SCA Flashcards
The Canadian Cardiovascular Society (CCS) classification for angina is defined as follows:
Classe 1 à 4
Class I—no angina with ordinary physical activity
Class II—minimal limitation of normal activity as angina occurs with exertion or emotional stress
Class III—severe limitation of ordinary physical activity as angina occurs with exertion under normal physical conditions
Class IV—inability to perform any physical activity without discomfort as anginal symptoms occur at rest or with minimal physical exertion
Définir angine de repos
Rest angina is defined as angina occurring at rest, lasting longer than 20 minutes, and occurring within 1 week of presentation.
Définir new onset angina
New-onset angina is angina of at least CCS classification class II severity, with onset within the previous 2 months.
Définir angine crescendo
Increasing or progressive angina is diagnosed when a previously known angina becomes more frequent, longer in duration, or increased by one class within the previous 2 months of at least class III severity.
Décrire la pathophysiologie de Angine instable et les caractéristique à l’ECG
1) Plaque rupture accompanied by 2) thrombus formation and 3) vasospasm illustrate the intracoronary events angine instable.
Anomalies à l’ECG:
including T wave and ST segment changes.
Décrire la physiopatho, les modes de soulagement et les changements à l’ECG de l’angine de prinzmetal
Caused by coronary artery vasospasm at rest with minimal fixed coronary artery lesions
Soulagée par exercise or NTG.
The ECG reveals ST segment elevation that is impossible to discern from STEMI clinically and electrocardiographically.
Considering the myriad clinical situations in which AMI is encountered, the five primary types of infarction are described by the following classification:
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
The actual definition, referred to as the universal definition of myocardial infarction, includes the following; either one of these criteria satisfies the diagnosis for an acute, evolving, or recent MI:
1.Typical rise and gradual fall or more rapid rise and fall of biochemical markers of myocardial necrosis, avec au moins 1 valeur > 99e percentile et au moins une des présentations cliniques suivantes:
- 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
Nommer 4 déterminants de la consommation en O2 du myocarde:
Myocardial oxygen consumption is determined:
Fréquence cardiaque
Post-charge
Contractilité
Étirement des fibres musculaire (wall tension)
À quel pourcentage une sténose coronarienne devient symptômatique:
Au repos
À l’effort
the reduction of coronary blood flow does not cause ischemic symptoms:
at rest until the vessel stenosis exceeds 95% obstruction to flow.
with exercise and increased myocardial oxygen consumption with as little as 60% vessel stenosis.
Nommer 3 most important factors in the infarction
Angiographic studies have demonstrated that the preceding coronary plaque lesion is often less than 50% stenotic, indicating that the most important factors in the infarction are the acute events of plaque rupture, platelet activation, and thrombus formation rather than the severity of the underlying coronary artery stenosis.
After significant coronary vessel occlusion, local mediators and vasoactive substances are released, inducing ….?
Vasospasme
Another important aspect of ACS is vasospasm. After significant coronary vessel occlusion, local mediators and vasoactive substances are released, inducing vasospasm, which further compromises blood flow. Central and sympathetic nervous system input increases within minutes of the occlusion, resulting in vasomotor hyperreactivity and coronary vasospasm. Sympathetic stimulation by endogenous hormones, such as epinephrine and serotonin, may also result in increased platelet aggregation and neutrophil-mediated vasoconstriction.
A prehospital 12-lead ECG offers high specificity ??? and positive predictive value ??? for STEMI in patients with atraumatic chest pain
Specificity (99%)
positive predictive value (93%)
for STEMI in patients with atraumatic chest pain while increasing the paramedic scene time by an average of only 3 minutes.
Nommer 4 avantages de faire ECG en pré-hosp pour dépister les STEMI
(1) earlier detection of STEMI;
(2) ability to base the destination on the availability of PCI;
(3) hospital-based preparation for patient arrival;
(4) more rapid initiation of hospital-based reperfusion therapy, either fibrinolysis or PCI.
ACS is significantly more likely if four of the five major risk factors. Nommer les 5 FR
ACS is significantly more likely if four of the five major risk factors—diabetes mellitus, smoking, hypertension, hyperlipidemia, and family history of AMI at an early age (usually <50 years)
There are several nontraditional risk factors for coronary disease (maladies chroniques) that should be considered in the appropriate patient.
Nommer en 4
Antiphospholipid syndrome
rheumatoid arthritis
human immunodeficiency virus (HIV)
particularly systemic lupus erythematosus (SLE) are associated with a higher risk of cardiovascular disease.
Women with SLE who are 35 to 44 years of age are more than 50 times more likely to have an MI than a similar age- and gender-matched Framingham population.
The Thrombolysis in Myocardial Infarction (TIMI) Score is used to determine the likelihood of ischemic events or mortality in patients with unstable angina or non–ST-segment elevation myocardial infarction (NSTEMI).
Nommer les 7 critères
Each of the following criteria constitutes one point for TIMI scoring (see Table 1):
1) Age ≥65 years
2) 3 ou plus: risk factors for coronary artery disease (CAD) (family history of CAD, hypertension, hypercholesterolemia, diabetes mellitus, tobacco use)
3) Known CAD (stenosis >50%)
4) Aspirin use in the past 7 days
5) Severe angina (≥2 episodes in 24 hours)
6) ST deviation ≥0.5 mm
7) Elevated cardiac marker level
Signification: TIMI Score
Risk of Death/MI/Urgent Revascularization by Day 14
Score 0-1 Risque 5%
score 2: 8%
Score 3: 13%
Score 4: 20%
score 5: 26%
Score 6-7: 41%
TABLE68.1 Clinical Characteristics of Classic Anginal Chest Discomfort
Voir tableau 68,1
Recognition that coronary ischemia may arise with an anginal equivalent rather than a classic symptom is the key to understanding the atypical presentation of ACS.
Nommer le symptôme d’équivalent angineux le PLUS fréquent et 3 moins fréquents
Dyspnea is the most common angina equivalent symptom presentation.
Isolated diaphoresis, nausea, and emesis are very uncommon sole presenting symptoms in ACS; weakness, dizziness, excessive fatigue, and anxiety likely do not occur as the single presenting complaint, or manifestation, in the ACS patient except, perhaps in the extreme older patient population.
Nommer 15 DDX de Infarctus
Acute myocardial infarction Stable angina Unstable angina Prinzmetal’s angina Myocardial or pulmonary contusion Pericarditis
Pneumonia Pulmonary embolism Pulmonary hypertension Pneumothorax Pleurisy
Boerhaave’s syndrome Gastroesophageal reflux Gastritis or esophagitis Mallory-Weiss syndrome Peptic ulcer disease Esophageal spasm Cholecystitis or biliary colic Pancreatitis
Aortic dissection
Herpes zoster
Musculoskeletal pain
Nommer 3 caractéristiques de DRS qui en font une DRS à très faible risque de SCA:
Indice 3 P
Pleuritic
Positional
Palpation reproducible by palpation
Nommer des complications aigues du STEMI (11 réponses)
1) Bradydysrhythmia and atrioventricular (AV) conduction block occur in 25% to 30% of patients with AMI; sinus bradycardia is usually seen.
2) Tachydysrhythmias
- atrial (TS ou FA) or ventricular ( Vtachycardia and fibrillation V)
3) Cardiogenic shock
4) Left ventricular free wall rupture
Clinically, free wall rupture may occur with sudden death, pulseless electrical activity, or precipitous deterioration in the presence of STEMI. Signs of pericardial effusion on the ECG or echocardiogram are suggestive of the diagnosis in the setting of an acute or recent MI.
5) Rupture of the interventricular septum
6) Pericarditis, when associated with AMI
Early (infarct-related pericarditis) or in a delayed (post-MI or Dressler’s syndrome)
Infarct-related pericarditis is associated with transmural insult and thus principally involves the pinnacle of the infarct zone near the epicardium.
Embolic complications are more common in patients with infarct pericarditis; linked to this is the higher rate of ventricular aneurysm development in this population.
7)Dressler’s syndrome
8) Stroke ischemic or thromboembolic.
+ Fréquent: Embolization from a left ventricular mural thrombus with decreased ejection fraction, embolization from the left atrial appendage with atrial fibrillation, and hypercoagulability with concomitant carotid arterial disease.
It is known that the rate of stroke is higher in the setting of MI (0.9%, tapering to 0.1% at day 28 after MI) than in similar non-AMI patients (0.014%).
9) Hemorrhagic stroke
-patient undergoing fibrinolytic therapy.
The rate of hemorrhagic stroke with varying fibrinolytic agents is less than 1%; the rate is marginally higher in older patients.
PCI lowers the overall risk of stroke compared with fibrinolytic therapy.
The difference in stroke rate is highly significant (1.6% in the fibrinolytic group vs. 0.7% in the PCI group). Hemorrhagic strokes: that the difference is again dramatic (1.0% in the fibrinolytic group vs. 0.1% in the PCI group).
10) Hemorrhage associated with medications resulting from invasive procedures. The various antiplatelet, anticoagulant, and fibrinolytic therapies are all associated with hemorrhage as a major complicating issue. Within a single class of medications, many of these agents are so similar in efficacy that superiority is determined by the rate of occurrence of adverse effects; this trend in an adverse reaction profile with anticoagulant-antiplatelet medication is most important to understand for agent selection.
11) PCI arterial injury
- the most typical is a pseudoaneurysm of the femoral artery with hemorrhage into the thigh compartment or retroperitoneal area
Cardiogenic shock post MI is defined as hypotension with end-organ hypoperfusion resulting from decreased cardiac output unresponsive to restoration of adequate preload.
Nommer des conditions qui rendent plus à risque de choc cardiogénique post MI
large infarctions prior MI low ejection fraction on presentation (<35%) older age diabetes mellitus.
Nommer 3 traitements qui améliorent la mortalité en choc cardiogénique post MI.
Nommer 1 traitement de l’infarctus aigu qui n’améliore pas la mortalité en choc cardiogénique
1) Vasopressor and inotropic support
2) intraaortic balloon counterpulsation
3) early revascularization
ATTENTION: fibrinolytic therapy does not decrease mortality in cardiogenic shock.
Rupture of the interventricular septum post MI
Décrire
1) La présentation clinique
2) L’examen diagnostic de choix
3) Le traitement
- New, harsh, loud holosystolic murmur heard best at the left lower sternal border
- Diagnosis by echocardiography with color flow Doppler imaging
- Presentation of acute catastrophic deterioration with a new, harsh systolic murmur should prompt immediate cardiac surgery consultation for repair of a septal defect or ruptured papillary muscle of the mitral valve. –Medical therapy: vasopressor and inotropic AND intraaortic balloon counterpulsation, is an important bridge to the definitive surgical treatments
Actions à poser en cas d’hémorragie post traitement médicamenteux du SCA:
-Héparine: Protamine
(The low-molecular-weight heparins (LMWHs) cannot be reversed.)
- Anticoagulant and antiplatelet: Fresh-frozen plasma (FFP) and platelet infusions
- Fibrinolytic agents also cannot be reversed; rather, therapy including FFP and packed red blood cell transfusions is most appropriate.
These various antidotal agents should be considered only with life-threatening hemorrhage.
TABLE68.3 Differential Diagnosis of Electrocardiographic ST Segment Elevation in the Adult Chest Pain Patient
Acute myocardial infarction Acute pericarditis Left ventricular hypertrophy Left ventricular aneurysm Ventricular paced rhythm Benign early repolarization Osborn wave of hypothermia Hyperkalemia Brugada’s syndrome Pulmonary embolism Acute cerebral hemorrhage Prinzmetal’s angina Postelectrical cardioversion Normal variant
The differential diagnosis of ST segment depression includes? (14 réponses)
myocardial ischemia or infarction repolarization abnormality of left ventricular hypertrophy (the so-called strain pattern) bundle branch block¸ ventricular paced rhythm (VPR) digoxin effect hyperkalemia hypokalemia PE intracranial hemorrhage myocarditis rate-related ST segment depression postcardioversion of tachydysrhythmias pneumothorax
The differential diagnosis of the tall T wave includes
hyperacute T waves of STEMI hyperkalemia benign early repolarization (BER) LVH LBBB acute pericarditis
Que signifie des deeply inverted or biphasic T waves in V2-3?
Wellens syndrome
Highly specific for a critical stenosis of the IVA
(left anterior descending artery (LAD).)
Nommer la localisation et le type de modification qui apparaissent pour le STEMI suivant:
Anterior wall STEMI
Lateral wall STEMI
Inferior wall STEMI
Right ventricular wall AMI
Posterior wall AMI
Anterior wall STEMI
-V1 - V4 Elevation
Lateral wall STEMI
-I, aVL, V5, V6 Elevation
Inferior wall STEMI
-II, III, aVF Elevation
Right ventricular wall AMI
-V4R Elevation
Posterior wall AMI
- V8, V9 Elevation et V1 - V3 Depression
Décrire la pathophysio du SCA en 5 étapes
1) Dommage endothéliale 2e bris de la plaque
2) Aggregation plaquettaire
3) Formation thrombus
4) Vasospasme coronarien
5) Dommage (injury) de reperfusion (cause: oxygène, calcium et neutrophile)
