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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

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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

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3
Q

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

A

Systemic hypertension - that increases the workload of the heart

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4
Q

How significant is IHD?

A

Is the leading cause of death globally

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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)

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6
Q

When is stenosis critical?

A

75% vessel occlusion - symptomatic during exercise

90% vessel occlusion - symptomatic even at rest

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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

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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
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9
Q

How soon is reperfusion needed to prevent cell loss?

A

<20 mins

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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

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11
Q

What are the 3 types of angina pectoris?

A
  1. Typical/stable 2. Crescendo/unstable 3. Variant/Prinzmetal
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12
Q

What characterises typical/stable angina?

A
  • Symptoms brought on at a predictable level of exertion - Relieved by rest / or nitrates (vasodilator)
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13
Q

What characterises crescendo/unstable angina?

A
  • Pain occurs with increasing frequency, or occurs at rest. - Lasts longer than “typical” angina
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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

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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

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16
Q

What characterises variant/prinzmetal angina?

A
  • Occurs at rest - Unrelated to exertion, heart rate or blood pressure
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17
Q

What is variant/prinzmetal angina due to?

A

Coronary artery spasm (can be seen in cocaine use)

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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.

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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)
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20
Q

What is sudden cardiac death?

A

A sudden, unexpected death caused by loss of heart function

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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

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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

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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
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24
Q

How can plaque rupture lead to acute ischaemia?

A

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

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25
How can plaque erosion or ulceration lead to acute ischaemia?
Causes endothelial injury and exposes the thrombogenic basement membrane to the blood -\> superimposed thrombus
26
How can haemorrhage into the plaque lead to acute ischaemia?
Expands its volume (non-occlusive -\> occlusive)
27
Which plaques are most at risk?
Lipid rich with a thin fibrous cap
28
What are extrinsic factors affect plaque rupture?
- Blood pressure - Emotional stress - Adrenaline (MI more common on waking)
29
What is transmural myocardial infarction? How does this differ from a subendocardial infarct?
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).
30
MI - Gross Morphology 1-2 days?
\<24h normal 1-2 days: Pale, oedematous, myocyte necrosis, neutrophils
31
MI - Gross Morphology 3-4 days?
Yellow with haemorrhagic edge, myocyte necrosis, macrophages
32
MI - Gross Morphology 1-3 weeks?
Red-grey to grey-white, pale, thin, granulation tissue then fibrosis
33
MI - Gross Morphology 3-6 weeks?
Dense fibrous scar
34
What is subendocardial MI usually caused by?
- 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
What is STEMI?
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
What is NSTEMI?
A less serious type of heart attack. NSTEMI stands for Non-ST-elevation myocardial infarction.
37
What do both STEMI and NSTEMI result from?
- Rupture of a vulnerable atherosclerotic plaque. - At the same time, endothelial dysfunction contributes to additional thrombosis and ineffective vasodilatation.
38
How does plaque rupture lead to STEMI/NSTEMI?
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
Diagnosing MI?
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
Key symptoms of MI?
Tachycardic, weak thready pulse, sweating, SOB, chest pain (radiating to jaw, left arm)
41
What is a silent MI? Who is it most common in?
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
What are the blood markers of cardiac myocyte damage ('cardiac enzymes')?
Measuring the blood levels of intracellular macromolecules that leak out of damaged myocytes Myoglobin, cardiac troponins (T & I), creatinine kinase, lactate dehydrogenase etc
43
What are the troponins?
Proteins that regulate the calcium mediated contraction of cardiac and skeletal muscle
44
Expected result of Troponins T & I in blood test of an MI? In what other conditions would you expect to see these raised?
Detectable 2 – 3h, peaks at 12-48h, detectable to 7 days Raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
45
Expected result of Creatine kinase MB in cardiac injury?
Detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
46
Expected result of myoglobin in cardiac injury?
Peak at 2h but also released from damaged skeletal muscle
47
Expected result of lactate dehydrogenase isoenzyme 1 in cardiac injury?
Peaks at 3days, detectable to 14days
48
Why is aspartate transaminase less useful as a marker in cardiac injury?
Also present in liver so less useful as a marker of myocardial damage
49
What is immediate treatment for STEMI?
PCI (percutaneous coronary intervention) This is a form of reperfusion therapy
50
What is the prognosis of MI?
\>35% fatal Of these deaths up to 70% are “sudden cardiac deaths” (within 1-2hrs)
51
Complications of MI?
- Arrhythmias - Contractile dysfunction - LV failure, cardiogenic shock - Rupture - Cardiac mural thrombus & emboli (endothelial damage plus altered blood flow/stasis - Ventricular aneurysm - Pericarditis
52
How can MI lead to rupture?
Occurs due to mechanical weakening of necrotic and inflamed myocardium
53
What is chronic ischaemic heart disease?
Progressive heart failure as a consequence of ischaemic myocardial damage Heart is enlarged and heavy with LVH and dilatation
54
What is familial hypercholesterolaemia?
A genetic disorder that means the body is unable to remove low density lipoprotein (LDL) cholesterol from the blood.
55
What are the causes of familial hypercholesterolaemia?
- LDL receptor gene mutation - Apolipoprotein B gene mutation
56
What type of inheritance is familial hypercholesterolaemia?
Autosomal dominant
57
Symptoms of familial hypercholesterolaemia?
- 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
Treatment for familial hypercholesterolaemia?
Heterozygotes: Early primary treatment with statins (hydroxymethylglutaryl CoA reductase inhibitors) is effective Homozygotes: treatment is more complex and less effective
59
What is heart failure?
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
Causes of congestive heart failure?
See lecture for list
61
Left and right heart failure
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
Signs and symptoms of heart failure
63
What is orthopnoea? What is it a common symptom of?
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
Heart failure investigations
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
Management of Acute Heart Failure
Basic measures include sitting the patient in an upright position with high concentration oxygen delivered via a face mask
66
Chronic heart failure management
67
Non-drug management for chronic heart failure
68
Complications of heart failure:
* 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
New York Heart Association (NYHA) Classification of severity of Heart Failure
70
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
1 --\> class 4 2 --\> class 1 3 --\> class 3 4 --\> class 2
71
What is the most common cause of heart failure?
Coronary artery disease
72
What is a 'high output' cause of cardiac failure?
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
In early stage heart failure, is the HR decreased?
No - compensatory state of heart in early failure (HR increases to try and maintain cardiac output)
74
Myocardial damage leads to the activation of sympathetic nervous system. What are the effects of this?
1. Renin-angiotensin system 2. Vasoconstriction 3. Increased heart rate and contractility 4. Direct cardiotoxicity
75
Effects of activation of RAS?
Fluid retention --\> increased wall stress --\> increased myocardial oxygen demand --\> **decreased contracility and myocardial hypertrophy**
76
Effects of vasoconstriction due to myocardial damage?
Increased wall stress --\> increased myocardial demand for oxygen --\> **myocardial hypertrophy** and **decreased contractility**
77
Effect of increased heart rate and contracility due to myocardial damage?
Increased myocardial oxygen demand --\> **myocardial hypertrophy and decreased contractility**
78
Effect of direct cardiotoxicity due to myocardial damage?
Myocyte damage
79

Yr 2 - EMS (60 decks)

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