Cardiovascular/Respiratory Integration Lecture 2

Question 1

What are the respiratory influences on the heart?

Answer 1

Mechanical Interaction

• Inspiration increases venous return to right ventricle (due to abdominal pressure)
• This increases right SV
• Corresponding increase in left EDV and hence SV

Neural interaction

-Inspiration increases HR (sinus arrhythmia)

Sinus arrhythmia are due to changes in cardiac vagal activty

Question 2

Describe the 2 main mechanisms that regulate the respiratory influence on the heart

Answer 2

Phasic inhibition of vagal activity during inspiration. Explained by two mechanisms:

1. Central Nervous Mechanism
   - Group of inspiratory neurons supply phrenic nerves to lower diaphragm and excite them
   - They also have collaterals to the NA and inhibit it, inhibiting vagal activity to the heart. Allowing heart rate to increase
2. Reflex Response
   - Pulmonary Stretch Receptors in the walls of airways are excited by breathing
   - They have vagal afferents which inhibit the NA via the NTS

These 2 mechainsms explain respiratory sinus arrhythmia, therefore when respiraiton increases, heart rate increases by these mechainsms. When respiration decreases, decrease in heart rate

Question 3

What are the peripheral chemoreceptor reflexes?

Answer 3

1. When respiration cannot increase
   - Primary cardiovascular reflex response to chemoreceptor stimulation dominants
   - HR decreases and vasoconstriction of peripheral tissue

This is O2 conserving

2. When inspiration can increase
   - Effects of increased respiration on HR dominate
   - This is because PSRs and CID both send inhibitory signals to NA which sends HR up by decrease of vagal activity

Question 4

When might someone get systemic hypoxia when respiration cannot increase?

Answer 4

Under muscle relaxant- ventilated at a constant rate and depth High spinal transection Long dive underwater Fetus in utero Severe respiratory disease Superimposed upon local effects of hypoxia- decrease HR and contractility, cerebral, muscle and coronary vasodilation, pulmonary basic instruction (pulmonary oedema, right ventricular failure, systemic oedema)

i.e. severe respiratory disease or fetus in utero

Chemoreceptors stimulated

• Increases afferent activity to NTS
• Reflex vasoconstriction and decrease in HR to conserve O2

Superimposed on Hypoxia effects

• Decreased HR and depressed contractility due to depressed SAN
• Cerebral, muscle and coronary dilatation due to local response (due to adenosine on P1 receptors)

O2 that is available directed to brain

-Pulmonary vasoconstriction may lead to oedema and eventually RV failure

Question 5

When might someone get systemic hypoxia when respiration can increase?

Answer 5

eg Hypoxia atmosphere High altitude Less severe respiratory disease

Increase in respiration and heart rate plus vasocontriction in GIT, kidney, helps to restore PaO2 so systemic tissues do not become as hypoxic and pulmonary vasoconstriction is less severe

Question 6

Describe the diving reflex

Answer 6

Reflex evoked by trigeminal receptors, Cold water on face/nose

Inhibition of central inspiratory neurones➡ expiratory apnoea and decrease HR (due to increase in vagal activity of NA), vasoconstriction (increased symp activity via RVLM) except brain

O2 conserving

Clinically receptors stimulated by sinus washing, irritant vapours, intubation, lumps of food in the pharynx

Mouth-mouth respiration/ventiliating thorax can terminate apnoea.