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When are the mitral, tricuspid, and semilunar valves open and closed in respect to pressure and systole/diastole?

A valve is open when the pressure in front of it exceeds the pressure behind it. A valve is closed when the pressure behind it exceeds the pressure in front of it.

The mitral and tricuspid valves are open when pressure in the atria is greater than in the ventricles. This allows for the ventricles to fill and occurs during ventricular diastole. The mitral and tricuspid valves are closed during ventricular systole when the pressure in the ventricles exceeds that in the atria.

The semilunar valves are open when the pressure in the ventricles exceeds that in the pulmonary artery and in the aorta which occurs during ventricular systole. The semilunar valves are closed when the pressure in the pulmonary artery and aorta exceed that in the ventricles which occurs during ventricular diastole.


What are chordae tendineae? What do they attach to and where are their attachments located? What is the fxn of their attachments?


Chordae tendineae are ligaments of the tricuspid and mitral valves that attach to palillary muscles in the ventricles. Papillary muscles contract during ventricular systole and pull on chordae tendineae so the mitral and tricuspid vavles are not everted into the atria.


What are the 2 types of valvular disease and what are their consequences?

stenosis: a stenotic valve is fibrotic and narrow and impeded the normal flow of blood. To preserve a roughly normal flow higher pressures must be developed prior to the stenotic valve. The heart must work much harder and cardiac reserve (the ability of the heart to increase its output, for example during exercise) is greatly reduced. Can cause hypertrophy (like left ventricular hypertrophy with aortic stenosis)

insufficiency: leaky valve. Valve is no longer one way and allows some blood to flow in the wrong direction. In mitral regurgitation, during ventricular systole part of the blood ejected form the left ventricle will flow back into the left atrium which leads to elevated left atrial pressure, left ventricular dilation, increased work of the heart and reduced cardiac reserve.


What restricts the backflow of blood from the heart into the superior and inferior vena cavae?


They do not have valves. Instead the thickening and contraction of the m uscle around their mouths prevent backflow of blood from the heart.


What are the definitions of left ventricular systole and diastole in regards to valve opening and closure (can be applied to right side with different names of valves)?

left ventricular systole: period from the start of ventricular contraction to the closing of the aortic semilunar valve (ventricular contraction)

left ventricular diastole: time from the closing of the aortic valve to the beginning of ventricular contraction (ventricle filling with blood)


______ flow through the heart is heard as a murmur and may be caused by an issue with a valve.


Turbulent. was seen on echocardiogram


The left side (left atrium and venticle) and right side (right atrium and ventricle) of the heart are 2 pumps in series. What is the consequence of this?

Since they are in series, flow through each side of the heart must be the same in a normal individual in steady state. (have same cardiac output) If not, then get fluid accumulation


Discuss vessels of the pulmonary circulation in relation to systemic cicrulation as it relates to compliance and pressure. Also, how do the pressures generated by the right and left heart differ and why?


Vessels of the pulmonary circulation are highly compliant and their pressures are much lower than those found in the systemic circulation. Similarly, pressures developed by the right ventricle are normally much less than pressures developed by the left ventricle. If this did not occur, would cause high pressure in pulmonary circulation and bc vessels are so compliant, they could explode.

note: the max pressure developed during systole by the right ventricle during rest is about 25 mmHg compared to 120 mmHg in the left ventricle


The systemic circulation system is made up of many _____ vascular beds. What is the result of this.


The systemic circulation system is made up of many parallel vascular beds (or regional circulations). The amount of blood entering each regional circulation is adjusted according to the needs of the tissue
(i.e. blood flow is not the same to each region, each region receives a portion of the cardiac output)


How is cardiac output (CO) calculated? What is the value of CO in a normal resting individual? What are the normal ranges for the values that determine CO?

CO= the amount of blood leaving each ventricle per minute


in a normal resting individual, HR is 70 bpm and SV is about 70-75 ml (SV is the amount of blood ejected from ventricles per heartbeat). Thus the CO is 5 L/min. Changes in heart rate and/or stroke volume can change CO.

Typical range for HR is 60-180 bpm and is 70-120 ml for SV


CO=HR x SV. What factors are HR and SV controlled by? What affects can changes in these factors cause?


HR is controlled by the autonomic nervous system inputs to the heart.

SV is determined by 3 variables-inotropic state (contractility) of the heart, preload, and afterload

preload: Amount the ventricles fill. The more the ventricles fill, the higher the SV. If ventricles fill more, the muscles stretch more, and the ventricle contract with more force.

afterload: the pressure your heart pumps against. The higher the pressur ein our arteries, the higher the afterload and the harder the heart is working.

inotropic state: controlled by 3 things:

-Ca2+ in the myoplasm

-number of functional myocytes (can be dc with MI)

-coronary artery supply (inadequate blood flow can reduce contractility)

Positive inotropic state: increasing myoplasmic Ca2+ Negative inotropic state: decreasing the number of functional myocytes or coronary artery supply

Increased inotropic state and increased filling of the heart (preload) both increase the force with which the heart contracts and therefore acts to increase stroke volume. Increased afterload will decrease stroke volume.



True or false: The filling of the heart is primarily determined by central venous pressure.



Blood and air both flow from high pressure to low pressure. However, the lungs create negative pressure and the heart creates positive pressure. What is the difference?

Negative pressure created during inhalation by contraction of the diaphragm and protrusion into the abdominal cavity to increase lung volume creates a negative pressure and causes air to be pulled in. Positive pressure created by the heart pushes blood out.


What happens to the lungs and chest wall when the chest is cut open? What balances the resting volume of the chest cavity? How can this change with lung disease?

The lungs have a tendency to collapse and the chest wall has a tendency to expand. Because the space btwn the chest wall and lungs is a vacuum, if this is disturbed the lungs will collapse and the chest wall will expand. The functional residual capacity is the resting volume of the lung (i.e. chest cavity). This is the point where the tendency of the chest wall to expand (elastic recoil of the chest wall) equals the tendency of the lungs to collapse (elastic recoil of the lungs). The balance of these forces leaves the lung at a normal volume with little or no effort. Any disruption of these forces such as in COPD, the chest can be either too large or too small leading to labored breathing.


What is minute ventilation and how is it calculated? How are its aspects controlled?

Minute ventilation is the volume of air which enters or leaves the lungs per minute.

Minute ventilation=f x VT

f=frequency (number of breaths)

VT: tidal volume: volume of air inhaled (or exhaled) per breath

Minute ventilation can be increased with taking deeper breaths (increasing tidal volume) or increasing frequency (number of breaths per minute)

Both aspects are regulated by metabolic need. Chemoreceptrs in teh carotid artery and the aortic arch sense arterial blood O2 and chemoreceptors in the brainstem sense CO2 with the brain tissue to regulate ventilation. Note that above equation is very similar to CO equation.


What are partial pressures of gas determined by? What are the partial pressures of N2 and O2 in the air? What is the PP of O2 in the lungs?

Ambient air is 79% N2, 21% O2, and minute quantities of CO2, argon, and other inert gasses. Gasses are described as partial pressures when talking about respiratory system. Dalton's gas law states that the sum of the partial pressures of individual gasses in the air must equal total pressure (1 atm or 760 mmHg).

PP of N2 (in atmosphere): 760 mmHg x 0.79= 600 mmHg

PP of O2 in atmosphere is 160 mmHg at sea level. During inspiration, the air is humified by the lungs and water is now taking up some of the partial pressure. The PP of water at body temperature is 47 mmHg which dilutes the other gasses. Because 47 mmHg of the 760 mmHg at sea level is now water, the PP of O2 sinks:

(760mmHg-47mmHg) x .21 =150 mmHg

This partial pressure sinks even further in the alveoli bc this is the site of gas exchange (O2 is being taken up by RBCs and CO2 is leaving RBCs and entering alveoli). The PP of O2 in the alveolus is ideally 102 mmHg


Discuss diffusion as it pertains to the alveolar-capillary network. What is the size of the barrier btwn the capillaries and alveoli? What does this barrier consist of? How is this related to the case study in which her pulmonary veins are visualized (pulmonary congestion) due to fluid accumulation?

Diffusion is most effective as a transport mechanism over short distances. A molecule which must diffuse 10 times farther takes 102 longer to diffues (100 times longer). Therefore, the barrier to exchange of O2 and CO2 within the blood must be extremely small. The barrier btwn gas in the alveoli and the blood is only 1-2 micrometers in thickness and consists of type I alveolar cells, capillary endothelial cells, and their respective basement membranes. Fluid in the pulmonary veins increases the distance for diffusion and is one of the causes for respiratory distress


How are O2 and CO2 transported in the blood?