all 3 sensory systems are available here, vision, somatosensory and the vestibular system, normal standing time is at least 30 sec)<br /> <br /> 2: eyes closed and firm surface, (2 sensory system are available here, somatosensory/vestibular. You take away the vision; patients who are dependent on vision become unsteady here. That is, condition 2 examines how well subjects maintain balance in the absence of vision)<br /> <br />3: eyes open, visual conflict (dome) and firm surface ( All three systems are available, but you have a conflict between eyes and vestibular information, patients who are dependent on vision are unsteady here; condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.) <br /> X <br /><br />4: eyes open and unstable surface (foam) ( if patients are dependent on surface/somatosensory inputs, they are unsteady in this position, and number 5 and 6; i.e . all positions on foam/unsteady surface; vision and vestibular system are available)<br /> <br />5: eyes closed and unstable surface ( you have taken away vision and the reliance on the surface/somatosensory system; patients with vision dependency due to somatosensory or vestibular loss are unsteady here)<br /> <br />6: eyes open, visual conflict and unstable surface ( visual conflict can create a problem for patients depending on their vision for balance, patients with somatosensory or vestibular loss are unsteady here)<br /> X <br /><br />In Summary: <br />• Patients dependent on vision become unstable in conditions 2,3, 5 & 6 where we either close the eyes, or have a conflict between vision and the vestibular system <br />• Patients dependent on surface/somatosensory inputs become unstable in conditions 4,5 & 6 because we stand the patient on a soft surface ( foam) <br />• Patients with vestibular loss become unstable in conditions 5 &6 because they can’t rely on vision or surface/ somatosensory function<br />• Patients with sensory selection problems become unstable in conditions 3-6. <br /><br /><br /><br /><br />Treatment: Treatments may involve the manipulation of sensory input while performing a task. This may be done for any of the three systems responsible for providing sensory feedback. For example, to encourage use of vestibular input, visual and somatosensory information may be challenged. Visual input is challenged by taking it away (e.g., eyes closed) or by destabilization (e.g., involving head and eye movements in the task). Unstable surfaces (e.g., rocker board or rough terrain) or compliant surfaces(e.g., foam) help to challenge somatosensory input. Vestibular input may be manipulated by changing the position of the vestibular organ (e.g., neck extension or repeated head movements).Unknownnoreply@blogger.com1