My lecture notes in pdf during MMed (Emergency Medicine) Phase I Conjoint Board Intensive Course in Universiti Malaya, 22 February 2010

1. Intensive Course For
Emergency Medicine Phase I
(MMed Professional Exam 2010)
KS Chew
School of Medical Sciences
Universiti Sains Malaysia

2. Cardiovascular Physiology Review:
Cardiac Output

3. • Stroke volume = End diastolic volume – End
systolic volume = 135 – 65 = 70 ml
• At rate of 70 beats/min, CO = 70 * 70 = 4900
ml
• Ejection fraction (EF) is the ratio of stroke
volume to end-diastolic volume (EDV),
expressed as a percentage:
• EF = (SV/EDV) * 100

6. Schematic Representation Of The Frog-
heart Preparation Used By Otto Frank

7. Frank-Starling Law

8. Effects On Stroke Volume Of Stimulating The
Sympathetic Nerves To The Heart

9. The pressure-volume cycle of the human left ventricle. The
area bounded by the pressure-volume curve gives the stroke
work of the heart. The lower confine of the pressure-volume
loop shown by the dotted line is defined by the passive
stretch of the relaxed ventricular muscle by the returning
blood.

11. Increased
Preload
Increased Increased
Afterload Contractility

16. Vascular Function and Cardiac
Function Curve

17. Vascular Function and Cardiac
Function Curve

19. Relationship Between End-diastolic
Ventricular Volume and Stroke
Volume

20. Pathophysiology of Acute Coronary
Syndrome

21. Onset of STEMI Hospital Management Modified from Libby. Circulation 2001;104:365,
- Prehospital issues - Medications Hamm et al. The Lancet 2001;358:1533 and
- Initial recognition and management - Arrhythmias Davies. Heart 2000;83:361.
in the Emergency Department (ED) - Complications
- Reperfusion - Preparation for discharge
Secondary Prevention/
Management Long-Term Management
Before STEMI
Chronology of the
interface between the
1 2 3 4 5 6 patient and the clinician
4 through the progression
of plaque formation and
the onset of
Presentation
Ischemic Discomfort
Working Dx Acute Coronary Syndrome
complications of
ECG No ST Elevation
UA NSTEMI
ST Elevation
STEMI.
Cardiac
Biomarker
Final Dx Unstable NQMI QwMI
Angina
Myocardial Infarction

22. Pathophysiology of ACS
Large
One example of atherothrombotic fissure
disease progression
Occlusive thrombus
Lipid pool (Q-wave MI)
Macrophages
Small
Stress, tensile, fissure
internal
Mural thrombus
Shear forces, Fissure (unstable angina/
external non-Q-wave MI)
Atherosclerotic
Plaque Thrombus
plaque disruption
Fuster V et al NEJM 1992;326:310–318
Davies MJ et al Circulation 1990;82(Suppl II):II–38, II–46

23. Atherothrombosis: a Generalized
and Progressive Process
Plaque Unstable
Fatty Fibrous
Athero- rupture/
sclerotic fissure &
angina
MI
}ACS
Normal streak plaque plaque thrombosis
Ischemic
stroke/TIA
Critical
leg
Clinically silent ischemia
Stable angina
Cardiovascular
Intermittent claudication death
Increasing age
ACS, acute coronary syndrome; TIA, transient ischemic attack

24. Platelet Inhibition With GP IIb/IIIa
Inhibitors
Reproduced with permission from Yeghiazarians Y, Braunstein JB, Askari A, et al. Unstable angina pectoris. N Engl J Med.
2000;342:101-114. Copyright © 2000, Massachusetts Medical Society. All rights reserved.

25. Mechanism of Action of Aspirin in Acute
Coronary Syndrome
Prostacyclin is produced by endothelial cells and thromboxane
A2 by platelets from their common precursor arachidonic acid
via the cyclooxygenase pathway.
Thromboxane A2 promotes platelet aggregation and
vasoconstriction, whereas prostacyclin inhibits platelet
aggregation and promotes vasodilation.
The balance between platelet thromboxane A2 and
prostacyclin fosters localized platelet aggregation and
consequent clot formation while preventing excessive
extension of the clot and maintaining blood flow around it.

26. Mechanism of Action of Aspirin in Acute
Coronary Syndrome
The thromboxane A2–prostacyclin balance can be shifted
toward prostacyclin by administration of low doses of aspirin.
Aspirin produces irreversible inhibition of cyclooxygenase.
Although this reduces production of both thromboxane A2 and
prostacyclin, endothelial cells produce new cyclooxygenase in
a matter of hours whereas platelets cannot manufacture the
enzyme, and the level rises only as new platelets enter the
circulation. This is a slow process because platelets have a half-
life of about 4 days.

31. The thrombus in STEMI is RBC & fibrin
rich and often called a red clot or red
thrombus
Unstable angina and NSTEMI often
precedes STEMI (preinfarction
angina). During this phase blood flow
in the coronary artery becomes
sluggish gradually, and therefore the
platelets get trapped within the
plaque. Hence in NSTEMI, thrombus is
predominantly a white thrombus
(platelet rich). Often, a central platelet
core is seen over which fibrin clot may
also be formed.

32. Fibrinolytics
• Why is streptokinase not used in treating UA/
NSTEMI?
• All available thrombolytic agents act basically
as a fibrinolytic agents, therefore it is difficult
to lyse the platelet rich clot.
• There is also a risk of these agents lysing the
fibrin cap and exposing underlying platelet
core and trigger a fresh thrombus (TIMI IIIb
trial)

33. STEMI, NSTEMI and UA
• STEMI - occlusive thrombus - ST elevation (and
Q waves) - Cardiac Enzyme elevation -
Fibrinolytics beneficial
• NSTEMI - non-occlusive thrombus - NO ST/Q -
Cardiac Enzyme elevation present -
Fibrinolytics not beneficial
• UA - non-occlusive thrombus - NO ST/Q -
Cardiac Enzyme elevation absent -
Fibrinolytics not beneficial

35. Electrophysiological Changes During
Cardiac Ischemia
• Ischemia/hypoxia causes an elevation in
extracellular K+. This occurs because K+ leaks
out through K+ - ATP channels and because of
decreased activity of the Na+/K+-ATPase
pump

37. Pathophysiology of Asthma and
COPD

38. • A chronic inflammatory disorder of the
airways
• Many cells and cellular elements play a role
• Characterized by airway hyperresponsiveness
that leads to recurrent episodes of wheezing,
breathlessness, chest tightness, and coughing
• Widespread, variable, and often reversible
airflow limitation

42. ASTHMA COPD
Allergens Cigarette smoke
YY Y
Ep cells Mast cell Alv macrophage cells
Ep
CD4+ cell Eosinophil CD8+ cell Neutrophil
(Th2) (Tc1)
Bronchoconstriction Small airway narrowing
AHR Alveolar destruction
Airflow Limitation
Reversible Irreversible
Source: Peter J. Barnes, MD