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I've got severe pain in my chest, posterior part of the right atrium…
I've got severe pain in my chest
Anatomy of the Coronary Circulation
Arteries
Right Coronary artery
Branches off
sinus atrial nodal artery
supplies
SA node
Right marginal artery
supplies
Right ventricle and apex
Atrioventricular nodal artery
supplies
AV node
Left Coronary Artery
Branches off
Circumflex artery
Branches off
Left marginal artery
supplies
Left ventricle
supplies
Left ventricle and left atrium
Anterior Interventricular artery
Branches off
Lateral artery
supplies
Left ventricle
supplies
Ventricles and anterior 2/3 of IV septum
drains areas of the heart supplied by the
Great cardiac vein
Dominance
posterior IV branches off the right coronary artery
dominance is
Right dominance
supplies
Ventricles and posterior 1/3 of the interventricular septum
drains
Middle cardiac vein
posterior IV branches off the circumflex artery
dominance is
Left dominance
Veins
Coronary sinus
drains into
Left atrium
Anterior cardiac veins
drains
Right ventricle and right atrium
Myocardial infarction
Nausea & Vomiting
Fatigue
SOB & Coughing
Cold Sweating
activate
sympathetic nerves system
release
adrenaline (stress hormone)
go to
bloodstream and cause vasoconstriction
leads to
1 more item...
Chest pain
characterized by
Tightness
Pressure
Squeezing
causes of MI
Atheroma
as a response to injury
monocytes converted to macrophages
engulf LDL
Foam cell
faty streak
turbulant flow
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Atheromatous plaque
Advanced stage of atheroma
Smooth muscle cells, fibrous tissue
Thrombus
injury
Vasoconstriction
Formation of a Platelet Plug
Coagulation cascade
Fibrinolysis which will break the clot
causes
Endothelial injury
Turbulent blood flow
Hypercoagulability state
mutation of the cascade factors
plaque
coronary artery occlusion
Obstructs blood flow
Ischemia
Cellular Injury
Necrosis
Investigation of MI
ECG
ST elevation
J point above 2mm
Determining location of MI
Leads effected
Vessels effected
Biomarkers
Myoglobin
Peak 4-12 hours
Early detection
Creatine kinase
Peak value within 24 hours
Cardiac troponin
Troponin T
Peak after 12-96 hours of MI
Troponin C
Not used due to low specificity
Troponin I
Found 2-8 hours after acute MI
Internal validity
History bias
Maturation bias
Testing bias
Selection bias
Attrition bias
Regression to the mean bias
Instrumentation bias
Social interaction
Pharmacology
Lipid lowering medications
Medications that lower lipid levels in the body
Types
HMG-COA reductase inhibitors
Statins
Lipoprotein Lipase Enhancers
Fibrates
VLDL & LDL reduction
Niacin
Bile Acid Sequestrants
Cholestryamine
Cholesterol Reabsorption Inhibitor
Ezteimibe
PCSK9 Inhibitors
Non medical management of MI
Non medical lifestyle and preventative measures to reduce the risk of MI and support overall health
Healthy lifestyle choices
Diet
Regular exercise
Weight management
Tabacco and alcohol cessation
Stress management
Meditation
Yoga
deep breathing exercise
Hobbies
Adequate sleep
Regular health check ups
Monitor BP, Diabetes and cholesterol
cardiac rehabilitation
Located at Qatar rehabilitation institute in HMC
Improve CVS health by administering treatment by assessing risk factors to make lifestyle changes inorder to prevent worsening of their condition
Team made op 28 specialists
Services
Outpatient cardiac rehab, Inpatient general and cardiac rehabilitation
Physiotherapy
Occupational therapy
Speech therapy
Death certificate and registry in Qatar
Process
!) Report the death to authorities
2) Obtain a medical certificate
3) Apply for death certificate
4) Registration of death
Notification of death in Qatar
Process
!) Contacting local authorities
2) Issuing a death certificate by MOPH
3) Contacting the embassy or consulate if foreign deceased
4) Funeral arrangements
5) Notifying authorities: employer, bank
6) Legal and administrative procedures: Inheritance etc
Emergenency managment of MI
Initial managment
Anticoagulation
Planned revascularization
Statins
P2Y12 inhibitor
Antiplatelet drug
Beta-blockers
chance of developing arrhythmias
Asprin
Antiplatelet drug
Sublingual nitrates
Vasodilation
:arrow_down: Preload
:arrow_down: Workload
oxygen consumption :arrow_down:
Supplemental O2
Saturation < 90%
Stable patient
Reperfusion therapy
within 12 hours post infarction
PCI
Thrombolysis
More than 12 hours
Reperfusion ineffective
Coronary artery bypass graft
1 more item...
Still patient acute
Unstable, sinus bradychardia, hypotension
IV Atropine
PNS
SNS takes over
Heart pumping more
Correcting bradycardia and hypotension
1 more item...
Pulmonary edema
IV Furosemide
Diuretic
Presistant pain, hypertension, heart failure
IV nitroglycerin
presistant severe pain not relieved
IV morphin
Pharmacalogical managment of MI
fibrinolytic
Convert plasimogen to plasmin
Dissolves thrombi
Streptokinease
Alteplase
Anticoagulants
LMWH
Heparin
:arrow_up: Antithrombin III activity
Factor Xa
Thrombin
Antiplatelets
Asprin
COX - 1 inhibitor
clopidogrel
P2Y12 inhibitor
Follow up of MI
Cardiovascular assessment
Psychsocial status
Review of symptoms
Referals to rehabilitations if not done
Types of shock
obstructive
obstruction of blood flow
distructive
widespread dilation of blood vessels
hypovolemic
decreased blood volume
cardiogenic
poor heart function
heart muscle cells die
can't contract as hard
decreased stroke volume
decrease cardiac output
releases vasoconstrictors
increase vascular resistance
help maintain blood pressure
reduction in CO
lowered blood flow
skin gets cool and clammy
Causes
MI
severe heart failure
cardiomyopathy
myocarditis
arrhythmia
stages and signs
stage 1: non progressive stage
neurohormonal mechanisms to maintain main organs
clinical outcomes
peripheral vasoconstriction
renal conservation of fluid
stage 2: progressive stage
tissue hypoperfusion
anaerobic glycolysis, production of lactic acidosis and decreased pH
clinical outcomes
mental confusion
decreased renal output
stage 3: irreversible stage
cellular and tissue injury
clinical outcomes
renal shutdown
survival not possible
complications of MI
left ventricular failure
extension of the infarcts
rupture of myocardium
mural thrombosis & embolism
cardiogenic shock
Angina
Investigations
Echocardiogram
Angiography
Blood test
ECG
Such as
Risk factors (CAD)
Signs + symptoms
Tx
Nitroglycerin
Beta blockers
CCB
Antiplatelet agents
Angina Pectoris
Definition
The heart muscle doesn't receive enough oxygen-rich blood temporarily.
Severity
less pain
lasts for a few minutes.
Types
Unstable Angina
Complications
• future heart attacks
• risk of arrhythmia
Variant Angina
Stable Angina
Myocardial Infarction
Definition
Sudden and prolonged lack of blood flow to a part of the heart muscle (necrosis)
Severity
• life-threatening
• more severe and prolonged chest pain
Types
1- Transmural MI
2- Subendocardial MI
Complications
• heart failure
Interventional cardiology procedures
PCI
Encompasses both
Angiography
Angioplasty
Plays a crucial role in
The management of acute myocardial infarction (STEMI)
Angioplasty
Involves
Balloon
stent
catheter
Angiography
Using
contrast dye
X-ray imaging
(angiograms)
posterior part of the right atrium and ventricles
drains
Small cardiac vein
clinical features
contain
to
form
lead to
cause
cause
lead to
activate the
then
caused by
lead to
formation of
thus
lead to
and
leading to
Indicated by
Measured at
Optimal for
measured at
first
second
Third
Useful for
gives insight on
Through observing
Has several
are
For example
For example
For example
For example
For example
Given if
Which is an
Which is an
Depends on
Reduces
causes
leading to
Which
Therfore
If there is
If there is
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If
Administer
Administer
Administer
Which is a
Administer
Blocks
Allows
Leads to
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Leads to
Requiring
Options include
Makes
An alternative is
Therfore inhibits
Examples include
Examples include
Examples include
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Which is a
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Work by
Which
Includes
due to
are
due to
due to
due to
leading to
therefore
the body
to
and
leads to
so
