Physiology 12.2

During isovolumetric ventricular contraction, which valves are open?

None-all are closed

During ventricular ejection, which valves are open?

the aortic and pulmonary valves

During isovolumetric ventricular relaxation, which valves are open?

none-all are closed

During ventricular filling, which valves are open?

AV valves

Cardiac output and equation for it

the volume of blood pumped out of each ventricle per unit time

-normal is about 5 liters per minute

CO=SV x HR

Mid to end Diastole

1. Left and right atria are relaxed but atrial pressure is slightly higher than ventricular pressure because atrium is filling with blood returning to the heart

2. AV valve is open due to pressure differences and blood entering the atrium from the pulmonary veins continues on into the ventricle

3. Aortic valve is closed at this time and throughout diastole (aortic pressure>ventricular pressure)

4. Aortic pressure is slowly decreasing because blood is moving out of the arteries and into systemic systems

5. Ventricular pressure is increasing slightly because blood is entering the relaxed ventricle from the atrium

6. Near the end of diastole, the SA node discharges and the atria depolarize (P wave)

7. Contraction of the atrium causes an increase in atrial pressure

8. End of ventricular diastole

Systole

1. From the AV node, the wave of depolarization passes throughout the ventricular tissue and triggers ventricular contraction (QRS Complex)

2. As the ventricles contract, ventricular pressure increases rapidly (exceeds atrial pressure) and the AV valve is forced to close to prevent back flow into the atrium

3. For a brief time, all valves are closed during this phase of isovolumetric ventricular contraction

4. This brief phase ends when the rapidly increasing ventricular pressure exceeds aortic pressure

5. The pressure gradient now forces the aortic valve to open and ventricular ejection begins

6. Ejection is rapid at first and then slows down. The volume and pressure in the aorta decreases as the rate of blood ejection from the ventricle slows

7. End of systole

Early Diastole

1. As the ventricles relax, ventricular pressure decreases below aortic pressure, which is higher due to the volume of blood that just entered. The change in pressure forces the aortic valve to close

   • Dicrotic Notch

2. AV valve also remains closed because ventricular pressure>atrial pressure. For a brief time, all valves are closed again during this phase of isovolumetric relaxation

3. This phase ends as the rapidly decreasing ventricular pressure decreases below atrial pressure

4. This change in pressure causes the AV valves to open

5. Venous blood that had accumulated in the atrium since the AV valve closed flows rapidly into the ventricles

How does blood travel?

high pressure→low pressure

Contraction of an area does what to the pressure of that area?

Contraction increases the pressure of the area

atrial pressure>ventricular pressure

AV valves open

ventricular pressure>atrial pressure

AV valves closed

ventricular pressure>aortic pressure

aortic valve open

aortic pressure>ventricular pressure

aortic valve closed

Stenotic Valve

narrowed valve with turbulent flow (still in the right direction) but causes a murmur

Insufficient Valve

leaky valve with turbulent back flow which causes a murmur

In the absence of any nervous or hormonal influences, what is the approximate bpm?

100 bpm

-this is the inherent autonomous discharge rate of the SA node

Activity in the parasympathetic system travels from where and does what to heart rate?

It travels within the vagus nerves and causes the heart rate to decrease

-has a lower membrane potential

Activity in the sympathetic system does what to heart rate?

causes heart rate to increase

-has a higher membrane potential

Antagonistic activity on heart rate via the parasympathetic and sympathetic systems is termed what?

chronotropic effects

Increases in plasma epinephrine causes…

-increased sympathetic activity

-decreased parasympathetic activity

-increased heart rate (SA node)

Stroke Volume

the volume of blood each ventricle ejects during each contraction

SV=EDV-ESV (end diastolic minus end systolic volumes)

What are the three factors that affect stroke volume?

• changes in the EDV (aka preload)

• changes in the magnitude of sympathetic nervous system input to the ventricles

  • increased contractility = increased SV

• changes in after load (arterial pressures against which the ventricles pump)

Frank-Starling Mechanism

relationship between stroke volume and end-diastolic volume where when all other factors are equal, stroke volume increases as the end-diastolic volume increases

-aka Starling’s law of the heart

-greater EDV=greater the stretch=able to pump harder (more forceful contraction)

-an increase in the venous return=increase in cardiac output by increasing EDV and therefore stroke volume

• more blood you get back from periphery=more to pump (more pumping)

Contractility

the strength of contraction at any given end-diastolic volume

What sympathetic neurotransmitters affect contractility and what effect do they have?

Norepinephrine acts on beta-adrenergic receptors to increase ventricular contractility

Plasma epinephrine also acts on these receptors to increase myocardial contractility

-sympathetic stimulation causes more powerful contraction and causes the contraction and relaxation of the ventricles to occur more quickly

Ejection Fraction (EF)

way to quantify contractility

EF=SV/EDV

-expressed as a percentage

-increased contractility=increased EF

What is after load and how does it affect stroke volume?

arterial pressure constitutes a “load” that contracting ventricular muscles must work against when ejecting blood

-greater load=less contraction of muscle fibers=less cardiac output/stroke volume

*it is harder for the heart to pump when there’s resistance

What effects do sympathetic nerves have on the SA node, AV node, Atrial muscle, and Ventricular muscle?

SA node: increased heart rate

AV node: increased conduction rate

Atrial muscle: increased contractility

Ventricular muscle: increased contractility `

What effects do parasympathetic nerves have on the SA node, AV node, Atrial muscle, and Ventricular muscle?

SA node: decreased heart rate

AV node: decreased conduction rate

Atrial muscle: decreased contractility

Ventricular muscle: no significant effect

Echocardiography

noninvasive technique that uses ultrasonic waves and can detect the abnormal functioning of cardiac valves or contractions of the cardiac walls

-can also be used to measure ejection fraction

Cardiac angiography

requires the temporary threading of a thin, flexible tube (catheter) through an artery or vein into the heart. A liquid containing radiopaque contrast material is then injected through the catheter

-technique is useful for evaluating cardiac function and for identifying narrowed coronary arteries

-same thing as heart cath

What are the different vessels of the vascular system?

arteries, arterioles, capillaries, venules, and veins

What is the major function of the vascular system?

regulate blood pressure and distribute blood flow to the various tissues

What is the one structural component that the entire circulatory system all have in common?

a smooth single-celled layer of endothelial cells (endothelium) that is in contact with the flowing blood

Arteries

-carry (oxygen-rich) blood away from the heart

-have large radii (low resistance)

-known as pressure reservoirs because of their elastic recoil (compliance)

-help maintain blood flow during diastole

-lot of musculature (smooth muscle and connective tissue)

Compliance

Compliance=change in volume/change in pressure

-higher compliance=more easily stretched

In terms of compliance, which has more: arteries or veins?

veins

-arteries have compliance, just not as much as veins do

As you age, what happens to systolic and diastolic pressure?

systolic pressure increases and diastolic pressure decreases

Pulse Pressure

the difference between systolic pressure and diastolic pressure

-can be felt as a pulsation or throb in the arteries of the wrist and neck with each heartbeat

-factors that determine pulse pressure:

• stroke volume

• speed of ejection of stroke volume

• arterial compliance

Arterial sclerosis

condition where there is a decrease in arterial compliance and arterial walls become more thickened/rigid as you age

• atherosclerosis: thickening of arterial wall due to plaque buildup; major cause of coronary artery disease

Mean Arterial Pressure

approximately equal to the diastolic pressure plus 1/3 of the pulse pressure

• pulse pressure=systolic-diastolic pressures

-important because it is the average pressure driving blood into the tissues averaged over the entire cardiac cycle

What is the sound heard when cuff pressure of sphygmomanometer is gradually lowered?

Korotkoff

Arterioles

Functions:

• determine where blood flows in respect to organs

• major factor in determining mean arterial pressure

Diameter is controlled by neural, hormonal, and local chemicals

If they contract, blood flow is diverted away from the downstream tissues

If they dilate, then blood flow to the tissues increases

Vasoconstriction and vasodilation effects on flow

Vasoconstriction: increases resistance of arterioles and flow to a tissue decreases

Vasodilation: decrease resistance of arterioles and flow to a tissue increases

What effects does active hyperemia have (local control)?

increased blood flow to the organ along with:

-increase in metabolic activity of the organ

-decreases O₂ but increases metabolites in the interstitial fluid

-anteriolar dilation

What effects does flow auto regulation have (local control) when there is a decrease in arterial pressure?

maintains constant blood flow in spite of different fluctuations

-decreased blood flow to the organ

-decreases O₂, increases metabolites, and decreases vessel-wall stretch in the organ

-ateriolar dilation

-restoration of blood flow toward normal

Flow auto regulation

automatic adjustment that ensures blood flow is going to get to all the organs

-regulated by local metabolic factors (which alters the diameter of local arterioles)

Increased norepinephrine in the extracellular fluid affects what type of receptors and causes what?

alpha adrenergic receptors

causes vasoconstriction

-this is sympathetic**

Increased plasma epinephrine affects what receptors and causes what?

alpha and beta adrenergic receptors

causes vasodilation if beta

causes vasoconstriction if alpha

Nitric oxide

released continuously in significant amounts by endothelial cells in the arterioles and contributes to arteriolar vasodilation in the basal state

-nitirc oxide does this by diffusing to vascular smooth muscle after being secreted by the endothelial cells

Capillaries

-smallest blood vessel with single layer of endothelial cells

-contain about 5% of blood

-permeate every tissue except the cornea

-main function is to exchange nutrients and gases (have lots of surface area to do so)

What is the implication of increased surface area in capillaries?

lot of surface area allows more more exchange to occur but makes it slower →slower means more exchange as opposed to fast

surface area has what effect on velocity

increased surface area=decreased velocity

Hydrostatic pressure

pressure blood exerts against the walls

-higher on the arteriole end of capillary to promote filtration

-lower on the venule end of capillary to promote absorption

Oncotic pressure

aka colloid osmotic pressure

pressure exerted by proteins in the blood (i.e. albumin)

-higher on the venule end of the capillary to promote absorption

-lower on the arteriole end of the capillary to promote filtration

Starling Forces and Net Filtration Pressure

Starling Forces:

• Capillary hydrostatic pressure (P_c)

• Interstitial fluid hydrostatic pressure (P_if)

• Osmotic force of capillary (π_c)

• Osmotic force of interstitial fluid (π_if)

If net filtration pressure is positive → favors filtration

If net filtration pressure is negative → favors absorption

capillary hydrostatic pressure and interstitial osmotic force favor filtration

interstitial fluid hydrostatic pressure and capillary osmotic force (plasma protein concentration) favor absorption

Venules and Veins

-capacity vessels (have large capacity for blood)

-have some permeability to macromolecules (i.e. leukocytes)

-thin walls and are very compliant

-considered blood reservoirs

What mechanisms exist to aid in venous return?

-Respiratory pump: pressure changes in the central cavity occur due to the pressure changes during breathing; produces a suction effect to move blood back to the heart

-Muscular pump: when muscles contract, they squeeze the veins, resulting in forward movement of blood towards the heart with backwards flow being prevented by one-way valves

The smooth muscle in the veins is under what type of control and why is that important?

sympathetic nervous system control

it contracts when stimulated, causing venous contraction which promotes venous return

Lymphatic System

network of small organs (lymph nodes) and tubes (lymphatic vessels) through which lymph (fluid derived from interstitial fluid) flows

-part of immune system

-lymphatic vessels carry the interstitial fluid back to the circulatory system

-lymphatic vessels scan also take up small amounts of protein and return them to the circulatory system

Mechanism of Lymph Flow

smooth muscle of the lymphatic vessels exerts a pump-like action by inherent rhythmic contraction that produce a one-way flow (due to valves) toward the point at which lymph enters the circulatory system

-this smooth muscle is innervated by sympathetic neurons

How does a hemorrhage affect things?

decreases blood volume, venous return and pressure, atrial pressure, EDV, stroke volume, cardiac output, and arterial blood pressure

Baroreceptors

monitor what your blood pressure is

-located in carotid artery and aortic arch

-pressure sensors:

• increased pressure=increased frequency of action potentials

• increased blood pressure=vasodilation

• increased chronic blood pressure=baroreceptors become less sensitive and lead to the creation of a new set point (blunted response)

How do beta blockers affect blood pressure?

they inhibit adrenaline and decrease heart rate to reset

Blood pressure is affected by what?

oxygen, CO₂, changes in blood flow to the brain, pain, eating, mood, sexual activity, and stress

Hypotension

low blood pressure

-causes include

• significant blood loss (i.e. hemorrhage)

• decrease in cardiac contractility

• strong emotion

• massive release of endogenous substances that relax arteriolar smooth muscle (allergic reaction)

Shock

any situation in which a decrease in blood flow to the organs and tissues damages them

-3 types:

• Hypovolemic shock: decrease in blood volume secondary to hemorrhage or loss of fluid other than blood

• Low-Resistance Shock: decrease in total peripheral resistance secondary to excessive release of vasodilators (allergy/infection)

• Cardiogenic Shock: extreme decrease in cardiac output from any variety of factors (i.e. heart attack)

Hypertension

chronically increased systemic arterial pressure above 140/90; contributing cause to some of the leading causes of disability and death

-primary hypertension: uncertain cause (most common etiology; ~40% of population)

secondary hypertension: identified cause

What are identified causes of secondary hypertension?

• damage to kidneys of their blood supply (renal hypertension)

• excess renal Na⁺ reabsorption

• hyper section of cortisol, aldosterone, or thyroid hormone

• abnormal nighttime sleeping pattern or sleep apnea

Hemostasis

the physiological mechanisms that stop bleeding

involves 3-step process:

1. Vascular spasm

2. Formation of platelet plug (sticking of collagen)

3. Coagulation of blood (fibrin protein to thicken blood and increase viscosity)