Ischemia sdr Flashcards

Question

Risk factors for atherosclerosis

Answer 1

``` Modificable Dislipidemia ↑ LDL-Cholesterol, ↑ Total Cholesterol ↓ HDL-Cholesterol ↑ Triglicerides Hypertension Smoking Diabetes, insulin resistance and metabolic syndrome ``` ``` Not Modificable Male sex Advanced age Family history of premature atherosclerosis Obesity and decreased physical activity Poverty, Psychosocial factors ``` Non-traditional risk factors: Rheumatoid arthritis, Collagen vascular disorders ``` Other ↑ Inflammation(hs-CRP, fibrinogen,IL-6, ICAM), etc. ↑ Prothrombotic factors ↑ Homocisteine ↑ Lipoprotein (a) ```

Answer 2

Definition: a syndrome characterized by  severe ischemic pain that usually occurs at rest  associated with transient Ecg ST-segment elevation caused by focal spasm of an epicardial coronary artery with  Coronary spasm results in ischemia and abnormal LV function  may lead to acute MI, ventricular arrhytmias, and sudden cardiac death  more frequent in Japan than in North America or Western Europe Patients profile  young  smoker  fewer coronary risk factors than do patients with NSTE-ACS Cardiac examination  Usually unremarkable in the absence of ischemia  Few patients associate migraine and/or Raynaud’s phenomenon Angiography + Hyperventilation or intracoronary acetylcholine → rest angina with transient ST-segment elevation on Ecg during pain  Atherosclerotic plaques in at least one proximal coronary artery occur in about 1/2 of patients

Answer 3

1. Type: sudden 2. Occurrence: at rest (Nocturnal angina may be a manifestation of unstable angina ) 3. Duration : > 20 (30) minutes 4. Intensity: mild, moderate, severe- not specific 5. Relived by nitroglicerin- generally NOT 6. Location : anterior thoracic (substernal) or on radiation area 7. Radiated to mandible, left ear, shoulder, scapular, both arms, both wrists Rarely: left laterothoracic

Answer 4

History and Physical Examination CHEST DISCOMFORT is typically severe and has at least 1 of 3 features:  Occurrence at rest (or with minimal exertion)  Lasting >10 min  relatively recent onset (i.e., within the prior 2 weeks) and/or  a crescendo pattern (distinctly more severe, prolonged, or frequent than previous episodes) NSTEMI → any of these features (without Ecg ST segment elevations) + evidence of myocardial necrosis=abnormally elevated levels of biomarkers  Located in the substernal region  Radiates to the left arm, left shoulder, and/or superiorly to the neck and jaw Anginal equivalents: dyspnea, epigastric discomfort, nausea, or weakness may occur instead of chest discomfort→ more frequent in: women, elderly, diabetes Physical examination  resembles that in patients with stable angina and may be unremarkable  large NSTEMI→ diaphoresis; pale, cool skin; sinus tachycardia; S3 and/S4; basilar rales; sometimes, hypotension.

Answer 5

Imbalance between myocardial oxygen supply and demand Thrombus formation: 4 processes that lead to that (1) disruption of an unstable coronary plaque due to:  Plaque rupture  Erosion  a calcified protruding nodule that leads to intracoronary thrombus formation (2) Coronary arterial vasoconstriction (3) Gradual intraluminal narrowing (4) Increased myocardial oxygen demand produced by conditions such as  Fever  Tachycardia  Thyrotoxicosis in the presence of fixed epicardial coronary obstruction

Answer 6

1. Chest pain 2. Clinical examination 3. 3 noninvasive tools  ECG  cardiac biomarkers  stress testing  coronary computed tomographic angiography CCTA may improve the accuracy Goals (1) Recognize or exclude myocardial infarction (MI) [ ↑cTn (cardiac troponin)=MI] (2) Detect rest ischemia (using serial or continuous ECGs) (3) Detect coronary obstruction at rest with CCTA and/ or myocardial ischemia using stress testing

Answer 7

UA is usually secondary to abrupt reduction in myocardial perfusion as a result of nonocclusive coronary thrombosis in which the nonocclusive thrombus that developed on a disrupted atherosclerotic plaque does not result in biochemical evidence of myocardial necrosis UA must be diagnosed from the clinical history (based on anamnesis) and negative biomarker 3 principal presentations of UA: (1) rest angina or angina with minimal exertion usually lasting at least 20 minutes (2) new-onset severe angina (Canadian Cardiovascular Society grade III or higher; Table 36–1) (3) crescendo angina, defined as previously diagnosed angina that has become distinctly more frequent, precipitated by less severe degrees of exertion, or more severe

Answer 8

Definition: Angiographic, intravascular ultrasound (IVUS), and angioscopic studies indicate that acute NSTEMI usually results from the disruption of an atherosclerotic plaque with a subsequent platelet-rich thrombus that obstructs microvascular blood flow and may transiently or partially obstruct epicardial blood flow. Diagnosis is based on cardiac chest pain from myocardial ischemia + the presence of abnormal concentrations of biomarkers indicative of myocardial necrosis, either the troponins (which are structural proteins) or creatine kinase- MB (which is a cardiac enzyme) The clearest separation between this end of the spectrum and ST-segment elevation myocardial infarction (STEMI) is made by the electrocardiogram (ECG).

Answer 9

* ~1/2 of AMI-related deaths occur before the patient reaches the hospital * ECG is a pivotal diagnostic and triage tool PATHOPHYSIOLOGY: ROLE OF ACUTE PLAQUE RUPTURE  occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis  Vulnerable plaques prone to disruptionare have a rich lipid core and a thin fibrous cap  Evolving precesses: platelet deposition and activation→conformational change in the glycoprotein IIb/IIIa receptor → high affinity for soluble adhesive proteins → activate fibrinogen& coagulation cascade → culprit coronary artery is occluded by a thrombus containing platelet aggregates and fibrin strands ``` Rare etiology  coronary emboli  congenital abnormalities  coronary spasm  inflammatory—diseases ```

Answer 10

The term acute myocardial infarction should be used when - there is acute myocardial injury with clinical evidence of acute myocardial ischaemia and - with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following:  Symptoms of myocardial ischaemia  ECG changes indicative of new ischemia (new ST/T-wave changes or new left bundle branch block [LBBB])  Development of new pathological Q waves  Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology  Identification of a coronary thrombus by Angiography or Autopsy (not for types 2 or 3 M )

Answer 11

Type I: Spontaneous Myocardial Infarction related to complicated atherosclerosis with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/ or demand Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable: Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic electrocardiogram (ECG) changes or new left bundle branch block (LBBB), but death occurring before blood samples Type 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention (PCI) Type 4b: Myocardial Infarction Related to Stent Thrombosis Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting (CABG)

Answer 12

 History  Prodromal Symptoms = Chest discomfort resembling classic angina pectoris, but it occurs at rest or with less activity than usual. A feeling of general malaise or frank exhaustion frequently accompanies other symptoms preceding STEMI  Predisposing Factors are present in 1/ 3- 1/2 of cases (vigorous physical exercise, emotional stress, or a medical or surgical illness)  Circadian periodicity especially in the morning within a few hours of awakening CHEST PAIN  deep and visceral (heavy, squeezing, and crushing; occasionally, it is described as stabbing or burning )  similar in character to the discomfort of angina pectoris but  commonly occurs at rest  is usually more severe  lasts longer  Location:  central portion of the chest and/or the epigastrium, and,  The frequent location of the pain beneath the xiphoid and epigastrium →mistaken impression of indigestion  Radiates  to the arms (on occasion)  Less common sites of radiation include the abdomen, back, lower jaw, and neck  The pain of STEMI may radiate as high as the occipital area but not below the umbilicus

Answer 13

CHEST PAIN  Onset  at rest ussually  when it begins during a period of exertion, it does not usually subside with cessation of activity  painless STEMIs: patients with diabetes mellitus; elderly ``` Accompaniing factors:  Anxiety  Sweating(diaphoresis)  Weakness  Nausea, Vomiting  a sense of impending doom  The respiratory rate may rise slightly soon after the development of STEMI; in patients without heart failure (HF) because of anxiety ``` Other presentation symptoms: sudden-onset dyspnea → may progress to pulmonary edema sudden loss of consciousness, a confusional state, a sense of profound weakness the appearance of an arrhythmia evidence of peripheral embolism an unexplained drop in arterial pressure

Answer 14

 Anxiety and restless  Altering their position  Moving about in bed  Stretching  Pallor + perspiration and coolness of extremities  The combination of substernal chest pain persisting for >30 min and diaphoresis strongly suggests STEMI  Vegetative manifestations of - sympathetic nervous system: hyperactivity (tachycardia and/or hypertension) → common with anterior infarct - parasympathetic hyperactivity (bradycardia and/or hypotension) → common with inferior infarction show evidence of  Apical impulse may be difficult to palpate  An abnormal systolic pulsation caused by dyskinetic bulging of infracted myocardium→ with anterior wall infarction (may develop in the periapical area within the first days of the illness and then may resolve

Answer 15

 Physical signs of ventricular dysfunction include - fourth and third heart sounds S3/ S4 - decreased intensity of the first heart sound ↓ S1 - paradoxical splitting of the second heart sound  Midsystolic or late systolic apical systolic murmur (transient ) due to dysfunction of the mitral valve apparatus may be present  Pericardial friction rub may be heard in patients with transmural STEMI  The carotid pulse: - often decreased in volume, reflecting reduced stroke volume  Temperature - elevations up to 38°C )may be observed during the first week after STEMI)  The arterial pressure is variable  SBP (systolic blood pressure) declines by ~10–15 mmHg in most patients with transmural infarction

Answer 16

STEMI temporal stages: (1) Acute (first few hours–7 days) (2) Healing (7–28 days) (3) Healed (≥29 days) The laboratory tests (1) ECG (2) Serum cardiac biomarkers (3) Cardiac imaging (4) Nonspecific indices of tissue necrosis and inflammation

Answer 17

Early Acute Phase → begins within minutes, persists, and evolves during hours T waves  increase in amplitude and widen over the area of injury (hyperacute pattern) ST segments  evolve from concave to straightened to convex upward patterns (acute pattern)  When prominent, the acute injury pattern of blended ST-T waves can take on a tombstone appearance  ST segment depressions that occur in leads opposite those with ST segment elevation are reciprocal changes

Answer 18

Evolved Acute Phase  ST segment elevation begins to regress  T waves in leads with ST segment elevation become inverted  pathologic Q or QS waves become fully developed (>0.03-second duration or depth >30% of R wave amplitude, or both) Chronic Phase  Resolution of ST segment elevation  Variable  usually complete within 2 weeks of inferior MI, but it can be delayed further after anterior MI  Persistent ST segment elevation may freeze with a large anterior MI  Symmetrical T wave inversions can resolve during weeks to months or can persist for an indefinite period  Q waves usually do not resolve after anterior MI but often disappear after inferior wall MI Early reperfusion therapy accelerates the time course of ECG changes  ST segments recede rapidly  T wave inversions and loss of R waves occur earlier  Q waves may not develop or progress and occasionally may regress

Answer 19

 Cardiac-derived troponin-I (cTnI) and troponin-T (cTnT) are proteins specific to sarcomeres  Serial measurement = the preferred approach for differentiating acute MI from unstable angina  Surrogate biomarkers: CK-MB, AST

Answer 20

 Abnormalities of wall motion  left ventricular (LV) function for prognosis evaluation  the presence of right ventricular (RV) infarction  ventricular aneurysm  pericardial effusion  LV thrombus  detection and quantitation of complications (ventricular septal defect & mitral regurgitation)

Answer 21

1.Myocardial perfusion imaging with [201Tl] or [99mTc]- sestamibi  → reveals a defect (“cold spot”) during the first few hours after STEMI 2.Radionuclide ventriculography [99mTc]-labeled red blood cells  demonstrates wall motion disorders and reduction in the ejection fraction 3.High-resolution cardiac MRI using late enhancement

Answer 22

``` slide 25 Rapid reperfusion therapy When CHEST PAIN + Characteristic ST elevation Or new LBBB 1. PRIMARY ANGIOPLASTY preferred 2. Fibrinolytic therapy ```