cardio physio Flashcards

Question

What is the formula for cardiac output?

Answer 1

CO= HR x SV

Answer 2

SV= EDV-ESV

Answer 3

So in exercise, you’ll have increases in cardiac output modestly, so when youre compensating with exercise in the SVT at very high heart rates. Even though the HR x SV drops so significantly in SVT that CO drops. So at very extremely high rates where you’re uncompensated in situations such as SVT, you will have a decrease in CO despite the fact that your HR is high. In compensated situations such as exercise, your cardiac output will actually stay the same nad SV will increase. In exercise, your HR doesnt just speed up, contractility speeds up, you know, your pre-load increases. There are situations where your strong contractility will not increase HR and thats in SVT for example. High HR results in a decrease in diastolic volume. In parasympathetic effects, a decrease in HR gives more tiem for filling, but HR is decreasing and therefor CO will decrease, despite decrease in EDV. Increase contractility, decrease ESV, so less blood left over after contraction and that’ll increase your cardiac output, because you have a very clear increase in stroke volume. When we increase HR a lot, we decrease end diastolic volume and therefore decrease cardiac output. During moderate increase in HR like in exercising, we increase cardiac output. In the parasympathetic nervous system, when we decrease contractility, it doenst have many effects. It doesn’t really do much in regards to our cardiac output but when you start to add in things like heart failure, where the muscles get stretched out and they really cannot contract, then you start to see decreases in SV like in cases of heart failure. This will lead to a decrease in cardiac output and the ejection fraction is decreased HR is really the biggest influence Vascular smooth muscle is essentially afterload Vasodilation is parasympathetic

Answer 4

Quantification of contractility. EF= SV/EDV, 50-70%. This is measured on echo, or cardio MRIs, etc. Percent of blood that the LV ejects during contraction

Answer 5

Arteries, arterioles, capillaries, venules, veins Artery use things like pressure, pumping of the heart, elasin and recoil to facilitate blood movement Veins have valves, some smooth muscle changes and skeletal muscles

Answer 6

Minimum arterial pressure reached just prior to ventricular ejection. Indicates recoil

Answer 7

Maximum arterial pressure reached during the peak of ventricular contraction and ejection (systole). Peak pressure during systole, aka when the left ventricle contracts and is ejecting blood. Indicates pressure

Answer 8

compliance= delta volume/ delta pressure. Arteries are often called pressure reservoirs and so arteries have stretchability or compliance

Answer 9

Is stated as SBP/DBP = 120/80. Arteries are elastic and the stretch out, so we can measure a pressure when they are returned back

Answer 10

This is a good indicator for cardiovascular health. Difference between SBP and DBP. PP

Answer 11

SBP-DBP=120-80= about 40-60 mmHg. Consider: SV, speed of ejection, arterial compliance. A PP >60 mmHg is considered widened and may suggest arterio-(arteries stiffen) or atherosclerosis (narrowing and increased peripheral resistance), hypertension, or aortic regurgitation. A PP <25 mmHg is considered narrow and may indicate low cardiac output or blood loss (hemorrhage, suggesting in adequate perfusion)

Answer 12

Decrease in firing of baroreceptors and that sensation goes back to the brain and the medulla will decrease output from the vagus nerve, through the sympathetic trunk. The barorecpetors reflex maintains MAP. We have a down regulation of sympathetic outputs from the sympathetic trunk and an increase in parasympathetic regulation.

Answer 13

It widens as we get older. What happens is, while the compliance decreases, the pressure inside increases. SVP is going to be higher. There is more stiffness

Answer 14

Average pressure driving blood to the tissues overcardiac cycle. Approximation formula: MAP = DBP + ⅓ PP= 80 + ⅓ (40) = 93 mmHg MAP = CO x total peripheral resistance (TPR) Vasodilation= decrease in MAP, decrease in total peripheral resistance Vasoconstriction= increase in MAP

Answer 15

In hemorrhage, SV decreases naturally. You see the sharp drop, your heart rate and baroreceptor response will go up. SV decreases because you dont have enough and you dont have enough preload. This is a great example. Your heart rate can bring out that CO only to a point. Your peripheral resistance will increase and so it will vasoconstrict because you have more volume. Peripheral resistance will increase, so you’ll vasoconstrict and have an increase in MAP. Hemorrhage causes decrease in peripheral resistance so there will be a parasympathetic response.

Answer 16

So, we will have decrease in parasympathetic response and decrease the SA node of the atrial heart an increased sympathetic response, so HR. Our peripheral resistance mostly has to do with our arteries, so we increase our peripheral resistance to try to increase our MAP, our arterial pressure. Increase blood volume, increase blood pressure so we will increase baroreceptor finding. This is a negative feedback mechanism. Increase in blood volume like drinking water

Answer 17

So increase in blood volume so increase in blood pressure, so increased baroreceptor firing so increase baroreceptor firing, laws of increase in venous pressure, venous return, we have more blood volume and we increase our EDV and try to increase our cardiac output which will increase our arterial pressure. We need to regulate arterial pressure. Regulation of MAP through baroreceptors. The RAAS system used ADH and aldosterone for longer term regulation of blood pressure. It takes a little bit longer. Drop in blood pressure, inhibits baroreceptors, then sympathetic nervous system activity and then the renin from the juxtaglomerulus complex and will cause the conversion of angiotensin to angiotensin I and ACE from the lungsto angiotensin II which goes to the adrenal cortex for aldosterone that helps with sodium reabsorption, ADH will be released by posterior pituitary, etc, etc

Answer 18

ANP is atrial naturetic peptide

Answer 19

Due to a decrease in blood volume secondary to hemorrhage or loss of fluid other than blood (hemorrhagic shock)

Answer 20

Due to a decrease in total peripheral resistance secondary to excessive release of vasodilators, as in allergy and infection (like septic, infection, anaphylaxis)

Answer 21

Due to an extreme decrease in cardiac output from any variety of factors (for example, during a heart attack)

Answer 22

Due to an obstruction in blood flow, such as a blood clot, a tumor, or a collapsed lung

Answer 23

Genetic problems with RAAS, regulation of endothelial cell function, and arteriolar smooth muscle contraction. Increased total peripheral resistance caused by reduced arteriolar radius, obesity, isulin resistance (characteristic of Type 2 diabetes), chronic high salt inatke leading to overstimulation of the sympathetic nervous system, stress, smoking, excess alcohol or caffeine consumption, poor diet, low birth weight and not being breast-fed as an infant.

Answer 24

Primary hypertension can be managed with diet, exercise, and lifestyle changes, and with medication

Answer 25

Damage to the kidneys or their blood supply can lead to renal hypertension, excess renal Na+ reabsorption, hypersecretion of cortisol, aldosterone, or thyroid hormone. The abnormal nightime sleeping pattern, sleep apnea. Secondary hypertension can be managed with medication.

Answer 26

Diastolic and systolic heart failure

Answer 27

Involves difficulty with ventricular filling, due to decreased compliance, reduced end diastolic volume leads to reduced stroke volume, often caused by the heart pumping against high arterial pressure (hypertension)

Answer 28

Involves difficulty with a ventricular ejection, due to damage to the myocardium, this can result from a heart attack, decreased contractility leads to a lower stroke volume at any EDV