Exam #2: Coronary Circulation & Temperature Regulation Flashcards
Where do the large coronary arteries lie? Where do they branch?
Coronary arteries lie on the epicardial surface of the heart & extend into the myocardium. Extensions of the coronary vessels in the myocardium are referred to as “mycocardial vessels” & deeper extensions are called “subendocardial vessels”
*Note that subendocardial vessels are the most sensitive to compressive forces exerted by ventricular dynamics.
What is the inlet pressure for the coronary circulation i.e. what is the pressure gradient that allows for flow through the coronary vessels?
Coronary vessels branch off the aortic pressure (i.e. aorta= inlet pressure) & empty into the right atrium (i.e. outlet pressure).
Thus, Flow= aortic pressure- RAP/ resistance
When is the LV maximally perfused? Why?
Diastole
Q=dP/R – because aortic (inlet) pressure is high during diastole & RAP (outlet) pressure is low during diastole
- High dP= High Flow
When is the minimally perfused?
Systole, at the end of isovolumic contraction
Which side of the heart is better perfused throughout the cardiac cycle?
Right because of smaller compressive forces
Draw the wall tension influences on the coronary circulation.
N/A
When is tension the greatest that will compress the coronary vessels? What is the effect on the coronary vessels?
- The end of isovolumic contraction
- Low perfusion
How will a dilated cardiomyopathy i.e. a big heart, affect the wall tension?
- It will increase wall tension–>compressive forces on the coronary vessels & poor perfusion
Remember, large hearts are never well perfused
Describe the cascade the follows from an increase in cardiac metabolism, from e.g. an increase in HR.
1) Increased metabolism
2) Hypoxia
3) ATP turnover
4) Adenosine accumulation
5) Vasodilation
What is adenosine a byproduct of?
ATP turnover
What does adenosine cause?
Vasodilation
How does the SNS regulate coronary flow? What is the difference between the direct effect & the indirect effect?
Sympathetic stimulation of the heart has two effects, a direct effect an an indirect effect.
Direct effect= NE mediated vasoconstriction by binding to alpha-1 receptors
Indirect effect= NE mediated increases in myocardial metabolism, which leads to the accumulation of metabolites that ultimately cause vasodilation (adenosine)
What is the temperature set-point?
Individual normal range for body core temperature
Average= 98.6 F
How does the core temperature compare to the skin temperature (core vs. shell)?
Basal core temperature is constant (within 1 degree F of 100F), except in the case of fever
- can change with activity & stress
- can change with circadian rhythm
Skin/shell temperature varies widely with changes in surrounding temperature
How is heat produced?
Metabolism
How is heat lost? How is heat loss prevented?
- Heat conduction through the body
- Heat conduction through skin
Fat prevents heat loss.
What is radiation?
Infrared heat rays (EM)
*Relies on a heat gradient.
What is conduction?
Direct contact between two objects, which will transfer down the thermal gradient
What is conductivity?
The rate of heat conduction
Air= low/ slow Water= high/ fast
How does the thermal conductivity of the skin vary?
Heat= vasodilation & increased conductivity
Cold= vasoconstriction & decreased conductivity
What is convection?
Loss of heat by current
What mechanism can the human body use to cool the body? What regulates sweating?
- Sweating i.e. evaporation (note that this doesn’t work if you’re dripping sweat–humidity)
- ACh is released from SNS to regulate sweating
Note that this it the ONLY mechanism that can result in cooling in an environment warmer than body temperature.
How does non-thermoregulatory “nervous” sweating occur? What is “special” about thermoregulatory sweating?
- Alpha-1 activation on sweat glands= nervous sweating
- Thermoregulatory sweating involves ACh release & M2 receptors in the SNS
What is the role of the CNS in thermoregulation? Draw the feedback loops for reduced body temperature & increase temperature.
N/A
