L28 Flashcards by Hayley 1234

what is pulmonary hypertension

Alteration in the structure and function of the pulmonary arteries
Primarily not in other arteries of the body

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what does pressure have to rise to in the pulmonary system to be classified as hypertension

> 25mmHg

normal = 15mmHg

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what is the prevalence of pulmonary hypertension

15/100 people in 1 million

about 3200 people in australia AND NZ

only 100 people in NZ

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describe the symptoms of hypertension

Non-specific symptoms such as breathless, fatigue and chest pain

Symptoms develop gradually, when the disease is very advanced

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there are 2 types of PH what are they and what % of the prevalence to they make up

primary pulmonary hypertension = 40%

secondary pulmonary hypertension = 60%

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what are the causes of primary and secondary pulmonary hypertension

primary = unknown

secondary = Chronic obstructive pulmonary disease (COPD )/ other lung conditions

Mitral valve disease

Sleep apnea

Sickle cell anemia

HIV

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what are the underlying causes of secondary pulmonary hypertension

Chronic obstructive pulmonary disease (COPD )/ other lung conditions

Mitral valve disease

Sleep apnea

Sickle cell anemia

HIV

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what form of remodeling do the pulmonary arteries undergo in PH

a combination of arteriosclerosis and atherosclerosis

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what does thrombosis indicate

role for inflammation

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what are the causes of remodelling in PH

Increased pressures - altered shear stresses and inflammation

this causes Endothelial dysfunction and proliferation

it could also be because of disturbed vasodilator/vasoconstrictor balance:
less Nitric oxide and/or Prostacyclin vs. more Endothelin and/or Thromboxane

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how does NO cause vasodilation

through cGMP

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what does endothelin cause

vasoconstriction by hypertrophy of the smooth muscle cells so they can have a larger contraction vasoconstrict

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what are the consequences of PH on the pulmonary system

More difficult to pump the blood into the lungs

Pulmonary Resistance increases theefore increase in Pulmonary Artery Pressure (PAP)

Severe bronchial obstruction

Decreased diffusion capacity for O2

Hypoxemia (decreased partial O2 pressure)

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normally the Pulmonary system is a….

Low pressure - low resistance
Receives ~100% of circulating blood

Pulmonary arterial tree
Compliance distributed over entire arterial system
Resistance distributed over entire arterial system

compeer this to the normal systemic system

Systemic arterial tree 
Compliance located in aorta
(80% of total compliance)
Resistance distributed over
all resistance arteries in
the different vascular beds

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overall resistance and blood pressures are lower in pulmonary system

however what happens when you increase the resistance

increases in pulmonary resistance result in relative larger increases in blood
pressures (with more disastrous consequences)

Although the pressures in the pulmonary system are lower it makes the increase in resistance much severe therefore has worse concequences

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what ventricle does PH affect

right ventricle

what is the difference between systemic hypertension and pulmonary hypertension in terms of the ventricles

In the left ventricle if you increase systolic pressure you increase the afterload and you decrease SV

In the right ventricle the graph is steeper therefore small changes in the resistance in the p arteries it causes a much larger afterload in the right ventricle than a similar change in the systemic arteries (afterload in the left ventricle)

there are 2 phases of PH cardiac remodelling

what are they

compensated (concentric)

2. decompensated (eccentric)

describe compensated PH cardiac remodeling

an increase in vascular resistance causing right ventricular hypertrophy

describe decompensated PH cardiac remodeling

RV hypertrophy (compensated)

will eventually wall stress (tension) will increase therefore causing an increase in RV workload causing chamber dilation.

eventually wall stress will increase again and this process will happen again and again until the chamber dilates too much and you get heart failure

which phases of PH cardiac remodelling are in the clinical phase and preclinical phase

compensated = preclinical

decompensated = clinical

describe what happens in compensated hypertrophy

We start with the compensated right ventricular hypertrophy. This will increase the pulmonary artery wall thickness therefore resistance

increase in resistance = increase in pulmonary arterial pressure and pulmonary vascular resistance. CO will decrease

In the compeastated state the wall of the right ventricle will increase in size (left will stay the same)

You will also get cellular hypertrophy (more sarcomear)

what causes the decompleansted state

Severe Pulmonary obstruction which leads to an increase in pressure and resistance

CO decreases

in the decompensated state why do you get dilation of the RV

In this stage we already have right ventricular hypertrophy and you start to get dilation of the right ventricle (because you cant maintain this)

why does cardiac remodelling of the heart eventually cause heart failure

If this continues then the right ventricle will continue to deteriorate and the pulmonary artery will become really obstructed this causes pulmonary artery pressure to drop which means that the right ventricle can't make the pressures required the right ventricular dilation will then cause a decrease in CO which leads to left ventricular dysfunction Healthy = the right and left contraction is synchronous (they contract at the same time) whereas in the end stage of PH the right and left are contacting at different times You can also see that the septum has become part of the right ventricle and then the right ventricle contracts it pushes into the left ventricle therefore impeding on the filling of the left ventricle decreasing the CO into the systemic arteries

when do you become systematic of PH

in the late stages of compensated remodeling

describe what the heart looks like in the late stages of cardiac remodelling because of PH

Healthy = the right and left contraction is synchronous (they contract at the same time) whereas in the end stage of PH the right and left are contacting at different times You can also see that the septum has become part of the right ventricle and then the right ventricle contracts it pushes into the left ventricle therefore impeding on the filling of the left ventricle decreasing the CO into the systemic arteries

In the late/end stages of Pulmonary Hypertension the end-diastolic volume: A. of the RV is increased, and of the LV remains the same. B. of the RV is decreased, and of the LV remains the same. C. of the RV is increased, and of the LV is decreased. D. of the RV is decreased, and of the LV is decreased

C is correct this is Because the right ventricle is dilated which impedes on the left ventricle

why is PH known as the insidious killer

because it has a 5-6 year survival rate used to be 70% of people die in this time but now it is more like 40% (which is still bad) because we understand it more

describe emphysema

Lung Emphysema (COPD) = Loss of alveoli --> induced vasoconstriction in poorly ventilated parts in lung –> reduction in capillary capacity -> increased total peripheral pulmonary resistance –> increased PAP --> development of PH this is a irreversible degenerative disease because When you are an adult you have a certain amount of alveoli and you don't make anymore therefore the ones that you loose you won't get back

how can we decide treatments for PH

Cause of pulmonary hypertension is because of the imbalance of the vasodilators and constrictors of the vessels therefore if we can synthetically replace/stimulate these we have a treatment

what are some possible treatments for PH could you use NO

You could inhale NO but that wouldn't last long

what are some things that would increase the effect of vasodilators (eg NO) as a treatment for PH

You could also look at guanylyl cyclase stimulators (to make more cGMP which causes vasodilation) or phosphodiesterase 5 inhibitors What happens when they inhibit phosphodiesterase 5 is is that it stops the breakdown of cGMP therefore the vasodilation pathways last longer

what could you do to stop the effects of vasoconstrictors as treatments for PH

You could also use prostaglandins and endothelin receptors antagonists to block the receptors of the vasoconstrictors

Sildenafil is a PDE-5 inhibitor what

Sildenafil opposes high altitude-induced pulmonary hypertension

who does Sildenafil opposes high altitude-induced pulmonary hypertension

Relaxes smooth muscle cells causing vasodilatation selectively in lung and penis it does this by blocking the breakdown of cGMP

what is the most effective theropy for PH

PDE5i (phosphodiesterase 5 inhibitors) and ERA (Endothelin Receptor Antagonists) when you combine these you increase the survival rate to 90%

During pulmonary hypertension the diffusion capacity for O2 decreases BECAUSE total pulmonary vascular resistance is decreased during pulmonary hypertension

the first statment is true and the second is false should say increased