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BRS 1b > Ishcaemic Heart Disease > Flashcards

Ishcaemic Heart Disease Flashcards

1
Q

What is ishcaemic heart disaese?

A

Refers to the occlusion of coronary arteries that supplies cardiomyocytes, reducing oxygen perfusion to satisfy the demand

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2
Q

What does ishcaemic heart disease manifest as?

A

Myocardial infarction

ishcaemic cardiomyopathy

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3
Q

How can sudden deaths occur in ishcaemic heart disease?

A

Acute coronary occlusion

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4
Q

What is angina type chest pain?

A

Aching, burning, fullness, heaviness, numbness, squeezing
Radiation in arms, back, jaw, neck, shoulder
High or low BP
Indigestion or heartburn is typically misperceived as angina.

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5
Q

What is s4 gallop?

A

A common early finding of diastolic dysfunction

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6
Q

What is s3 gallop?

A

An indication of reduced left ventricular function and a poor prognostic sign

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7
Q

What heart rhythm disorders are associated with ishcaemic heart disease?

A

Palpitations (irregular heartbeats or skipped beats)
Heart murmurs
Tachycardia (Acute coronary syndrome, ACS, acute myocardial infarction AMI)
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation

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8
Q

What general signs are associated with ishcaemic heart disease?

A

Nausea, sweating, fatigue or shortness of breath, weakness or dizziness.
Reduced exertional capacity
Leg swelling (when left ventricular dysfunction is present)
Diaphoresis

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9
Q

What is s3 ventricular gallop?

A

S3 is head during early ventricular diastole caused by the oscillation of blood back and forth between the walls of the ventricles initiated by the inflow of blood from the atria.
• Blood striking compliant left ventricle.

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10
Q

What is a DALY?

A

DALY: Disability-adjusted Life Year
A sum of Years of Life Lost (YLL) and Years Lost to Disability (YLP)
• DALY is a more accurate measure to quantify the burden of disease than prevalence and mortality. IHD is the leading cause of disability and years of life lost globally.

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11
Q

Why does myocardial ischaemia occur?

A

Myocardial ischaemia occurs when there is an imbalance between the supply of oxygen and the myocardial demand for these substances.

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12
Q

What may cause obstruction of coronary flow?

A
  • Atheroma
  • Thrombosis
  • Spasm
  • Embolus
  • Coronary Ostial Stenosis
  • Coronary Arteritis
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13
Q

Which molecule is oxidised by macrophages and implicated in athersclerosis?

A

Low-density lipoproteins

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14
Q

Hows does a lipid necrotic core form?

A

Atherosclerosis is a complex inflammatory process that involves the accumulation of lipids and oxidised low-density lipoproteins within the subendothelial space, potentiated by macrophage activity.
• Macrophage phagocytosis of OxLDLs form foam cells  Lipid necrotic core
• In intimal plaques in the large and medium sized coronary arteries
• Process refers to atherogenesis

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15
Q

What are the triggers for atherogenesis?

A
  • Endothelial dysfunction
  • Mechanical sheer stress (HTN) – Turbulent flow reduces the shear stress exerted onto the endothelial potentiating release of pro-coagulant factors.
  • Biochemical abnormalities (elevated and modified LDL, DM, elevated plasma homocysteine)
  • Immunological factors (free radicals from smoking)
  • Inflammation (Infection such as chlamydia, helicobacter)
  • Genetic alterations
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16
Q

What is mechanical sheer stress?

A

Turbulent flow reduces the shear stress exerted onto the endothelial potentiating release of pro-coagulant factors.

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17
Q

What happens during the fatty streak phase of athersclerosis?

A
  1. Dysfunctional endothelial cells + retention of lipoproteins (LDL, VLDL)
  2. Increased expression of monocyte chemotactic protein-I (MCP-I) which facilitates the macrophage migration into intimal space.
  3. Other immune cells mediate the internalisation of OxLDLs to form foam cells.
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18
Q

Which factor is increased , resulting in macrophage migration during the fatty streak phase?

A

Monocyte chemotactic protein I

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19
Q

Macrophage phagocytosis of oxidised LDLs, forms what?

A

Foam cells

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20
Q

Tunica media smooth muscle cells secrete which two main factors?

A

TGF-bETA

fibroblast growth factor

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21
Q

How does a stable plaque form due to SMC?

A

Plaque Progression
There is an infiltration and proliferation of tunica media smooth muscle cells that secrete growth factors including TGF-B, and FGF.
• Smooth muscle cells are recruited to the luminal side of the lesion to form a barrier between lesional prothrombotic factors.

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22
Q

What supports a stable plaque?

A

Fibrous cap

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23
Q

What is a fibrous cap?

A

The fibrous cap is composed of layers of smooth muscles ensconced in a substantial extracellular matrix network.
• Provides an effective barrier preventing plaque rupture.
• Stable plaques have small necrotic cores.
• The production of TGF-beta by T-regulatory cells and macrophages maintains fibrous cap quality by being a potent stimulator of collagen production in smooth muscle cells.

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24
Q

Which factor secreted by T-regulatory cells and macrophages maintain the fibrous cap?

A

TGF-beta

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25
Q

What does TGF-beta do?

A

Potent stimulator of collagen production in smooth muscle cells

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26
Q

Why does a vulnerable plaque form?

A

It Is a result of increases and unresolved inflammatory status of core. This unresolved inflammation causes thinning of the fibrous cap.
• Areas of thin fibrous cap are prone to rupture exposing prothrombotic components to platelets and pro-coagulation factors leading to thrombus formation and clinical events.

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27
Q

What is the consequence of a vulnerable plaque?

A

Plaque rupture, leading to thrombus formation

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28
Q

How does an atherosclerotic plaque cause coronary heart disease?

A

Presentation of coronary/ischaemic heart disease
Atherosclerotic plaques can minimally obstruct the arteriole lumen; therefore, blood flow can continue to perfuse cardiac tissue, manifesting as asymptomatic.
• Chronic  Fixed atherosclerotic plaque  Reduced lumen  Occludes blood flow.

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29
Q

What are the three categories of acute coronary syndrome?

A

Unstable Angina
Non-ST elevation MI
ST-elevation MI

30
Q

What is acute coronary occlusion?

A

Acute coronary occlusion occurs in individuals with underlying atherosclerotic disease, potentiated by thrombus formation.

31
Q

What happens when an atherosclerotic plaque breaks through the endothelium?

A

Blood platelets adhere to it
Fibrin is deposited
RBCs entrap to form a blood clot

The fibrin mesh network is insoluble, eventually occluding the lumen of the vessel.
• A local muscular spasm of the coronary artery can also occur, participating to the luminal occlusion.

32
Q

Which factor is released in hypoxic conditions?

A

Hypoxia inducible factor

33
Q

What does hypoxia inducible factor do?

A

Hypoxia inducible factor is released under hypoxic conditions to stimulate angiogenesis in which collaterals form as a compensatory mechanism to maintain blood perfusion to the cardiac muscle.

34
Q

What happens to collaterals during an acute episode?

A

Dilation - doubling by the second or the day to reach normal coronary flow, within a month

35
Q

In chronic athersclerotic patients, what happens to the collaterals?

A

• Slow occlusion-collateral vessels can develop at the same time while the atherosclerosis becomes progressively severe.

36
Q

What happens after an acute occlusion to the heart?

A

After an acute occlusion, the area of cardiac muscle that is hypoperfused cannot sustain cardiac function  Infarcted  Myocardial infarction.

37
Q

How does engorgement occur in athersclerosis?

A

Pathogenesis
• A proportion of collaterals dilate, facilitating blood to flow into the infarcted area.
• Local blood vessels dilate, and area becomes overfilled with stagnant blood
• Muscle fibres uptake remaining oxygen, and haemoglobin becomes deoxygenated  Bluish brown hue and blood vessel engorgement occurs despite lack of blood flow.

38
Q

How does an oedema form in late stage IHD?

A

The coronary vessel endothelium increases in permeability fostering the leakage of fluid into local tissues forming an oedema

Cardiac muscle cells swell and due to insufficient blood supply. undergo necrosis within hours.

39
Q

How much oxygen does cardiac muscle require?

A

Cardiac muscle requires 1.3ml of oxygen per 100g of muscle tissue
• 8ml of oxygen per 100g delivered to normal resting ventricle each minute such that the cardiac muscle does not necrose.
• 15-30% of blood supply remains  Muscle is preserved except in the central portion of a large infract with no collaterals.

40
Q

What are the main causes of death post-MI?

A

• Decreased cardiac output-systolic stretch and cardiac shock.
During ventricular systole, cardiac contraction will cause non-functional muscle to be forced outwards by pressure inside the ventricle.

The necrosed cardiac muscle in the left ventricle is pulled given that there is no elasticity resulting in a ballooning effect.

  • Cardiac failure arises due to an insufficient pumping mechanism such that stroke volume decreases and peripheral ischaemia arises.
  • Low cardiac flow  Low blood flow to kidneys  Fail to excrete water leads to congestive symptoms and pulmonary oedema (damming of the venous system).
  • Rupture of infarcted area: Infarcted area begins to degenerate, heart walls become thin stretched and are unable to sustain stretch during systole  cardiac rupture.

Ventricular fibrillation – can occur during the first 10 minutes – an hour.

41
Q

What can occur within the first 10-60 minutes post-MI?

A

Ventricular fibrillation

42
Q

Why can a cardiac rupture occur in a patient post-MI?

A

• Rupture of infarcted area: Infarcted area begins to degenerate, heart walls become thin stretched and are unable to sustain stretch during systole  cardiac rupture

43
Q

Why is the venous system affected in a post-MI?

A

• Low cardiac flow  Low blood flow to kidneys  Fail to excrete water leads to congestive symptoms and pulmonary oedema (damming of the venous system).

44
Q

What are the consequences for a small area of ischaemia?

A

There is minimal cell death, potential to become functional temporality due to nutrient restriction.

45
Q

What are the consequences for a large area of ischaemia?

A
  • Cardiac cells in the centre necrose rapidly within 1-3 hours due to complete loss of blood supply.
  • Immediately peripheral to the centre is non-functional area failure of contraction and impulse conduction.
  • Surrounding non-functional still contraction however weak due to mild ischaemia.
46
Q

Who is the NHS health check programme eligible for?

A

• Aged 40-74 years who have not been diagnosed with CVD, diabetes or CKD is invited every 5 years for a free health check

47
Q

How should a person’s 10-year CVD risk be assessed?

A

QRISK assessment tool

48
Q

What clinical examinations are performed on patients presenting with chest pain?

A

Heart auscultation
Blood pressure
BMI
General physical examination

49
Q

What lab-tests are performed for patients presenting with chest pain?

A

LDL, HDL
Triglycerides
Lipoprotein A
C-reactive protein

50
Q

What serum markers are elevated in patients with suspected acute cardiac events?

A

Troponins (I or T)
Creatine kinase with MB isozymes
Lactate dehydrogenase & isozymes
Serum aspartate aminotransferase

51
Q

What are the biomarkers for predicting death?

A 
B-type natriuretic peptide
CRP
Homocysteine
Renin 
Urinary albumin-to-creatinine ratio.
52
Q

What test should be done for a patient with stable angina, before an ECG?

A

Exercise stress test - ST-elevation indicating IHD

53
Q

What ECG changes are seen in a patient with an unstable angina?

A

ST depression and T-wave inversion

54
Q

What ECG changes are seen in patients with an acute MI/STEMI?

A

St-segment elevation with T wave inversion,

Q waves

55
Q

What investigation is conducted in individuals to evaluate haemodynamics in patients with stenosis?

A

Echocardiography

56
Q

What is the purpose of transthoracic echocardiography?

A
  • Left ventricular function
  • Wall-motion abnormalities in the setting of ACS or AMI
  • Mechanical complications of AMI
57
Q

How can an aortic dissection be assessed?

A

A transoesophageal echocardiography

58
Q

What is a stress echocardiography?

A

Stress echocardiography: Can be used to evaluate haemodynamically significant stenoses in stable patients who are thought to have coronary arterial disease.

59
Q

What is coronary angiography?

A

An iodinated contrast agent is injected through a catheter placed at the ostium of the coronaries.
• Visualised through radiographic fluoroscopic examination of the heart.
• Coronary angiography remains gold standard for detecting stenoses that may be revascularized through percutaneous or surgical intervention

60
Q

What is the gold standard investigation for detecting stenosis, prior to PCI?

A

Coronary CT angiography

61
Q

What are doppler velocity probes?

A

Doppler Velocity Probes
Applied technique for measuring coronary flow.
• Doppler guidewire measures phasic flow velocity patterns and tracks linearly with flow rates in small, straight coronary arteries.
• Doppler velocity probe use includes determining the severity of intermediate stenosis (40-60%).
• Evaluates whether the normal blood flow has been restored after percutaneous transluminal coronary angioplasty (PTCA).

62
Q

What is the mechanism of HMG-CoA reductase inhibitors?

A

Lower LDL-C levels. Lower triglyceride levels and raise serum HDL levels.
• Atorvastatin (Lipitor)

63
Q

What is the mechanism of calcium channel blockers?

A

Relaxes coronary smooth muscle and produces coronary vasodilation which in turns improves myocardial oxygen delivery.
• Amlodipine (Norvasc)

64
Q

What is the mechanism of action for bile acid sequestrants?

A

The bile acid sequestrants block enterohepatic circulation of bile acids and increase faecal loss of cholesterol.
• Cholestyramine (Questran, LoCholest, Prevalite)

65
Q

What is the mechanism of action of ACE inhibitors?

A

Hypertension and atherosclerosis may be intimately linked through their effects on vascular endothelial dysfunction.
• Captopril (Captoten), enalapril (Vasotec), and lisinopril (Zenstril)

Inhibit the conversion of angiotensin-I to angiontensin-II.

66
Q

What is the mechanism of action for beta-blockers?

A

Inhibit sympathetic stimulation of the heart, reducing heart rate and contractility; this can decrease myocardial oxygen demand and thus prevent or relieve angina in patients with CAD.

67
Q

What are antianginal agents?

A

Ranolazine is a novel antianginal agent  Relieve ischaemic by reducing myocardial cellular sodium and calcium overload via inhibition of the late sodium current of the cardiac action potential.

68
Q

What are platelet aggregate inhibitors?

A

Exert protection against atherosclerosis through inhibition of platelet function and through changes in haemorrhagic profile.
• Clopidogrel
• Aspirin

69
Q

What function do nitrates have with treating IHD?

A

Nitrates are effective in the treatment of acute anginal symptoms.
• Sublingual GTN
• Primary anti-ischaemic effect of nitrates is to decrease myocardial oxygen demand by producing systemic vasodilation.

70
Q

What is a PCI?

A

Percutaneous coronary intervention
Involves angiography and stent placement:
• Treat stable CAD
• Improves blood flow by placing a stent and compressing the plaque – dilates vessel.
• PCI conducted in patients with the ability to revascularize to bypass the clot.

71
Q

What is a CABG?

A

CABG
A vessel from another part of the body to create a graft- allowing blood to flow around the blocked or narrowed coronary artery.
• Used of patients with several narrowed coronary arteries.

BRS 1b (62 decks)

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