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Alterations in Cardiac Function (Acute Coronary Syndrome (chest pain and…
Alterations in Cardiac Function
Cardiac Cycle
one heartbeat
ventricular contraction (systole)
S1：AV valve closure produces a sound that can be heard at the chest wall.
stroke volume (SV)：blood ejected with each contraction of the ventricle
amount of blood that remains in the ventricle after ejection is the end- systolic volume (ESV).
The volume of blood in the ventricle before ejection is the end-diastolic volume (EDV)
ejection fraction (EF), which is calculated by dividing SV by EDV
A normal EF is 60% to 80%; patients with systolic heart failure often an EF of less than 40%.
relaxation (diastole)
S2.：Closure of the semilunar valves causes the second heart sound
−dP/dt：the rate of ventricular relaxation is indicated by the drop in ventricular pressure per unit time
includes ventricular, atrial, and aortic (or pulmonic)
mean right atrial pressure, also called the central venous pressure (CVP)
Arterial pressures fall to their lowest value just before semilunar valve opening. This lowest pressure is called diastolic blood pressure.
Arterial pressure reaches its maximum during ventricular ejection and is called systolic blood pressure
Pressure changes
valvular opening and closing
unidirectional movement of blood through the heart
pressure- volume loop
evaluate left ventricular function
Abnormalities waveforms：changes in blood volume, or changes in pumping capacity
Coronary Circulation
driving pressure and vascular resistance to flow
driving pressure (P)
through the coronary arteries is determined by aortic blood pressure and right atrial pressure
P=ABP-RAP
increases blood flow (Q)
increase in resistance (R)
(1) coronary artery diameter
(2) the varying degrees of external compression attributable to myocardial contraction and relaxation
Coronary Heart Disease
ischemic heart disease (IHD)
coronary artery disease (CAD)
Atherosclerosis of coronary arteries is the source
-progressive narrowing of the arterial lumen,
-predisposes to a number of processes that can precipitate myocardial ischemia
When ischemia of cardiac, the oxygen supply is insufficient to meet metabolic demands
Myocardial cells are unable to store much energy in the form of adenosine triphosphate (ATP)
Myocardial workload depends on heart rate, preload,afterload
ACS occurs when sudden obstruction of coronary blood flow results in acute myocardial ischemia
-A high fibrinogen level, as occurs in smokers, and enhanced platelet adhesivenes
-enhance the risk of thrombus formation
The platelets that initially attach release chemicals that attract more platelets, which aggregate and form a plug
Chemicals released by activated platelets include several vasoactive products (e.g., serotonin, thromboxane)
may present as unstable angina, MI, or sudden cardiac arrest
thrombus formation
coronary vasospasm
endothelial cell dysfunction
1.Endothelial cells secrete variable quantities of vascular relaxing and contracting factors
2.controlling myocardial blood flow
As the plaques acquire more free lipid within the arterial wall, they are more vulnerable to rupture, thrombus formation, and progressive plaque growth.
Stable plaques usually are asymptomatic
ay be associated with exercise-induced angina pain (stable angina pectoris)
plaques are vulnerable to rupture orerosion, can initiate thrombus formation and acute coronary occlusion
angina, infarction, ischemic cardiomyopathy, and sudden cardiac arrest
Acute Coronary Syndrome
chest pain and evidence of acute ischemia on the electrocardiogram (ECG) (ST-segment elevation [STEMI])
acute reperfusion therapy
Differentiation between unstable angina and NSTEMI： after obtaining cardiac necrosis markers
unstable angina and no ST elevation on the ECG may not benefit from reperfusion strategies
antiplatelet drugs are a cornerstone of therapy
diagnosed with unstable angina
An MI may occur at any age
Females younger than 45 years have a sixfold lesser risk than men of the same age
After menopause, the rate of MI in women approaches that of their male counterparts and becomes essentially equal by age 80
Platelets passing by the surface of the ruptured plaque adhere to it, initiate formation of a platelet plug, and activate the clotting cascade
occludes the vessel and triggers the transmural MI
irreversible cell injury occurs after 30 to 40 minutes of complete occlusion
Nearly all infarcts are located in the left ventricular walls
Occlusion of the left anterior descending artery causes 40% to 50% of acute MIs
After 18 to 24 hours, the area of infarction becomes paler than surrounding tissues
The diagnosis of MI
signs and symptoms
Severe crushing, excruciating chest pain that may radiate to the arm, shoulder, jaw, or back
electrocardiographic changes
elevations in the levels of specific marker proteins in the blood
The MB band of creatine kinase (CK-MB) and troponin I are the most specific of the protein markers
Myoglobin is an early marker but is not very specific.
it turns yellowish and soft with a rim of red vascular connective tissue