4. Ischaemic Heart Disease And Failure Flashcards
What is Ischaemic heart disease (IHD)
Inadequate blood supply to heart
What is IHD caused by
Reduced coronary blood flow due to atheroma mostly/ can be thrombus
Myocardial hypertrophy- may be due to high b.p n overworking
What percentage of a coronary vessel lumen being occluded would be considered critical stenosis
75 % or more
Therefore have symptoms at this stage
What is door to balloon time
The time between getting symptoms to getting a coronary angioplasty of the coronary artery
What is the percentage increase in mortality if the door to balloon time is increased over 2 hrs
20 percent to 60 percent
After how long after a coronary occlusion would myocardial necrosis be seen
30 minutes
How many minutes is considered rapid perfusion (which would prevent cell loss and can limit infraction size/ area of risk)
20 mins
What are the three types of angina pectoris
Typical/ stable
Crescendo/ unstable
Variant/ prinzmetal
Which types of angina pectoris can happen at rest
Crescendo
Variant/ prinzmetal
How can a typical/ stable angina be relieved
By rest (symptoms occur OE) Nitrate (vasodilator - cos of chronic narrowing due to atherosclerosis)
What can a crescendo angina be caused by
Disruption of the atheromatous plaque eg rupture with partial thrombus/ embolism
- happens usually before MI
What causes variant angina pectoris
Due to coronary artery spasm, caused by transient myocardial ischaemia
Unrelated to exertion
What is acute coronary syndrome
unstable angina, non-ST-segment-elevation myocardial infarction (NSTEMI) and ST-segment-elevation myocardial infarction (STEMI) that are due to a sudden reduction of blood flow to the heart.
What is ST elevation referring to
Abnormality seen in an ECG ST segment (interval between ventricular depolarisation and re polarisation) is raised
What can acute ischaemia lead to
Trans mural MI
What is a trans mural MI
Ischaemi necrosis involves the full thickness of the ventricular wall
What is a subendocardial MI
Ischaemia involved a small area (on the inner layers) of teh myocardial wall not all the layers - only the subendocardium
Which type of MI has ST elevation
Trans mural
What does STEMI stand for
ST-segment elevation myocardial infarction
What does the heart look like at 1 to 2 days of an MI
Pale
Odeamatous
Myocyte necrosis
Neutrophils
What does teh heart look like at 3-4 days of an MI
Yellow with haemorrhagic edge
Myoctye necrosis
Macrophages
What does the heart look like 1-3 weeks after an MI
Red grey to pale- white
Thin
Granulation tissue then fibrosis
3 to 6 weeks of an MI, heart looks like?
Dense fibrous scar
What can cause a subendocardial MI
Plaque rupture
Coronary thrombosis where the necrosis doesn’t spread full thickness
Prolonged reduction in systemic blood pressure
Hypotensive meaning
Abnormally low blood pressure
In which people may an MI be silent/ atypical
Women
Elderly
Diabetics
Tests for MI
ECG Cardiac enzymes Echo Angio Pulse, breathing
What are cardiac enzymes and when can they leak out
Blood markers of cardiac myocyte damage that leak out when myocytes become damaged
Give 5 examples of cardiac enzymes
Tropnonins T and I Creatine kinase MB Myoglobin Lactate dehydrogenase isoenzmye 1 Aspartate trasnaminase
Why might the cardiac enzyme aspartate transaminase be a less useful marker of myocardial damage
It is also present in the liver
What do troponins T and I do
Regulate Ca mediated contraction
Tissue specific
When are levels of troponins T and I raised
Post MI
PE
Heart failure
Myocarditis
What else apart from teh heart is myoglobin also released from
Damaged skeletal muscle
Treatment of MI
MONA= Morphine Oxygen Nitrates Aspirin Reperfusion (eg, PCI, balloon angioplasty, stenting, coronary artery bypass grafting)
What that is the main aim of the treatment given for an MI
Reduce total ischamic time
What treatment can be given as a secondary prevention for MI
Ace- I = help to dilate vessel
Anti platelets = stops platelets from sticking - reduce clot formation
Anticogaltion = slow process of clot formation
Antiarrhythmics= restore normal heart rhythm
Beta blockers = reduce activity of the heart
Statins = lower blood choesltrol levels
What % of MIs are fatal
Over 35%
What % of fatal cardiac deaths are sudden cardiac deaths (in 1 to 2 hrs)
70%
Who may be at more risk of MI
Women
Elderly
Diabetics
Had a previous MI
How can an MI cause a myocardial rupture
Due to weakening of the necrotic muscle
What is tamponade
Compression of the heart by an accumulation of fluid in the pericardial sac
What is an aneurysm
Excessive localised swelling of an artery wall
What is chronic IHD
Progressive heart failure due to ischaemic myocardial damage
What is familial hypercholestrolaemia
Mutations in genes involved in cholesterol metabolism:
- low density lipoprotein receptor gene
- apoliprotein B
Symptoms of familial hyper cholesterolaemia in heterozygotes and thier treatment
Xanthomas = yellow patch/ nodule on skin caused by lipid deposition
Periocular corneal arcus
Early progressive atherosclerosis
Treatment = statins (hydroxymethyl CoA reductase inhibtors)
What is heart failure
Heart is unable to pump blood at required demand
End stage of all disease of the heart
In the western world what are the two most common causes of HF
Coronary artery disease (CAD)
Hypertension
Symptoms/ signs of HF
Dilated pupils Infarct Low bp Weak pulse Pitting oedema Confusion Falling 02 saturation Cough Dyspnea Orthopnea etc.
Give some causes of HF
CAD
Hypertension
Alcohol and drugs
Cardiomyopathy etc.
Investigation for HF
Initial: CXR ECG Echo Bloods
What does the New York Classifaction of heart failure severity do
Tells us about survival probability
Four classes:
I= no symptoms, normal functional status II= mild symptoms with normal activity, comfy at rest, slight limit of functionality III= moderate symptoms IV= sever symptoms even at rest, sever limitation of functional status
