Afterload or preload, that is the Q
the R&L coronary A meet and are called the _ of the heart.
- which artery, R OR L, suplies the posterior aspect of the ventricle?
Crux of the heart
- R coronary A goes down and supplies the posterior aspect of the ventricl 80-85
what is minute oxygen consumption (VO2)?
what is it a measure of?
whats its equation?
vo2 is the measure of aerobic fitness ( need oxygen)
as it increases, that means you are more fit!
- VO2= cardiac output (Q) x (Arterial = venous) difference
what is the atrial septal defect?
there is an opening btwn the R & L atria so there will be a mixing of oxygenated and deoxygenated blood
what is the ventricular septal defect (hint what side of the heart does it effect)
ventricualr septal defect is when there is an opening of the heart
what are some risk factors that are modifiable and non modifibale when it comes to Hypertension HTN
modifiable (you can change)
1. stress, obesity, poor nutrition, k deficieny (decreases the excess Na & watr in blood so it can raise BP when theres a def)
nonmodifiable ( not something you can change)
1. age
2. gender
3. race
factors that influence the Heart during exercise : Preload
1. what is preload
2. is it a stretching or relaxing force?
3. what does preload depend on?
preload is the amount of blood in the heart (whats coming back to the heart is preload)
- its the actual amount of blood in the heart
- it is the STRETCHING force that elongates the resting sarcomeres before activation
- preload depends on the venous return and end diasolic volume. like any other muscle, when stretched, it gets better contractility. so when we exercise and get increased venous return to our heart, it puts a little extra stretch on the heart and the heart can genrate more force
with exercise training V02 increases. What part of the formular increases with ST training?
a) SV
b) Q (Cardiac output)
c) (A-v)o2
d) HR
C . because avo2 changes (increases) with short term training
what is the coarctation of the aorta
what is the dextroposition of aorta
the aorta OVERRIDES both R&L ventricular septum & receives blood from both the R&L ventricle
- this means that the Aorta is receiving oxygenated blood from LV & deoxygenated blood from RV
1. asymptomati until BP is very high
2. occipital headache
3. vertigo 4. flushed
5. visual changes
6. increased nocturnal urinary freq (this is bc during the day there is an increase in renal A resistnce and decreased BF to the kidney--> causing decrease urine. but at night --> there is a decrease in catecholamines and BP decreased but theres now increase urine
factors that influence the Heart during exercise : afterload
1. what is afterload
2. is it a stretching or relaxing force?
3. what does afterload depend on?
-afterload is the amount of FORCE the heart has to overcome to EJECT the blood - its basically what its pumping against
- its the total instantaneous force the heart must generate to elevate the intraventricular pressure to aortic pressure (systolicc)
-the velocity and extent of shortening decreases as afterload increases ( ex: just like when doing bicep curls, if you hold a weight thats too heavy it will be difficulty to move fast)
Congenital cardiac disorders
1. what are they/how do they occur?
congenital heart disease is a result of altered embryonic development of a normal structure or failure of a normal structure to progress beyond its early stage of embryological development
in coarctation of the aorta, what does the primary pathology cause a problem with?
a) preload
b) afterload
c) contractility
afterload (ejection of the blood is harder)
what is right ventricualr hypertrophy
right ventricular hypertrophy is a heart disorder characterized by thickening of the walls of the right ventricle.
-It can be caused by excessive stress on the right ventricle because its pumping against the stenosis (narrowing)
what are some non-pharmacological and pharmalogic treatemnet for HTN
nonpharmacological aka lifestyle changes
1. Wt reductions, 2. Na restricition 3. regular aeroboic exercise 4. relaxation
pharmacological
1. diuretics ( drug that eliminat fluid from systm) 2. vasodilators (nitroglycerine makes the Arteries dilate so the P lowers)3. Beta-adrenergic blockers (ex: metropanol)
what is the contractility state?
what happens to preload when the contractility increases?
its the hearts innate ability to contract
(the innate intensity and rate of force)
- increased contractility results in greater VELOCITY of shortening and force development at a given preload ex: a 25 yr old will have better contractility than a 70 yr old
what is a ventricular septal defect? * VSD
- how does it occur?
ventricular septal defect is a defect in the septum between the R & L ventricles.
- this is the MOST COMMON congenital defect of the heart
- the baby while inside the mother deosnt pump blood to lungs bc the mother is oxygenating the baby thru the palcenta. but when the baby takes their first breathe, they need to pump their own blood and breath, so the pressure btwn the R&L ventricle change. BUT, if there is a little hole left btwn them, the lV blood is going to flow into the RV and will cause HIGH PRESSURE in the RV and pulmonary hypertension
can you name the 4 types of Tetralogy of fallot /fallow/ "flow"
1. pulmonary valve ( aka pulmonary artery stenosis/narrowing)
2. Ventricular septal defect
3. Dextroposition of aorta
4. Right ventricular hypertrophy
what is hypertension ?
what are the #s that determine it?
how is it dx ?
hypertension is high blood pressure
greater than 120-129 systolic/diastolic less than 80
-you need to have at least 2 occassions at least 2 wks apart
what is Coronary artery disease CAD?/what is it caused by?
CAD is caused by build up of plaque in the arteries
what is Cardiac output?
what is the formula?
the total amount of blood ejected from the heart per minute
Q= stroke volume x heart rate
(stroke volume = the amount of blood pumped out per contraction)
when a baby is developing they have a patent ductus arteriosus. How does it close?
- what causes it?
the ductus arterious is an opening btwn the pulmonary A and aorta.
- if it fails to close, you will get a mix of venous (deoxygenated blood) in the areterial blood
- hereditary or environmental expsoure to rubella
what is the pulmonary valve or pulmonary artery stenosis(narrowing) abnormality of the heart? (hint: think WHICH side of the heart/chamber it effects)
the R side of the heart is going to have difficulty ejecting blood
- remember the R side of the heart already has a low pressure so its not made to genrate a lot of force
what is the difference btwn primary/essential hypertension, secondary HTN and Labile (unstable) /boarder line HTN ?
1. primary HTM = its idiopathic! we dont know what caues it
2. secondary = its cause can be identified. ex: renal A dise, oral contraceptive w/ smoking, hyperthyroidsim, etc
3. labile/borderline HTN: intermittent! they can have one High BP 1 day but not the next
can you explain atherosclerosis development
in early stages: fatty streaks form in intima
- its scattered at first but as it progresses it can become prevalent and start to cover the inner layer of the artery (intima)
- overtime, cholesterole particles in arteries can become more frequent and can form a plaque
- the plaque can then block the artery and if it gets too big and no blood can pass, it can break off or cause MI or necrosis