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Cardiovascular System > CHD, MI and embolism > Flashcards

CHD, MI and embolism Flashcards

1
Q

How does coronary artery disease present?

A
  • Sudden cardiac death
  • Acute coronary syndrome
    Acute MI
    Unstable angina
  • Stable angina pectoris
  • Heart failure
  • Arrhythmia
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2
Q

What two main categories does sudden onset chest pain fall under?

A
  • MI

- Progressive unstable angina

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3
Q

What are the consequences of CAD?

A
  • Damage of the heart muscle leading to heart failure (cannot pump)
  • if there is scar tissue formation within the myocardium then this is an important substrate for the development of arrhythmia which leads to sudden cardiac death
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4
Q

Describe the epidemiology of CVD?

  • worldwide
  • mortality
  • death number worldwide
  • women?
  • age?
A
  • number one cause of death worldwide
  • leading cause of death in women
  • leading cause of death in over 70
  • affects more women
  • mortality has decreased by 50% over 50 years
  • 17 million death yearly
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5
Q

UK burden of CHD

A
  • 88,000 CHD deaths in UK yearly
  • Commonest cause of premature death
  • mortality falling but higher than rest of Europe
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6
Q

What are the risk factors of CHD?

A
  • tobacco
  • physical inactivity
  • alcohol abuse
  • hypertension
  • obesity
  • diabetes
  • hyperlipidaemia
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7
Q

What is angina pectoris?

causes, relieved by?

A
  • clinical diagnosis
  • discomfort in chest, jaw, shoulders, arms or back
  • provoked by stress or exertion
  • rest or GTN (inorganic nitrate vasodilator)
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8
Q

Describe the epidemiology of stable angina

A
  • incidence increasing
  • 2 million cases in the UK
  • affects more people as age increases
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9
Q

What is myocardial ischaemia?

A
  • Mismatch between myocardial oxygen supply and demand
  • Primary reduction in blood flow
  • Inability to increase blood flow to match an increase in metabolic demand
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10
Q

What is the job of the coronary circulation?

A
  • To make sure that over a wide range of perfusion pressures, flow remains constant - autoregulation
  • To make sure that coronary blood flow matches myocardial demand
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11
Q

What is the purpose of investigations for stable CHD?

A
  • To confirm the clinical diagnosis

- To assess risk of future adverse cardiovascular events (severity, heart function)

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12
Q

What are some of the categories of investigations into CHD?

A

Functional - demonstrate that there is an imbalance between supply and demand
Anatomical - look at anatomical severity of the narrowing within the artery then make an inference about how it is affecting flow

Some of these tests are invasive and others are not

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13
Q

Give examples of functional invasive and non invasive tests

A

invasive - FFR (guided pressure wire), iFR

non invasive - exercise ECG, stress echo, PET/CT

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14
Q

Give examples of anatomical invasive and non invasive tests

A

invasive - coronary angiogram

non invasive - CT coronary angiogram, CT coronary calcium score

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15
Q

What are the treatment strategies for CHD?

A
  • prevent atherosclerosis progression and MI risk through education, lifestyle and aspirin/ACE inhibitors/statins
  • reduce heart oxygen demand (meds to reduce heart rate, wall stress and metabolic modifiers)
  • improve blood supply (vasodilators, revascularisation)
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16
Q

UK MI epidemiology

A
  • 124,000 per year
  • 33,600 death yearly
  • cost 3.6 billion yearly
17
Q

Describe the functional anatomy of the coronary circulation

A
  • Epicardial coronary arteries (those running on the surface) are conductance vessels that are dependent on arterial pressure.
  • Overall coronary resistance is 50% in large arteries and 50% in the smaller arteries and capillaries.
  • Seperated into: epicardial and intracardial components.
18
Q

What is the effect of epicardial stenosis on resting TPR and blood flow?

A
  • With stenosis in the epicardial compartment, the resistance here increases
  • This is compensated to some degree by an increase in vasodilation (reduction in R) in the intramyocardial vessels, however, after around 70% stenosis, coronary blood flow decreases rapidly.
19
Q

What is the coronary flow reserved and how is it calculated?

A
  • The ratio of resting blood flow: blood flow achieved under maximal stress = coronary flow reserve
  • This reserve is the ability of the coronary circulation to adapt to an increasing demand in the face of increasing stenosis
  • Past 50% stenosis, the ability of the coronary circulation to increase blood supply in response to a vasodilator falls
20
Q

Mechanisms of Myocardial Infarction- what causes interrupted blood flow to heart?

What are the ways in which mycoardial death occurs?

A
  • Coronary plaque rupture (this is the most common cause of MI – 70-80% cases)
  • Coronary plaque erosion
  • Coronary dissection
  1. Oncosis – Ischaemic cell death
  2. Apoptosis – Programmed cell death
21
Q

What are the types of thrombus and how is it formed?

A

WHITE Thrombus:

  • Platelet rich.
  • Common in arterial thrombosis.
  • Treated by anti-platelet therapy.

RED thrombus:

  • Fibrin rich (with trapped erythrocytes).
  • Common in venous thrombosis.
  • Treated by anti-coagulants.

Thrombus Formation:
Tissue factor plays a key role and is made by either the plaque itself or ischaemic muscle cells.
TF can trigger the cascade of factor activation leading to coronary thrombosis (10a and 2a are important).

22
Q

What is the effect of coronary stenosis on sheer stress and blood flow type?

A

The blood focuses to go into the narrowing which slows the blood flow down and decreases shear stress, then inside the stenosis, a high shear stress exists where the blood accelerates and then upon exiting, turbulent flows are created which decreases shear stress which can have an affect on deregulating the endothelium

23
Q

What is the universal definition of an acute myocardial infarction?

A

Detection of a rise or fall in a biomarker (troponin) with at least one value >99th percentile reference limit and at least one of: symptoms, ECG changes or heart muscle change

24
Q

What are some of the symptoms of MI used in the definition?

A
  • Symptoms suggestive of ischaemia
  • New or presumed new ST-T changes or LBBB (left branch bundle block) on ECG
  • Development of pathological Q wave on ECG
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of intracoronary thrombus or angiography autopsy
25
Q

Troponin as a marker for MI diagnosis

A
  • Cardiac Troponin (cTn) is the part of the thin filament of the sarcomere and it comes in 3 isoforms:
    I, T and C with I and T being specific to cardiac muscle
  • I and T are used to diagnose MI
  • After the onset of symptoms, cTn rises and falls after a period of time (>2 weeks is undetectable)
26
Q

Acute Coronary Syndrome and their Associated ECG changes

A

There are 2 types of ACS:

  1. ST Elevation – Complete occlusion of the lumen
  2. No ST Elevation – Partial occlusion which then embolises distally resulting in MI cell death and troponin elevation
27
Q

How does the MI develop?

A

Essentially, the myocardial necrosis zone post-MI will begin at the inner layers of the myocardium as this is where the most work occurs. The infarct if left can become a transmural infarct which is very bad.

28
Q

What is reperfusion injury?

A

The act of opening an artery following a period of ischaemia associated with heart muscle damage

No reperfusion = 70% cell death
Reperfusion = 30% cell death due to lethal perfusion
Reperfusion with cardioprotection = 5%

29
Q

Left ventricular remodelling following myocardial death: what is it and what does it result in?

A
  • Remodelling results in expansion of the heart muscle, thinning of the
    scar and impairment of heart function
  • Accompanied by an increased risk of heart failure and arrhythmias
  • Results in: LV dilation = increased wall tension (to maintain CO
  • In non damaged myocardium inflammation and myofilament disruption, LV hypertrophy etc may occur affecting heart function even more
30
Q

What are the consequences of adverse LV remodelling?

A
  • Increased systolic and diastolic wall tension/stress.
  • Increased MVO2
  • Reduced myocyte shortening
  • Reduced sub-endothelial perfusion
  • Heart blocks
  • Mitral regurgitation
  • Ventricular arrhythmias and fibrillation
31
Q

How is an acute and recurrent thrombosis managed?

A

Acute:

  • Thrombectomy
  • Drugs e.g. IV antiplatelets

Recurrent:

  • Oral antiplatelet drugs
  • Anticoagulants e.g. F10a inhibitor
32
Q

How are plaques managed (stabilised)?

A

Mechanical:
- Stent

Drugs:

  • Statins (high dose) – anti-inflammatory effect
  • ACE inhibitors
33
Q

How is LV re-modelling managed?

A

Non-drug:

  • Pacemakers or Defibrillators
  • Progenitor cells

Drugs:

  • Beta blockers
  • ACE inhibitors
34
Q

What is an embolism?

A

An obstruction in a vessel due to a travelling thrombus

35
Q

Arterial embolus - causes and forms

A

Caused by transient ischaemic attack or stroke

  • Comes in embolic or haemorrhagic forms
36
Q

What are other forms of embolus and what can cause them?

A

Air embolism – e.g. compression sickness

Fat embolism – e.g. trauma

Amniotic fluid embolism – e.g. sudden CV collapse due to maternal amniotic fluid embolus

Cholesterol embolism – e.g. plaque rupture and cholesterol embolus

37
Q

Deep vein thrombosis: incidence, aetiology, diagnosis, complication, prevention, treatment

A

Incidence: 1.6 per 1000 a year

Aetiology: Trauma, malignancy, orthopaedic surgery, immobility, autoimmune disease

Diagnosis: CT, MRI, venography

Complications: Pulmonary embolism, post thrombotic syndrome, venous ulcer

Prevention: TEDS (drugs)

Treatment: anticoagulants, fibrinolysis, thrombectomy

38
Q

Pulmonary emoblism: symptoms, diagnosis, complications and treatment

A

Symptoms: dyspnoea, chest pain, hypotension and shock

Diagnosis: clinical, ECG, echo, MRI and pulmonary arteriogram

Complications: death, shock. pulmonary hypertension, RV failure

Treatment: anticoagulation, fibrinolysis, IVC filter

39
Q

What is PPCI – Primary Percutaneous Coronary Intervention?

A

Used to treat ST Elevation acute coronary syndrome

-A guide wire is passed through the thrombus and a stent is put in to re-canalise the vessel.

Cardiovascular System (19 decks)

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