Last Patho Exam Flashcards
Preload
Stretch of LV myocardial fibers at end of diastole
Fills the volume of the heart
Preload is mainly determined by
venous return
Frank Starling Law
the greater the strech the greater the force of contraction
As preload increases
SV and CO increase
There is an increase in preload if..
increased blood volume occurs as in fluid volume deficit and heart valve regurg/ septal defects
There is a decrease in preload if
decrease in blood volume as in dehydration
Afterload
resistance to ventricular ejection; the pressure the ventricle must overcome to pump out blood
EX: pushing
What is afterload largely determined by
BP- total peripheral resistance and resistance to pulmonary flow
As afterload increases,
there is a decrease in SV and CO
hypertension and high peripheral resistance can cause
increased afterload
decreased afterload results in what condition
arteriolar dilation
Systole
period of ventricular contraction and ejection of blood
at the end of systole
ventricles relax causing inraventricular pressure to fall
end systolic volume should be what ml
50
Diatole
period of ventricular relaxation and filing
end diastolic volume amount of blood in ml
120
CHD
coronary heart disease: occurs mainly from impaired blood flow in the coronaries
main cause of CHD
atherosclerosis
CHD includes:(5)
angina, MI, dysrhythmias, heart failure, sudden death
Two main coronary arteries
left and right that arise from aortic arch
Left coronary artery splits to become:
- Left anterior desceding to supply LV and portion of septum and papillary muscle.
- circumflex- to supply the left lateral wall of LV
Right coronary artery supplies what? and ext3ends to where
SA node and RV
extends to back of the heart
coronary arteries are mainly perfused during
diastole
coronary circulation is affected by..
aortic pressure- autoregulation allows constant blood flow to coronary arteries at mean arterial pressure of 60-180
metabolic control of coronary circulation
heart needs aerobic metabolism and fatty acids for energy
blood flow is regulated by O2 needs of myocardium
metabolic mediators for coronary circulation and how is it released..
K, lactic acid, CO2, adenosine-
released from myocardial cells in response to decreased O2 supply R/T demand and cause of vasodilation
endothelial cells that line coronary artieries secrete factors that..
affect blood flow.
vasodilating factors: endothelial control
nitric oxid- released when endothelium comes in contact with aggregating platelets, thrombin, products of mast cells, increased shear force
vasoconstricting factors: endothelial control
endothelin release stimulated by thrombin, epi and vasopressin
anti-thrombinogenic factors: endothelial control
imhibits platelet aggregation and clot formation
as larger arteries occlude,
smaller ones increase in size
What is atherosclerosis
the major cause of CHD, narrowing of coronary arteries due to buildup of plaque
people with atherosclerosis can do really well until what percentage of blockage
75
Atheromas/ Plaques in the heart, brain and peripheral arteries cause
angina in the heart
TIA in the brain
intermittent claudication in the peripherals
Two types of artherosclerotic lesions
- ) Fixed-stable, obstructs blood flow
2. ) Unstable- rupture spontaneously due to stress or presure
Risk factors for atherosclerosis
hemodynamic changes- BP, HR, increase in SNS activity, force of contraction, coronary blood flow
Diurnal changes- rupture first thing in the morning due to stress
In atherosclerosis, the lipid core provides,,
stimulus for platelet aggregation and thrombus formation
White platelet containing thrombi
found in patients with unstable angina
Red fibrin containing thrombi
found in vessel occlusion in Mi
CHD can occur in normal arteries, TRUE or FALSE
TRUE
CHD is due to an increase in what and a decrease in what..
increase in heart muscle demand, decrease in perfusion pressure (aortic stenosis)
Commonly occurs in those who have increased metabolic demands (hyperthyroidism, pregnancy, severe exertion, sepsis.
Chronic ischemic heart disease: CHD
stable angina, variant angina, silent MI
Acute coronary syndrome: CHD
unstable angina, MI (STEMI and NONSTEMI)
What is angina
chest pain or pressure associated with transient myocardial ischemia
anginal pain lasts for how long
2-10 min and is relieved with rest or NITRO
Where is angina pain typically felt
in the pericardial and substernal area of chest, radiating to shoulder, jaw, arm, epigastrum or back
Atypical presentation of angina
common with women and elderly: fatigue, SOB, heartburn, nausea, weakness, dizziness, faintness, confusion
Angina can be silent. and is due to
sedentary lifestyle, development of adequate collateral circulation or inability to perceive pain (diabetes)
Stable Angina
short lived, lasting 2-10 minutes, relieved by rest, occurs during exertion, cold, or stress.
Stable angina is caused by
fixed obstruction due to atherosclerosis resulting in disparity between supply and demand
Unstable Angina
unpredictable, may occur at rest and is prolonged.
no relieved by rest or NITRO
New onset (
unstable angina is caused by
atherosclerotic plaque disruption (ruptured plaque)
Variant Angina/ Vasospastic angina is caused by and may be associated with
vasospasms rather than atherosclerotic plaque.
May be associated with coronary stenosis but can occur without presence of disease
Variant Angina/ Vasospastic angina
occurs at rest, during sleep, with minimal exercise or stress. Pain follows a cyclic pattern and happens that the same time every day.
Variant/ Vasospastic angina is treated with
calcium antagonists
STEMI
ST elevation Myocardial Infarction
tramural/ Q wave- involves FULL THICKNESS of ventricular wall, most common with obstruction of single coronary artery.
Most MI’s are transmural and involve LV
NON-STEMI
NON-ST elevation MI
subendocaredial/non-Q wave- involves inner 1/3 or 1/2 of ventricular wall, most common when arteries are severely narrowed but still patent
Pathophysiology of ischemia/ MI
loss of blood flow= anaerobic metabolism
cell dysfunction and contractile function decrease within a minute of onset
Cell changes start within minutes with irreversible cell death after…
20-40 minutes
microvascular injury occurs in about how many minutes
60
reestablish blood flow within an hour of infarct leads to..
minimal cell death
reestablish blood flow within 6-12 hours of onset of symptoms decreases
mortality and morbidity
where does ischemic necrosis begin
subendothelial area and progresses through the muscle wall
Area of injury
surrounding area has some blood flow and some cells will recover
iIshcemic zone
if blood flow is reestablished this area can be salvaged so there will be no cell death
Acute inflammatory response can occur within
the first 3 days
Macrophages remove..
necrotic tissue in the inflammatory response
Whe is the center of the infarct area soft/weak and can rupture
4-7 days post MI
In 6-8 weeks, necrotic tissue is replaced wtih
scar tissue
Anginal pain versus MI pain
angina is short lived.
12 Lead EKG
detects dysrhythmias due to ischemia
provides evidence about a previous MI
identifies pattern changes with ischemia, injury and infarction (ST elevation or depression)
used for STEMI
In Non-stemi patients this may appear normal
In a 12-lead EKG, ischemia alters ..
myocardial repolarization (T wave changes), no polarization from necrotic tissue (Q Waves)
Cardiac Catheterization
insert the cath into a vein if viewing the rt heart, or an artery if viewing the left heart and thread into pulmonary capillaries or coronary arteries
Inject dye to visualize obstructions
Can measure pressures and o2 sats
what electrolytes should be monitored
K and Mg
Main way to diagnose a non-ST segment elevation is by
assessing cardiac markers (Troponin)
what are cardiac markers
they are enzymes and muscle proteins that are released from myocardial cells as they die
Creatine Kinase (CK): begins to rise, peak and return to normal in…
where is it found
rise- 4-8 hours
peak- 12-24 hours
return to normal- 2-4 days
found in the brain, heart and skeletal muscle cells
CK-MB (isoenzyme): begins to rise, peak, and return to normal in..
found in
rise- 4-8 hours
peak- 12-24 hours
return to normal- 2-3 days
found in heart
myoglobin: begins to rise, peak, return to normal
found in
rise- 1-2 hours… RISES EARLY
peak-4-8 hours
return to normal- 24-36 hours
found in heart, skeletal muscle
Troponin T versus Troponin I
Troponin T- rises in 2-6 hours, peaks in 12-24 hours, returns to normal in several weeks
Troponin I- rise in 2-6 hours, peaks in 12-36 hours, returns to normal in 7-10 days
both found in heart muscle and increase in MI
