ngina Flashcards

1
Q

angina and heart attacks

A
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2
Q

typical angina pain?

A
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3
Q

unstable angina pain?

A

diaphoratic

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4
Q

coronary stenosis, cause of angina?

A

Coronary stenosis as a cause of angina. It is now recognized that coronary artery obstructions are capable of changing caliber, and constriction or narrowing of a preexisting lesion can be a factor in precipitating angina and myocardial ischemia.If the coronary segment has sufficient smooth muscle (media) that is not involved in the atherosclerotic process, the vessel can dilate or constrict at the site of the stenosis. In general, vasoconstriction is most likely to occur with eccentric or asymmetric lesions, which consist of coronary atherosclerotic plaque in a segment of the vessel wall, with some relatively normal media intact. Concentric stenoses are less likely to constrict further or dilate. In concentric atherosclerosis, the atherosclerotic plaque circumferentially involves the entire area of the vessel. It is believed that at least 25% of an arc or rim of media in the coronary artery must be preserved to allow for stenosis vasomotion.This figure shows how the caliber of eccentric coronary artery stenoses may change, with considerable variation in the degree of stenosis resistance and the propensity to produce angina. Both increased vascular tone (first two examples) and decreased vascular tone (third example) are depicted. This phenomenon has been called dynamic coronary obstruction by some, emphasizing the variability and transitory nature of the actual “obstruction.” (Adapted from Epstein and Talbot [26].)

References:

[26]. Epstein S, Talbot T, Dynamic coronary tone in precipitation, exacerbation and relief of angina pectoris. Am J Cardiol 1981 48 797-803

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5
Q

conditions associated with angina?

A
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6
Q

angina investigations?

A

NB ECG Often normalBloodsCholesterol and GlucoseHbRenal Function

Exercise ECG NB: Useful for Risk stratification Poor as Diagnostic tool

Many causes of ST change on ETTAbnormal resting ECG eg BBBDrugs eg DigoxinLV hypertrophyWPW etc etc

Many causes of ST change on ETTUse other marker of ischaemia eg perfusion defect or change in LV function ( eg new WMA)Radio-isotopes or EchoSome patients unable to exerciseUse pharmacological stresseg Dobutamine

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7
Q

typical exercise ECg patterns at rest and at peak exertion?

A

Typical exercise electrocardiographic (ECG) patterns at rest and at peak exertion. The computer-processed incrementally averaged beat corresponds with the raw data taken at the same time during exercise. The patterns represent a gradient of worsening ECG response to myocardial ischemia. In the column of computer-averaged beats, ST-80 displacement (top number) indicates the magnitude of ST-segment displacement 80 ms after the J-point relative to the PQ junction or E point. ST-segment slope measurement (bottom number) indicates the ST-segment slope at a fixed time after the J-point to the ST-80 measurement. At least three noncomputer averaged complexes with a stable baseline should meet criteria for abnormality before the exercise ECG can be considered abnormal.The first two tracings illustrate normal and rapid upsloping ST segments; both are normal responses to exercise. Minor ST depression can occur occasionally at submaximal workloads in patients with coronary disease; in the illustration, the ST segment is depressed 0.9 mm (0.09 mV) 80 ms after the J-point. A slow upsloping ST-segment pattern often demonstrates an ischemic response in patients with known coronary disease or those with a high clinical risk before testing. Criteria for slow upsloping ST-segment depression include J-point and ST-80 depression of 1.5 mV/s or greater and an ST segment slope of 0.7 to 1.0 mV/s or greater.Classic criteria for myocardial ischemia include horizontal ST-segment depression observed when J-point and ST-80 depression are 0.1 mV or greater and the ST-segment slope is within the range of ± 0.7 to 1.0 mV/s. Downsloping ST-segment depression occurs when J-point and ST-80 depression are 0.1 mV or greater and ST-segment slope is -0.7 to -1.0 mV/s or greater. ST-segment elevation in a non-Q-wave non-infarct territory lead occurs when J-point and ST-60 are 1.0 mV or greater and represents a severe ischemic response. ST-segment elevation in an infarct territory (Q-wave lead) indicates a severe wall motion abnormality and is usually not an ischemic response. (Courtesy of Bernard R. Chaitman.)

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8
Q

stress radionuclide imaging?

A

Principle of stress radionuclide imaging for the detection of coronary artery disease. Shown are 1) a normal coronary artery and an artery with significant stenosis (top), 2) the myocardial territory (perfusion image), and 3) the ventricular wall (wall motion image) supplied by each artery. The graph (bottom) depicts coronary blood flow both at rest and during stress. At rest, coronary blood flow is similar in the normal artery and in the artery with stenosis. Resting coronary blood flow in the diseased artery is maintained at a normal level and is sufficient to meet resting metabolic myocardial demands because of recruitment of coronary reserve (dilatation of the resistance vasculature) in the distal coronary bed. If the patient does not have angina pectoris, coronary myocardial perfusion is homogeneous and global and regional left ventricular function is normal.During exercise, myocardial metabolic demands increase and more myocardial nutrient blood flow is required. Coronary reserve is increased as a result of dilatation of the coronary resistance vessels in the peripheral coronary bed. In the territory of the normal coronary artery, the resistance vessels dilate and coronary blood flow is increased by 2 to 2.5 times. In the abnormal coronary bed, which is distal to the significant coronary stenosis, resistance vessels are already dilated and little if any further dilatation is possible. Increased metabolic demands thus cannot be met, and the relatively hypoperfused myocardium becomes ischemic.The distribution of regional myocardial blood flow in the myocardium is heterogeneous, ie, there is less blood flowing in the ischemic myocardial bed (blue area) than in the normal myocardial bed. This heterogeneity of myocardial perfusion can be visualized noninvasively using radionuclide imaging with Tl-201 or a Tc-99m perfusion agent like sestamibi. When exercise-induced ischemia is severe enough, regional and global left ventricular dysfunction occurs. This can be assessed noninvasively using radionuclide ventriculography by either first-pass radionuclide angiocardiography or equilibrium radionuclide angiocardiography. (Courtesy of Frans J. Th. Wackers.)

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9
Q

normal first pas radionuclide angiography at rest and during exercise

A

Normal first-pass radionuclide angiography at rest and during exercise. In this illustration the left ventricular end-diastolic (ED) outline (white) in the anterior position is superimposed on the end-systolic (ES) image. This display allows assessment of regional wall motion from a static image; such images are best interpreted by dynamic display as an endless loop cine on a computer screen. Here, maximum count activity is yellow and the lowest activity is green. Resting left ventricular ejection fraction (LVEF) in this patient is 60% (A), and peak exercise LVEF is 80% (B). Regional wall motion shows uniformly increased contraction. In order to meet the increased demand during exercise, cardiac output must increase; this is achieved by increasing heart rate and LVEF (LVEF = ED volume - ES volume/ED volume). A normal LVEF response is defined as an increase in LVEF of 5% or greater compared with baseline LVEF and a uniform increase of regional wall motion. (Courtesy of Frans J. Th. Wackers.)

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10
Q

norma right coronary artery anatomy?

A

Normal right coronary anatomy. Shown are left (A) and right (B) anterior oblique views in a patient whose anatomy demonstrates typical right coronary artery distribution. The artery reaches the crux and gives rise to the posterior descending and atrioventricular node branches. A few small posterolateral branches to the left ventricular posterior wall are present.

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11
Q

modified seldinger technique?

A
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12
Q

commonly used catheters?

A
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13
Q

techniques for catheterization?

A

Techniques for catheterization of the left and right coronary arteries using preformed Judkins catheters in a left anterior oblique projection. A, Catheterization of the left coronary artery is performed by advancing the catheter into the ascending aorta while the curves of the catheter are kept in the profile shown. The catheter is advanced until the tip sits in the coronary ostium. B, Engagement of the right coronary artery is somewhat more complex. The catheter is first advanced to the level of the aortic valve with the tip pointed away from the right coronary ostium. The catheter is turned 180° in a clockwise direction as the tip is lifted slightly above the aortic valve. Arterial pressure is monitored continuously from the tip of the coronary catheter. Immediately after engagement (or suspected engagement) of either artery, pressure is checked to be certain that no damping or ventricularization of the pressure has occurred.

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14
Q

coronary angiography indicitation?

A
  1. Limiting angina despite full medical treatment
  2. Unstable Angina
  3. Other ‘high risk patterns of Angina
    - Post MI
    - ETT positive at low work load
  4. Patients undergoing other cardiac op
  5. Diagnostic ( eg equivocal non- invasive tests )
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15
Q

ventriulography?

A

Ventriculo-graphy is performed by injection of a contrast agent into the left ventricle; the injection and subsequent clearance of contrast over several cardiac cycles are filmed. Ventricular volume can be calculated, and normal and abnormal patterns of ventricular contraction can be identified by comparing end-diastolic (A) and end-systolic (B) images. The images shown are from a patient with normal ventricular function.

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16
Q

extent of coronary disease in determining prognosis?

A

The extent of coronary disease is an important determinant of prognosis for patients with coronary disease. The relationship between annual mortality and the extent of coronary artery disease in patients with angina pectoris is depicted. Both the number of diseased vessels and the presence of left ventricular (LV) dysfunction have an important influence on risk of death. The greatest risk is in patients with left main coronary artery disease (LMCD) and abnormal LV function. In contrast, patients with one-vessel disease and normal ventricular function have a very low risk of death (1.5%). (Adapted from Silverman and Grossman [23]; with permission.)

References:

[23]. Grossman W, Angina pectoris: natural history and strategies for evaluation and management. N Engl J Med 1984 310 1712-1717

17
Q

angina treatment?

A

Beta blockers + + +
Ca Antagonists
Diltiazem/Verapamil + +
Dihydropyridine
long acting + +
short acting -
Nitrates +
Nicorandil +

Newer anti-anginals eg Ivabradine Role not fully established

If ‘Limiting Angina despite full medical therapy consider revasc’
CABG + + +
Angioplasty + + +

Statins ++
Aspirin +
Clopidogrel +/-
Anticoagulants +/-
ACE-I +

CABG if severe CAD ie 3 VD, LMS, 2VD including LAD

PCI does not improve prognosis in stable angina

18
Q

saryof treatment?

A

Aggressive Risk Factor Management incl Statin
Life-style modification eg smoking cessation
Aspirin

Anti-anginal Medication
Beta blocker + Calcium Antagonist (di-hydropyridine) +GTN
Rate limiting Ca Antagonist if BB C/I
?Nicorandil, ?Ivabradine, ?Long acting Nitrates

Revasc (CABG or PCI)
“If ‘limiting’ Angina despite full medical treatment

Anti-ischemic mechanisms of medical therapy in stable angina. It is traditionally believed that all classes of drugs act predominantly through lowering myocardial oxygen consumption, thereby lessening cardiac energy demands. The ß-blockers are the most potent in this regard. The nitrates and calcium antagonists increase coronary blood flow and thus are used in the presence of coronary artery vasoconstriction. Coronary atherosclerotic stenosis constriction is believed to be an important cause of angina in some patients. Data regarding drugs other than the nitrates in preventing or reversing stenosis constriction are limited. The nitrates are the favored drugs for patients with angina and left ventricular dysfunction or congestive heart failure. The a-blockers and calcium antagonists are ideal for angina occurring in the presence of hypertension. (Courtesy of Jonathan Abrams.)

19
Q
A