Brainscape's Knowledge GenomeTM

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


See full index

Yr 2 - EMS > Ischaemic Heart Disease & Heart Failure > Flashcards

Ischaemic Heart Disease & Heart Failure Flashcards

1
Q

What is ischaemic heart disease?

A

Inadequate blood supply to the myocardium, resulting in lack of oxygen and decreased availability and removal of metabolites

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

What is cause of ischaemic heart disease in 90% of cases?

A

Decreased coronary blood flow due to obstruction of the coronary arteries by atheroma

Often referred to as coronary heart disease

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

Why is there often a coexisting component of myocardial hypertrophy in IHD?

A

Systemic hypertension - that increases the workload of the heart

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

How significant is IHD?

A

Is the leading cause of death globally

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

Difference between acute and chronic IHD in terms of coronary atherosclerosis?

A

Chronic: due to a progressive narrowing of the lumen leading to stenosis (chronic, fixed, blockages) Acute: due to acute plaque disruptions with thrombosis (sudden)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When is stenosis critical?

A

75% vessel occlusion - symptomatic during exercise

90% vessel occlusion - symptomatic even at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When may collateral vessels develop during IHD?

A

Slowly developing occlusions may lead to the development of collateral vessels over time, which can be protective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When does myocardial necrosis begin after coronary occlusion? What type of necrosis is this (histologically)?

A
  • Approx 30 mins after coronary occlusion with class features of an MI seen after reduced perfusion for 2-4 hours
  • Of coagulative type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How soon is reperfusion needed to prevent cell loss?

A

<20 mins

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

What is angina pectoris?

A

Complex of symptoms characterised by paroxysmal attacks of chest pain (constricting, squeezing, choking, knife-like) caused by transient (secs-to-minutes) myocardiac ischaemia that doesn’t induce the cellular necrosis that defines ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 types of angina pectoris?

A
  1. Typical/stable 2. Crescendo/unstable 3. Variant/Prinzmetal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What characterises typical/stable angina?

A
  • Symptoms brought on at a predictable level of exertion - Relieved by rest / or nitrates (vasodilator)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What characterises crescendo/unstable angina?

A
  • Pain occurs with increasing frequency, or occurs at rest. - Lasts longer than “typical” angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is typical/stable angina due to?

A

Due to reduction of coronary perfusion to a critical level by chronic narrowing by atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is crescendo/unstable angina due to?

A

Due to disruption of an atherosclerotic plaque (plaque rupture) with partial thrombosis and or embolism and or vasospasm Often occurs before an acute MI

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

What characterises variant/prinzmetal angina?

A
  • Occurs at rest - Unrelated to exertion, heart rate or blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is variant/prinzmetal angina due to?

A

Coronary artery spasm (can be seen in cocaine use)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is acute coronary syndrome?

A

Encompasses a range of conditions that are due to a sudden reduction of blood flow to the heart.

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

What are 3 types of acute coronary syndrome?

A
  1. Non-ST elevation myocardial infarction (NSTEMI) 2. Unstable angina 3. ST elevation myocardial infarction (STEMI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is sudden cardiac death?

A

A sudden, unexpected death caused by loss of heart function

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

What is sudden cardiac death usually due to?

A

Usually due to a lethal cardiac arrhythmia: - Could be due to ischaemia impinging on the conduction system itself - Usually due to electrical irritability of the myocardium away from the conduction system

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

What is the acute ischaemia underlying unstable angina or acute MI, or even sudden cardiac death usually due to?

A

An abrupt change in the atherosclerotic plaque, followed by thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 3 possible abrupt changes to the atherosclerotic plaque?

A
  1. Plaque rupture 2. Plaque erosion or ulceration 3. Haemorrhage into plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can plaque rupture lead to acute ischaemia?

A

Exposes the thrombogenic components of the plaque to the blood -> superimposed thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How can plaque erosion or ulceration lead to acute ischaemia?

A

Causes endothelial injury and exposes the thrombogenic basement membrane to the blood -> superimposed thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How can haemorrhage into the plaque lead to acute ischaemia?

A

Expands its volume (non-occlusive -> occlusive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which plaques are most at risk?

A

Lipid rich with a thin fibrous cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are extrinsic factors affect plaque rupture?

A
  • Blood pressure - Emotional stress - Adrenaline (MI more common on waking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is transmural myocardial infarction? How does this differ from a subendocardial infarct?

A

Transmural: - Results when myocardial necrosis extends throughout the entire thickness of the myocardium - Due to complete occlusion of an epicardial coronary artery (i.e. STEMI) Subendocardial: - Results in necrosis exclusively involving the innermost aspect of the myocardium. - Usually a result of a partially occluded epicardial coronary artery (i.e. NSTEMI).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MI - Gross Morphology 1-2 days?

A

<24h normal 1-2 days: Pale, oedematous, myocyte necrosis, neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MI - Gross Morphology 3-4 days?

A

Yellow with haemorrhagic edge, myocyte necrosis, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MI - Gross Morphology 1-3 weeks?

A

Red-grey to grey-white, pale, thin, granulation tissue then fibrosis

33
Q

MI - Gross Morphology 3-6 weeks?

A

Dense fibrous scar

34
Q

What is subendocardial MI usually caused by?

A
  • Stable atheromatous occlusion of the coronary circulation - Plaque rupture and and coronary thrombus that becomes lysed before myocardial necrosis can spread full thickness through the wall OR Can result from sufficiently prolonged and severe reduction in systemic blood pressure
35
Q

What is STEMI?

A

An ST-segment elevation myocardial infarction (STEMI) is a serious form of heart attack in which a coronary artery is completely blocked and a large part of the heart muscle is unable to receive blood

36
Q

What is NSTEMI?

A

A less serious type of heart attack. NSTEMI stands for Non-ST-elevation myocardial infarction.

37
Q

What do both STEMI and NSTEMI result from?

A
  • Rupture of a vulnerable atherosclerotic plaque. - At the same time, endothelial dysfunction contributes to additional thrombosis and ineffective vasodilatation.
38
Q

How does plaque rupture lead to STEMI/NSTEMI?

A

Ruptured plaque exposes the circulating blood to highly thrombogenic substances, which induces clot formation. The lumen of the affected coronary artery gets occluded by thrombus –> deprived myocardium

39
Q

Diagnosing MI?

A
  1. Clinical history: ischaemic type chest pain lasting for more than 20 minutes) 2. Examination: pulse, breath 3. Investigations: ECG, cardiac enzymes (creatine kinase-MB fraction and troponin), echo, angio
40
Q

Key symptoms of MI?

A

Tachycardic, weak thready pulse, sweating, SOB, chest pain (radiating to jaw, left arm)

41
Q

What is a silent MI? Who is it most common in?

A

A silent heart attack is a heart attack that has few, if any, symptoms or has symptoms you don’t recognise as a sign of a heart attack. Most common in women, elderly and those with diabetes

42
Q

What are the blood markers of cardiac myocyte damage (‘cardiac enzymes’)?

A

Measuring the blood levels of intracellular macromolecules that leak out of damaged myocytes Myoglobin, cardiac troponins (T & I), creatinine kinase, lactate dehydrogenase etc

43
Q

What are the troponins?

A

Proteins that regulate the calcium mediated contraction of cardiac and skeletal muscle

44
Q

Expected result of Troponins T & I in blood test of an MI? In what other conditions would you expect to see these raised?

A

Detectable 2 – 3h, peaks at 12-48h, detectable to 7 days Raised post MI but also in pulmonary embolism, heart failure, & myocarditis.

45
Q

Expected result of Creatine kinase MB in cardiac injury?

A

Detectable 2 – 3h, peaks at 10-24h, detectable to 3 days

46
Q

Expected result of myoglobin in cardiac injury?

A

Peak at 2h but also released from damaged skeletal muscle

47
Q

Expected result of lactate dehydrogenase isoenzyme 1 in cardiac injury?

A

Peaks at 3days, detectable to 14days

48
Q

Why is aspartate transaminase less useful as a marker in cardiac injury?

A

Also present in liver so less useful as a marker of myocardial damage

49
Q

What is immediate treatment for STEMI?

A

PCI (percutaneous coronary intervention) This is a form of reperfusion therapy

50
Q

What is the prognosis of MI?

A

>35% fatal Of these deaths up to 70% are “sudden cardiac deaths” (within 1-2hrs)

51
Q

Complications of MI?

A
  • Arrhythmias - Contractile dysfunction - LV failure, cardiogenic shock - Rupture - Cardiac mural thrombus & emboli (endothelial damage plus altered blood flow/stasis - Ventricular aneurysm - Pericarditis
52
Q

How can MI lead to rupture?

A

Occurs due to mechanical weakening of necrotic and inflamed myocardium

53
Q

What is chronic ischaemic heart disease?

A

Progressive heart failure as a consequence of ischaemic myocardial damage Heart is enlarged and heavy with LVH and dilatation

54
Q

What is familial hypercholesterolaemia?

A

A genetic disorder that means the body is unable to remove low density lipoprotein (LDL) cholesterol from the blood.

55
Q

What are the causes of familial hypercholesterolaemia?

A
  • LDL receptor gene mutation - Apolipoprotein B gene mutation
56
Q

What type of inheritance is familial hypercholesterolaemia?

A

Autosomal dominant

57
Q

Symptoms of familial hypercholesterolaemia?

A
  • Develop xanthomas (fatty skin deposits over parts of the hands, elbows, knees, ankles and around the cornea of the eye) - Cholesterol deposits in the eyelids (xanthelasmas) - Chest pain (angina) or other signs of coronary artery disease may be present at a young age.
58
Q

Treatment for familial hypercholesterolaemia?

A

Heterozygotes: Early primary treatment with statins (hydroxymethylglutaryl CoA reductase inhibitors) is effective Homozygotes: treatment is more complex and less effective

59
Q

What is heart failure?

A

Also known as congestive cardiac failure Common end stage of all diseases of the heart Heart unable to pump blood at the rate requires to meet the demands of the tissues

60
Q

Causes of congestive heart failure?

A

See lecture for list

61
Q

Left and right heart failure

A

N.B. RHF usually occurs as a result of LHF but can be caused by severe pulmonary hypertension (cor pulmonale) when there is increased resistance in the pulmonary circulation

62
Q

Signs and symptoms of heart failure

A
63
Q

What is orthopnoea? What is it a common symptom of?

A

Shortness of breath (dyspnea) that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair.

Common symptom of heart failure

64
Q

Heart failure investigations

A

Initial

  • CXR
  • ECG
  • Echo
  • Bloods

–FBC, U&Es, LFTs, TFTs, Glucose

–Cardiac enzymes (if recent infarction is suspected)

Other

  • Radionuclide imaging
  • CPX
  • Cardiac catheterisation
  • Myocardial bx -? myocarditis
65
Q

Management of Acute Heart Failure

A

Basic measures include sitting the patient in an upright position with high concentration oxygen delivered via a face mask

66
Q

Chronic heart failure management

A
67
Q

Non-drug management for chronic heart failure

A
68
Q

Complications of heart failure:

A
  • Arrhythmias – AF, VF, VT, bradyarrhythmias
  • Thromboembolism – stroke, DVT, PE
  • GI – hepatic congestion & dysfunction, malabsorption
  • Musculoskeletal – muscle wasting
  • Respiratory – pulmonary congestion, resp muscle weakness, Pul HTN (rare)
69
Q

New York Heart Association (NYHA) Classification of severity of Heart Failure

A
70
Q

What are the NYHA classifications for the following symptoms:

  1. Severe symptoms and minimal physical activity
  2. No symptoms and no limitation in physical activity
  3. Moderate symptoms and less than normal physical activity
  4. Mild symptoms and no limitation in physical activity
A

1 –> class 4

2 –> class 1

3 –> class 3

4 –> class 2

71
Q

What is the most common cause of heart failure?

A

Coronary artery disease

72
Q

What is a ‘high output’ cause of cardiac failure?

A

Increase in body’s demand for oxygen even though heart is working normally

  • Pregnancy (high metablic state)
  • Anaemia
  • Thyrotoxicosis (high metabolic state due to increased thyroid hormones)
73
Q

In early stage heart failure, is the HR decreased?

A

No - compensatory state of heart in early failure (HR increases to try and maintain cardiac output)

74
Q

Myocardial damage leads to the activation of sympathetic nervous system. What are the effects of this?

A
  1. Renin-angiotensin system
  2. Vasoconstriction
  3. Increased heart rate and contractility
  4. Direct cardiotoxicity
75
Q

Effects of activation of RAS?

A

Fluid retention –> increased wall stress –> increased myocardial oxygen demand –> decreased contracility and myocardial hypertrophy

76
Q

Effects of vasoconstriction due to myocardial damage?

A

Increased wall stress –> increased myocardial demand for oxygen –> myocardial hypertrophy and decreased contractility

77
Q

Effect of increased heart rate and contracility due to myocardial damage?

A

Increased myocardial oxygen demand –> myocardial hypertrophy and decreased contractility

78
Q

Effect of direct cardiotoxicity due to myocardial damage?

A

Myocyte damage

79
Q
A

Yr 2 - EMS (60 decks)

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