Exercise Effects on HR & Circulation Flashcards
What is the initial cardiac response at onset of exercise?
- initial cardiac response to increased workload is to increase HR and SV to account for the need for an increased CO
- HR increases more so than SV (only ~15%)
- HR increases linearly w/ O2 consumption (work done by body) up until hit the max HR
How does the autonomic nervous system effect exercising heart?
-at rest PNS & vagal nerve act on heart to decrease SA node intrinsic firing from 100bpm to 70bpm
-when begin exercising, withdraw PNS initially until hit 100bpm, then need to activate SNS to increase HR up to max
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What does SNS augmentation act on in the heart? What is the role of B-1 receptors & blockers?
- SNS innervates SA node, AV node, and cardiac myocytes to increase rate of contraction& contractility
- SNS acts on B-1 receptors and only activated when exercising
- means at B-1 blockers have no effect on Resting HR
How does an athletes heart differ from an average persons heart?
- athletes have an increased SV compared to avg pop, is why resting HR is ~50bpm but CO is sufficient
- when exercise HR has same max as everyone else, but SV increases so have more CO at a specific HR than a non-ahtelte at the same HR
How does a patient w/ CHF heart differ from an avg persons heart?
- venticle can’t create enough force to eject a normal preload level regardless of SNS augmentation
- require an increased pre-load, ventricle can eject a lower SV but one that will allow body to not go into hypovolemic shock
- this means that very low SV and require higher HR at rest to maintain MAP
What are the cardiovascular adjustments to exercise?
1) increased SV
2) increased CO
3) increased HR
4) MAP remains relatively constant (MAP= CO x SVR)
5) SVR decreases
6) whole body O2 consumption increases
How does SVR relate to body’s O2 consumption?
- SVR is inversely proportional to O2 consumption
- due to local metabolite vasodilation systemically (active hyperemia)
How do CO and SVR relate?
- CO is inversely proportional to SVR (MAP= CO x SVR)
- as resistance increases, less Co can occur
- reflects baroreceptor heart regulation
What is Cardiac output limited by? (equation of CO?)
- the stoke volume and heart rate
- CO= SV + HR
How does Mean arterial pressure change during exercise?
-it remains relatively constant since elevated CO made up for by decreased SVR
How is increased cardiac output matched with an increased venous return?
- SNS venoconstriction due to baroreflex
- sk. muscle pumps
- respiratory pumps
How does the Frank-Starling curve change during exercise?
- shifts up and to the left
- the ESV decreases (due to greater contractility), while EDV remains same increasing the PP
- SV increases
What is the main function of the pulmonary circulation?
- CO2 and O2 gas exchange
- to bring cardiac output into close proximity to the atmospheric air that fills the alveoli
What is main difference between pulmonary and cardiac circulation?
- main difference is that pulmonary circulation is a low pressure- low resistance system
- cardiac circulation is a high pressure-high resistance system
How does blood flow into lungs?
- deoxygenated blood arrives to the lung via the pulmonary artery and enters into capillaries that act as mesh around the alveoli
- leave alveoli well oxygenated and go to through pulmonary vein into the LA
How does Cardiac output and the lungs relate?
- all CO has to flow through the lungs & systemic circulation
- means all factors that effect CO will affect blood flow to the lungs
- pulmonary capillaries hold ~75mL of blood, CO is ~75mL; so pulp capillaries refill w/ each heart beat
what are alveoli?
- smooth, very thin walled vessels
- contain layer of surfactant to decrease the surface tension and help them expand when inspiring
What does it mean that the pulmonary circulation is optimized for diffusive exchange?
- that pulmonary system has all key features (seen by Fick’s Law of Diffusion) to have rapid diffusion
- air/plasma barrier very thin, short diffusion distance, large concentration gradient, O2/CO2 diffuse across membrane rapidly
What is the path of oxygen from the alveoli to the hemoglobin in RBC? How long take to this?
1) surfactant layer
2) alveoli epithelial
3) basal lamina
4) alveoli endothelial
5) air/plasma space
6) RBC–> Hemoglobin
- takes
What would happen if the blood/air barrier was NOT super thin?
-would have a slower diffusion
What does it mean that pulmonary circulation is low pressure & low resistance?
- pulmonary arteries/arterioles have low resistance to blood flow & transmit all CO under low (hemodynamic) pressure
- this system ensures fluid absorption in pulp capillaries
Why do CHF patients have pulmonary edema>
- failing LV can’t develop sufficient contraction at any degree of stretch
- LV needs to operate at high filling pressure & volume to have a SV that satisfies baroreceptors
- high filling pressure backs up into pulmonary cap, increases its pressure and causes fluid pushed out into interstium= pulomary edema
effects of pulmonary edema?
-decreases cardiac function and impairs gas exchange
How do perfusion(Q) and ventilation (V) change with gravity and location in the lung?
when standing amount of gravity(hydrostatic pressure) effects distribution of blood flow
- more hydrostatic pressure at base of lung than at lung apex (top)
- when standing blood flow to lungs is unequal with 10x more going to base than apex
Apex vs base of lung blood flow?
at base: cap are thin wall & distensible; increased hydrostatic pressure causes vasodilation, reduces resistance, and increases flow
-at apex: reduced hydrostatic causes capillaries to collapse during diastole so only perfused during systole
What happens when have local ischemia/hypoxia in the lungs?
- they vasoconstrict
- so that the blood flow goes to alveoli with sufficient O2 to saturate blood
- provides optimal gas exchange, better matches flow (Q) with ventilation (V)
What happens when have local ischemia/hypoxia in the systemic tissue?
-causes increased vasodilator metabolites and get vasodilation to get hyperemia or increased blood flow
What is ventilation perfusion matching?
- blood will take the most direct route to become fully saturated with O2 by air-filled alveoli
- they bypass O2 deficient alveoli by capillary vasoconstriction in response to hypoxia
What is HAPE?
- high altitude pulmonary edema
- its a positive feedback cycle instigated by widespread hypoxic vasoconstriction (ex when mountainclmbing and P02 is very very low)
- widespread hypoxia causes increased pulomary pressure since only a few cap route are open to blood
- increased pressure promotes filtration over absorption so get Pulmonary Edema
- pulmonary edema impairs gas exchange which leads to more hypoxic vasoconstriction (+ feedback cycle)
What happens if HAPE is initiated? How prevent HAPE?
- death can come quickly if the climber is not immediately brought down to lower elevation and given 100% O2
- best way to treat is to prevent by slowly acclimated before climbing everest
Why do you get pulmonary edema in CHF?
- heart is operating at a very high pressure to eject a small SV
- high pressure back sup into pulmonary capillaries and is enough to switch from absorption to filtration preference
- **check notes Starling curve
What are causes of pulmonary edema originated in the pulmonary artery?
- pulm artery deoxygenated blood go to lungs
- pulmonary hypertension due to high altitude, hypoxemia (COPD) hypoventilation
- results in vasoconstriction in hypoxic capillary beds & greater flow/pressure to other capillary beds
What are causes of pulmonary edema originated in the pulmonary vein?
- oxygenated blood going to the heart
- CHF (left heart failure) or stenotic mitral valve
- get pulmonary venous hypertesion which clogs up the capillary bed, increases pressure and get leakage of fluid out
What is a pulmonary embolism?
- another cause of pulmonary edema
- when an embolism (blood clot, cell debris or bubble) develop in systemic veins & flow into the lungs where can occlude smaller pulmonary arterioles blocking their blood flow
- leads to pulmonary hypertension & pulmonary edema
What are symptoms/signs of PE?
- dyspnea(difficulty breathing)
- chest pain on inspiration
- low blood O2 saturation
- tachypnea (rapid breathing)
- cough/hemoptysis (cough up blood)
- tachycardia
what is a thrombus?
- aggregate of platelets in a meshwork of fibrin
- blood coagulates whenever not toughing the endothelial cells surface
- can lead to pulmonary embolism & edema
What is the cutaneous circulation?
the blood circulation to the skin
- main function is to remove heat from exothermic (releasing heat) metabolic reactions occurring in the body from the surface of the skin
- once blood moves heat to skin, it can be released by conduction, convection, radian, sweating/evaporation
What is the skins main function?
- to remove the heat byproducts of cellular metabolism
- rate of heat
what is the global thermal regulation?
-the idea that heat loss=rate of heat production so that the core temp in body remains constant regardless of ambient/local temperature
How does the body handle too high of a core temp?
- thermostat in the hypothalamus activates cooling mechanisms, decreases SNS vasoconstrictor innervation
- arterioles and AVA dilate, dermal papillae capillaries & venous plexus fill w/ warm blood
- get warm (red) skin , like when you plush
- sweat glands activated to increase evaporative cooling
How does the body handle too high of a core temp?
- thermostat in the hypothalamus activates cooling
- hypothalmus increases SNS vasoconstrictor system
- arteriorles & AVA vasoconstrict
- dermal papillae and venous plexus collapse
- get cold, pale skin
- sk muscles activated so start shivering to generate more heat
What happens when have cardiogenic hypovolemic shock?
- is when have poor perfusion/low blood volume
- have cold, pale skin since not enough blood to feed the skin so is becoming cold/pale
- similar to when body has too high of a core body temp and responses are activated
What happens in distributive shock?
- causes loss of SVR due to cytokine release so have systemic vasodilation & patients have warm-red skin similar to the response of the body when core temp is too low
What are dermal papillae?
- they are projections close to the skin that increase SA for capillary loops
- they are loaded with capillaries, so highly vascular
What is the venous plexus?
- a very distensible reservoir for warm blood near the skin surface
- has 2 components the distensible plexus (Reservoir) and the arterial plexus (for constriction/dilation)
What are some characteristics of the skin?
- 2nd largest organ maintains 1/3 of BW
- low workload/energy consumption so has low nutritional blood flow demand
- cutaneous flow not dependent on local metablolism but the hypothalmus and SNS nerves
What happens in the skin during hypotension?
- baroreflex gets activated causes strong cutaneous vasoconstriction and prevents blood flow to the skin so it can be redirected to more important places
- vasocostrciton important also for thermal regulation
What are AVA?
- arteriovenous anastomoses
- connect arteries and veins to help move blood between them
- vasoconstrict/dilate to increase or decrease blood flow
- help dissipate heat
