Theme 4: Cardiorespiratory (CVS/Resp) Flashcards

1
Q

What is the primary function of the respiratory system?

A

O2 and CO2 exchange so that tissues can receive O2 and the waste product of respiration, CO2, can be disposed of.

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2
Q

What factors affect the rate of diffusion of gases in the body?

A
Surface area (capillary density)
Diffusion resistance (nature of barrier; diffusion path)
Concentration gradient (rate of blood flow)
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3
Q

Regarding gases, what is Boyle’s Law?

A

Pressure is inversely proportional to volume (at constant °C) (more collisions - smaller smace).

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4
Q

Regarding gases, what is Charles’ Law?

A

Pressure is proportional to temperature (more kinetic energy, therefore increased likelihood of harder collisions).

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5
Q

What is saturated vapour pressure?

A

Vapour pressure is the partial pressure of H2O, as a gas.

It becomes saturated when the rate of molecules moving and leaving the water are equal.

Gases enter the body at a saturated vapour pressure; they will not dry out the respiratory tract.

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6
Q

What is the content of gas in a liquid determined by?

A

Solubility (volume of gas that can dissolve in a liquid) multipled by tension (‘how readily a gas will leave a liquid’; at equilibrium: tension = partial pressure).

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7
Q

How would you calculate cardiac output and therefore blood pressure? What is a normal cardiac output in a resting person?

A

CO = SV x HR;
BP = CO x TPR (or SV x HR x TPR)
5L/min

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8
Q

Which blood vessels can restrict flow?

A

Arterioles and pre-capillary sphincters.

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9
Q

In terms of the cardiovascular system, what is capacitance?

A

A store of blood that can be called upon to make up for an imbalance in blood pumped out of, and returning to, the heart. The veins display capacitance (2/3 of the bodies’ blood is stored there at rest).

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10
Q

What is tidal volume?

A

The amount of air displaced between normal inspiration and expiration.

(n.b. approximately 500 cm3 at rest)

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11
Q

Is the pulmonary circulation under low or high pressure?

A

Low pressure. There is low resistance due to short, wide bronchi, which are connected in parallel. The arterioles also have less smooth muscle surrounding them.

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12
Q

What is hypoxic pulmonary vasoconstriction?

A

Alveolar hypoxia leads to vasoconstriction of pulmonary vessels. This increased resistance results in reduced flow to poorly ventilated areas and more to the well ventilated areas.

It helps maintain the ventilation/perfusion matching ratio (normally 0.8).

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13
Q

Pathologically, what can chronic hypoxic pulmonary vasoconstriction result in?

A

This may result in pulmonary hypertension (an increased afterload on the right ventricle), which can lead to right heart failure (Cor Pulmonale).

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14
Q

What are conducting arteries? How do distributing arteries differ?

A

Conducting (or elastic) arteries carry blood away from the heart. They expand slightly with each heartbeat. Distributing (or muscular) arteries are connected to conducting arteries. They can contract, regulating blood flow, and are continuous with arterioles.

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15
Q

How is the diameter of arterioles controlled?

A

By the autonomic nervous system: action of a1-receptors result in vasoconstriction.

Specificially in vascular smooth muscle: Gaq subunit - PIP2 –> DAG + IP3; IP3 leads to Ca2+ influx via SR); Ca2+ binds to calmodulin; calmodulin associates with MLCK.
Phosphorylation of regulatory light chain occurs (from ATP) - enables actin-mysoin interaction (then known as MLCP); the myosin head inactivates as Ca2+ levels decrease. This process results in contraction.

DAG leads to PKC production which inhibits MLCP, inhibiting contraction.

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16
Q

In the parasympathetic nervous system, which neurotransmitters and receptors are found at the pre- and post-ganglionic synapses?

A

Pre-ganglionic: ACh; Nicotinic

Post-ganglionic: ACh; Muscarinic

17
Q

In the sympathetic nervous system, which neurotransmitters and receptors are found at the pre- and post-ganglionic synapses?

A

Pre-ganglionic: ACh; Nicotinic.

Post-ganglionic: NA; Adrenergic (n.b. except to the sweat glands which is ACH; Muscarinic).

18
Q

What is the parasympathetic input to the heart? What does increased parasympathetic stimulation result in?

A

CN X (Vagus Nerve) which synapses at the epicardial surface or within the walls of the heart at the SA and AV node. Post-ganglionic cells release ACh which acts on M2-receptors, resulting in decreased AV node conduction and therefore chronotropy.

19
Q

What is the sympathetic input to the heart? What does increased sympathetic stimulation result in?

A

Post-ganglionic fibres from the sympathetic trunk innervate the SA and AV node as well as the myocardium. They release NA which acts on ß1-receptors, resulting in an increased chronotropic and inotropic effect.

20
Q

What are the layers of arteries/veins from inner to outermost?

A

Tunica Intima - often contain endothelial cells and sub-endothelium of connective tissue.
Media - often contains the bulk of elastic/muscular fibres.
Tunica Adventitia - often contains vasa vasorum (‘vessels of vessels’), lymphatic vessels and nerve fibres.

21
Q

Ventilation-perfusion mismatch can lead to respiratory illness. What could be the cause of decreased perfusion to the alveoli and how could this result in Type 1 Respiratory Failure?

A

A pulmonary embolism can lead to decreased perfusion. Affected parts of the lungs will have sufficient oxygen but not enough blood. There is poor oxygenation. This is consistent with Type 1 Respiratory Failure where there is hypoxaemia but there is not hypercapnia (i.e. there is no failure in breathing, e.g. hypoventilation).

22
Q

Heart Failure

A

CVS Session 11; Integrative Session 7

23
Q

What is the definition of heart failure?

A

The heart fails to maintain an adequate circulation despite an adequate filling pressure.

24
Q

What is preload?

A

It is the end diastolic volume that stretches the heart to its fullest. It is affected by venous blood pressure and venous return.

25
Q

What is afterload?

A

Afterload is the force that the ventricles must overcome to eject blood out of the heart.

It is composed of the aortic pressure that the left ventricle must overcome to eject blood into the aorta - therefore a high aortic pressure will increase afterload.
If the left ventricle is dilated it must generate more force to overcome the aortic pressure - therefore a dilated left ventricle will increase afterload.