Ex Phys final: Cardiovascular 1

Function of Valves

Prevent back flow

T or F: Valves get stiffer with age

True

1 multiple choice option

Stenosis

Valve openings become smaller

Regurgitation

Backflow, caused by improper valve closure

Functions of capillaries

Gas and energy exchange

What is the BP inside of the LV

120/80

What is the BP inside of the RV

25/12

T or F: The RV is more vulnerable to failure

True

1 multiple choice option

Functions of the tunica interna

Coats arteries and veins

Endothelium

1. Mediates health and size of vessel

2. Regulates blood flow through vessel tone (dilation/constriction)

3. Prevent clotting

4. Damage to this causes the vessel to not be able to control itself

What is the biggest risk to damage endothelium

Hypertension

Tunica Media in the arteries

1. A thick muscle layer which controls diameter of vessel to control resistance and therefore blood flow

2. Becomes particularly important in exercise to direct blood flow to where it is needed and redirect where it isn't which is generated through metabolic demand

Tunica media in the veins

1. Very then

2. Veins do not need to redistribute blood anywhere, it is all headed to the same destination so you don't need as much control

Cardiac output

1. Amount of blood being pumped out to the body

2. Product of HR and SV

Stroke volume

Volume of blood pumped out of LV per beat

Cardiac output at rest

5 L/min

Cardiac output at max exercise

~35 L/min

What is the autonomic control of the heart

Control how fast and how hard the heart is beating

What is the effect on HR from sympathetic stimulation on the SA node

Increase HR

What is the result of exercise on the sympathetic system

1. Activates SNS to stimulate SA node, which increases ventricular depolarization and in turn increases contraction, which increases HR

2. Generates calcium production (depolarization) and more myocyte activation (stronger force contraction)

What is the parasympathetic effect on HR

1. Decrease HR, but not from actually acting on monocytes

When resting, how do you bring HR down

1. Not through parasympathetic, because it does not affect force of myocyte contraction

2. Through less activation of sympathetic NS-> take foot off gas

Describe preload

1. Stretch of the heart

2. How much blood is in the chamber

3. How heavy is the hikers backpack for mountain

4. More blood= more stretch

Describe afterload

1. Amount of work that the heart has to do to push the blood out/ to empty a chamber

2. If hypertensive/ arrowing of aorta, heart has to work harder

3. How steep is the man

What is exercise capacity limited by

The L ventricle

Systole

Ventricular contraction, emptying

As ventricular volume decreases, pressure

increases

1 multiple choice option

What has to occur with ventricular pressure to open the aortic valve

Ventricular pressure must exceed aortic pressure

1 multiple choice option

In systole, what valves are open, and which is closed

Mitral valve is closing, aortic valve is opening once pressure is high enough

1 multiple choice option

Describe pressure changes in systole

Atrial pressure decreases as ventricle starts to contract-> ventricular pressure exceeds atrial pressure causing AV (mitral) valves to prevent back flow towards low pressure system in atrium

1st heart sound

systole

Diastole

Ventricular relaxation, filling, volume is increasing, pressure is decreasing

Which valves are open and closing during diastole

Aortic valve closes, Mitral valve opens

1 multiple choice option

Why does the aortic valve close during diastole

Closes as ventricle is relaxing because pressure falls below aortic pressure

Why does mitral valve open during diastole

1. because atrial pressure exceeds ventricular pressure, the atria has been filling as ventricle has been relaxing/ contracting

2. Ventricle almost all the way to 0 before pressure is low enough for the mitral valve to open

Describe atrial contraction

1. Push blood from the atrium through valve to ventricle

2. Ventricular relaxation sucks blood from atrium and then atria contracts to " top off"

Effect of atrial disease on ventricular filling

Ventricle can fill most of the way by itself but topping off won't be there

What is the pressure in the venous system

Very low

What occurs to the valves of the venous system in peripheral vascular disease

1. Valves become incompetent so blood starts to stagnate inside the venous system which leads to concern of clots

2. When veins start to clot, they start to bulge (varicose veins)

Varicose veins

High risk of DVT to embolus to heart, but doesn't get stuck until lungs where it meets very small vessels aka pulmonary capillaries

Muscle pump effect on venous return

1. Causes compression of vein

2. Squeeze/ pump/ work muscles which squeeze your veins--activity and movement prevent blood pooling

Diminished venous return leads to

Decreased cardiac output

Respiratory pump effect on venous return

1. Inspiration when you expand thorax, volume increases, and pressure decreases causing air to be sucked into lungs and blood puled up through veins due to pressure changes

2. As you take a deep breath in, venous return increases so HR increases a little to clear blood as blood returns to the heart through veins

How do veins function as a reservoir

1. Veins are more compliant than arteries, they are stretchy and expand as more blood is given

2. 60% blood volume is in the venous side

3. Allows veins to compensate for volume loss through sympathetic venoconstriction: smooth muscle can contract and stiffen even pushing bloodback to heart when needed

What are specific blood reservoirs in the body on the venous side

1. Spleen

2. Liver sinuses

3. Large abdominal veins

4. Cutaneous venous plexus

Describe starlings law

more cross briges= more tension the muscle can generate, pull the actin filaments together to shorten the muscle

Describe starlings law with a overly stretched muscle

Fewer cross bridges form-> less tension able to generate, less able to shorten

What occurs with starling law when muscle is to short

actin filaments start to overlap, fewer cross bridges, less tension

How does preload relate to starlings law

1. fill a chamber with blood stretches the wall and will contract harder because actin and myosin in a better relationship

2. If the heart has less volume, not stretching enough, myosin doesn't create tension which causes less preload

3. Dilated cardiomyopathy-> overstretched muscles

4. Add preload, add volume, add stretch to heart= bring heart into optimal alignment and more tension

5. venous return increases with muscle pump, increase preload, increases stretch of chamber wall, harder contraction, increases cardiac output

Describe LVEDP

1. If you have more blood coming back to the heart (increased venous return), the pressure in the L ventricle after filling is directly correlated to the amount of blood pumped out of the heart when the heart contracts

2. Increased venous return (exercise) leads to higher LVEDP which leads to greater preload, leading to a more forceful contraction

3. Deceased venous return leads to lower LVEDP because less volume coming back, thus leading to actin and myosin not aligning well= decrease in SV

4. More cross bridges= more tension= higher SV

T or F: LV output and RV output do not need to match

False

1 multiple choice option

What occurs when RV> LV output

1. Blood going to stall in LV causing a distended LV= blood will regurgitate into LA and then into the lungs

2. LV failure= pulmonary edema-> volume overload lung= SOB, pulmonary edema

Correction of when RV> LV output

Pulmonary circulation pressure rises leading to increased LV filling pressure leading to dissension of LV leading to increased contractility leading to LV output raising

hypotensive BP

90/60 mmHg

normal BP

120/80 mmHg

Hypertensive BP

>130/89 mmHg

What occurs as a result of hypotension

1. Inadequate perfusion pressure

2. Orthostatic hypotension-> low BP when standing up

3. More susceptible with aging and lack of baroreceptor reflex

What occurs as a result of hypertension

1. Vascular (vessel damage)

2. Endothelial dysfunction

3. Increase cardiac strain/failure

What are effects of hypertension on LV

Causes strain when the LV is trying to adapt and results in a maladaptions of walls becoming very thick which causes too much pressure

What 2 things can effect SVR

Blood viscosity or vascular tone

What is BP

cardiac output x systemic vascular resistance

What 3 things effect stroke volume

1. Preload

2. Contractility

3. Afterload

Iontrophy

Contractility

Describe blood viscosity

Number of red blood cells in the blood--more RBCs= increased load on heard

Describe vascular tone

Smooth muscle layer-> contracts to make vessel smaller or relaxes to make vessel bigger

Blood viscosity and hypoxia

Want more RBCs from stimulated bone marrow which creates thicker or more viscous blood

What causes the most profound change in resistance and flow

radius

What occurs to resistance when you decrease the radius

increase vascular tone and in return resistance

Major role of the baroreceptor reflex

Brining BP back down after steressure/ stimulation through sympathetic innervation of the heart and vasculature

Describe generally how baroreceptor reflex works

1. Brings down BP after a stressor, or stimulation, there is receptors inside of the aortic arch and carotid sinus that pick up pressure or more stretch changes that cause nerve endings to fire

2. This stimulates vagal tone to the SA node which is directly associated with PNS

3. PNS acts to decrease CO (HR and SV) to lower BP- decrease HR to lower CO and in turn pressure (not SV because doesn't affect myocardium) it just takes foot off the gas

4. Overall, it decreases sympathetic drive to the myocardium through SNS inhibition to SA node to decrease CO by reducing HR and SV, and decreases sympathetic tone of vessels

5. Once BP reduced, baroreceptors stop firing

Describe the ban bridge reflex

1. Prevents atrial congestion

2. Stretch of the atria inducing vaguely mediated increase in heart rate

3. Increase in BP

4. Baroreceptors inside atrial wall-> neural endings feel congestion/ stretch/ pressure, they signal to brainstem to increase HR

Describe chemoreceptor reflex

1. Indications that there isn't enough tissue perfusion (increased CO2, increased metabolic waste

2. Raising BP in response to hypoxia, hypercapnia or acidosis

3. Increase BP to increase tissue perfusion

What is long term control of BP

Changes in volume; hormonally controlled and kidney influenced

What is aortic pulse pressure

Difference between systolic pressure and diastolic pressure in the aorta when the ventricle is relaxed and when ventricle contracts

Increase SV= greater volume in aorta=

greater change in pressure in aorta

Slower heart rate= longer time for ventricle to fill= increase in

Stroke volume

SO slower HR= increase SV= increase change in

APP

What are 3 factors that can cause a decrease in aortic compliance

1. Age

2. Arteriosclerosis

3. Hypertension

What does decreased aortic compliance do to APP

The aorta can't stretch as much so it loses some compliance which causes an in crease in APP and volume doesn't move as easy so pressure increases

What occurs if the aorta is highly compliant

can push volume in and it will stretch so pressure won't go up as much (this is how aorta typically is)

What is MAP

Mean between diastolic and systolic pressure over time

What is the MAP equation

Pdias + 1/3(Psys-Pdias)

Why is MAP divided by 1/3

because 1/3 of cardiac cycle is spent in systole

Arterial system: sympathetic activity and vascular compliance

1. Add a little volume to the arterial system, pressure increases tremendously-> non compliant/ not stretchy

2. Pretty stiff system= big muscular wall

Venous system: sympathetic activity and vascular compliance

1. Add volume to venous system, pressure doesn't change as much= compliant/ stretchy

T or F: you cannot change compliance of vessels with SNS activity

False

1 multiple choice option

How does SNS activity affect vessels

Constrict vessel/ smooth muscle contracts and become less compliant, same amount of volume with increase pressure anymore

What happens to vasculature when you inhibit SNS activity

Relax vessel/ dilate-> become more compliant, more volume with less pressure

Why does PP change at rest vs exercise

PP changes because the systolic pressure increases as the heart is required to contract harder with exercise so the heart has to work harder to perfuse tissues-HR, SV, BP increases to circulate-> increase SV

PP increases significantly with exercise due to

1. Increase SV

2. Enhanced ventricular contractility

3. Reduced arterial stiffness effects during dynamic exercise

Why does MAP only increase a little during exercise

1. because it takes time in account and the heart only spends 1/3 of time contracting

2. Increase in SV to change diastole

3. Diastolic doesn't change much because even though you add more work, vessels dilate during exercise which results in decrease in peripheral resistnace

MAP increases modestly because

1. CO rises

2. Total peripheral resistance decreases during to vasodilation in active muscle

3. This balance maintains adequate perfusion without excessive pressure load

What may excessive rise in MAP indicate

Abnormal vascular response

What does a abnormally high PP at rest suggest

arterial stiffness or elevated CV risk

Tachycardia at rest

>100