Unit 2 Lecture 8: High Systolic BP Flashcards
What are the consequences of High Systolic BP?
- Aneurysm
- Myocardial Infarction
What is an aneurysm?
- Rupture in the wall of the aorta
- Pressure in the aorta being extremely high (Next to LV in systole)
What is an aortic dissection?
Blood flow from lumen of aorta penetrating the wall of the aorta
Who is more susceptible to aneurysms?
- Older patients
- Males more than females (<60 years)
Why are males more susceptible to abdominal aorta aneurysms?
Estrogen of females has a protective feature while testosterone of males has more detrimental effects on the walls of the aorta
What is Marfan Syndrome?
Also known as “spiderman” where there is a mutation in the ECM protein “fibrillin-1”
* Elastin protein is not directly affected; it attaches to fibrillin-1 but a weak protein means elastin does not do its job properly (terrible recoil)
Note: This is a genetic mutation to the protein fibrillin not elastin; high risk of aneurysm
Characteristics of people with Marfan Syndrome?
- Tall, thin, arm span exceeds height
- Patients have skin that can stretch and have poor recoil
In someone with a mutated fibrilin, how are the elastic fibres organized?
They’re very disorganized unlike in a structure without a mutated fibrilin
In the aorta it causes a high risk of aneurysm
How is Myocardial Infarction a consequence of High Systolic BP?
Workload of heart is too high ==> Oxygen demand is not met
* LV must contract harder to maintain cardiac output
What is “Afterload?”
The pressure that LVP has to overcome in order for ventricular ejection to occur
When MAP increases why does SV immediately decrease?
When diastolic pressure of Aortic pressure becomes very high, the LVP must contract significantly to overcome Aortic Pressure
* LV works much harder to contract and eject blood & the heart is under isovolumetric contraction for a longer period of time where diastolic pressure is now way too high
* Shorter ventricular ejection duration ==> Less blood is ejected out when MAP increases and aortic pressure increases
* LVP can only be greater than aortic pressure for such a short amount of time due to it already working hard enough
* Therefore, SV decreases when MAP increases
REMEMBER: What causes SV decrease during pre-compensation to high aortic pressure is shorter ventricular ejection duration
How does LV compensate for high Aortic pressures?
LV contracts stronger, develops more LVP and therefore maintains SV
- More intense contraction requires more oxygen & energy which causes increase in SNS activity to compensate
Increasing SNS allows for Ca2+ to be released and allow LV to contract harder. This also means that cardiac afferents are activated and they will be sensing changes such as?
- mechanoreceptors sensitive to stretch and contraction
- Sensitive to metabolites (Metaboreceptors respond to changes in muscle from La- or H+) ↑SNS
- Changes in O2 and CO2 ==> ↑ SNS
- Frank-Starling Mechanism: Increasing contractility of the heart means you’re increasing tension and therefore the force & pressure and this can be due to ↑SNS causing increased stretch
PURPOSE: These all lead to ↑ SNS or due to increased SNS
Compensation of aortic pressure requires a longer systolic time. What does that mean for time that we’re in diastole?
Decreases
When SV decreases what happens to coronary blood flow and oxygen delivery?What about when SV increases?
Both will decrease which causes deprivation of oxygen to cardiac muscle cells
- When we increase contractility, we increase SV and increase oxygen demand but coronary blood flow remains low
- Coronary blood flow in this case stays low because the blood vessels contract that it decreases the amount of blood flow to the heart itself (similar to exercise and blood vessels in muscle)
Both cases: Lead to oxygen deprivation in cardiac muscle cells (cardiac myocytes)
Why does the area in which blood flow in the coronary artery is blocked important?
- If blood flow is blocked more further down then the cells in that region will die
- If blood flow in the coronary artery is blocked further up, it can cause death to the entire heart ==> Myocardial infarction far more likely and far more worse
NOTE: Cardiac myocytes receive oxygen, nutrients through the coronary artery network, NOT by direct diffusion of substances from the chamber of the heart.
What is happening to the blood vessels during systole?
The blood vessels are being squeezed and blood flow is being slightly impeded
* We see this in weight lifting when someone is contracting the vessels are squeezing increasing the amount of pressure
Why does coronary blood flow drop in the picture below?
During systole, coronary artery blood flow can drop so low b/c the heart contracts so hard that it excludes any blood going to the coronary arteries
- Decreased blood flow ==> Decreased oxygen to myocytes ==> Decreased ATP ==> Myocytes can’t repolarize or relax ==> Myocardial infarction
- Outer layer not as affected as that is where blood supply usually goes to and is not affected by pressure as compared to the inner most layer of the cardiac myocyte
Note: Happens mostly in the endocardial region - innermost layer of the heart and is compressed by contraction & the pressure in the LV
