Heart murmurs and skipped beats are pertinent to heart disease
Mitral stenosis: is the stiffening of the bicuspid valve. It's caused by the increased back pressure into the leftatria.
The stretch of the left atria caused by mitral stenosis causes it to undergo hypertrophy to thicken. This causes for decreased space within the atria
Mitral regurgitation: improper closure of the bicuspid valve so blood backflows into the left atrium. This causes less blood to be available for the rest of the body and decreases pressure within the heart.
Mitral valve prolapse: occurs when the mitral valve opens and gets stuck in the extended position. Asymptomatic for the first few years with females having a higher risk. You could also hear a mid-systolic click
Aortic stenosis is similar to mitral stenosis is associated LVH and left sided heart failure instead of right
Aortic stenosis is occurs in people aged 70 to 90 and could lead to angina due to decreased cardiac output.
Aortic regurgitation causes an increase in EDV/ESV which leads to LVH. This can result in bounding radial due to increased stroke volume.
Aortic prolapse doesn't exist cuz someone would be dead if they had it
70% of the population is right dominant for the RCA with 10% being left and 20% being codominant; if ur codominant ur chilling frfr
Coronary bloodflow is regulated centrally by the ANS and locally regulated by autoregulation.
Q=perfusion, P=drivingpressure and R=resistance; the formula is Q=P/R
Metabolic hypothesis states that if there is an increased O2 demand or decreased O2 supply, chemical mediators are released
Vasodilatory substances: adenosine, H+, K+, Co2, NO and prostaglandins
NO is produced by coronary arteries and its a very potent vasodilator
NO decreases R which in turn increases Q. It's release always increases with hypoxemia
SNS stimulation does not allow coronary arteries to vasoconstrict
Systole decreases coronary perfusion because while driving pressure is increased, resistance is increased a lot more
BCP contributes to increasing the chance of getting ischemicheart disease
Factors that decrease O2 supply: atherosclerosis, thrombosis, vasospasm, shock, poor perfusion pressures, respiratory pathologies and anemia
Factors that increase demand of O2: increase in preload/afterload, SNS stimulation, stress, exercise, sex, fever and sympathomimetics
Patho of ischemia is decreased P, decreased vessel diameter, decreased Q time, increased metabolic demands decreased glycogen stores and a loss of Ca+/K+ ions
Zones 1 is infarction, zone 2 is hypoxiccell injury and zone 3 is ischemic zone
The cells in zone 1 are dead, cells in zone 2 can recover if the issue is fixed.
Cardiac impulses can't be sent through zones of infarction which means they bounce around and are uncoordinated
Myocardial stunning occurs when blood flow is ok but the tissue is stunned and not functioning that well; temporary loss of fxn and contractility, this could last for hours to days after reperfusion
Myocardial hibernation: persistently ischemic cells are ignored so demand is brought down to meet supply.
Myocardialhibernation can be seen as low power mode and its seen with chronic angina or after an MI
Myocardial remodeling is hypertrophy of myocytes caused by the RAAS/catecholamines
Coronary syndromes are: stable angina, unstable angina, prinzmetal/variant angina, AMI(splits off into STEMI and NSTEMI) and sudden cardiacdeath
Anginas don't have infarctions but have ischemia of heart tissue
Atherosclerosis is the build up of plaque within an artery
Arteriosclerosis is the hardening of arteries
Cardiac pain travels up the afferent fibers and travels via the cardiac plexus and sympathetic chain
The pleura are innervated but the lungs are not
25% of cardiac events have reproducible effects so don't use only this as a tool of diagnosis
Silent MIs have no s/s and make up about 1/3 of them
Prinzmetal/variant angina is a temporary spasm that can happen in healthy vessels
Don't get angina PTs to lie down
Giving NTG to someone with stable angina reduces R