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 rezervă

B. Volumul maxim de aer care poate fi ventilat într-un minut

C. Volumul expirator de rezervă

D. Capacitatea reziduală funcţională

E. Volumul de aer vehiculat în cursul respiraţiei 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 toată aria pulmonară

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

- D 1 - MS dr. MS stg.- D 2 - MS dr. MI stg.- D 3 - MS stg. MI stg.

- aVR - MS dr.- aVL - MS stg.- aVF - MI stg.

Tipuri de derivatii in ECG de suprafata

- V1 –sp.4 parasternal. dr.- V2 – sp.4 parasternal stg.- V3 – ½ 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

Derivatiiunipolare

Dreivatiibipolare

Derivatii precordiale unipolare

right left

Pozitionare electrozi periferici

Pozitionare electrozi precordiali

LR

Interpretare ECG

1. ritm cardiac2. frecventa cardiaca3. ax electric4. analiza unda P5. analiza interval P-R / P-Q6. analiza interval si complex QRS7. analiza segment S-T8. analiza unda T9. analiza unda U10.durata interval Q-T

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

Date tehnice

Ritm cardiac

ritm regulat / neregulatregulat ritm sinusal / jonctional / idioventricular

- se cauta unda P in deriv. D1, D2, V1neregulat exista / nu periodicitate sau pattern recognoscibil

Bradicardie sinusalaFibrilatie atriala

- 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

Frecventa cardiaca

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.

↑1

↑2

↑3

↑… ..

↑30

↑1

↑2

↑3

↑4

↑5

↑6

↑7 x 10 ~ 70 / min

6 secunde

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 hexaaxialmet. 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 stangavariatie normala variatie normala

inspir expir

emfizem diafr.ascens sarcina

HVD ascita, tum. abd.

HBPS HBAI

BRD BRS

dextrocardie lez. congenitale

WPW WPW

ritm ventr. ectopic ritm ventr. ectopic

hiperpotasemie

Analiza unda P

- prima unda de pe ECG- prima ½-depol. AD, a doua ½-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 ½ negat. D3, V1 dilat. AS

• P bifid, durata >0.12s, amplit. D1>D3

P mitral (HAS)

• P amplit2.5mm, vf. ascutit, D3>D1

P pulmonar (HAD)

• 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 QRS larg = sdr. WPW

• + QRS ingust = sdr. de P-R scurt sdr. LGL tahiaritmii

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

prelungire scurtare

varianta normal varianta normal

BAV prin BCI, RAA ritm atrial inf.,jonct.A-V

hipertiroidie WPW, LGL

ritm de pacemaker glicogenoze

digitala 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 – 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 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 QRSV1-V2 – R/S < 1, de fapt rSV3-V4 – R/S = 1V5-V6 – R/S > 1, de fapt Rs

• semnificatie unde componente QRSQ – depolar. septalaR, 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 Tvizualizare optima V3evidentiere: 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 J-wave, 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 Ve afectat de: influente autonome, catecolamine, momentul zilei,

somn, sex, varstafrecventa cardiaca det. cea mai mare variabilitate formule de corectie = QTcrapid, QT < ½ interv. RR precedentmatematic, QTc = Qt real/ RR – Bazett

QTc = QTreal + 0,154(1 – RR) – FraminghamQTc > 0.44 sec. este considerat crescutQT lung - idiopatic / dobandit – predispune la fen. reintrare tahiaritmii SV maligne (torsada vf., TV), sincope, moarte subita

idiopatic - sdr. surdocardiac - sdr. Romano-Ward

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.

Cauze de QT lung Cauze de QT scurt

tulb. electrolit. - HCa++, HK+medicamente digitala

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.atrialeetiol.: 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, aVFhipervoltaj >3mm

P pulmonar simetricaascutita, cu aspect de cortdilat. 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,V2durata >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 mVdurata TADI = 0.06 sec. V5, V6durata 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. 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

afectarea retea Purkinje

• 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. clare2) 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.= 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

HVD avansata

Criterii de dg.HVD volum HVD presiune

V1, V2 V5, V6 V1, V2 V5,V6

asp. de BRD, nu identic, config. rR',

p.2 a QRS neregulata si durata usor

crescuta

 

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

R/S < 1 (asincronism patologic, inversat

stg. - dr.

R/S ~ 1, unda S usor neregulata (echiv. R'

din V1, V2) 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. ax Qrs hiperdeviat la dr.

modif. sec. de faza term.

fara modif. de faza term.

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

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

Treatment of sinus tachycardia associated with a Treatment of sinus tachycardia associated with a pathologic condition must be directed at the underlying pathologic condition must be directed at the underlying cause cause (e.g., infection, hyperthyroidism, CHF, or alcohol (e.g., infection, hyperthyroidism, CHF, or alcohol withdrawal). 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) Drugs that increase vagal tone (e.g., digitalis) or that decrease sympathetic tone (e.g., beta blockers)or that decrease sympathetic tone (e.g., beta blockers)• Calcium channel blockers such as diltiazem and Calcium channel blockers such as diltiazem and

verapamil may cause marked sinus bradycardia. verapamil may cause marked sinus bradycardia. • Hypothyroidism Hypothyroidism • Sick sinus syndrome Sick sinus syndrome • Vasovagal reactions Vasovagal reactions

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

Narrow QRS complexNarrow QRS complex Sinus tachycardia Sinus tachycardia Paroxysmal supraventricular tachycardias Paroxysmal supraventricular tachycardias

• Atrial tachycardiasAtrial tachycardias• AV nodal reentrant tachycardiaAV nodal reentrant tachycardia• AV reentrant tachycardia AV reentrant tachycardia

Atrial flutter Atrial flutter Atrial fibrillation Atrial fibrillation

Wide QRS complexWide QRS complex Ventricular tachycardiaVentricular tachycardia Any supraventricular tachyarrhythmia, Any supraventricular tachyarrhythmia, with with aberrantaberrant ventricular conduction ventricular conduction usually caused by either of the following: usually caused by either of the following:

• Bundle branch block Bundle branch block • Atrioventricular bypass tract (WPW) Atrioventricular bypass tract (WPW)

Major TachyarrhythmiasMajor Tachyarrhythmias

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 failure- or 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 FibrillationCauses 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 and Multiform VPBs• Uniform 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 TachycardiaDuration

• 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 sine-wave 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 life-threatening 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 VF is the most common cause of

sudden cardiac death 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 BradyarrhythmiasMajor 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 A prolonged PR interval does not produce symptoms or significant change in cardiac function 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 Most factors that produce PR prolongation

can also produce second- and third-degree can also produce second- and third-degree

block 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 ToxicityCommon 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

• Tachycardias – Accelerated junctional rhythm (nonparoxysmal junctional tachycardia)

– Atrial tachycardia with block

– Ventricular ectopy

• 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., hoxiesevera = afect. depol. + repol.

Tipuri de modif. ECG: ischemieischemie leziuneleziune

necrozanecroza

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 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 curentilor 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/T-

asoc. 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 antsantul 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

- 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.

Infarct cu supra ST

- 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, inferiordiagn. 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 - ½ 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-V4Infarct 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 indirecteProblema 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 localizataspre partea endocardica si nu se traduce electric prin prezenta deunda 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.