Mecanismele fiziopatologice implicate in astmul bronsic includ urmatoarele, cu exceptia:

A. cresterea rezistentei la fluxul de aer B. hiperventilatie pulmonara C. hipoventilatie zonala cu scaderea PaO2 alveolar si cresterea Pa CO2 D. ventilatie inegala a diferitelor zone E. creste travaliul muschilor respiratori

Volumele pulmonare statice includ urmatoarele cu exceptia:

A. Volumul inspirator de rezerv
B. Volumul maxim de aer care poate fi ventilat ntr-un minut C. Volumul expirator de rezerv

D. Capacitatea rezidual funcional

E. Volumul de aer vehiculat n cursul respiraiei de repaus

Semne de gravitate definitorii pentru astmul acut grav sunt:

A. Hipercapnie B. Sputa perlata C. Agitatie psihomotorie D. Folosirea muschilor sternocleidomastoidieni E. Hipersonoritate pe toat aria pulmonar

In tratamentul crizei de astm bronsic se utilizeaza:

A. Prednison B. Salbutamol C. Montelukast D. Bromura de ipratropium E. Formoterol

In pericardita acuta apar, cu exceptia:

A. Supradenivelare de segment ST in toate derivatiile cu exceptia aVR si V1 B. Supradenivelare de segment PR C. Subdenivelare de segment PR D. Supradenivelare de segment PR in aVR E. Un raport intre amplitudinea supradenivelarii de segment ST si amplitudinea undei T mai mare de 0.24 in V6.

ELECTROCARDIOGRAMA

ELECTROCARDIOGRAMA de suprafata

Definitie: inregistrarea la suprafata corpului a curentilor electrici generati la nivelul cordului

suma vectoriala curenti reproductibilitate universala aparatura + interpretare

ECG standard - ritm, ax electric, morfologie unde, intervale - poate orienta catre alte forme complexe de ECG sau catre alte investigatii ECG cu inregistrare de durata (Holter, 24 ore) - ambulator - tulburari de ritm la bv. suspectati - modificari ischemice
ECG computerizata - ECG standard cu amplificare digitala - potentiale tardive (risc aritmogen ) - analiza digitala frecventa cardiaca la Holter variabilitate ritm cardiac ritm fix (ex. Hcatecolamine) = fact. risc de moarte subita

Explorare electrofiziologica prin cateterism cardiac - mapping endocavitar mod depolarizare inducere aritmii

Proba de efort ECG - ECG in timp ce pacientul face un efort dozat si imediat dupa (recovery) - modificare ritm cardiac - tulburari de ritm - modificari de segmente si unde

Tipuri de derivatii in ECG de suprafata

Dreivatii - D 1 - MS dr. MS stg. Derivatii - aVR - MS dr. bipolare - D 2 - MS dr. MI stg. unipolare - aVL - MS stg. - D 3 - MS stg. MI stg. - aVF - MI stg. Derivatii precordiale - V1 sp.4 parasternal. dr. - V2 sp.4 parasternal stg. unipolare
- V3 distanta V2 V4 - V4 sp.5 pe LMC stg. - V5 oriz. prin V4 LAA stg. - V6 oriz. prin V4 LAM stg. - V7 oriz. prin V4 LAP stg. - V8 oriz. prin V4 vf. scapula - V9 oriz. prin V4 paravert. stg. - V3R - V4R simetrice V3,V4,V5 - V5R R, S, q = 0

Pozitionare electrozi periferici

right

left

Pozitionare electrozi precordiali

Interpretare ECG 1. ritm cardiac 2. frecventa cardiaca 3. ax electric 4. analiza unda P 5. analiza interval P-R / P-Q 6. analiza interval si complex QRS 7. analiza segment S-T 8. analiza unda T 9. analiza unda U 10.durata interval Q-T

Date tehnice
viteza hartie = 25 mm/s uzual orizontal 1mm = 0.04s, 5mm = 0.2s vertical 1cm = 1mV

Ritm cardiac
ritm regulat / neregulat regulat ritm sinusal / jonctional / idioventricular - se cauta unda P in deriv. D1, D2, V1 neregulat exista / nu periodicitate sau pattern recognoscibil

Fibrilatie atriala

Bradicardie sinusala

Frecventa cardiaca
- 1500 (mm) /dist R-R (mm)/ (medie pe 10 cpx) - 300/150/100/75/60/50/43/37/33/30 (300 x 1/5 = 60 sec =1 min) - nr. cicluri card. intre 2 puncte considerate ca interval cunoscut de timp aplicabil cand complexele cad pe liniile groase

Care e frecventa ?
1. Masoara 6 secunde pe derivatia de analiza a ritmului derivatia continua (numara 30 de patrate mari)
2. Numara complexele QRS din acel interval 3. Inmulteste numarul de complexe QRS cu 10.

 12 3

6 secunde

..30

3 4 5 6 7 x 10 ~ 70 / min

Ax electric
- se det. in deriv. membrelor (plan frontal) - reprez. ax complex QRS - se det. avand la dispoz. min. 2 derivatii, util 6 derivatii - triunghi Einthoven sistem hexaaxial met. vizuala - impulsul electric se inscrie max. in deriv. paralela cu el si min. in deriv perpendiculara pe el (sau echidifazic) met. bisectoarei - determ. cu exactitate a ax. compar 2 deriv. adiacente din cadran. in care se afla ax. - ax 0 +90 grade = ax normal - ax +90 +180 grade = ax deviat la dreapta - ax 0 -90 grade = ax deviat la stanga - cpx. izoelectrice in toate deriv. ax el. nedet. in plan frontal

Cauze de deviere a axului electric

dreapta
variatie normala

stanga
variatie normala

inspir emfizem HVD HBPS BRD dextrocardie WPW ritm ventr. ectopic

expir diafr.ascens sarcina ascita, tum. abd. HBAI BRS lez. congenitale WPW ritm ventr. ectopic hiperpotasemie

Analiza unda P
- prima unda de pe ECG - prima -depol. AD, a doua -depol. AS - normal pozitiva D1, D2, V4-6, aVF negativa aVR variabil D3, aVL - amplitudine max. 2-3 mm - durata = 0.08 0.12 sec - forma rotunda, fara varfuri - repolarizarea atriala = T p, se inscrie in QRS

-anormal:

inversiuni de sens P depol. atriala inferioara

(ectopie atriala, ritm jonctional superior) crestere amplitudine P hipertrofie / dilat. A (valvulop. A-V, HTA, cord pulm., congenit.) crestere durata P dilat. AS, miopatii

P difazic, a 2-a negat. D3, V1 dilat. AS

P bifid, durata >0.12s, amplit. D1>D3 P mitral (HAS) P pulmonar (HAD) P amplit.>2.5mm, vf. ascutit, D3>D1

P absent, ritm regulat ritm jonct., bloc SA

Analiza interval P-R / P-Q

timp scurs de la inceput P la inceput Q / R durata normala 0.12-0.20 sec., variaza cu frecv. card. scade la ritmuri rapide P-R are loc prin suprimarea tonus parasimpatic la efort P-R la tahicardizare tulburare de conducere atrii in ritm de pacemaker digitala P-R > 0.20 sec. = BAV grad I P-R < 0.12 sec. + unda d+QRS larg = sdr. WPW + QRS ingust = sdr. de P-R scurt sdr. LGL tahiaritmii

Cauze de modificare a duratei P-R / P-Q

prelungire varianta normal BAV prin BCI, RAA hipertiroidie ritm de pacemaker digitala scurtare varianta normal ritm atrial inf.,jonct.A-V WPW, LGL glicogenoze HTA feocromocitom

Analiza QRS
- reprezinta depolarizarea intrgii mase ventriculare - 1deflexiune negativa = unda Q - 1deflexiune pozitiva = unda R - deflexiune negativa aparuta dupa deflexiune pozitiva = unda S - excursii subsecvente pozitive = R, R - excursii subsecvente negative = S, S - QRS format dintr-o unda negativa mare = QS - aspectele q, Q, r, R, s, S depind de amplitudinea undei - interpretarea QRS: durata amplitudine (voltaj) prezenta Q axa elctrica in plan frontal zona de tranzitie in deriv. precordiale deflexiune intrinsecoida aspectul general al undelor

 durata QRS: - 0.06 - 0.10 sec. in deriv.membrelor - 0.11 0.12 sec. HV, B incompl. de ram > 0.12sec. B intraventr., B compl. de ram voltaj QRS minim S deflexiunii si + > 5 mm in D1-D3, V1, V6 > 7 mm in V2, V5 > 9 mm in V3, V4 anormal: BCI difuza, IC, liq. peric., mixedem, amiloidoza maxim greu de stabilit - 20 30 mm D2 - 25 30 mm precord. anormal criterii de hipertrofie fact. de influentare: pozitie + contact electrozi, marime torace, emfizem,etc.

 unda Q - q < 2 mm in D1, aVL, aVF, V5, V6 = normal derivatii inferioare inspir = elimina q pozitional - Q in aVR <1/4 R = unda R din alte deriv. - normal - durata maxima de 0.03 sec. - Q patologic >1/4 R in deriv. respect. > 0.04 sec. absenta unda d in WPW = q BRS major D2,D3,aVF,V1-V3 = Q cord pulmonar cronic emfizem q V1 V4 axa electrica in plan frontal zona de tranzitie rotatii in plan transversal - normal QRS echidifazic in V2 V3 - rotatie orara aspect QRS dr. in V3, V4 - rotatie antiorara aspect QRS stg. in V2, V3

 deflexiune intrinsecoida (TADI) - timpul scurs de la debut. depolar. ventric. unda exciatie epicardica + inregistrarea ei prin electrodul explorator cel mai apropiat - V1-V2 < 0.035 sec., V5-V6 < 0.045 sec. - V1-V2 HVD, BRD, WPW - V5-V6 HVS, BRS, WPW aspect morfologic al QRS V1-V2 R/S < 1, de fapt rS V3-V4 R/S = 1 V5-V6 R/S > 1, de fapt Rs semnificatie unde componente QRS Q depolar. septala R, S depolar. in masa ventriculara

Analiza segment ST
- punct de emergnta din QRS = punct J - 2 elemente se urmaresc: translatarea fata de linia izoelectrica forma - linia izoelectrica este considerata segmentul TP - supradenivelari permise: 1 mm D1-D3, 2 mm V1-V2 indiv. afroamericani, tineri, sanatosi patologic: leziune subepicardica - subdenivelari permise: 0,5 mm patologic: leziune subendocardica, modif. sec. HVS, HVD, BRS, BRD, WPW -forma: linie, curbata usor catre panta undei T patologic: - linie perfect orizontala suspic. ischemie mioc. - translatare franca ischemie tranzitor supradenivelare - postcardioversie

Analiza unda T
- expresia ECG a repol. ventric. - acelasi sens cu QRS, axul el. cu 30 60 grade mai la stg - pozit. D1,D2,V3,V6 // neg. aVR // var. aVL,aVF,V1,V2 T neg. - 30% in V1, 5% in V2 tendinta de inversiune catre deriv. stg. cu varsta - amplitudine aprox. 1/3 R, < 5 mm D1 < 10 mm precord. patologic: - ischemie epicardica, supraincarc.V, Hk+, Hvagotonii, AVC, psihotici -BCI difuza, digitala, supraincarc. V, obezit. - forma asimetrica, cu panta ascend. mai lina, panta descend. abrupta, vf. rotunjit patologic: simetric, vf ascutit ischemie miocardica, HK+ crestat pericardita (uneori)

Analiza unda U
acelasi sens cu unda T vizualizare optima V3 evidentiere: hK+, cu polaritate nemodif. ischemie, incarc. VS din HTA, IMi, IAo negat. la ECG de repaus, U neg. stenoza TC sau IVA

In hypothermia, a small extra wave is seen immediately after the QRS complex (best seen in Lead I in this example). This x-tra wave is called a Jwave, or Osborne wave after the individual who first described it. This wave disappears with warming of body temperature. The mechanism is unknown.

Analiza interval QT

masurat de la inceput QRS la sf. T durata totala a sistolei V e afectat de: influente autonome, catecolamine, momentul zilei, somn, sex, varsta frecventa cardiaca det. cea mai mare variabilitate formule de corectie = QTc rapid, QT < interv. RR precedent matematic, QTc = Qt real/ RR Bazett QTc = QTreal + 0,154(1 RR) Framingham QTc > 0.44 sec. este considerat crescut QT lung - idiopatic / dobandit predispune la fen. reintrare tahiaritmii SV maligne (torsada vf., TV), sincope, moarte subita

Cauze de QT lung

Cauze de QT scurt

idiopatic - sdr. surdocardiac tulb. electrolit. - HCa++, HK+ - sdr. Romano-Ward medicamente digitala IC, BCI, RAA, miocardita, PVM AVC hemoragic tulb. electolit. - hK+ asoc. hCa++ - hMg++ hipotermie medicamente chinidina, procainamida, disopiramida amiodarona, sotalol fenotiazine, ADTc sulfamide antiDZ eritromicina pentamidina, etc.

When the long QT interval is due to a long ST segment with a delayed onset of the T wave, it is specific for hypocalcemia. Besides, the T waves are tall, narrow, and pointed and are highly suggestive of hyperkalemia. This combination of electrolyte problems is common in patients with chronic renal failure, which this patient has. The serum potassium level was 8.2 mEq/L and calcium 5.4 mg/dL at the time.

ELECTROCARDIOGRAMA IN DILATATII SI HIPERTROFII

Supraincarcari atriale
ECG = modif. ale undei P - depol.atriale etiol.: SMi, STri, insuf. fct. prin dil. cavit. solicit. volum congenit.- DSA, desch. anorm. VP in AD, VC / VAzig in AS HTP sec. boli pulm. cr. solicitare de presiune

Supraincarcare AD (SAD)
CPcr., SP, DSA, Fallot, sdr. Ebstein, STri, ITri modif. raport de masa intre atrii, modif. 1 moment de depol.A ECG: modif axa P = + 75 - +900 orient. dr, ant. jos modif. morfologie P in V1, V2, D2, D3, aVF hipervoltaj >3mm P pulmonar simetrica ascutita, cu aspect de cort dilat. AD in V1-V2, cu deflex. poz. > 2mm

Supraincarcare AS (SAS)
SMi, IMi, DSA, mixom AS

2 parte a depol. A este modificata, cu amplitud. ECG: modif. ax P cu deviere la stg.,orient. stg., post., jos modif. morfologie P in D1, aVL, V5, V6, indirect V1,V2 durata >0.11 sec. P mitral crosetata, asincronismului AD-AS > 0.02 sec. P neg. in V1, V2

Supraincarcare AD + AS (SAD +SAS)

elemente sumate de la SAD, SAS in functie de predom. uneia ECG: morfologie P durata >0.11 sec. hipervoltata > 3 mm, mai ales in deriv. mb. hipervolatjul ambelor deflexiuni +,- V1, V2

Supraincarcari ventriculare
reprezinta un mecanism adaptativ in prima faza, ca raspuns la suprasolicitarea volemica sau presionala, cu ingrosarea , alungirea sau hiperplazia fibrelor miocardice

Suprasolicitarea VS
suprasarcina de volum: IMi, IAo, PCA suprasarcina de presiune: HTA, SAo valv./subvalv., CoAo, CMH stari dismetabolice: BCI, miocardite, etc. fen. anatomice: - hipertrofie ventriculara = ingrosare perete - dilatare cavitati - fortare VS = strain = HV / dilat. + tulb. metabol. si electrofiziol. modif. faza term. fen ECG: durata QRS, TADI, amplit. QRS rotatie antiorara prin dilat. VS, cu extindere model epicardic stg. catre deriv. dr. R/S = 1 in V1, V2 modif. faza term. ST, T

 electrofiziologie - asincronism ventricular, cu depol. intarziata a ventric. Htrof. - nu e modificata ordinea de depol. nici ordinea undelor - modif. faza term. sunt sec. perturb. depol. - imgini directe: D1,aVL,V5,V6 Hvoltaj + - imagini indirecte: V1,V2 Hvoltaj criteriile de diagnostic a HVS includ informatii despre amplit. QRS, durata TADI, modif. ST,T elemente de hipertrofie VS: imag. directa - V5,V6 R >2.5 mV (3.5) - aVL R >1.3 mV - D1 R >1.5 mV imag. indirecta - V1,V2 S >2 mV durata TADI = 0.06 sec. V5, V6 durata QRS = 0.12 0.13 sec. modif. faza term. S-T, T - D1, aVL,V5, V6

Indice Sokolow Lyon: R (V5/V6) + S (V1/V2) >3.5 mV (4.5 mV la copil) Indicele Cornell: R (aVL) + S (V3) > 2.8 mV (B), 2 mV (F) Scorul Romhilt Estes: 1) R sau S deriv. mb. > 2 mV S V1, V2, V3 > 2.5 mV 3 p. R V4, V5, V6 > 2.5 mV 2) S-T in opoz. de faza cu QRS 3 p. (fara digitala) S-T, T de tip strain 1 p. (cu digitala) 3) deviere ax.stg > -15o 2 p. 4) duarata QRS > 0.09 sec. 1 p. 5) TADI V5, V6 > 0.04 sec. 1 p. 6) panta termina P > 0.04 sec. 3p. Total 13 p.; HVS = 5 p. ; probabil = 4 p.

 evolutia suprasarcinii VS - incipient - tulb. repol. T hvoltat / subdeniv.oriz.ST cu T izoel. - avansat - majorit. criterii de dg. - strain = fortare - Hvoltaj QRS + tulb. faza term. subdeniv ST T Hvoltat - masa ventriculara ecografic - ischemie mioc., tulb. cond. intramioc. - apare o data cu dilatarea + insuf. VS - HVS + BRS incomplet = durata QRS 0.12-0.14 sec. TADI 0.08 sec. afectarea retea Purkinje Hvoltaj excesiv QRS absenta q V5, V6, aVL, D1 - HVS + BRS major - e mascata Htrofia in deriv stg. - imag. indirecta - S > 2 mV in V1,V2 - HSV + BRD - mascheaza imag. indirecta - S mari in V1, V2 de asp. rSr / rSR - HVS + IM sechelar ant. / lat. TADI

 asocierea la HVS a HAS este uzuala, inclusa in crit. dg. ECG nu diferent. HVS concentr. de dilat. VS. marire de VS ECG nu este de cele mai multe ori sufic. pt. caract.marirea de VS formule de expunere: 1) HVS = crit. dg. clare 2) elem. de HVS = unele crit., dar nu majorit. 3) posibil HVS = prea putine criterii, cu specificit.

In this example of LVH, the precordial leads don't meet the usual voltage criteria or exhibit significant ST segment abnormalities. The frontal plane leads, however, show voltage criteria for LVH and significant ST segment depression in leads with tall R waves. The voltage criteria include: 1) R in aVL >11 mm; 2) R in I + S in III >25mm; and 3) (RI+SIII) - (RIII+SI) >17mm (Lewis Index).

Suprasolicitarea de VD
mecanism compensator, in final maladaptativ, de lunga durata, aparut ca urmare a solicitarilor de volum si de presiune impuse miocardului VD etiologie: incarcare de volum - DSV, Fallot, PCA (sunt stg. dr.) incarcare de presiune HTP esent., HTP sec.(emfizem, TBC, bronsiectazii bilat., fibroze pulm., SMi) fiziopatol.- balanta vectoriala VD-VS se schimba pana la predom. VD, in cazuri extreme de HVD - inversarea asp. normal pe ECG: R in V1, V2 + S in V5, V6 - rotatie orara, catre anterior a VD + rotatie posterioara a vf. inimii - prin masa VD asincronism VD-VS

 consecinte ECG: - devierea ax. dreapta QRS - modif. modele epicard. HVD moderat - hvoltaj QRS - nemodif. TADI - asincronism inversat = Hdeviatie dr. HVD avansata = invers. modele epicard. HVD concentric - Htrof. masa septala dr. QS V5, V6, aVL, D1 - tulb. sec. faza term imag. dir. V1,V2, imag indir. V5, V6, D1, aVL difera asp. electrofiziol. intre HVD de orig. volemica (parietala) si cea presionala (rezistenta, concentrica) in HVD volemica se asoc. un grad de dilat. VD

Criterii de dg.
HVD volum V1, V2 asp. de BRD, nu identic, config. rR', p.2 a QRS neregulata si durata usor crescuta R/S < 1 (asincronism patologic, inversat stg. - dr. R/S ~ 1, unda S usor neregulata (echiv. R' din V1, V2) V5, V6 V1, V2 HVD presiune V5,V6

invers. completa a modele. epicard. - model dr. de tip rS, model stg. de tip qR

R/S <1

R/S <1

R > 0.7 mV

S>0.7 mV

R>0.7 mV

S>0.7 mV

ax QRS Hdeviat la dr. modif. sec. de faza term. fara modif. de faza term.

ax Qrs hiperdeviat la dr. modif. sec. faza term ST - T

Criterii simplificate: 1) deviatie axiala > 900 2) R V1 > 7 mm 3) R V1 + S V5/V6 > 10 mm 4) R/S V1 >1 5) S/R V6 >1 6) TADIi V1 > 0.035 sec. 7) aspect de BRD 8) ST T strain D2, D3, aVF 9) P pulmonar / P congenital 10) Aspect S1S2S3 la copii spre deoseb. de HVS, aici asp. complet de HVD este rar HVD se pot insoti si de dilat. AD, cu asp. de SAD in caz de SMi, cu apar. de P mitral asociat dg. diferential: a) sdr. WPW unda d b) BRD masurare de TADI c) IMA postero-bazal si posterolatera strain: asociaza tulbur. independente celor strict de HVD

Note the qR pattern in right precordial leads. This suggests right ventricular pressures greater than left ventricular pressures. The persistent S waves in lateral precordial leads and the RAD are other finding in RVH.

In this case of severe pulmonary hypertension, RVH is recognized by the prominent anterior forces (tall R waves in V1-2), right axis deviation (+110 degrees), and "P pulmonale" (i.e., right atrial enlargement). RAE is best seen in the frontal plane leads; the P waves in lead II are >2.5mm in amplitude.

Supraincarcre de VS + VD

Criteriile ECG: Criterii de voltaj pt HVS in precordiale + Hdeviatie ax spre dr. Criterii de voltaj pt HVS + R V1, V2 S putin adanc V1 + S mai adanc V2 SAS ca expresie a HVS + oricare din: S/R >1 V5,V6 S > 7 mm V5, V6 deviere ax. dr.

TULBURARILE CARDIACE DE RITM SI CONDUCERE

Normal Sinus Rhythm

Normal Sinus Rhythm

normal sinus rhythm the P wave is negative in lead aVR and positive in lead II The heart rate is between 60 and 100 beats/min.

Sinus Tachycardia

Sinus Tachycardia
Sinus tachycardia is simply sinus rhythm with a heart rate exceeding 100 beats/min In adults the heart rate with sinus tachycardia is generally between 100 and 180 beats/min

Sinus tachycardia. Each QRS complex is preceded by a P wave. Notice that the P waves are positive in lead II. With sinus tachycardia at very fast rates the P wave may merge with the preceding T wave and become difficult to distinguish.

In general, sinus tachycardia occurs with any condition that produces an increase in sympathetic tone Or a decrease in vagal tone.

conditions commonly associated with sinus tachycardia:

Anxiety, excitement, exertion, and pain Drugs that increase sympathetic tone Drugs that block vagal tone (e.g., atropine Fever, many infections, and septic shock Congestive heart failure (CHF) Pulmonary embolism Hyperthyroidism Alcohol intoxication or withdrawal

Treatment of sinus tachycardia associated with a pathologic condition must be directed at the underlying cause (e.g., infection, hyperthyroidism, CHF, or alcohol withdrawal).

Sinus Bradycardia

Sinus Bradycardia
sinus rhythm is present and the heart rate is less than 50 beats/min

This arrhythmia commonly occurs in the following conditions:

Drugs that increase vagal tone (e.g., digitalis) or that decrease sympathetic tone (e.g., beta blockers) Calcium channel blockers such as diltiazem and verapamil may cause marked sinus bradycardia. Hypothyroidism Sick sinus syndrome Vasovagal reactions

Moderate sinus bradycardia usually produces no symptoms. If the heart rate is very slow (40 to 50 beats/min), light-headedness and even syncope may occur. Treatment requires decreasing medication doses or even discontinuing drug therapy. If inappropriate bradycardia causes symptoms (as in sick sinus syndrome), an electronic pacemaker may be needed

Sinus Arrhythmia

Sinus Arrhythmia
Respiratory sinus arrhythmia. Normally the heart rate increases slightly with inspiration and decreases slightly with expiration

Sinus Pauses, Sinus Arrest, and Escape Beats

Sinus Pauses, Sinus Arrest, and Escape Beats

sinus node fails to stimulate the atria for one or more beats a missed beat (no P wave or QRS complex) at occasional intervals,
Sinus pause in a patient with sick sinus syndrome. The monitor lead shows sinus bradycardia with a long pause (about 2.4 seconds).

Major Tachyarrhythmias

Major Tachyarrhythmias
Narrow QRS complex Sinus tachycardia Paroxysmal supraventricular tachycardias Atrial tachycardias AV nodal reentrant tachycardia AV reentrant tachycardia Atrial flutter Atrial fibrillation Wide QRS complex Ventricular tachycardia Any supraventricular tachyarrhythmia, with aberrant ventricular conduction usually caused by either of the following: Bundle branch block Atrioventricular bypass tract (WPW)

Supraventricular Arrhythmias

Supraventricular Arrhythmias,

Premature atrial and AV junctional beats, paroxysmal supraventricular tachycardias, AV junctional rhythms

Atrial and AV Junctional (Nodal) Premature Beats

Atrial and AV Junctional (Nodal) Premature Beats

APBs have the following major features
The atrial depolarization is premature, occurring before the next normal P wave is due The QRS complex of the APB is often preceded by a visible P wave that usually has a slightly different shape and/or different PR interval from the P wave seen with normal sinus beats. The PR interval of the APB may be either longer or shorter than the PR interval of the normal beats. In some cases the P wave may be "buried" in the T wave of the preceding beat

After the APB a slight pause generally occurs before the normal sinus beat resumes. * The QRS complex of the APB is usually identical or very similar to the QRS complex of the preceding beats. Remember that with APBs the atrial pacemaker is in an ectopic location but the ventricles are usually depolarized in a normal way. This contrasts with VPBs, in which the QRS complex is usually very wide because of abnormal depolarization of the ventricles

Notice the atrial premature beat (APB) after the fourth sinus beat (arrow). B, Notice also the blocked atrial premature beat, again after the fourth sinus beat (arrow). The premature P wave falls on the T wave of the preceding beat and is not followed by a QRS complex because the atrioventricular node is still in a refractory state.

Atrial bigeminy in which each sinus beat is followed by an atrial premature beat (or premature atrial complex).

Paroxysmal Supraventricular Tachycardias

Paroxysmal Supraventricular Tachycardias

Premature supraventricular beats may occur singly or repetitively A sudden run of three or more beats constitutes a paroxysmal supraventricular tachycardia (PSVT) -nonsustained (i.e., lasting from three beats up to 30 seconds) -Sustained episodes (greater than 30 seconds) may last minutes, hours, or longer

In summary, a PSVT should be suspected when a rhythm strip shows a rapid and typically very regular rate at about 200 beats/min (range: 100 to 250 beats/min).

The mechanism may be due to reentry in the AV node (AVNRT) atrioventricular reentrant tachycardia (AVRT) with a concealed bypass tract ectopic AT.

A, The reference is normal sinus rhythm. B, With atrial tachycardia (AT), C, With atrioventricular (AV) nodal reentrant tachycardia

P waves are usually hidden in the QRS comple

because the atria and ventricles are activated simultaneously.

In other cases the P waves may appear just before or just after the QRS complex and therefore may be difficult to see. Because of
this retrograde (bottom-to-top) activation of the atria, the P waves are negative in lead II

AVNRT may cease spontaneously or may require treatment.

Initial therapy usually involves attempts to increase vagal tone that can be increased with the Valsalva maneuver or with carotid sinus massage

AV Junctional Rhythms

AV Junctional Rhythms the ectopic pacemaker is located somewhere in the atria outside the SA node When the AV junction is the cardiac pacemaker, the atria are stimulated in a retrograde fashion, from bottom to top This retrograde stimulation of the atria produces a positive P wave in lead aVR and a negative P wave in lead II . With AV junctional rhythm the ventricles are depolarized normally resulting in a narrow QRS complex.

AV junctional beats can be recognized on the ECG by one of the following patterns Retrograde P waves (positive in lead aVR , negative in lead II) immediately preceding the QRS complexes Retrograde P waves immediately following the QRS complexes Absent P waves (buried in the QRS), so that the baseline between QRS complexes is flat

Atrioventricular junctional (nodal) beats produce P waves that point upward in lead aVR and downward in lead II. The P wave may just precede the QRS complex (A), follow it (B), or occur simultaneously with it (C). In the last instance no P wave is visible

AV JUNCTIONAL ESCAPE RHYTHMS

An AV junctional escape beat is simply a beat that comes after a pause when the normal sinus pacemaker fails to function. The AV junctional escape beat therefore is a "safety beat." An AV junctional escape rhythm is a consecutive run of AV junctional beats. The heart rate is usually slow (30 to 50 beats/min).

Atrial flutter and atrial fibrillation

Atrial flutter and atrial fibrillation

they are ectopic the atria are being stimulated not from the sinus, or sinoatrial (SA), node but from an ectopic site or sites With PSVT the atria are stimulated at a rate generally between 140 and 250 beats/min With atrial flutter the atrial rate is even faster, generally 250 to 350 beats/min AF the atrial depolarization rate is typically between 400 and 600 beats/min

Atrial Flutter

Atrial Flutter

stimulation rate is about 300 beats/min the ventricular rate with atrial flutter is about 150, 100, or 75 beats/min Atrial flutter with a ventricular response of 150 beats/min is called 2:1 flutter the atrial rate in atrial flutter may be
considerably less than 250 beats/min (as low as 200 to 220 beats/min) in patients taking drugs that slow atrial conduction

With atrial flutter, the ECG shows the following:

Characteristic "sawtooth" flutter waves instead of discrete P waves A constant or variable ventricular rate (e.g., one QRS complex with every fourth flutter wave, 4:1 flutter; one QRS with every two flutter waves, 2:1 flutter, and the ventricular rate half the atrial rate; or the rare 1:1 flutter, in which the ventricles contract about 300 times a minute)

Atrial Fibrillation

Atrial Fibrillation

most commonly seen arrhythmias the atria are stimulated (depolarized) at a very rapid rate, up to 600 beats/min This fibrillatory activity produces a characteristically irregular wavy pattern in place of the normal P waves The irregular waves are called fibrillatory or f waves

 the AV junction in patients with AF is bombarded by innumerable stimuli from the atria the AV junction is refractory to most of these impulses and allows only a fraction to reach the ventricle normal AV junction the ventricular rate is generally between 110 and 180 beats/min

In summary, AF has two ECG characteristics:

An irregular wavy baseline produced by the rapid

f waves (fibrillatory waves) instead of P

waves A ventricular (QRS) rate that is usually quite irregular.

AF occurs paroxysmally and may last only minutes, hours, or days chronic and may persist indefinitely
CLINICAL ASPECTS symptomatic (typically complaining of palpitations, weakness, or dyspnea -heart failureor stroke ) no specific complaints ( AF may first be discovered during a routine examination )

CLINICAL CONSEQUENCES Decreased Cardiac Output Atrial Thrombi and Embolization

ETIOLOGY lone atrial fibrillation = AF in patients without clinical evidence of heart disease changes in autonomic tone organic (structural) heart disease
coronary artery disease hypertensive heart disease valvular heart disease

Causes of Atrial Fibrillation Alcohol ("holiday heart") Autonomic factors

Sympathetic (during exercise or stress) Vagotonic (occurring during sleep)

Cardiothoracic surgery Cardiomyopathies or myocarditis Congenital heart disease Coronary artery disease Hypertensive heart disease

 Idiopathic ("lone" atrial fibrillation) Paroxysmal supraventricular tachycardias or the Wolff-Parkinson-White preexcitation syndrome Pericardial disease (usually chronic) Pulmonary disease (chronic obstructive pulmonary disease) Pulmonary emboli Sick sinus syndrome Thyrotoxicosis (hyperthyroidism) Valvular heart disease (particularly mitral valve disease)

Ventricular Arrhythmias

Ventricular Premature Beats

VPBs have two major characteristics * : They are premature and occur before the next normal beat is expected. They are aberrant in appearance. The QRS complex is abnormally wide (usually 0.12 second or more), and the T wave and QRS complex usually point in opposite directions.

VPBs may occur in various combinations Two in a row are referred to as a pair or couplet Three or more in a row are, by definition, VT

Coupling Interval

The term coupling interval is frequently applied to the interval between the VPB and the preceding normal beat When multiple VPBs are present, fixed coupling often occurs, with the coupling interval approximately the same for each VPB At other times, VPBs may show a variable coupling interval.

Compensatory Pause

VPBs are usually followed by a pause before the next normal beat The pause after a VPB is usually but not always longer than the pause after an APB A fully compensatory pause indicates that the interval between the normal QRS complexes immediately before and immediately after the VPB is exactly twice the basic RR interval

 Uniform Uniform and Multiform VPBs VPBs have the same appearance in any lead and arise from the same anatomic site (focus) Uniform VPBs are uni focal Uniform VPBs may occur in normal hearts and hearts with underlying organic heart disease

 multiform VPBs have different morphologies in the same lead Multiform VPBs often but not always arise from different foci Multiform VPBs usually indicate that organic heart disease is present

R on T Phenomenon The R on T or VPB on T phenomenon refers to VPBs that are timed so that they fall near the peak of the T wave of the preceding normal beat

CLINICAL SIGNIFICANCE
VPBs are among the most common arrhythmias They may occur - in normal hearts - with serious organic heart disease Individuals with VPBs may be - Asymptomatic - palpitations (i.e., sensations of a "skipped" or "extra beat).

Ventricular Tachycardia

Ventricular Tachycardia
VT is, by definition, simply a run of three or more consecutive VPBs

Classification of Ventricular Tachycardia Duration Nonsustained (lasting three beats to 30 seconds) Sustained (lasting 30 seconds or more, or somewhat shorter runs if associated with symptoms of syncope or near-syncope) Morphology Monomorphic Polymorphic With long QT(U) syndrome: torsade de pointes Without long QT(U) syndrome: for example, polymorphic VT with acute ischemia

Sustained VT (typically lasting more than 30 seconds) is usually a life-threatening arrhythmia for two major reasons: Most patients are not able to maintain an adequate blood pressure at very rapid ventricular rates and eventually become hypotensive. The condition may degenerate into VF causing immediate cardiac arrest.

VT, whether sustained or not, can also be characterized as monomorphic ( A) or polymorphic, depending on whether consecutive VPBs have the same or a variable appearance in a single lead. Very rapid VT with a sinewave appearance is sometimes referred to as ventricular flutter. This arrhythmia often leads to VF

 Despite pharmacologic therapy, some patients are at high risk for life-threatening recurrences of sustained VT or VF. For these patients a special device called an implantable cardioverter defibrillator (ICD) has been developed to deliver an electric shock directly to the heart during a lifethreatening tachycardia

Accelerated Idioventricular Rhythm

Accelerated Idioventricular Rhythm

AIVR the heart rate is usually between 50 and 100 beats/min, and the ECG shows wide QRS complexes without associated P waves. The arrhythmia is generally short lived, lasting minutes or less, and usually requires no specific therapy. particularly common with acute MI it may be a sign of reperfusion after the use of thrombolytic agents

Torsade de Pointes

Torsade de Pointes: Specific Form of Polymorphic Ventricular Tachycardia the direction of the QRS complexes appears to rotate cyclically, pointing downward for several beats and then twisting and pointing upward in the same lead. torsade de pointes occurs in the setting of delayed ventricular repolarization, evidenced by prolongation of the QT intervals or the presence of prominent U waves

Ventricular Fibrillation

Ventricular Fibrillation

VF is the most common cause of sudden cardiac death

the ventricles do not beat in any coordinated fashion but instead fibrillate or quiver asynchronously and ineffectively No cardiac output occurs, and the patient becomes unconscious immediately VF is one of the three major ECG patterns seen with cardiac arrest ( The other two are bradyasystolic patterns and electromechanical dissociation )

 The ECG in VF shows characteristic fibrillatory waves with an irregular pattern that may be either coarse or fine VF requires immediate defibrillation with an unsynchronized DC shock.

Bradyarrhythmias

Major Classes of Bradyarrhythmias Sinus bradycardia and its variants, including sinoatrial block Atrioventricular (AV) heart block * or dissociation
Second- or third-degree AV block Isorhythmic AV dissociation and related variants

Junctional (AV nodal) escape rhythms Ventricular escape rhythms (idioventricular rhythms) Atrial fibrillation or flutter with a slow ventricular response

Atrioventricular Heart Block

Atrioventricular Heart Block

Heart block is the general term for atrioventricular (AV) conduction disturbances Heart block occurs when transmission through the AV junction is impaired either transiently or permanently

Classification of AV Heart Blocks First-degree block = Uniformly prolonged PR interval Second-degree block = Intermittent conduction failure - Mobitz type I (Wenckebach) : progressive PR prolongation - Mobitz type II: sudden conduction failure Third-degree block = No atrioventricular conduction

First-Degree Heart Block

Prolonged PR Interval (First-Degree Heart Block)

With first-degree heart block the PR interval is prolonged above 0.2 second and is constant from beat to beat

 A prolonged PR interval does not produce symptoms or significant change in cardiac function mild PR interval prolongation is seen as a normal variant, especially with physiologic sinus bradycardia during rest or sleep occur with acute rheumatic fever ischemic heart disease during inferior wall infarction tend to be transient drugs: digitalis, which has a vagal effect on the AV junction Most factors that produce PR prolongation can also produce second- and third-degree block

Second-Degree AV Block

Second-Degree AV Block two types: Mobitz type I block (also called Wenckebach block) and Mobitz type II block.

MOBITZ TYPE I (WENCKEBACH) AV BLOCK

each stimulus from the atria to the ventricles appears to have a more difficult time passing through the AV junction. Finally the stimulus is not conducted at all. This blocked beat is followed by relative recovery
of the AV junction, and the whole cycle starts again.

ECG :progressive lengthening of the PR interval from beat to beat until a beat is "dropped." The dropped beat is a P wave that is not followed by a QRS complex, indicating failure of the
AV junction to conduct the stimulus from the atria to the ventricles.

Mobitz Type I AV Blocks

Clinically

Patients with the Wenckebach type of AV block are usually without symptoms unless the ventricular rate is very slow The pulse rate is irregular.

Common causes
a physiologic increase in vagal tone may cause Wenckebach AV block in athletes at rest ischemic heart disease drugs : digitalis, beta blockers, and calcium channel blockers (diltiazem and verapamil) is not uncommon with acute inferior wall MI (usually transient and generally does not require any
treatment except observation)

Occasionally these patients may progress into complete heart block

MOBITZ TYPE II AV BLOCK

Its characteristic feature is the sudden appearance of

a nonconducted sinus P wave

MOBITZ TYPE II AV BLOCK

is generally a sign of severe conduction system disease involving regions below the AV node (i.e., His-Purkinje system) not seen with digitalis excess or inferior MI may be seen with anterior wall MI often progresses into complete heart block indication for a pacemaker

Advanced second-degree AV block

= refers to the ECG finding of two or more consecutive nonconducted P waves
For example, with sinus rhythm and 3:1 block, every third P wave is conducted; with 4:1 block, every fourth P wave is conducted

Third-Degree (Complete) Heart Block

Third-Degree (Complete) Heart Block

no stimuli are transmitted from the atria to the ventricles the atria and ventricles are paced independently The atria generally continue to be paced by the sinus node The ventricles are paced by an escape pacemaker located somewhere below the point of block in the AV junction The resting ventricular rate with complete heart block may be lower than 30 beats/min or as high as 50 to 60 beats/min The atrial rate is generally faster than the ventricular rate.

ECG with sinus rhythm and complete heart block has the following three characteristics: P waves are present, with a regular atrial rate faster than the ventricular rate. QRS complexes are present, with a slow (usually fixed) ventricular rate. The P waves bear no relation to the QRS complexes, and the PR intervals are completely variable because the atria and ventricles are electrically disconnected.

Complete heart block may also occur in patients whose basic atrial rhythm is flutter or fibrillation. In these cases the ventricular rate is very slow and almost completely regular.

QRS complexes may be - of normal width or - abnormally wide with a BBB pattern The width of the QRS complexes depends in part on the location of the block in the AV junction As a general clinical rule complete heart block with wide QRS complexes tends to be less stable than complete heart block with narrow QRS complexes because the ventricular escape pacemaker is usually slower and less consistent.

 narrow QRS = If the block is in the first part (the AV

node), the ventricles are stimulated normally by a junctional pacemaker and the unless the patient has an underlying bundle branch block

wide QRS complexes = If the block is within, or

particularly below, the bundle of His, the ventricles are paced by an idioventricular pacemaker

Complete heart block is a potentially life-threatening arrhythmia = If the ventricular rate becomes too slow the cardiac output drops and the patient may faint Fainting spells associated with complete heart block (or other types of bradycardia) are referred to as

Stokes-Adams attacks

In some patients, complete heart block is a chronic and persistent finding OR may occur transiently and may be recognized only with
more prolonged monitoring.

ETIOLOGY
most commonly seen in

older patients who have chronic degenerative changes (sclerosis or fibrosis) in their conduction systems
not related to MI.

Digitalis intoxication open-heart surgery bacterial endocarditis

ETIOLOGY complication of MI -inferior MI =Transient *Occlusion of the right coronary artery with inferior MI also
often leads to temporary ischemia of the AV node, sometimes resulting in complete heart bloc

* inferior wall MI is often a transient and reversible complication

that does not usually require a temporary pacemaker unless the patient is hypotensive

-anterior MI = idioventricular escape rhythm that develops is

usually slow and unstable = temporary pacemaker

(and subsequently a permanent one)

Common Arrhythmias in Digitalis Toxicity Bradycardias

Sinus bradycardia, including sinoatrial block Junctional (nodal) escape rhythms Atrioventricular (AV) heart block, including the following:

Mobitz type I (Wenckebach) AV block Complete heart block

Accelerated junctional rhythm (nonparoxysmal junctional tachycardia) Atrial tachycardia with block Ventricular ectopy

Tachycardias

Ventricular premature beats Monomorphic ventricular tachycardia Bidirectional tachycardia

Ventricular fibrillation

ELECTROCARDIOGRAMA in BOALA CARDIACA ISCHEMICA

Modificarile ECG in cardiopatia isch. sunt II intensit. hipoxiei, rapidit. de instal., hoxie moderata = afect. repol., hoxie severa = afect. depol. + repol. Tipuri de modif. ECG: ischemie leziune necroza

Ischemie
expresia hoxie. moderata afect. repol., depend. de metab.aerob terit. afectat e depol. = negat., cel vecin e repol. = pozit. vectorul de ischemie localiz. - isch. subepicardica = epicard endocard - isch. subendocardica = endocard epicard ax. electr. T este deviat prin S normal + patologic asp. ECG - schimb. polaritatii - simetrica

Leziune
hoxie severa afect. depol. + repol. depol. lenta a z. afectate electro. pozit. curent de leziune: z. norm. z. afect.; repol.: $unui curent similar celui de ischemie curent sistol. det. supra/subdeniv. ST, curent diastol. det. modif. T ECG: subepicardic = supradenivelare de ST subendocardic = subdenivelare de ST

Necroza
rezult. suprimarii aport O2, tesutul el. deservit = inactiv electr. ECG: unda Q patologica - S > 25-30% R in aceasi deriv. - durata > 0.04 sec. teorii electrogenet. - teoria ferestrei el. (aplic. IMA transmurale) - teoria vectoriala = dezeq. forte el., unda Q / modif. raport R/S / modif. ax electr. vectorul de necroza Scurentilor existenti la momentul depol., sensul sau fiind divergent cu z. de necroza

Angina stabila = Angina pectorala

in per. intercritice, sdr. anginos determina aspecte ECG diverse tipuri traseu: 1. normal QRS normal ST-T normal 2. modif. minore de repol. QRS normal T + simetrica, Hvolt. / aplatiz. /difazica / 3. modif. majore de repol. QRS normal modif. tip lez. subendocard., isch. subepicard. 4. modif. de depol. v. BRD, BRS, HBSA, HVS modif. mixte / primare tip isch. lez. subendocard. cele mai frecv.: lez. subendoc.(subdeniv. ST) +/- isch. subepic.(T -) T + in criza, cu T in afara crizei = pseudonormal alungire tranzit. QT tulb. ritm parox. FlA, FiA, ExV, TV specificit. ECG de repaus e folos. ECG in durere / ECG de efort

Angina varianta = Angor Printzmetal

forma particulara de angina, aparuta adesea cu orar fix, durata mai lunga de 15 min., nedeclansata de efort sau stres emotional expresia unei stenoze coronariene epicardice ECG: lez. subepicardica supradeniv. de ST, T inglobat in ST/Tasoc. tulb. cond. intraventr. BAV 2, Mobitz I

Infarctul Miocardic
forma anatomoclinica cea mai severa a cardiopatiei ischemice, corespunzand unei necroze miocardice var. ca intindere mec. patogenice: marcata sau 0 a flux sgv. intr-un anum. terit. cu corespunz. a aport O2 la cel. cauze: - tromboza coronara completa - stenoza severa a coronarelor prin placi de aterom - ocl. coronara prin hematom subintimal +/- tromboza sec. - ocl. embolica ( endoc. bact, embolii gaz., gras.,Aotite lues) topografie infarct: - VS, VD, rar atrial - infarct VS cel mai frecv., cu implic. clinice cele mai import.

 a. coronara stg: - a circumflexa santul A-V post - a interventriculara ant.santul IV a. coronara dr.santul A-V post crux cordis - a IV post. - a post.lat. teritorii de vasc. - IVA sept IV f. ant. + lat. VS - LCx f. stg. + post. VS ` - CD f. ant. + lat. + post. VD f. inf. VS sept IV post.

evidentiere ECG: V1 V4 ant.= IVA V5,V6, aVL, D1 lat. = LCx V3R V5R ant VD = CD proxim. V7 V9 post = LCx term., CD D2,D3,aVF inf. = CD distal

Infarct cu supra ST
- necroza - leziune - ischemie ECG se urmareste in dinamica necroza flux 0 - expresie ECG = unda Q patol. leziune flux minim pastrat expresie ECG = supradenivelare ST ischemie flux pastrat expresie ECG = T -, ascutita, simetrica necroza = singur marker al IM vechi, celelalte pledand pt. faza ac. imag. ECG dir. = Q, ST supra ,T imag. ECG reciproca = R, ST sub, T + stadializ. temporala a IM: stadiu acut ( < 2-3 sapt.) N,L,I - supaacut - acut constit.

- supraacut (0 4 h) = a) T +, , simetr. = I b) ST sub, T+, simetr. c) ST supra, T+, ample, concav sus d) marea unda monofazica ST supra, convexa sus, inglob T - acut constit (4h 2-3 sapt) = N,L,I, domina ST supra, convexa sus apare Q T , simetr. stadiu subacut (2-3 sapt 2-3 luni) = N,I de la revenire ST la izoel. event. revenire la norm. T stadiu cronic (> 3 luni) = N unda Q persista Evolutie: - persist. indef. ST supra, T - = N,L = imag ingetata - persist. indef. a T - = N,I = ischem. reziduala periIM - dispar in timp Q (20%)

topografie ECG cele mai frecvente sunt IM anterior, inferior diagn. se pune uzual pe semne directe, rareori pe reciproce IMA ant intins per ant.lat. VS, parte per ant VD, parte sept ocl. IVA la orig. vector de necroza stg dr, ant. post., cranio caudal ECG - imag. directa - D1, aVL, V1-V6 - imag. indirecta D2, D3, avF, V7 V9 - planul de necroza este predom. in plan trsv., deriv mb.inregistrand putin semnal el. imagine reciproca de amplit. N, L predom in V1,V2, I in V5, V6 = IMA ant. cu extindere lat.

Infarct anteroseptal - ant.sup. sept, extins paraseptal dr. + stg. - ocl. ram septale din IVA - vector de necr. perpendic plan frontal ant. post ECG - imag. directa V1 V3 - D1, aVL imag indiferente, normale - Q V1, ST supra V2,V3, T - V3,V4 - aspect de BRD poate insoti acest IM Infarct anterior localizat - 1/3 medie sept per.ant. - vector necroza ant. post - ECG deriv. V2-V4 Infarct lateral - z. de IMA in terit LCx. - necroza este pe per. later, extinsa la per ant - vector de necroza stg. dr. - ECG: imag directe D1, aVL, V5,V6 daca IMA lat. inalt, deriv folosite pot fi cu 1 spatiu mai susV5x, V6x

Infarctul inferior - ocl IVP, ram CD - vector de necroza caudocranial inainte - ECG: imag. directe.: D2, D3, aVF imag. indirecte: R/S >1, ST sub, T + simetr V2-V4. - in general, daca aria de necroza e mica, imag. indirecta nu se inregistreaza Infarctul posterior - rar singur, insoteste IMA anterior sau lateral - ECG: imag. directe V7, V8, D1, aVL imag. indirecte V1, V2 Infarctul septal profund - sept, de la per. inf. la per. ant. - ocl. ambe aa. IV - vector de necr. dr. stg., caudocranial - ECG imag.directe D2,D3,aVF,V1-V3 - forma clinica grava - insuf. card. - soc cardiogen - tulb. ritm / conduc.

Infarct de VD - ECG - ST supra V4R, la pacientii cu IMA inf. - ST supra > 1mm V4R V6R e specific - intinderea supra ST in deriv. dr. se coreleaza cu riscul de BAV Infarct atrial - uzual insoteste IMA inf. - ECG - aspect de IM ventr. + aritmie atriala brusca - contur anorm. unda P - modif. de la linia izoel. a segm PR in imag. directe si indirecte Problema de diagnostic IMA VS + BRS QRS - Q in deriv. laterale D1,aVL,V6 - S crestat V3, V4 - amplit. R de-a lungul deriv stg. - analiza in dinamica a ECG ST - supra / sub disproportionat pentru BR - pierderea concavit./ convexit. ST

Infarctul fara supradenivelare ST

necroza nu e completa pe toata grosimea miocardului, e localizata spre partea endocardica si nu se traduce electric prin prezenta de unda q si supradeniv. ST se admite ca o leziune subendocardica (ST subdenivelat > 1mm) persistenta se considera infarct subendocardic ECG frecvent: - ST subdeniv. , T - T -, , persistente, alungirea QT - ischemie subepicardica, T + simetr., fara unda Q pentru IM fara ST supradeniv. criteriul ECG nu este un criteriu de baza remodelajul ventricular este mic pacientii sunt predispusi la completarea trombozei coronare

ELECTROCARDIOGRAMA de EFORT in BOALA CARDIACA ISCHEMICA

Definitie: Inregistarea ECG la intervale diferite de timp in timpul si imediat dupa un efort fizic real sau simulat cu scopul evidentierii modif. de ischemie / inducerii unor aritmii. Utilitatea probei: obiectivarea fenomenelor ischemice nerelevate la repaus evidentierea ischemiei reziduale dupa un episod de sdr. coronarian acut inducere de aritmii cardiace Criterii de pozitivitate: subdeniv. ST orizontala /descendenta, 1- 2 mm, cu durata >0.08 sec. supradeniv. ST >1 mm, durata >0.08 sec.

Contraindicatii absolute - IMA / modif. recente de repaus - AI in evolutie - Aritmii card. semnificative - Pericardita ac. - Endocardita - StAo severa - Disfct. severa VS - TEP / infarct pulmonar
Contraindicatii relative: - HTA / Htp semnificative - valvulop. moderate - CMH - obstr. TC / echivalente - aritmii mai putin semnif. - tulb. psihice semnific.