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case 1: cardiac arrest > Ischaemia/ Infarction (Friday 27th) > Flashcards

Ischaemia/ Infarction (Friday 27th) Flashcards

1
Q

Ischaemia

A

Organ/ tissue has lowered perfusion relative to metabolic needs.

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2
Q

Infarction

A

Need ischaemia for infarction. Localised area of tissue necrosis due to ischaemia.

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3
Q

Vascular Occlusion

A

The most important cause of ischaemia and infarction. It can be arterial, venous or capillary.

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4
Q

Arterial Ischaemia Causes/ Aetiology

A
  1. Atheroma and thrombrosis
  2. Low flow infarction: occurs in cardiovascular shock. E.G. Blood lost due to trauma. The heart does not have enough blood to pump to the tissues.
  3. Other - embolism, vasculitis, hypertension, spasm
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5
Q

Susceptibility factors in Arterial Ischaemia

A
  • Adequacy of organ function
  • Arterial supply: dual like in lung and liver may protect, single like heart is more susceptible

-Type of onset:
Slow / gradual - collaterals may develop (In anatomy, a collateral is a subordinate or accessory part. A collateral is also a side branch, as of a blood vessel or nerve. After a coronary artery occlusion, collaterals (that is, collateral vessels) often develop to shunt blood around the blockage).
Fast / sudden - more susceptible

  • Tissue susceptibility: Brain most susceptible. Also heart.
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6
Q

Clinical Syndromes of Arterial Ischaemia

A
  • Depends on whether vascular narrowing/ occlusion is sudden or gradual
  • GRADUAL = angina but SUDDEN = myocardial infarction
  • GRADUAL = hypertensive renal disease but SUDDEN = renal infarct
  • GRADUAL = claudification but SUDDEN = gangrene
  • GRADUAL = dementia but SUDDEN = brain infarction
  • GRADUAL = ischaemic colitis but SUDDEN = gut infarct infarct
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7
Q

The four ways in which IHD can manifest

A
  1. Chronic Ischaemic Cardiopathy
  2. Cardiac Sudden Death
  3. Angina
  4. Acute Coronary Syndromes
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8
Q

Aspects of MI by different techniques

A

BIOCHEMISTRY:
- Markers of myocardial cell death recovered from blood samples

ELECTROCARDIOGRAPHY:

  • Evidence of myocardial ischaemia (ST-T segment changes)
  • Evidence of loss of electrically functioning cardiac tissue (Q waves)

IMAGING:

  • Reduction or loss of tissue perfusion
  • Cardiac wall motion abnormalities
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9
Q

Capillary Ischaemia Causes/ Aetiology

A

Blocked or damaged capillaries can lead to local ischaemia
EXAMPLES:
Frostbite
Cryoglobulinaemia
Disseminated intravascular coagulation (DIC)
Diabetic microangiopathy

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10
Q

Venous Ischaemia Causes/ Aetiology

A

Venous obstruction ultimately leads to cessation of arterial inflow, and infarction results.

The best known example of this is gut infarction in a strangulated hernia. The arrow shows a hernia in the inguinal canal.

The herniated intestines can strangulate at the OS (arrow) of the hernia, obstructing venous return, resulting in ischaemia and infarction.

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11
Q

ISCHAEMIC HEART DISEASE EPIDEMIOLOGY

A

see cvd death rates across classes
Under 40 = 10%
Under 65 = 45%
Frequency rises progressively with age and when predisposition to atheromatosis are present (hypercholesterolemia, smoking diabetes, HTS)
Women are “protected” against MI during reproductive years.

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12
Q

CHRONIC ISCHAEMIC CARDIOMYOPATHY

A

Cardiomyopathy refers to diseases of the heart muscle. These diseases have many causes, signs and symptoms, and treatments. The heart muscle becomes enlarged, thick or rigid in cardiomyopathy, and in rare cases the muscle tissue is replaced with scar tissue.

Causes of CM:

  • Post- infarct (silent or not)
  • Myocardial degeneration (old people)

Histology of CM:

  • Myocyte atrophy
  • Patchy interstital fibrosis
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13
Q

SUDDEN CARDIAC DEATH

A

Unexpected death due to heart problems, which occurs within one hour from the start of any cardiac-related symptoms. Due to massive transmural acute myocardial infarction or fatal arrhythmia [i.e. ventricular fibrillation, asystolia …]

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14
Q

ANGINA (Angor Pectoris)

A

Paroxysmal and usually recurrent attacks of subesternal or precordial chest discomfort (constricting, squeezing, choking …) caused by transient (15’’ to 15’) myocardial ischemia that falls short to induce cellular necrosis*.

  • Cellular necrosis defines infarction from the pathological point of view.

STABLE ANGINA – is the most common type. Atheromatosis with luminal stenosis <50%. Subendocardial ischemia. ST depression.

PRINZMETAL OR VARIABLE ANGINA – due to spam in artery with severe atheromatosis (>50%), occurring at rest.

UNSTABLE OR CRESCENDO – progressively increasing frequency of the pain with less effort. Disruption of plaque with superimposed partial thrombosis.

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15
Q

ACUTE CORONARY SYNDROMES

A

The term acute coronary syndrome (ACS) refers to any group of clinical symptoms compatible with acute myocardial ischemia and includes unstable angina (UA), non—ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).

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16
Q

Flowchart for if a patient has acute coronary syndromes to identify if they have MI

A

Do ECG: if no elevated ST than they have incomplete/transient occlusion. Do blood test, check for elevation of bio-markers for Myocardial Necrosis. If no bio-markers, and no ST segment elevation then have unstable angina. However if no ST- segment elevation, but bio-markers in blood test for myocardial necrosis then have Non-ST-segment Elevation Myocardial Infarction (NSTEMI) caused by partial thickness MI.

Do ECG: if elevated ST- segment, and blood test will show elevated biomarkers of myocardial necrosis. They have STEMI (Q waves usually present) caused by transmural MI.

17
Q

Myocardial Infarction

A
  • Death of portion of heart tissue due to lack (block) of blood supply
  • The main cause (99.8%) is thrombosis over an atheromatous plaque.

-The right coronary artery (RCA) serves the posterior left ventricle and 1/3 posterior interventricular septum
The left coronary artery (LCA) divides into the left circumflex (LCX) and left anterior descending (LAD) arteries.
The LAD serves the anterior left ventricle and anterior 2/3 interventricular septum.
The LCX serves the lateral wall of the left ventricle.
Coronary artery thrombi cause infarcts in the areas served

  • Atheromatosis is the most common cause.
  • Subendocardial infar.ction: not full thickness/ extension. 10% of the cases
  • Transmural Infarction: characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. 90% of the cases
18
Q

Complications in MI

A 
Can be early phase 2-10 days:
Reinfarction [extension MI]
Arrhythmia
Acute cardiac failure [cardiogenic shock]
Acute Pericarditis
Aneurysm
Thrombosis/Embolism
Cardiac rupture
Free wall
Interventr. septum
Papillary muscle
Or late.p (10+ days)
Aneurysm
Recurrent M.I.
Chronic cardiac failure
Dressler syndrome
Pericarditis 2-10 months post MI
Immunological mechanism
Elevated ESR

Expanded info on some complications:

  1. Arrhythmia
  2. Asystole (a cardiac arrest rhythm in which there is no discernible electrical activity on the ECG monitor- a “flat line.”)
  3. Ventricular fibrillation
  4. Free wall rupture, heamo-pericardium, cardiac tamponade.
  5. Papillary muscle infaction, papillary muscle rupture, severe mitral regurgitation
  6. Mural thrombus (a thrombus in contact with the endocardial lining of a cardiac chamber or, if not occlusive, with a wall of a large blood vessel) leading to Systemic Embolism (blockage causing material in arterial CV system).
19
Q

Macroscopic Appearances in MI

A

Time from Onset
18-24h = Pallor of myocardium (little to see)
24 - 72h = Pallor with some hyperemia
3 - 7 days = Hyperemic (an excess of blood in the vessels supplying an organ or other part of the body) border with central yellowing
10 - 21 Days = Maximally yellow and soft with vascular margins
7 weeks = White fibrosis

20
Q

Microscopic Appearances in MI

A

Time from Onset
1 – 12 Hours: None
12 - 24 Hours: Wavy myocardial fibers. Complement activation (ICC to C9, C4d)
18 - 24 Hours: Coagulation necrosis (early loss of myocyte nuclei and striations), haemorrhage, nuclear pyknosis and early neutrophilic infiltrate
24 - 72 Hours: Total loss of nuclei and striations along with heavy neutrophilic infiltrate
3 - 7 Days: Macrophage and mononuclear infiltration begin. Fibrovascular response (granulation tissue) begins
10 - 21 Days: Fibrovascular response with prominent granulation tissue
7 weeks: Fibrosis

C-reactive protein (CRP) is a substance produced by the liver that increases in the presence of inflammation in the body. An elevated C-reactive protein level is identified with blood tests and is considered a non-specific “marker” for disease. Complement activation is due to the presence of CRP

case 1: cardiac arrest (21 decks)

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