3. โข Stroke volume = End diastolic volume โ End
systolic volume = 135 โ 65 = 70 ml
โข At rate of 70 beats/min, CO = 70 * 70 = 4900
ml
โข Ejection fraction (EF) is the ratio of stroke
volume to end-diastolic volume (EDV),
expressed as a percentage:
โข EF = (SV/EDV) * 100
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.
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;326:310โ318
Davies MJ et al Circulation 1990;82(Suppl II):IIโ38, IIโ46
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 ยฉ 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 A2โprostacyclin 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.
27.
28.
29.
30.
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
โข Why is streptokinase not used in treating UA/
NSTEMI?
โข All available thrombolytic agents act basically
as a fibrinolytic agents, therefore it is difficult
to lyse the platelet rich clot.
โข 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
โข STEMI - occlusive thrombus - ST elevation (and
Q waves) - Cardiac Enzyme elevation -
Fibrinolytics beneficial
โข NSTEMI - non-occlusive thrombus - NO ST/Q -
Cardiac Enzyme elevation present -
Fibrinolytics not beneficial
โข UA - non-occlusive thrombus - NO ST/Q -
Cardiac Enzyme elevation absent -
Fibrinolytics not beneficial
34.
35. Electrophysiological Changes During
Cardiac Ischemia
โข 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
38. โข A chronic inflammatory disorder of the
airways
โข Many cells and cellular elements play a role
โข Characterized by airway hyperresponsiveness
that leads to recurrent episodes of wheezing,
breathlessness, chest tightness, and coughing
โข Widespread, variable, and often reversible
airflow limitation
39.
40.
41.
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