CVS Session 10 Flashcards
How is cardiovascular chest pain located?
Central
What type of pain is caused by myocardial ischaemia?
Tightening and diffuse
What is the typical radiation of myocardial ischaemic pain?
L and/or R arms/shoulders Neck Jaw Back Epigastrium
What type of pain is caused by pericarditis?
Sharp
What type of pain is caused by aortic dissection?
Tearing
Where does the pain from an aortic dissection radiate to?
Backwards b/w shoulder blades
Down spine - following aorta
Where is respiratory chest pain located?
Lateral - localised to affected side
What is pleuritic pain?
Pain which is worse on inspiration and coughing
Give three causes of respiratory chest pain.
Pneumonia
Pulmonary embolism
Pneumothorax
Where is GI chest pain localised?
Chest and epigastrium
What makes GI chest pain worse?
Bending and/or lying down
Give four causes of GI chest pain.
Reflux oesophagitis
Gastric disease
Gall bladder disease
Pancreatic disease
What indicates that chest pain is due to musculoskeletal injury?
Hx of trauma
Hx of excessive use
Movements may increase pain
Give three MSK causes of chest pain.
Trauma
Muscle pain
Bone metastases
What is the most common cause of myocardial ischaemia?
Atheromatous coronary artery disease
What does coronary blood flow depend on?
Coronary artery resistance Perfusion pressure (diastolic BP)
What does myocardial oxygen supply depend on?
Coronary blood flow
Oxygen carrying capacity of blood
What does myocardial oxygen demand depend on?
HR
Wall tension
Contractility
What determines wall tension?
Pre load
After load
Give a circumstance when after load will be increased.
Pumping against stenosis
Which area of cardiac muscle is most vulnerable to ischaemia?
Subendocardial
Describe the collateral circulation of the heart.
Absent between major arteries
Present between smaller coronary arteries and arterioles
How does the collateral circulation change with ischaemia?
Expansion and development of new collaterals over time
What can cause IHD if coronary circulation is perfect?
Severe hypotension Non-atheromatous causes of coronary artery narrowing Severe anaemia Tachycardia Aortic stenosis Thyrotoxicosis
What are non-modifiable risk factors for CAD?
Age
Male gender - females catch up after menopause
FHx - especially in 1st degree relatives at an early stage
What are modifiable risk factors for CAD?
Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes mellitus
What is the structure of a stable atheromatous plaque?
Atheroma with a small necrotic core and thick fibrous cap
How can a stable atheromatous plaque present clinically?
Asymptomatic
Stable angina
Why does thyrotoxicosis increase myocardial oxygen demand?
Increased HR
Increased BMR
Is there myocyte injury and necrosis in stable angina?
Nope
What is used to determine the cause of chest pain?
Anatomical sieve
What is stable angina?
Transient ischaemia during periods of high oxygen demand
Relieved when demand stops
Can progress to severe, fixed narrowing
Predictable pain
What does stable angina indicate?
High risk of acute coronary syndrome
How quickly is the ischaemic pain of stable angina relieved by rest or nitrates?
~5 mins
What are the specific signs of stable angina on examination?
There are none
What is the clinical diagnosis of angina based on?
Hx
What signs of risk factors for stable angina may been seen on presentation?
High B.P.
Corneal arcus
Signs of atheroma elsewhere
Left ventricle dysfunction
What test can be used if the diagnosis of stable angina is uncertain?
Exercise stress test
Describe the exercise stress test for stable angina.
Patient has ECG continuously taken whilst undertaking graded exercise on a treadmill
Stop when target HR reached/ECG changes/chest pain/ other problems (arhythmias, low BP)
+ve if ST depression > 1 mm
How can the exercise stress test be used to determine the prognosis of stable angina?
Speed of development of ST depression correlates
What are the 5 mechanisms of stable angina treatment?
Decease preload and afterload
Decrease HR
Decrease myocardial contractility
Increase blood flow by revascularisation
Prevent progression and thrombosis and stabilise plaque
How can oral nitrates be used to treat stable angina?
Decrease preload
Why are calcium channel blockers used to treat stable angina?
If beta-blockers cannot be tolerated they decrease afterload
How can beta-blockers treat stable angina?
Decrease HR and myocardial contractility
How is PCI used to treat stable angina?
Percutaneous coronary intervention by stent
Femoral puncture –> aorta –> coronary artery
Which blood vessels can be used in CABG?
Radial artery
Internal mammary artery
Reversed saphenous vein
Why must the saphenous vein be reversed for use in CABG?
So the valves open in the right way
Which imaging technique influences whether PCI or CABG is used for revascularisation?
Angiography
Why are statins given to stable angina patients?
Decrease LDL levels
Reduce progression
Less necrotic core
Why is aspirin given in stable angina?
Prevent thrombosis
What is acute coronary syndrome?
A medical emergency when an atheromatous plaque fissure causes a sudden reduction in artery lumen which may be sufficient to cause myocyte injury/necrosis
How does ACS present?
Same pain as angina but much more severe
May have had preceding symptoms of atheroma
Can be asymptomatic until point of rupture
Which three conditions does ACS include?
STEMI
Unstable angina
NSTEMI
How does sudden plaque fissuring cause a STEMI?
Occlusion complete
Persistent
Large area of myocardium w/out collateral circulation affected
Severe ischaemia w/myocardial necrosis
How does sudden plaque fissuring cause unstable angina/NSTEMI?
Non occlusive thrombus Brief occlusion Small area of myocardium affected Collaterals present Less severe ischaemia +/- necrosis
What treatments are used for a STEMI?
Aspirin and colpidogrel IV nitrates Beta-blockers ACEI Statins
Why are ACEI used in treatment for a STEMI?
To prevent harmful heart remodelling in L ventricle dysfunction
Which areas of the heart are affected by a STEMI?
Sub-endocardial to sub-epicardial
What are the three types of unstable angina?
Crescendo
Angina at rest
Recent onset of new, effort limiting
What is crescendo unstable angina?
More frequent, more severe and longer lasting angina pain
What treatments are used for unstable angina/NSTEMI?
Anticoagulants - heparin Non-urgent PCI/CABG Antiplatelets - aspirin Statins ACEI
How does the presence of biomarkers differ between STEMI, NSTEMI and unstable angina?
STEMI: +ve
NSTEMI: +ve
Unstable angina: -ve
Which area of the heart is affected in NSTEMI/unstable angina?
Subendocardial areas
What ECG changes are seen in NSTEMI and unstable angina?
ST depression
What percentage of arterial occlusion is considered total artery occlusion?
90
Which proteins present in myocytes that are important in the myosin/actin interaction are released in myocyte death?
Cardiac troponin I and T
When are cardiac troponin I and T seen in the blood following MI?
4 hrs after onset of pain
When do cardiac troponin I and T levels peak following MI?
18-36 hrs after initial pain
How long does it take for cardiac troponin I and T to be returned to normal levels in the blood?
Up to 10-14 days
Why are cardiac troponin T and I a good biomarker for detecting MI?
V. Specific and sensitive
What is the cardiac isoenzyme of creating kinase?
CK-MB
When would CK-MB be used as a biomarker of myocyte damage?
When troponins are unavailable e.g. when new episodes of chest pain occur w/in 10 days of initial MI
How do the levels of CK-MB vary over time?
Rise 3-8 hrs after onset of pain
Peak at 24 hrs
Back to normal after 48-72 hrs
What is the typical Hx given by a patient suffering an MI?
Central, crushing chest pain w/typical radiation
‘Feeling of impending death’
Persistant pain often w/ no precipitant
Autonomic features e.g. nausea, vomiting, faint
Signs of LV dysfunction - breathlessness, lung base crackles, low BP, S3/S4
Why are aspirin, beta-blockers and statins used as long term treatments for MI?
Decrease mortality
Decrease risk of reinfarction
Why are ACEI used as a long term treatment following MI?
Increase survival
What non-medicine long term treatment can be used following an MI?
Management of risk factors
Why are pathological Q waves seen in myocyte damage?
‘Window’ created by necrotic tissue so don’t see depol moving towards view
What is the criteria of a pathological Q wave?
Wide = >1 small square wide Deep = >25% of QRS
Why are pathological Q waves not always deep?
Not always followed by R wave
What causes the T wave inversion on an ECG showing myocyte damage?
Ischaemia
Describe the progression of ECG changes with myocyte damage.
Hyperacute T-wave in mins/hrs –> ST elevation in 0-12 hrs –> Q wave in 1-12 hrs –> ST elevation w/T wave inversion in 2-5 days –> recovery after weeks-months
What are the complications of MI?
Sudden cardiac death - V. Fib/asystole Arrhythmias Heart block Re-entry circuits/ increased automaticity --> V. tachy/fib Heart failure Cardiogenic shock
What is cardiogenic shock?
When >40% of myocardium is infarcted –> severely decreased cardiac output –> systolic BP
What causes heart failure as a complication of MI?
Decreased contractility
If the area of infarction in MI is inferior, which ECG leads and which artery will be affected?
II, III, aVF
RCA
If the area of infarction in MI is anteroseptal, which ECG leads and coronary artery will be affected?
V1-V2
LAD
If changes are visible in the V3-V4 ECG leads, which area of the heart and coronary artery have been affected?
Anteroapical
LAD (distal)
If the I, aVL, V5-V6 ECG leads have noticeable changes in them following MI, which area of the heart and coronary artery have been affected?
Anterolateral
Cm
If the proximal LCA has been occluded in MI, which area of the heart and ECG leads will be affected?
Extensive anterior
I, aVL, V2-V6
If the RCA is occluded in MI, which area of the heart ands hat change is seen in V1?
True posterior
Heightened R wave
