Pathophysiology of Heart Failure

Question 1

What is heart failure?

Answer 1

• Syndrome of insufficient CO (low vol failure, valve problems, sys/diastolic dysfunction of lateral myocytes)
• Collection of symptoms (exercise intolerance, breathlessness, oedema)
• Left, right or both (congestive), as well as systolic/diastolic dysfunction

Question 2

Describe blood pressure

Answer 2

• Pressure drives perfusion
• Adequate driving pressure- perfuse body
• CO- amount of blood pumped in system
• Total peripheral resistance- total res to blood flow
• Mean arterial press= CO X TRP
• TRP- how constricted arteries
• CO- combination- stroke vol and HR big influence on sys pressure

Question 3

Describe the baroreceptor reflex

Answer 3

• BP drops, CO drops
• Pressure in aorta- less stretch of baroreceptors in carotid sinus- less firing
• Central- medulla- response to decreased firing
• Drop in PNS (vagal) output- increases HR
• Raises SNS- drives vasoconstriction, peripheral res, venoconstriction, force of contraction + preload
• Independently ionotropic
• Chronotropic
• Increased CO and BP

Question 4

Compare contractility and preload

Answer 4

• SNS increases preload + force of contraction
• • Ionotriopic
• • Rise in LAP–> rise in SV
• • Expand heart, myocytes align and contract with force
• • So, venous return = CO
• Adr release increases contractility
• • Any given preload- larger SV
• • Larger SV- increases preload and contractility- independent mechanisms (so additive)

Question 5

What is the cardiac response to low pressure?

Answer 5

• HF syndrome of low CO
• Failing heart ‘curve’ shifts down, vol decreased- CO decreased
• Baroreceptor reflex- increase in contractility- SNS outflow- normalise SV
• Despite drop in SV, can be offset by increasing contractility as part of reflex

Question 6

What factors increase renin release?

Answer 6

• Low arterial bp (SNS activation via baroreceptor reflex, infrarenal stretch receptor)
• Low blood vol (SNS flow pressure receptors)
• Altered sodium handling (detected by infrarenal mechanism- macula dense)

Question 7

Describe the renin-angiotensin system

Answer 7

• Renin release drives
• Increased angiotensin
• Increased vasoconstriction
• Leads to aldosterone release
• Increased Na and water retention–> vasoconstriction
• Increased BP

Question 8

What is ADH and what does it do?

Answer 8

• Anti-diuretic hormone- increase permeability of cells to water- aquaporins in collecting duct
• Decreased fluid loss in urine
• Secreted from posterior pituitary- response to changes in osmolality
• Rise in osmolality–> ADH secretion–> water resorption–> plasma diluted, osmolality falls–> triggered by Ang too
• Also called vasopressin

Question 9

Describe cardiac response to low pressure involving ADH

Answer 9

• Volume drops in HF
• Quick contractility response
• Long term: Ang, aldosterone and ADH drive vol expansion; increase vascular vol and preload; normalise CO
• Maintain SV- expanding blood vol and increased atrial pressure

Question 10

Describe what happens with decreasing cardiac output

Answer 10

• Flattened curve
• Ang, aldosterone and ADH maintain resting volume
• Expand volume –> increase preload, so venous return
• Cardiac function drops- chronic failing heart- more AAA
• Function maintained by expanding plasma volume
• Eventually curve flattens more- SV maintained
• If further deterioration- flat line- no plasma vol increase would maintain normal resting SV

Question 11

Describe volume overload/hypervolaemia

Answer 11

• Fluid volume too high in vascular compartment (initially)
• Unlikely to stay like that indefinitely
• Common occurrence in renal/heart failure
• Increased Na and water retention–> secondary complication–> chronic baroreceptor reflex- chronic RAS
• Benefit- maintain CO, massively compromised by expanding vascular compartment
• Oedema

Question 12

Describe capillary dynamics

Answer 12

• Movement of fluid from capillary to lymphatics
• Vol expansion–> greater pressure in capillary (plasma)
• Oncotic press decrease–> decreased protein grad
• Larger plasma grad- net grad considerably larger
• Overwhelms lymphatic drainage
• Fluid collection in interstitium
• LHF- pulmonary oedema
• RHD- ankle oedema (bilateral)- gravity

Question 13

Describe the release of ANP

Answer 13

• Atrial natriuretic peptide (or BNP, CNP)
• Release with increased plasma vol
• RA press increases
• Increased ANP
• Increased Na loss, decreased osmolality
• Correction of plasma vol
• Important because markers of vol overload- good indicators of HF and vol expansion

Question 14

What are natriuretic peptides?

Answer 14

• Several
• ANP tested more often, also BNP (brain) and CNP
• Primarily regulate blood vol, and oppose some RAD actions
• Release in response to atrial stretch (fluid overload)
• Inhibits Na+ resorption- promotes excretion, decreases osmolality

Question 15

Describe decompensated heart failure

Answer 15

• Decreased cardiac function
• Maintained SV by expanding plasma vol
• Curve can no longer maintain
• Heart can’t reach SV anymore (decompensated HF)
• β-blockers- despite decreasing pressure- but at this point no vol expansion can improve heart
• -> So RAS stimulation no longer beneficial- builds up Ang- drives myocardial remodelling
• Dropping preload to normal will not have consequences- but can reduce remodelling