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Flashcards in deck_862009 Deck (62):
1

Describe the structure of atheromas in stable angina?

Atheromatous plaques with a necrotic centre and fibrous cap

2

What is the effect of atheroma in IHD?

Occlude more and more of the lumen as they build up in coronary vessels. This leaves less space for passage of blood and ischaemia in myocardium

3

At what point does an atheromatous plaque cause angina?

When it occludes more than 70% of the lumen

4

What occurs in stable angina?

Brief episode of ischaemia pain brought on by stress.Predictable pain, relieved by rest or nitrates within five minutes. Presence of risk factors

5

What is brief chest pain in ischaemic heart disease typically caused by? How is it described?

brought on by exertion, emotion particularly after meals and in cold weather. It is described as mild to moderate pain.

6

What is the treatment of acute episodes of anginapreventative episodes of angina

Preventative - B blockers, Ca2+ channel blockers, oral nitratesPrevent cardiac events- Aspirin, statins, ACE inhibitors Long term - consider revascularisation

7

In basic terms, what is the use of Nitrates Ca2+ blockerACE inhibitors Beta blockers In stable angina

Nitrates - decreased preload, venodilation Ca2+ blocker - decreased after load, peripheral vasodilationACE inhibitors - reduced after loadBeta blockers - Reduced HR and contractility

8

How does unstable angina form?

Develops from stable angina, due to increased occlusion of lumen

9

Define unstable angina

Ischaemic Chest Pain that occurs at rest (or with minimal exertion) described as severe pain and occurring with a crescendo pattern (distinctly more severe, prolonged, or frequent than before)

10

Define MI

A MI is a complete occlusion of a coronary vessel, leading to an infarct (death) of the myocardium it supplies.

11

What can happen to an atheroma to form a thrombosis which will occlude a vessel?

The fibrous cap of the Atheromatous plaque can undergo erosion or fissure, exposing blood to the thombogenic material in the necrotic core.The platelet ‘clot’ is followed by a fibrin thrombus, which can either occlude the entire vessel where it forms or break off to form an embolism.

12

How does MI present?

MI presents with typical ischaemic chest pain that is very severe, persistent, at rest and often with no precipitant. It is not relieved by rest or nitrate spray. The patient may also be breathless, faint, feeling of impending doom and autonomic features.

13

Describe the autonomic features of an MI (adrenaline)

Sweating, pallor, nausea and vomiting

14

What is an NSTEMI

Non ST Elevated Myocardial InfarctionInfarct is not full thickness of myocardium

15

What is a STEMI

ST Elevated Myocardial InfarctionInfarct is full thickness of myocardium

16

What is the clinical diagnosis of angina based on ?

History

17

What are the four risk factors for angina which can be revealed from a cardiovascular exam?

Elevated BPCorneal arcusLV dysfunction Signs of peripheral vascular disease

18

What is the resting ECG of someone with stable angina usually like?

Normal, but may show signs of previous MI (pathological Q wave)

19

How do you confirm stable angina if a resting ECG is normal?

Exercise stress test

20

What is an exercise stress test? How long does it go on for?

Graded exercise on a treatment connected to an ECG until:Target heart rate reachedORChest PainORECG changesOROther problems – arrhythmias, low BP etc…

21

QUESTION What is a positive ECG after exercise stress test for stable angina? Why do you get st depression, cell death?

Shows ST depressions of >1mm. A strong positive test indicates critical stenosis

22

What is acute coronary syndrome? What is it a result of?

Acute Coronary Syndrome (ACS) relates to a group of symptoms attributed to the obstruction of the coronary arteries. ACS is a result of:Unstable AnginaNSTEMISTEMI

23

Describe unstable angina Occlusion by thrombosis?Myocardial necrosis?ECG character?Biochemical blood markers?

Occlusion by thrombosis?PartialMyocardial necrosis?NoneECG character?May have ST segment depression, T wave inversion or normalBiochemical blood markers?None

24

Describe NSTEMIOcclusion by thrombosis?Myocardial necrosis?ECG character?Biochemical blood markers?

Occlusion by thrombosis?PartialMyocardial necrosis?SomeECG character?No ST segment elevationBiochemical blood markers?Troponin

25

Describe STEMIOcclusion by thrombosis?Myocardial necrosis?ECG character?Biochemical blood markers?

Occlusion by thrombosis?TotalMyocardial necrosis?Large myocardial infarctECG character?ST segment elevationBiochemical blood markers?Troponin

26

How can initial ECG be used to to differential STEMI from NSTEMI/Unstable Angina

SEE DIAGRAM!

27

What causes ST depression in NSTEMI and unstable angina?

K+ leak from injured subendocardial (partial thickness, highest intensity area!) causes depolarisation as ST segment depolarises in ECG lead facing area

28

What do you get minutes to hours after an MI?

ST elevation T wave upright

29

What happens after STEMI diagnosed?

Either primary PCI or fibrinolytic therapy

30

What do you get hours to days after MI?

ST elevation, decreased T waveDecreased R wavePathological Q wave begins

31

What causes ST elevation in STEMI?

K+ leak from injured subepicardial (full thickness!) myocyte, causing depolarisation + ST segment elevation in ECG leads facing injured area

32

What do you get days 1-2 after MI?

Deep pathological Q waveST elevation, decreased T waveDecreased R wave

33

What do you get over 2 days after an MI?

ST normalisesT wave invertedPathological Q wave

34

What do you get weeks after an MI?

ST & T normalQ wave persists

35

How can previous MIs be identified?

Persistence of pathological, deepened Q wave

36

How can you determine where someone's had an MI?

The site of an MI can be localised using an ECG, as abnormalities will be seen due to the infarcted, dead myocardium. Look at which lead the abnormality is on and where that lead’s view is allows localisation of the MI.

37

What causes pathological q wave?

Q moves from left to right side and vice versa of inter ventricular septum Area of necrosis in left myocardium provides 'window' - only depolarisation going AWAY from lead view shown, so Q depolarisation away massively depolarised down

38

See other deck of flashcards for lead view Mis

yay..

39

Name two troponins important in MI detection

Cardiac Troponin I (cTnI) and Troponin T (cTnT) are proteins important in actin/myosin interaction, which are released in myocyte death.i

40

Why is it good to test for cardiac troponins?

Very sensitive and specific marker, rising 3-4hrs after the first onset of pain and peaking at 18-36 hrs. They will then decline slowly for up to 10-14 days.

41

What is the iso-enzyme found in the blood after MUI?

CK-MB, rising 3-8 gours after onset, peaking at 24hrs.

42

What does the prescence of troponin or creatine kinase indicate?

Death of the myocardium. It therefore distinguishes between unstable angina and NSTEMI, as there is no tissue death in unstable angina and there is in NSTEMI.

43

How do you treat unstable angina?

Prevent UA from progressing to MI and limiting muscle loss in MIPrevent progression of thrombosisRestore perfusion of partially occluded vessels

44

How do you prevent progression of thrombosis in unstable angina/MI?

Anti Thrombotic therapyAnti platelet agents: AspirinAnticoagulants: Heparin

45

How do you restore perfusion of partially occluded vessels in unstable angina/MI?

High riskEarly Percutaneous Coronary Intervention (Angioplasty) (PCI)Coronary Artery Bypass Graft (CABG)Low RiskInitially medical treatment

46

What are some general treatments for coronary artery syndrome in unstable angina/MI?

O2Organic NitratesB-blockersStatinsACE-Inhibitors

47

What are three surgical treatmeants for CAD?

AngiographyPercutaneous coronary interventionCoronary bypass grafting

48

What is angiography used for?

to view any vessel occlusions, and from the findings choices can be made about revascularisation surgeries.

49

What does aspirin do?

Reduced platelet aggregation, decreased thrombus formation

50

What is percutaneous coronary intervention?

Angioplasty and stenting. Inflation of a balloon inside the occluded vessel expands a mesh that holds the vessel open, increasing the lumen size and allowing for more blood to flow.

51

What is involved in a CBPG?

involves taking an artery from elsewhere in the body, e.g. internal mammary artery, radial artery, saphenous vein (reversed because of valves) and grafting it to the heart.

52

Describe 5 causes of acute pericarditis?

Infections (viral, TB)Past MI/cardiac surgeryAutoimmuneUraemia (kidney failure)Malignant Deposits

53

Describe the symptoms of acute pericarditis

Central/left sided chest painSharp, worse than inspirationImproved by leaning forward

54

What vessels are used in CABG

Reversed great saphenous vein Radial artery

55

What happens after NSTEMI diagnosed?

Anti thrombotic therapyEarly PCI

56

Give some complications of MIl

Arrythmia-tachycardia (anxiety)-bradycardia (SA node ischaemia£ -heart block (av node ischaemia) - Ventricular tachycardia (recently looping) - Atrial fibrillation Heart failure (decreases myocardial contractility) Cardiogenic shock

57

What would you see in the ECG of someone with pericarditis?

ST elevation with upward concavity in all leads

58

What is a complication of pericarditis?

Pericardial effusion

59

What would be the treatment of pericarditis?

Pericardiocentesis

60

What is aortic dissection ?

Tear in the intima of aorta

61

What are four causes of aortic dissection?

HypertensionTraumaMarfan's syndrome Iatrogenic catheterisation

62

What is acute coronary syndrome? What is the priority and initial treatments?

Chest pain lasting longer than 15 minutes, priority is to separate into STEMI or NSTEMI/unstable angina ECG, cardiac biomarkers