Why does heart rate increase in inspiration?

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SUMMARY

The heart rate increases during inspiration due to the creation of negative intrathoracic pressure, which enhances blood flow to the lungs while temporarily reducing left atrial input and stroke volume. This physiological response is characterized by a heart rate increase, often exceeding 50 bpm during inhalation, while heart rates can drop below 40 bpm during exhalation. The aortic valve closes before the pulmonary valve during inspiration due to the dynamics of blood flow and pressure changes in the thoracic cavity. Additionally, the lungs function as an accessory cardiac pump, facilitating blood pooling in the pulmonary vasculature.

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  • Understanding of pulmonary circulation and its low-pressure characteristics
  • Knowledge of cardiac physiology, specifically stroke volume and heart rate dynamics
  • Familiarity with the mechanics of respiration and intrathoracic pressure changes
  • Awareness of physiological shunts, including the bronchial and thebesian veins
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  • Research the mechanics of negative intrathoracic pressure during respiration
  • Study the physiological implications of pulsus paradoxus in clinical settings
  • Explore the role of the diaphragm in cardiac and pulmonary function
  • Investigate the effects of hypoxia on pulmonary vascular resistance
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Medical students, healthcare professionals, and anyone interested in understanding the relationship between respiration and cardiovascular dynamics.

sameeralord
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Hello everyone,

Can anyone explain simply why heart rate increases in inspiration. Also why does the aortic valve close before pulmonary valve in inspiration? In inspiration does superior vena cavae get more blood? From what I read there was something to do with blood pooling inside the lungs during inspiration? Why does blood pool I don't understand?

Thanks :smile:
 
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Lungs are described as an accessory cardiac pump.
In inspiration, there is a depression (diaphragm) and blood goes more easily in lungs.
 
Hey somasimple did you mean blood goes less easily in lungs in inspiration. We learned this in class today!
 
I said the contrary:
http://www.nda.ox.ac.uk/wfsa/html/u12/u1211_01.htm
Blood supply

The lungs have a double blood supply, the pulmonary circulation for gas exchange with the alveoli and the bronchial circulation to supply the parenchyma (tissue) of the lung itself. Most of the blood from the bronchial circulation drains into the left side of the heart via the pulmonary veins and this deoxygenated blood makes up part of the normal physiological shunt present in the body. The other component of physiological shunt is from the thebesian veins, which drain some coronary blood directly into the chambers of the heart.

The pulmonary circulation is a low-pressure (25/10mmHg), low-resistance system with a capacity to accommodate a substantial increase in blood flowing through it without a major increase in pressure. Vascular distension and recruitment of unperfused capillaries achieve this. The main stimulus which produces a marked increase in pulmonary vascular resistance is hypoxia.

A pressure gradient is required to generate flow. In spontaneous respiration inspiratory flow is achieved by creating a sub-atmospheric pressure in the alveoli (of the order of -5cmH2O during quiet breathing) by increasing the volume of the thoracic cavity under the action of the inspiratory muscles. During expiration the intra-alveolar pressure becomes slightly higher than atmospheric pressure and gas flow to the mouth results.
 
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In my case there seems to be a rather big difference. My heart rate is now about 45 bpm, but I notice that when I'm breathing in, it is above 50 bpm (the beats come almost every second). When I'm exhaling, my heart rate becomes very slow, below 40 bpm.
 
Heart rate and blood pressure are different things. :wink:
 
Heart rate increases whereas primarily, it is the blood pressure that decreases. During inspiration, negative intrathoracic pressure fills the pulmonary vasculature temporarily reducing the left atrial input and therefore the stroke volume. An increase in heart rate is a consequence of this.

In the clinical condition known as pulsus paradoxus, there is exaggeration of these events.
 

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