Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y4 Cardiology > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

Define what ischaemic heart disease (IHD) is

A

IHD is a term synonymous with coronary heart disease and coronary artery disease. It describes the gradual build up of fatty plaques within the walls of the coronary arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the pathophysiological stages of IHD development ?

A
  1. Initially endothelial dysfunction - triggered by CV risk factors
  2. Endothelial dysfunction results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
  3. Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles - fatty streak
  4. Monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process. - Fatty plaque
  5. Smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 2 main problems which ischaemic heart disease leads to ?

A

The build up of fatty plaques within the walls of the coronary arteries leads to:

  1. Gradual narrowing resulting in angina, i.e. chest pain - due to less blood & therefore oxygen reaching the myocardium at times of exertion.
  2. Risk of sudden plaque rupture (ACS) - The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the risk factors for the development of IHD ?

A

Unmodifiable:

  • Increasing age
  • Male gender
  • Family history

Modifiable:

  • Smoking
  • Diabetes mellitus
  • Hypertension
  • Hypercholesterolaemia
  • Obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define what acute coronary syndrome (ACS) is and what it encompasses

A

Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of IHD. It encompasses:

  • ST elevation myocardial infarction (STEMI)
  • Non-ST elevation myocardial infarction (NSTEMI)
  • Unstable angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the typical signs & symptoms of acute cornoary syndrome ?

A
  • Acute central/left sided chest pain lasting > 20mins which may radiate to the jaw or left arm
  • Chest pain often described as ‘heavy’, ‘constricting’ or ‘crushing’
  • Chest pain not relieved by rest of GTN (ACS can happen at anytime unlike stable angina which cannot happen at rest as its releived by it - if pain < 20 mins but at rest think unstable angina)
  • Nausea and vomiting
  • Sweatiness/clamy, pale
  • Dysponea
  • Palpitations
  • May be tachycardic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the atypical signs & symptoms of acute cornoary syndrome and in whom are these more likely to occur in?

A

In diabetes and elderly patients they may present without chest pain. There presentations may include:

  • Syncope
  • Pulmonary oedema
  • Epigastric pain and vomiting
  • Post-op hypotension
  • Oligouria
  • Acute confusional state
  • Stroke
  • Diabetic hyperglycaemic state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the characteristic symptoms of angina as opposed to ACS ?

A
  1. Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in about 5 minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How should someone presenting with chest pain be diagnosed with or have ACS excluded ?

A

1st line = 12 lead ECG + and a blood sample taken for high-sensitivity troponin I or T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the stages of ECG changes which occur during MI ?

A
  1. hyperacute T waves (big and tall) - only persist for a few minutes
  2. ST elevation may then develop
  3. The T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
  4. pathological Q waves develop after several hours to days. This change usually persists indefinitely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define what pathological q waves are

A
  • They are any q wave in leads V1-3
  • Q wave ≥ 0.03s in leads I, II, aVL, aVF, V4, 5 or 6
  • They must be present in any 2 continguous leads and be > 1mm in depth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What ECG changes indicate ischaemic or previous MI ?

A
  • Pathological Q waves (in particular).
  • Left bundle branch block (LBBB).
  • ST-segment and T-wave abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Specifically what T wave changes can indicate ischaemia ?

A
  • Tall tented
  • Biphasic (up and down)
  • Inverted
  • Flattened

Pic shows biphasic t wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the potential causes of ST segment depression?

A
  • secondary to abnormal QRS (LVH, LBBB, RBBB)
  • ischaemia
  • digoxin
  • hypokalaemia
  • syndrome X
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does widespread and deep ST segment depression generally indicate in the context of myocadial ischaemic ?

A

It is a very poor prognostic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What ECG changes define an STEMI ?

A
  • >1mm ST elevation in 2 adjacent limb leads
  • >2mm ST elevation in at least 2 contiguous precordial leads
  • New onset bundle branch block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Using ECG how can the part (location) of the heart being affected by ACS be determined and what artery is then affected?

A
  • Anteroseptal: V1-V4 - Left anterior descending (LAD)
  • Inferior: II, III, aVF - Right coronary
  • Anterolateral: V4-6, I, aVL - Left anterior descending or left circumflex
  • Lateral: I, aVL +/- V5-6 - Left circumflex
  • Posterior: Tall R waves V1-2 - Usually left circumflex, also right coronary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What should always be done as follow up investigation in ACS patients ?

A

A second ECG (at 12hrs or day 2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

List some of the other causes of ST segment elevation to be aware of

A
  • Benign early repolarisation
  • LBBB
  • LVH
  • Ventricular aneurysm
  • Coronary spasm/printzmetals angina
  • Pericarditis
  • Burgada syndrome
  • Subarachnoid haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Differentiating between new LBBB and actue changes suggestive of STEMI are beyond what I need to know.

What should I basically know to consider with patients with new changes suggestive of LBBB?

A

In patients with new LBBB, acute MI should be considered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In patients with a posterior MI, what changes do we see?

A

ST segment depression in V1-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the criteria for diagnosing a STEMI in the presence of LBBB? (prob dont need to know as bit too complicated)

A
  • A) ST depression > 1mm in V1-3
  • B) ST elevation > 1mm in leads with positive QRS complex
  • C) ST elevation > 5mm in leads with a negative QRS complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diagnose what is wrong

A

Anterior MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diagnose what is wrong

A

Inferior MI

25
Q

What is the initial management of ACS?

A

MONAH + C (ticagrelor then pasurgel preferred now)

  • O2 also only given if sats < 94%
  • M stands for morphine & metoclopramide now
  • H = fondaparinux or LMWH
  • For Killip class I ACS in the absence of bradycardia or hypotension consider bet-blockers

Anti-emetic given also

26
Q

Following initial management of ACS what is the definitive treatment of STEMI ?

A

1st line = PCI to patients who present within 12 hours of onset of symptoms, if it can be delivered within 120 minutes of the time when fibrinolysis could have been given.

2nd line = fibrinolysis (altepase (tPA) > streptokinase)

27
Q

Following initial management of ACS what treatment is then done for someone with a NSTEMI ?

A

A risk stratification score (such as GRACE) is used to decide upon further management:

Early coronary angiography and revascularisation should be done in those within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0% (i.e. they are medium or high risk) OR if they are clinically unstable.

28
Q

In patients with NSTEMI undergoing revascularisation therapy what is done ?

A
  1. Coronary artery bypass graft surgery should be considered for - patients with diabetes mellitus, left main-stem disease or multivessel coronary artery disease
  2. PCI should be considered for - patients with a SYNTAX score of 22 or less or those with a high surgical risk
29
Q

When are Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) used in patients whom have had a NSTEMI?

A
  • Patients at higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%) (& ==> who are scheduled to undergo angiography within 96 hours of hospital admission)
30
Q

Following ACS what is the long-term secondary prevention management ?

A
  • Dual anti-platelet therapy for 6 months - Aspirin + (ticagrelor and prasugrel > clopidogrel)
  • Long-term statin
  • Long-term Beta-blocker
  • Long-term ACEi

SABA + C

31
Q

What can be added to the long-term treatment for secondary prevention of MI if the patient has symptoms and/or signs of heart failure and left ventricular systolic dysfunction?

A

An aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone)

32
Q

What are the risk of thromblytic therapy used in ACS ?

A
  • Failure to re-perfuse
  • Haemorrhage - ICH rates 0.5 – 2.0%
  • Hypersensitivity
33
Q

For patients who fail to respond to thrombolytic therapy for STEMI what needs to be done ?

A

Transfer to somewhere for rescue PCI

34
Q

What complications can develop following MI?

A
  • Cardiac arrest
  • Cardiogenic shock
  • Chronic heart failure
  • Tachyarrhythmias
  • Bradyarrhythmias
  • Pericarditis
  • Left ventricular aneurysm
  • Left ventricular rupture
  • Ventricular septal defect
  • Mitral regurgitiation
35
Q

What are the 4 stages of the KILLIP classification and what is it used for ?

A

Used to determine risk of mortality in patients with acute MI:

  • I - No signs of heart failure 6%
  • II - Crepitations < 50% of lung fields 17%
  • III- Crepitations > 50% of lung fields 38%
  • IV- Cardiogenic shock 81%
36
Q

What is the main cause of cardiac arrest in patients with MI and how is it managed?

A
  • This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI.
  • Patients are managed as per the ALS protocol with defibrillation.
37
Q

What tachyarrhytmias commonly arise following MI ?

A

Ventricular fibrillation and ventricular tachycardia

38
Q

What are the characterisitc features of pericarditis ?

A
  • Occurs within 48hrs following MI
  • Pleuritic chest pain (worse on inspiration) which is worse when lying flat and relieved by sitting forward
  • Pericardial rub
  • Pericardial effusion may be demonstrated with an echocardiogram.
39
Q

What are the ECG changes suggestive of pericarditis compared to MI ?

A
  • Upward concave ST segment elevation (saddle shaped), the changes then do not evolve like in MI
  • The ST segment changes are widespread covering > 1 vascular territory
  • Also PR depression
40
Q

What are the characterisitc features of dresslers syndrome ?

A
  • Occurs 2-6 weeks following MI
  • Fever
  • Pleuritic chest pain
  • Pericardial effusion and a raised ESR.
41
Q

What is left ventricular aneurysm formation associated with and what does it increase the risk of?

A
  • Typically associated with persistent ST elevation and left ventricular failure.
  • Thrombus may form within the aneurysm increasing the risk of stroke.
42
Q

What are the characterisitc features of left ventricular free wall rupture ?

A
  • Occurs around 1-2 weeks afterwards.
  • Present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds).
43
Q

What urgent treatment is required for left ventricular free wall rupture ?

A

Pericardiocentesis and thoracotomy are required.

44
Q

What are the characterisitic features of ventricular septal defect following MI ?

A
  • Usually occurs in the first week
  • Features: Acute heart failure associated with a pan-systolic murmur.
45
Q

What is used to diagnose a ventricular septal defect and then what is done to treat it ?

A
  • Dx = echo
  • Tx = surgical correction
46
Q

What is the characterisitic feature suggestive of mitral reguritation following MI and what is done to treat it ?

A
  • Early-to-mid systolic murmur
  • It often needs surgical repair
47
Q

Define what angina is based on the 3 key symptoms

A
  1. Central chest tightness or heaviness, which may radiate to the neck, shoulders, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in about 5 minutes
  • If all 3 features = typical angina
  • If 2 of the above features = atypical angina
  • If ≤ 1 feature = non-anginal chest pain
48
Q

What are the associated symptoms of anginal chest pain ?

A
  • Dysponea
  • Nausea
  • Sweatiness
  • Faintness
49
Q

Based on initial clinical assessment of someone presenting with potential anginal chest pain how can a diagnosis of angina be excluded ?

A

If clinical assessment indicates non-anginal chest pain i.e. ≤ 1 of the 3 key features of anginal chest pain

50
Q

If clinical assessment alone cannot exclude angina what is done next ?

A

ECG

51
Q

For patients in whom stable angina cannot be excluded by clinical assessment (e.g. symptoms consistent with typical/atypical angina OR ECG changes) what is done?

A
  • 1st line: CT coronary angiography
  • 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
  • 3rd line: invasive coronary angiography
52
Q

What is the management of stable angina ?

A

All patients - Aspirin + statin + GTN PRN

  • 1st line = Beta-blocker or a CCB (rate-limiting)
  • 2nd line = add either a Beta-blocker or CCB (needs to be dihydropyridine CCB e.g. nifedipine due to risk of rate-limiting in combo with beta-blocker causing complete heart block)
  • 3rd line = if cannot tolerate combo then consider a long-acting nitrate, ivabradine, nicorandil or ranolazine
  • 4th line = a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
53
Q

What is the management of unstable angina ?

A

Manage as per ACS

54
Q

Interpret the following ECG

A
  • Marked ST seg elevation in V1-3 & 4,5
  • Early Q wave formation in V1-3

Dx = actue STEMI affecting LAD artery affected

55
Q

Interpret the following ECG

A
  • ST Segment elevation - V2-3, aVF
  • Reciprocal ST segment depression in V1 & aVL
  • Rhythm - mobitz type I

Dx = inferior STEMI with secondary mobitz type I

56
Q

Interpret the following ECG

A
  • Sinus tachycardia
  • ST segment depression over inferior, septal and later leads
  • LVH identified using voltage criteria (check aVL which shows QRS complex > 11mm)

This is in keeping with severe HTN caused by possible critical aortic stenosis

57
Q

Interpret the following ECG

A
  • ST segment elevation in leads I,II,III & V3-6 (possible saddle shape)
  • PR depression most easily seen in V3 which is characterisitic of pericarditis

Dx = pericarditis

58
Q

Interpret the following ECG

A
  • ST segment elevation in anterior & lateral lead with some evidence of PR depression
  • Q waves esp in lead III & aVF

Dx = in the context of recent CABG likely to be dresslers syndrome or pericarditis

Y4 Cardiology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions