Case 4 Flashcards
what is clinical heart failure
a state in which the cardiac output fails to meet the body’s demands. extracellular fluid composition and movement off fluid between compartments
what is the extracellular fluid divided into
plasma and interstitial
how much of the body is made up of fluid
60%
what are the two phases of fluid movement
- the blood and associated plasma
2. movement from capillaries into interstitial fluid or space
what is the composition of ECF
- na+
- cl-
- HCO3-
- glucose
how much of the ECF is plasma
1/5
how far away are cells in the body from capillaries
50um
How do water molecules pass through the capillary
pores and will include ions like sodium and chloride
how does water move
area of high concentration to an area of low concentration
what does the capillary pressure do
tends to drive fluid out from the capillary
what is capillary pressure opposed by
interstitial fluid pressure which Is usually lower and in fact is sub atmospheric
what does capillary pressure push out
water
what does colloid pressure do
pulls water into the capillary
what pulls water into the capillary
plasma proteins, largely albumin pulling water towards them
what is colloid pressure opposed by
interstitial fluid colloid pressure
how big is the interstitium
1/6 of the body’s volume,e
what has the interstitium got in it
loosely packed proteins, things like collagen fibre bundles and proteoglycan filaments
what consistency is the interstitium
gel like consistency
components of intracellular fluid compartment
- K+
- Mg++
- Phosphates
- Proteins
why do proteins draw on ions such as sodium and potassium
because proteins are negatively charged and sodium and potassium are positively charged and water follows them into the cell
what is required for active transport
kinetic energy
what molecules can cross the lipid bilayer freely
fat soluble molecules
what channel proteins transport water into the cell
aquaporines, they have a pore inside them which allows water molecules to traverse the cell membrane in single file. red blood cell has aquaporins in it
what are the factors impacting diffusion
- concentration
- charge - ions are negatively charged and inside membrane is positively charged.
- pressure affects movement of substances (capillaries and interstitial space)
what is the protein involved in facilitated diffusion
carrier proteins that are specific to substances and bind, allowing them to diffuse form one side of the membrane to another after going through a conformational change.
what is the rate limiting factor in facilitated diffusion
the carrier protein needs to change shape twice
what is the max rate of transportation denoted as
Vmax
how many potassiums does the Na-K-ATPase pump bind to
2 potassiums
how man sodiums does the Na-K-ATPase pump bind to inside the cell
3 sodiums
what activates the ATP pump
binding of potassium and sodium
what is the ATP pump function
breaks down adenosine triphosphate which is a high energy phosphate substance
what does the ATP pump break adenosine triphosphate into
adenosine diphosphate and a phosphate ion
what does the ATP pump release
energy
does the ATP channel go under a conformation change by using energy
yes
what does the conformational change do in the ATP pump
makes 3 sodium leave the cell and 4 potassium enter the cell
why does the inside of the cell membrane become negatively charged in ATP channel
there is a net loss of one positive ion every time
what does losing one sodium ion result in in the ATP pump channel
allows some water to follow it from the inside to outside of the cell. partly responsible for it not bursting
what 3 things regulate the cardiac output
Frank Sterling, Autonomic nervous system, endocrine system also
cascade of events if patient has a heart attack and develops important amounts of damage to left ventricle
Left ventricle pumps blood to the systemic circulation normally, so if there is significant amount of damage to it, this will reduce the amount blood it pumps and reduce the cardiac output
Output of the heart will not be sufficient to reach body’s needs (stroke volume)
Causes a reduction in systemic blood pressure which the body will sense
Because forward force is reduced, the heart is not getting rid of the blood that is inside the left ventricle
The blood is stagnating there and makes it difficult for blood to enter the left ventricle because forward flow is poor
This cause the pressure in the left atrium to increase, which normally of loads its blood into the left ventricle
Blood that wants to return into the left atrium from the lungs also struggles to enter as pressure is increased
Creates a back flow of pressure
The right ventricle is pumping against an increased pressure, and the right atrium is also increased in pressure
Difficult for blood to return into the heart from inferior and superior vena cava because of pressure in right ventricle
what is the neurohormonal response to a reduced cardiac output
- sympathetic nervous system
- RAAS
- ADH
What receptors detect low blood pressure
baroreceptors
where are the baroreceptors found
aortic arch and carotid Sinus
which nerves do the baroreceptors send signals via
the vagus and glossopharyngeal nerves
when the vasomotor sends signals to the heart to increase heart rate how many times is the cardiac output increased
2-3 fold
what else does sympathetic activation cause
innervates the vasculature and causes vasoconstriction in the arteries and veins and also increases the blood pressure
RAAS mechanism
- renin is released by the kidneys in response to decreasing blood pressure
- vasoconstriction
- salt and water retention increases circulating volume in the body
- chronic activation results in progressive water retention
- increasing circulating volume should increase stretch of the heart muscle
what does angiotensinogen form
angiotensin 1
what does angiotensin II lead to
- renal retention of salt and water
- vasoconstriction
- angiotensinase
what enzyme converts angiotensin I to angiotensin II
ACE
where is ADH released from
posterior pituitary
what does ADH result in
fluid retention, thirst and dilution of the blood
what does activation of SNS in heart attack lead to
increased heart rate and increased myocardial contractility
what do SNS and RAAS lead to
vasoconstriction
what do AHD and RAAS lead to
ECF expansion
what causes natriuretic peptides
increased myocardial stretch
example of a natriuretic peptide
BNP
function of BNP
passes sodium into urine which causes loss of salt and water which counteracts fluid expansion
what does BNP cause
vasodilation - counteracts vasoconstriction which is damaging to heart in long run
what is maladaptive process
chronic fluid retention
what does chronic fluid retention lead to
- no further improvement in the cardiac output
- increased workload on already damaged heart
- pulmonary and peripheral oedema
mechanism of oedema
- back flow of pressure and venous pressures eventually increase causing an increase in the capillary pressure which will tend to cause more fluid to filtrate out of the capillaries
- also more circulating volume, salt and water retention, which will again cause more fluid to cross capillary membrane
why is oedema common in lower limbs
- elevated venous pressure in legs due to gravity
- pressure also elevated in the capillaries leading to leakage of fluid into the tissue spaces (oedema)
- lowest limbs have highest capillary pressure
what does chronic sympathetic activation cause
- increased energy demand
- vasoconstriction: increased after load
- worsening schema
- apoptosis/necorisis of heart cells
what does chronic RAAS activation lead to
- hypertrophy of heart muscle
- fibrosis
- apoptosis
what gets rid of the fluid overload
diuretics
which layer is the heart formed in
the mesoderm
what does the ectoderm give rise to
skin and neural tissues
what does the mesoderm give rise to
most of the muscles
what does the endoderm give rise to
internal organs like GI tract
where is heart development visible
ventral surface
cardiac development summary
cardiac development begins with the initiation of structures called heart fields
These heart fields then converge at the midline of the embryo to form something called the cardiac crescent which assort of an ’n’ shaped structure in the embryo
Those cardiac crescent cells come together to form a linear heart tube
That tube goes under a series of morphological changes called looping so that it takes on the correct position within the embryo
It then further subdivides into the different chambers and we can see structures such as the cardiac cushions, form the valves, begin to develop within that tube
We also get grooves forming on the surface of the tube which will represent the premature or primitive formation of the chambers
Following these events we get the formation of the great vessels and the heart acquires the anatomy it needs for the adult
development of cardiac stages
- cardiac cell fate acquired
- angiogenic cells located in cariogenic plate - cranial and lateral to neural plates
when is cardiac crescent developed
at 15 days post fertilisation
what are the two heart fields
primary and secondary
what is different about the secondary heart fields
they move into the heart and contribute to outflow tract and right ventricle cardiac structures
cardiac crescent fusion
- cardiac crescent fuses at the mid-line to form the cardiac tube
- elongate at the midline of the embryo
- forms primary heart tube
when does linear heart tube form
21 days
where are ventricles and atria located in heart tube
developing ventricles are situated more cranial. atria is at the bottom of the tube and ventricle is in the mid region
what are the heart tube structures in order from top to bottom
1 dorsal aorta 2 aortic sac 3 bulbus cordis 4 primitive ventricle 5 atrioventricular sulcus 6 primitive atria 7 sinus venous
when does cardiac looping occur
23-24 days
what does cardiac looping do
brings atria more upwards and behind the presumptive ventricle.
what shape is cardiac looping
dextral C-shape loop