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I've Got Severe Pain in My Chest, named after, because it, arise from,…
I've Got Severe Pain in My Chest
Antianginal drugs
Ca+2 channel blockers
Intracellular Ca+2 influx inhibition
Dihydropyridine
Selectively on vascular smooth muscle
Nifedipine
Nimodipine
Amlodipine
Non-dihydropyridine
On both vascular and cardiac smooth muscles
Diltiazem
Verapamil
Slow AV conduction and decrease HR, contractility and BP
Organic nitrates
Dilation of large veins and coronary vasculature
Increase blood flow to the heart
Sublingual nitroglycerin
Isosorbide mononitrate
Decrease preload
β-Blockers
Blocking beta receptors
Decrease in HR and contractility
Decrease O2 consumption
Reducing frequency and severity of angina
Adverse effects
Erectile dysfunction
Hypotension
Bradycardia
Fatigue
Ranolazine
Inhibiting the late phase of the sodium current
Improving the O2 supply and demand equation
Angina pectoris
Risk factors
Tobacco use.
Diabetes.
hypertension
Older age.
Obesity.
Types
Stable, effort-induced, classic
Most common
Caused by
the reduction of coronary perfusion
due to
a fixed obstruction of a coronary artery
Characterized by
a short-lasting burning, heavy, or squeezing feeling in the chest
Unstable angina
considered between
stable angina and MI
Chest pain occurs with
increased frequency, Duration and Intensity
suggestive of unstable angina
Any episode of rest angina longer than 20 minutes
any increasing angina
sudden development of SOB
is a form of
ACS
requires
more aggressive therapy
to prevent progression to MI and death.
hospital admission
Prinzmetal, variant, vasospastic, or rest angina.
Uncommon
occurs
at rest
due to
coronary artery spasm
Symptoms are due to
decreased blood flow to the heart muscle
by
the spasm of the coronary artery
.
May also present with
dyspnea
atypical symptoms
such as
Indigestion
Nausea
vomiting.
Is a characteristic
sudden, severe, crushing chest pain
that may
radiate to the neck, jaw, back, and arms.
Internal validity & forensic medicine
Refers to trustworthiness of the research
Chance
Randomization
Increase sample size
Bias
Information bias
Selection bias
Study design bias
Confounding
Ensure adequate similarity in baseline characteristics of the sample
The branch of medicine dealing with the application of medical knowledge to establish facts in civil or criminal legal cases
Investigation into the cause and time of a suspicious death
Autopsies
DNA analysis
Control of coronary circulation
high metabolic rate
contractile force
basal metabolic processes
ionic homeostasis
high capillary density
high oxygen extraction
by increasing blood flow
coronary driving force
coronary driving force = Aortic root pressure - LVEDP
physicsl factors
redistribution of blood flow during systole
blood flow reduces during systole
compression of coronary vessels due to myocardium contraction
entrance of coronary vessels is partially blocked by opening of aortic valve
metabolic factors
blood flow
coronary vasodilators
adenosine
myocardial oxygen balance
O2 supply
coronary blood flow
O2 content in blood
O2 comsumption
afterload
heart size
myocardial contractility
heart rate
Cardiogenic shocks & angioplasty
Cardiogenic shock
Life-threatening condition in which the heart suddenly can not pump enough blood
Symptoms
Pale skin
Rapid breathing
Causes
Aortic Stenosis
Myocardial infraction
Pathogenesis
There is decreased blood volume and blood pressure and co
Inadequate amount of oxygen reaching the tissue
Ischemia followed by necrosis
Organ failure
Angioplasty
Angioplasty uses a tiny balloon catheter that is inserted in a blocked blood vessel to help widen it and improve blood flow
Procedure
The tube is thread to the affected artery using x-ray
Small amount of dye through the catheter to help locating the narrowing artery
A catheter with a ballon on tip inserted to reopen the artery
A stent then placed in artery
A thin tube (catheter) inserted in an artery in the groin or wrist
Atherosclerosis
Theories of Atherosclerosis
Theory of endothelial dysfunction
Theory of Autoimmune
Theory of lipoprotein infiltration:
Theory of Monoclonal
pathogenesis
endothelial injury
foam cell formation
hardening of vessel wall
intimal SMC proliferation
fibros cup that will cause blood vessel narrwing
thrombosis
A vessel wall thickening
the accumulation of WBCs, fatty streak and proliferation of intimal- smooth muscle cell
creating an athermatous plaque
Anatomy of coronary arteries
aortic sinus
right coronary artery
posterior IV artery
Right marginal artery
AV nodal artery
SA nodal artery
left coronary artery
anterior IV artery
diagonal artery
left marginal artery
circumflex artery
crown
encircle heart and allow for clollateral circulation
both atria & ventricles
cardiac veins
small cardiac vein
anterior cardiac vein
middle cardiac vein
venae cordis minimae
thebesian veins
great cardiac vein
coronary sinus
Myocardial infarction
Occurs when blood flow to a part of heart muscle stops, causing damage or necrosis
Endothelial cell dysfunction
Atherosclerosis
Cot formation
Ischemia & necrosis in the area under the clot
Subendocardial infarction
Transmural infarction
Pathological changes
12 to 72 h
Microscopic changes
Neutrophils infiltration
Loss of nuclei
Complication
Pericarditis
Macroscopic changes
Appearance of coagulative necrosis
3-7 days
Microscopic changes
Reabsorption of necrotic cells by macrophages
Complication
Myocardial rupture
Macroscopic changes
Well-defined soft yellow necrosis
Onset of infarction to 12 h
Microscopic changes
Loss of striation
Karyorrhexis
Wavy myocyte
Release of intracellular proteins
Complication
Arrhythmia
No macroscopic changes
After weeks to months
Microscopic changes
Dense fibrous tissue scar formation
Complication
Heart failure
Macroscopic changes
Firm pale/gray scar
MI Cardiac Markers
CK-MB
4-6 hours
24 hours
48-72 hours
Diagnose re-infarctions
Myoglobin
4-12 hours
24 -36 hours
1 hour
Earlier detection of MI
Cardiac troponins
Troponin T
2-8 hours
12-96 hours
Re-expressed in skeletal muscle diseases
14 days
Troponin I
24 hours
7-10 days
2-8 hours
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