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case two > ischaemia and infarction > Flashcards

ischaemia and infarction Flashcards

1
Q

define ischaemia

A

an inadequate supply of blood to a tissue, resulting in an insufficient supply of oxygen and other metabolic needs for that tissue

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2
Q

define infarction

A

an insufficient supply of blood carrying oxygen and other metabolic needs leading to cell/tissue necrosis

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3
Q

name the types of occlusion in ischaemia

A

partial complete - more severe and often leads to infarction

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4
Q

what factors make tissues more susceptible to ischaemia?

A
  1. previous damage to organ/tissue 2. single blood supply 3. onset of blood supply affected 4. type of tissue affected
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5
Q

what is the most common cause of ischaemia?

A

occlusion of blood flow - tissue isn’t getting enough oxygen to meet its metabolic demands

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6
Q

what are the main causes of occlusion?

A

atheroma thrombosis embolus spasm

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7
Q

name types of venous ischaemia

A

strangulated hernia volvulus - bowel twists around itself, blocking off its own venous supply

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8
Q

name examples of capillary ischaemia

A

frostbite diabetic microangiopathy disseminated intravascular coagulation

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9
Q

name the 2 non-vascular (not occlusion of a blood vessel) causes of ischaemia

A
  1. decrease in oxygenated blood flow 2. increased tissue demand
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10
Q

what can cause a decrease in oxygenated blood flow?

A
  1. Hypotension
  2. Anaemia – there are fewer red blood cells in the blood so fewer cells with oxygen carrying capacity
  3. Carboxyhaemoglobinaemia – i.e. carbon monoxide poisoning
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11
Q

what can cause increased tissue demand?

A
  1. Thyrotoxicosis – overactive thyroid
  2. Tachyarrhythmias – the heart is beating faster so needs more oxygen to meet its demands
  3. Marked Myocardial Hypertrophy – the heart is larger so needs more oxygen to maintain its contractile force
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12
Q

which clinical syndromes cause gradual occlusion?

A
  • angina
  • hypertensive renal disease
  • claudication
  • ischaemic colitis - blood vessels supplying large intestine
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13
Q

which clinical syndromes cause sudden onset of ischaemia/infarction?

A
  • myocardial infarct
  • renal infarct
  • gangrene
  • brain infarct
  • gut infarct
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14
Q

describe the pathophysiology of hypoxic damage

A
  1. narrowing/blockage of artery means not enough oxygen can get to the heart (inadequate perfusion)
  2. lack of oxygen (hypoxia) means heart cells shift to anaerobic metabolism, producing less ATP but more lactic acid
  3. this leads to a rise in sodium, calcium and water levels in the cell as pumps require ATP
  4. this leads to cell oedema and activation of degenerative lipases and proteases, which leads to cell death
  5. myocardial function is decreased within 2 mins dye to lack of ATP impairing contractile function
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15
Q

what are the non-modifiable risk factors for ischaemic heart disease?

A
  • increasing age
  • male (prior to age 60)
  • ethnicity (south asians who live in UK)
  • family history
  • social deprivation
  • type 2 diabetes
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16
Q

what are modifiable risk factors for ischaemic heart disease?

A
  • smoking
  • diet
  • sedentary
  • overweight/obesity
  • HBP
  • high cholesterol levels
  • excessive stress or alcohol consumption
17
Q

what are the two divisions of ischaemic heart disease?

A
  • chronic ischaemic heart disease
  • acute coronary syndrome
18
Q

name the 3 divisions of chronic ischaemic heart disease

A
  • stable angina
  • variant angina
  • silent angina
19
Q

name the 3 divisons of acute coronary syndrome

A
  • unstabke angina
  • NSTEMI
  • STEMI
20
Q

describe the pathophysiology of stable angina

A
  • narrowed coronary arteries due to build-up of atherosclerotic plaques
  • when patient does activity that puts stress on the heart, metabolic demands of the heart increase
  • due to narrowed coronary arteries, not enough blood can reach heart to meet its metabolic demands
  • leads to build-up of metabolites, causing chest pain (which can be releived by rest or GTN spray (causes vasodilation)
21
Q

what are the symptoms of stable angina?

A
  • central precordial chest pain, which may raidate to arms/jaw
  • pain can be ‘heavy, gripping, tight’
  • dyspnoea
  • palpitations
  • chest pain occurs on exertion and subsides after rest
22
Q

describe the pathophysiology of variant angina

A
  • caused by spasms of the coronary artery
  • can occur without provocation (i.e. at rest)
  • due spasm, coronary arteries are narrowed and metabolic demand of the heart can’t be met
  • build-up of metabolites, causing chest pain
23
Q

what is the difference between stable and variant angina?

A

stable = upon exertion

variant = at rest

24
Q

name possible reasons for lack of chest pain in silent angina

A
  • autonomic neuropathy - nerves are damaged
  • may not be enough myocardium involved to produce pain
25
Q

describe the pathophysiology of silent angina

A

same as the other types of angina, minus the chest pain

26
Q

describe the management of angina

A

lifestyle management

medications

  • to improve blood flow by dilating blood vessels
  • slow heart rate or reduce contractility to redyce demands from the heart/tissue for oxygen
  • secondary medication to reduce platelet aggregation, BP and blood cholesterol

surgery

  • cardiac revascularation (e.g. stenting)
  • improves passage of blood through arteries affected by occlusion
27
Q

why are the acute coronary syndromes grouped together?

A

all caused by acute disruption of a coronary artery plaque which leads to sudden occlusion of the artery via platelet aggregation

28
Q

list the types of acute coronary syndrome in order of severity (least to most)

A
  • unstable angina
  • NSTEMI
  • STEMI
29
Q

describe the pathophysiology of acute coronary syndrome

A
  1. atherosclerotic plaque within coronary artery ruptures due to blood flow, exposing soft material inside
  2. soft material is thrombogeneic (likely to form clots), leading to thrombus formation
  3. this leads to partial or complete occlusion of coronary arteries
30
Q

what are the symptoms of acute coronary syndrome?

A
  • dyspnoea
  • nausea
  • central chest pain - not all patients (some have a silent MI - more common in females, the elderly and diabetics)
31
Q

how can you diagnose acute coronary syndrome?

A

blood marker - troponin T

  • troponin is released when there is cardiac muscle damage due to necrosis
  • marker is taken multiple times during an admission and a significatn rise is diagostic of a myocardial infarction (NSTEMI or STEMI - no rise in unstable angina as there is no necrosis)

ECG changes

  • differentiate between STEMIs, NSTEMIs and unstable angina
  • e.g. in STEMIs, there is an elevation of the ST segment
32
Q

what are the ECG findings for unstable angina and NSTEMI?

A
  • can be normal
  • potential ECG changes = ST depression, T wave inversion
  • no ST elevation
33
Q

how is ACS managed?

A

immediate management

  • oxygen, vasodilator and analgesia (painkillers)

acute management - revascularation

  • improves passage of blood through arteries affected by occlusion
  • insertion of a stent into coronary arteries
  • bypass graft (attaching a vessel which bypasses the area of blockage within the artery)

longer term management

  • controlling modifiable risk factors
  • medication to reduce platelet aggregation, control BP and reduce/control blood cholesterl level
34
Q

name the possible complications following a myocardial infarction

A

Death

Arrhythmias – e.g. ventricular tachycardia/ventricular fibrillation.

Rupture – of ventricular septum (i.e. between the 2 ventricles), papillary muscles

Tamponade – accumulation of fluid within the pericardium (sac-like tissue surrounding the heart) leading to compression of the heart

Heart Failure – damage to the heart muscle due to the necrosis

Valve Disease – mitral regurgitation

Aneurysm – of the ventricle

Dressler’s Syndrome – pericarditis (inflammation of the pericardium i.e. sac like tissue surrounding the heart)

thromboEmbolism – mural thrombus = adhering to blood vessel wall

Recurrence – further MI

35
Q

name the symptoms of variant angina

A
  • central precordial chest pain, which may raidate to arms/jaw
  • pain can be ‘heavy, gripping, tight’
  • dyspnoea
  • palpitations
  • chest pain at rest usually, rather than exertion
  • more common in women
36
Q

what are the ECG findings for STEMIs?

A

ST elevation

case two (10 decks)

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