L18: Heart Failure Flashcards
What is heart failure
The inability of the heart to supply adequate blood flow and therefore oxygen to peripheral tissue and organs
What are the symptoms of heart failure
Weight gain Shortness of breath Increased swelling Trouble sleeping frequent cough Loss of appetite
What happens in the heart failure which tries to increase CO
Increase SNS
Increase volume loading
Hypertrophy
What are the common causes heart failure
Myocardial infarction
What is myocardial infarction
When a thrombus forms in the coronary artery
So the myocardium is perfumed by one artery
What occurs when there is no blood flow to a specific area of the muscles
Ischaemia
What is ischaemia
No blood flow
What happens to the tissue when there is ischaemia
Hypoxic
Hypercapnic
Acidotic
Nutrient depleted
What is the tissue at risk of if ischaemia occurs
Necrosis
What is necrosis
Tissue death
How does a thrombus develop in the coronary arteries
1) as we age we develop fatty plaques in the arteries
2) the plaque ruptures and releases substances to platelet activation
3) platelet forms a thrombus which completes block the coronary artery
What is the treatment for MI
Percutaneous coronary intervention (PCI)
What does a PCI involve
Inserting a catheter into the coronary artery which punctures the thrombus
Catheter inflates the ballon so vessel is stretched
A stent is fitted so the vessel remain open and blood flows
What happens to the tissues when we re-introduce blood flow via PCI
Tissue can die further due to sudden reperfussion
Do we have any interventions in place to stop the cell death after PCI
No
What are the other causes of heart failure
Hypertension
Contractile dysfunction
Why does hypertension cause heart inability to pump
Increases the afterload (pressure that the heart has to work against)
How does a contractile dysfunction lead to Heart failure
Cant pump
What happens to the starling curve in heart failure
Decreases
Why does the starling curve decrease
We lose our inability to stretch sacromere and stretch to give a contraction to increase the SV
Where are baroreceptors found in the body
Aortic arch
Carotid sinus
What is the afferent nerve of the carotid sinus
CN9/ glossopharyngeal nerve
What is the afferent nerve of the aortic arch
Vagus nerve /CN10
If there is a fall in stroke volume due to a change in the starling curve what happens to the ABP
Abp= co X TPR
Abp= (SV X HR) X TPR
Decreases
What happens to the afferent nerve activity of the baroreceptors when they detect a decrease in the ABP
Afferent activity decreases
Where does the afferent nerve input into
The CNS to NTS
What happens after inputting into the NTS
1) NTS inhibits the nucleus ambiguus so the PNS vagal activity to the SAN decreases
2) RVLM is activated which increases the sympathetic pre-ganglionic nerve to the SAN and heart rate increases
3) sympathetic activity also causes vasoconstriction
4) SNS also causes an increase in SV by increasing the contractility of the cardiac myocytes
5) SNS causes adrenaline release form the adrenal gland which increase the HR and SV
What does an increase in SV and HR do
Increase cardiac output
What is the consequence of the persistent activation of the SNS to the heart
Hypertrophy
Loss of adregenic sensitivity due to less beta receptors expressed
Dysfunction with calcium homeostasis
How do we get a calcium homeostasis dysfunction due to the persistent activation of SNS
1) SNS leads to sarcoplasmic reticulum overload with calcium as it open voltage gated calcium channels
2) the overload of calcium causes calcium to lead during diastole
3) calcium becomes removed by the NA+/CA2+ exchanger
4) sodium is brought into the cell which causes depolarisation
5) we get a small contraction during the diastole interval and if it meets the threshold it leads to an ectopic AP
6) SNS also causes increases PKA activity which brings in calcium back to the sarcoplasmic reticulum by stimulating SERCA
When there a reduced ABP what happens in the kidney
1) renin is released
2) renin coverts angiotensinogen to angiotensin 1
3) ACE converts angiotensin 1 to angiotensin 2
4) angiotensin 2 causes the release of aldosterone which brings in water by bringing in sodium and therefore water follows
What does the effect of bringing in water do to the EDV
Increase it
What effect does increase in EDV have to the SV
Increase it to maintain CO
What happens to the SV in late stage heart failure
Decreases because we lose sacromeres which cannot stretch despite the increase in the EDV
What happens when we get a mismatch in the left and right CO
Oedema
Where can oedema occur
Pulmonary
Systemic
In left heart failure where do we get the oedema
Pulmonary
In right heart failure where do we get the oedema
Systemic
Why do we get an oedema forming when there is an increased blood volume
An increase in blood volume increases the hydrostatic pressure in the capillaries
Fluid moves into the interstitial space to give oedema
When we get pulmonary oedema what happens to diffusion of oxygen
Decreases due to an increases diffusion distance created by the fluid
Which receptors does a decrease in oxygen stimulate
Peripheral chemoreceptors
What is the treatment for pulmonary oedema
100% o2 supply
Diuretics
Ace inhibitors
AT1 receptor antagonist
Why do we get hypertrophy of the heart
Due to an increase in blood pressure or SNS activity
How can we lower BP
Give vasodilator
How can we stop the stimulation of SNS
Beta blockers
