cardio Flashcards
Définition d’un IAM
- Typical rise and gradual fall or more rapid rise and fall of biochemical markers of myocardial necrosis, with at least one value above the 99th percentile of the upper reference limit (URL) and with at least one of the following clinical parameters: • Ischemic symptoms • Electrocardiographic changes indicative of ischemia (T wave changes or ST segment deviation) • Development of pathologic Q waves on the ECG and/or • Imaging evidence of presumably new findings, such as a loss of viable myocardium or a regional wall motion abnormality 2. Pathologic findings of an AMI
5 types de SCA
Type 1—spontaneous MI related to ischemia resulting from a primary coronary event, such as plaque erosion rupture, erosion, fissuring, or dissection with accompanying thrombus formation and vasospasm. Type 1 infarctions represent the true ACS event.
Type 2—MI secondary to ischemia caused by increased oxygen demand or decreased supply, as seen in coronary artery spasm, coronary embolism, severe anemia, compromising arrhythmias, or significant systemic hypotension related to a range of causes.
Type 3—sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST segment elevation or new left bundle branch block (LBBB) pattern. Fresh coronary thrombus is noted via angiography or autopsy; death occurs before appropriate sampling of the blood to detect the abnormal cardiac biomarker.
Type 4—MI associated with coronary instrumentation, such as occurring after percutaneous coronary intervention (PCI). For PCIs in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of periprocedural myocardial necrosis. By convention, increases of biomarkers greater than three times the 99th percentile URL are designated as defining PCI-related MI. A subtype related to a documented stent thrombosis is similarly recognized.
Type 5—MI associated with coronary artery bypass grafting (CABG). For CABG in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of periprocedural myocardial necrosis. By convention, increases of biomarkers greater than five times the 99th percentile URL, plus any of the following, are designated as defining CABG-related MI:
•
New pathologic Q waves or new LLLB
•
Angiographically documented new graft or native coronary artery occlusion
•
Imaging evidence of new loss of viable myocardium
Nommer des complications d’un SCA
- Rupture ventriculaire
- Rupture du septum interventriculaire
- Rupture d’un muscle papillaire
- Péricardite (précoce ou tardive/dressler, dressler 1 sem à plusieurs mois après)
- Arythmies (TV, FA, Bloc)
- Mort subite
- Choc cardiogénique
- Anévrysme ventriculaire
- complications emboliques, stroke
- thrombus mural
- Complications hémorragiques reliées au traitement
- complication PCI - pseudoanévrysme a. fémorale
Ddx sus décalage segment ST
Ddx ondes T hyperaigues
- ischémie précoce
- hyperkaliémie
- HVG
- BBG
- péricardite aigue
DxD d’un sous-décalage segment ST
- ischémie sous-endocardique
- HVG
- hyper ou hypokaliémie
- embolie pulmonaire
- hémorragie intracrânienne
- bloc de branche
- rythme de pace
- arythmies post cardioversion
- myocardite
- PTX
- digitale
décrire les trouvailles à l’ECG d’un syndrome de wellens
- Inversion des ondes T symmétriques ou biphasiques en précordial
- segment ST isoélectrique ou minimalement susdécalé < 1 mm
- Absence d’ondes Q
DxD d’une inversion des ondes T
T wave inversion is broad and includes ACS, ventricular hypertrophy, bundle branch block, VPR, myocarditis, pericarditis, PE, pneumothorax, Wolff-Parkinson-White syndrome, cerebrovascular accident, hypokalemia, GI disorders, hyperventilation, persistent juvenile T wave pattern, and normal variants
Décrire la présentation à l’ECG d’un syndrome de Winter
Décrire les changements à l’ECG d’une occlusion de la coronaire D et d’un infarctus du VD
ST segment elevation inferiorly that is greater in lead III than in lead II, accompanied by ST segment depression in lead aVL, I, or both, is 90% sensitive and 71% specific for right coronary artery occlusion. ST segment elevation in lead V1 in the presence of an ST segment elevation inferior MI (with elevation greater in lead III than in lead II) suggests concomitant right ventricular infarction.
Décrire les changements à l’ECG lors d’un IAM postérieur
Isolated posterior wall acute myocardial infarction (PMI)—complexes from right precordial leads and posterior leads. The right precordial leads V1 and V2 reveal typical findings of PMI with prominent R wave (A), ST segment depression (STD; B), and upright T wave (C). The posterior leads V8 and V9 in the same case demonstrate ST segment elevation (STE) (arrows), confirming isolated PMI.
Nommer 5 caractéristiques à l’ECG de la repolarisation précoce
BER includes the following electrocardiographic characteristics: (1) ST segment elevation; (2) upward concavity of the initial portion of the ST segment; (3) notching of the terminal portion of the QRS complex at the J point (ie, junction of the QRS complex with the ST segment); (4) symmetric concordant T waves of large amplitude; (5) diffuse ST segment elevation on the ECG; and (6) relative temporal stability over the short term, although these changes may regress with advancing age. J point elevation is usually less than 3.5 mm, and the concave ST segment is usually elevated less than 2 mm in the precordial leads (although it may be elevated as much as 5 mm in some cases) and 0.5 mm in the limb leads. Maximal ST segment elevation in BER is typically seen in leads V2 to V5. Isolated BER in the limb leads is rare and should prompt reconsideration of STEMI
Nommer caractéristiques à l’ECG d’un anévrisme du VG
electrocardiographic changes of LVA tend to be regional rather than diffuse. Anatomically, LVA is usually found anteriorly, and changes are most often seen in leads V1 to V6 and leads I and aVL. ST segment elevation may be of any morphology (eg, convex or concave), and Q waves may be present (Fig. 68.14). The calculation of the ratio of the amplitude of the T wave to the QRS complex may help distinguish acute anterior MI from LVA. It has been shown that if the ratio of the amplitude of the T wave to the QRS complex exceeds 0.36 in any single lead, the ECG probably reflects STEMI. If the ratio is less than 0.36 in all leads, however, the findings are probably the result of a ventricular aneurysm.
3 critères de Scarbossa pour l’ischémie en BBG
(1) ST segment elevation of at least 1 mm that is concordant with the QRS complex (Fig. 68.16); (2) ST segment depression of at least 1 mm in lead V1, V2, or V3 (see Fig. 68.16A): and (3) ST segment elevation of at least 5 mm that is discordant with the QRS complex
Nommer des causes non cardiaques d’élévation des troponines
Troponin level elevations can also be seen in noncardiac conditions, including PE, sepsis, extreme physical exertion, renal insufficiency, and even essential hypertension
Nommer les 5 étapes de la pathophysiologie d’un SCA
ACS pathophysiology includes the following: (1) endothelial damage through plaque disruption, irregular luminal lesions, and shear injury; (2) platelet aggregation; (3) thrombus formation causing partial or total lumen occlusion; (4) coronary artery vasospasm; and (5) reperfusion injury caused by oxygen free radicals, calcium, and neutrophils
Nommer les délais recommandés en STEMI pour la fibrinolyse et la coro
AHA recommends that all patients with STEMI receive fibrinolytic therapy within 30 minutes of arrival or undergo primary PCI (ie, device across the culprit artery) no later than 90 minutes after arrival.
Quel est le mécanisme d’action de l’héparine non fractionnée?
UFH binds to antithrombin III, forming a complex that is able to inactivate factor II (thrombin) and activate factor X. This prevents the conversion of fibrinogen to fibrin, thus preventing clot formation.
dose: bolus 60u/kg puis 12u/kg/hr
Quel est le mécanisme d’action des héparines de bas poids moléculaire?
LMWHs inhibit the coagulation system in a fashion similar to that of UFH. Approximately one-third of the heparin molecules bind to antithrombin III and thrombin. The remaining molecules bind only to factor Xa.
Plus facile à administrer, meilleure biodisponibilité, plus longue demi-vie et réponse thérapeutique plus équivalente entre patients. Préférable en NSTEMI. Pour STEMI, utiliser UFH
Dans quelle situation clinique utilise-t-on le fondaparinux?
, this drug may be considered as a reasonable alternative to UFH in the care of NSTEMI patient receiving non-invasive management; however, the increased risk of catheter-associated thrombi during PCI prevents its use without additional UFH administration when an invasive strategy is chosen.
Quand doit-on thrombolyser un STEMI (délais)?
In the absence of contraindications, fibrinolytic therapy should be considered in patients with STEMI and the onset of ischemic symptoms within the previous 12 hours when it has been anticipated that primary PCI cannot be performed within 120 minutes of first medical contact
Définition à l’ECG d’un STEMI
These findings include diagnostic ST elevation in the absence of LVH or LBBB, including ST elevation at the J point in at least two contiguous leads more than 2 mm in men or more than 1.5 mm in women in leads V2and V3 and/or more than 1 mm in other contiguous chest or limb leads.4 Other electrocardiographic findings that should be considered for fibrinolytic therapy include the following: (1) ST elevation in aVR with coexistent multilead ST depression, concerning for proximal LAD or left main coronary artery occlusion; and (2) evidence of posterior transmural injury (posterior STEMI) indicated by ST segment depression in two or more precordial leads (V1–V4)
Quels sont les délais acceptables pour PCI vs thrombolyse selon le temps écoulé x début sx
- sx < 2 hr
< 2hr sx < 3hr
sx >3-12hr
If presentation is within 2 hours or less of symptom onset, consider immediate fibrinolysis unless transfer time for PCI is anticipated to be no more than 60 minutes (AHA class IIB recommendation).
•
If presentation is within 2 to 3 hours of symptom onset, consider immediate fibrinolysis or PCI if time to transfer time for PCI is anticipated to be no more than 60 to 120 minutes (AHA class IIB recommendation).
•
If presentation is within 3 to 12 hours of symptom onset, consider PCI as opposed to initial fibrinolysis if time to transfer time for PCI is anticipated to be no more than 120 minutes (AHA class IIB recommendation).
Décrire les mouvements ioniques sur la courbe de dépolarisation d’une cellule myocardiaque
Décrire la vascularisation du noeud sinusal et du noeud AV
décrire vascularisation de la branche D et G anté et G post
Noeud sinusal 55% CD, 45% circonflexe
Noeud AV 90% CD, 10 % circonflexe
Branche D + G anté = IVA
G post= CD ou circonflexe
Décrire les 3 mécanismes d’arythmies avec des exemples pour chacun
- Augmentation de l’automaticité: tachy atriale/jonctionnelle associée à la digitale, rythmes idioventriculaires associés à l’hyperK
- Triggered activity: earlyafterdepolarization = torsades de pointes, delayed afterdepolarization lors tachy surtout intox digitale ou post reperfusion myocardique
Nommer des agents de classe 1A-1B et 1C et nommer leur effet sur la dépolarisation/conduction et repolarisation/durée potentiel d’action
Class IA
Moderate slowing of depolarization and conduction; prolong repolarization and action potential duration.
Procainamide
Quinidine
Disopyramide
Class IB
Minimally slow depolarization and conduction; shorten repolarization and action potential duration.
Lidocaine
Phenytoin
Tocainide
Mexiletine
Class IC
Markedly slow depolarization and conduction; prolong repolarization and action potential duration.
Flecainide
Encainide
Lorcainide
Propafenone (shares properties with class IA agents)
Vernakalant (atrial-specific, investigational)
Nommer des agents de classe 3 et leur effet sur la repolarisation/durée potentiel d’Action
Antifibrillatory agents—prolong action potential duration and refractory period duration with antifibrillatory properties.
Bretylium (historical significance)
Amiodarone
Dofetilide
Ibutilidea
Sotalolb
Dronedarone
Azimilide
Comment administre-t-on la procainamide
In stable patients, the recommended administration is a rate of 20 to 30 mg/min until the dysrhythmia is terminated, hypotension occurs, or the QRS complex widens (to 50% of the pretreatment width), up to a total dose of 18 to 20 mg/kg
Habituellement, bolus sur 1 heure
Nommer le principal effet 2nd de la classe 1C
Effet proarythmogène
Nommer 10 effets secondaires de la cordarone et nommer 5 médicaments dont le niveau sérique est altéré par la cordarone
Acute Effects
Hypotension
Slowing of heart rate
Decreased contractility
Long-Term Effects
Common Effects
Corneal deposits
Photosensitivity
Gastrointestinal intolerance
Less Common Effects
Hyperthyroidism
Heart failure
Pulmonary toxicity, fibrosis
Hypothyroidism
Bradycardia
Prodysrhythmic effect
Drug Interactions
Increased Levels
Phenytoin
Procainamide
Warfarin
Digoxin
Flecainide
Nommer le mécanisme d’action de la digitale et 2 effets arythmogènes
Inhibe la pompe NaKATPase qui entraine une augmentation du Ca intracellulaire
Augmente l’automaticité et triggered activity
Nommer 10 effets secondaires de la digitale
Common Effects
Gastrointestinal intolerance (eg, nausea, vomiting, abdominal pain, diarrhea, anorexia)
Fatigue
Drowsiness
Visual color disturbances
Headache
Depression
Apathy
Less Common Effects
Psychosis
Cardiac symptoms
Heart block
Increased ectopy
Combined block and ectopy (multifocal atrial tachycardia with block or complete atrioventricular block with accelerated junctional rhythm, usually in overdose setting)
Ventricular tachycardia
Nommer 5 causes de brady sinusale pathologique
Sinus bradycardia occurs in a variety of pathologic conditions associated with vagal stimulation, ranging from autonomic-mediated syncope to hemoperitoneum or acute inferior wall myocardial infarction. Other pathologic causes of sinus bradycardia include hypothermia, hypoxia, drug effects (especially β-adrenergic blockers and calcium channel blockers), and intrinsic sinus node disease
Atropine 0.5mg IV q 3-5 min PRN max 3mg
Compléter le tableau des différentes caractéristiques entre le bloc AV 2e degré type 1 et type 2
Nommer 3 causes de QRS groupés
Wenckebach mechanism (usually at atrioventricular node, but can occur elsewhere)
Sinoatrial exit block
Atrial tachycardia or flutter with alternating conduction
Frequent extrasystoles
Nonconducted atrial trigemini
Concealed or interpolated extrasystoles
Commer différentier un Mobitz 1 de 2 lorsque la conduction est 2:1
When the conduction ratio is exactly 2 : 1, it is hard to distinguish type I from type II second-degree AV block on the surface ECG. In general, the presence of a prolonged PR interval makes type I block more likely, whereas the presence of wide QRS complexes makes type II block more likely.
Nommer 5 caractéristiques pouvant différentier un ESA d’un ESV
Nommer 10 causes d’ESV / TV
Comment pouvez-vous décrire le phénomène d’Ashman
The Ashman phenomenon refers to aberrant ventricular conduction of an early-arriving atrial impulse following a relatively long R-R interval, the result of a partially refractory His bundle. Such aberrantly conducted impulses are commonly seen in atrial fibrillation but can occur in any irregular rhythm in which long-short cycle sequences occur; they typically assume an RBBB pattern
Quel est le syndrome de Lown-Ganong-Levine?
The Lown-Ganong-Levine syndrome is an uncommon accessory pathway syndrome associated with paroxysmal narrow-complex tachycardia, short PR interval, and normal QRS complex without a delta wave. The treatment parallels that for the WPW syndrome
Nommer 10 causes de QT long
Nommer les indications de classe 1 de pacemaker et de pace défib
Classe 1 défib: arrêt, TV soutenue et pas, syncope
1.
Cardiac arrest resulting from VF or VT not caused by a transient or reversible event
2.
Spontaneous sustained VT
3.
Syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiologic study when drug therapy is ineffective, not tolerated, or not preferred
4.
Nonsustained VT with coronary artery disease, prior myocardial infarction, left ventricular dysfunction, and inducible VF or sustained VT at electrophysiologic study that is not suppressible by a class I antiarrhythmic drug
Avantages et désavantages des sondes unipolaires et bipolaires
Unipolaires: plus petites, moins de fracture, tendance à oversensing
Bipolaires: plus grosses, plus de fracture, moins de oversensing
Nommer les 3 grandes catégories de dysfonction de pacemaker et des examples pour chacun
Undersensing: post infarctus du VD ou 2nd fibrose dans contexte CMP
Nommer des causes d’exit block de pacemaker
ischémie, hyperkaliémie, antiarythmiques de classe 3
Nommer 3 causes d’augmentation inappropriée du nombre de choc d’un pace-défib
- Détection de TSVP comme une TV et choc 2nd
- Choc durant TV non soutenur
- Oversensing des ondes T avec interpération de tachy et choc
Nommer les indications de pace biventriculaire
Indications for biventricular pacing have expanded to include patients with New York Heart Association (NYHA) class II, III or IV heart failure, left ventricular dysfunction, and left bundle branch block, or patients with AV block and ventricular systolic dysfunction with NYHA class I, II, or III heart failure
3 principales causes d’insuffisance cardiaque
CMP ischémique, dilatée et maladies valvulaires
Nommer 12 causes de péricardite
Principaux néo qui donnent métastases au péricarde
poumon, seins, lymphome et leucémie
Traitement de la maladie de Chagas
Benznidazole et nifurtimox
Trichinose:
Pathogène impliqué:
présentation classique
Traitement
Trichinella spiralis
Myalgies, fièvres, DEG, oedème périorbitaire. 20% atteinte cardiaque avec IC/arythmies/blocs/anomalies ST-T
Mebendazole ou albendazole
Traitement de l’atteinte cardiaque secondaire à la diphterie
Carnitine PO
Facteurs de risque de CMP dilatée
Alcool, tabac, sexe masculin, hypertension, post myocardite, origine africaine, grossesse
Étiologies de CMP restrictive
Principale: amyloidose
Autres: sarcoidose, sclérodermie, maladie du collagène, hémochromatose, infiltration néoplasie, maladie de Fabry et Gaucher.
FR de CMP péripartum
Multiparité, grossesse gémellaire, âge avancé, obésité, cocaine, myocardite, tocolyse, prédisposition génétique
Décrire les trouvailles cliniques indiquant un mauvais pronostic de récupération après ROSC ( après délai 72 hrs)
- Absence de réflexe pupillaire à la lumière
- Absence de potentiels évoqués positifs
- Status myoclonique
- EEG en burst suppression ou status epilepticus
- Absence de réactivité aux stimulis à EEG
- perte importante différenciation cortico-sous corticale au TDM dans les 2hrs après l’arrêt
- Restriction importante à la diffusion à L’IRM 2 à 6 jours après l’événement
Décrire le HEART score et un bas risque
cf med calc
