case 2 - clinical symposium Flashcards
the 2 types of causes of chest pain
visceral
somatic
the 3 types of visceral chest pain
Cardiac
Pulmonary
Gastrointestinal
the 2 types of somatic chest pain
Musculoskeletal
Spinal
what are the 2 different types of pain
visceral pain
referred pain
examples of visceral pain
*Deep sensation
*Discomfort, pressure,
tightness, squeezing, dull,
aching, boring
*Poorly localized
*Sense of malaise
*Strong autonomic reflexes eg.
Sweating, nausea, dizziness
examples of referred pain
*Superficial sensation
*Numbness, tingling,
aching
*Localized to dermatomes
relating to the affected
viscus
what does angina feel like
‘strangling’ or ‘throttling’ pain (angere)
in cardiac ischaemia, myocardial oxygen supply is equal to or less than or more than myocardial oxygen demand?
myocardial oxygen supply is less than myocardial oxygen demand
what increases myocardial oxygen demand in cardiac ischaemia?
Exercise – Heart rate and contractility go up.
Emotional stress – Sympathetic activation = increased HR and BP.
Peripheral vasoconstriction – Increases afterload = more work for the heart.
Ventricular hypertrophy – More muscle mass = more oxygen needed.
what decreases myocardial oxygen supply in cardiac ischaemia?
Coronary atheroma – Plaque buildup in coronary arteries = reduced blood flow.
Coronary spasm – Transient narrowing of coronary arteries = sudden drop in supply.
Microvascular dysfunction – Small vessels don’t dilate properly = poor perfusion.
Anaemia – Low hemoglobin = less oxygen carried in the blood.
Blood redistribution – Conditions like shock or vasodilation in other areas can “steal” blood from the heart.
MEDIATORS
OF CARDIAC
ISCHAEMIC
PAIN - name 3
The heart is insensitive to touch,
cutting, cold and heat.
Reduced coronary perfusion activates
coronary presso-receptors.
Hypoxia activates myocardial presso-
receptors and chemo-receptors.
Pain-producing substances and
metabolites, e.g Lactic acid, K+, kinins, Adenosine.
Distension of cardiac chambers and
large vessels
PHYSIOLOGY OF CARDIAC
ISCHAEMIA
*Resting myocytes use up to 65% of oxygen
delivered to them
*Most tissues use only 25% of oxygen delivered
*Increased myocardial oxygen demand can
therefore only be met by increased coronary
blood flow and oxygen delivery
*Stress requires an increase in coronary blood flow of x3-4 (250mls/min to 1000mls/min) to meet increased myocardial oxygen demand
equation for coronary blood flow
Coronary blood flow = Change in Pressure/Resistance
equation for blood resistance
resistance=1/r^4 (r for radius)
consider the equations for coronary BLOOD FLOW AND RESISTANCE… if an artery or arteriole constricts to half its original
radius its resistance to blood flow is increased…
increased by 16 times
REDUCTION IN CORONARY BLOOD FLOW due to what
Epicardial narrowing
*Atherosclerosis
*Vasospasm
Microvascular
*Endothelial dysfunction
*Widespread in the arteriolar circulation (microvasculature)
CORONARY ATHEROSCLEROSIS
AND CORONARY BLOOD FLOW
*Even severe coronary stenosis can be asymptomatic at rest
*Autoregulation maintains coronary blood flow at normal levels at rest across a wide
range of perfusion pressures
*Reduced coronary reserve during stress
mechanism of action of REFERRED PAIN
Visceral afferent pain fibers from the heart travel along the thoracic cardiac branches of the sympathetic trunk, primarily entering the spinal cord at levels T1 to T4 (especially T1–T3).
At these same spinal cord segments, somatic sensory afferents from the T1 to T3 dermatomes — which include areas of the chest wall and medial aspect of the upper arm — also enter the spinal cord.
Both visceral and somatic afferents have their cell bodies in the dorsal root ganglia of these spinal segments (T1-T3) and transmit signals through the posterior/dorsal roots into the spinal cord.
Within the dorsal horn of the spinal cord, visceral and somatic afferent fibers synapse on the same second-order neurons.
The central nervous system can’t distinguish whether the pain originated from the heart (visceral) or from the skin/muscles (somatic), so it interprets the pain as coming from the somatic region, typically the left chest, shoulder, or inner arm → hence referred pain
Late Presentation of
a NSTEMI - Will require?
Coronary artery investigations
Echo Cardiogram (ECG)
Lipid lowering medication (statin)
Antiplatelet medication (possible ACEi and
beta blockers)
Diagnostic criteria of NSTE-ACS?
all ACS’s without significant ST elevations are classified as NSTE-ACS. in most cases, there’s ST-segment depressions and/r T-wave inversions. A minority of patients with NSTE-ACS display normal ECG through the course
pathophysiology of NSTE-ACS?
partial occlusion causing ischaemia located to the subendocardium
pathophysiology of STE-ACS?
total occlusion in a coronary artery. this causes extensive ischaemia which is transmural (i.e stretches from endocardium to epicardium). these infarctions are large and usually lead to development of pathological Q-waves in leads with ST elevation
diagnostic criteria of STE-ACS?
All ACS’s with significant ST elevations are classified as STE-ACS. The ECG will usually also display ST-segment depressions and/or T-wave inversions
describe what AORTIC DISSECTION CHEST
PAIN feels like (name 1 or 2 bullet points)
Severe pain -agony, writhing, unbearable
‘Tearing’ or ‘ripping’
Migration with propagation of the dissection
Anterior chest with proximal dissection
Interscapular and back with distal dissection
Prominent autonomic symptoms
*Nausea, vomiting
*Sweating
*Fainting, hiccups
