heart failure and oedema Flashcards
- The lifetime risk for development of HF is 20% for
Americans ≥40 years of age. - Absolute mortality rates for significant HF remain
approximately 50% within 5 years of diagnosis
– i.e. same as colonic carcinoma!
– 30–40% of patients die within 1 year of diagnosis !! - No need to remember figures but do remember
A patient presenting in heart failure has a — illness which is at an – stage !!
life threatenig
advanced
(from up to down)
Pathophysiology
* — [Index Event] → — → —
– Index Event:
* Reduces – or —
– Compensation:
* May mask – disease — at presentation
* — and — systems
– Decompensation:
* Characterised by —
– Myocyte hypertrophy - contractility – desensitisation - loss – replacement
– Ventricular wall – perfusion – papillary muscle – AV ring
insult
compensation
decompensation
conreacility or compliance
severity
advanced
adrenergic and Renin angiotensin aldosterone
by remodelling
Heart failure occurs when the heart is unable to —
blood at a – [cardiac output] sufficient to meet the — demands of the tissue
*Heart failure –> complex clinical syndrome resulting from:-
–Impairment of :-
* —
– poor venous return, poor volume, Frank - Starling law
* —
– of blood from the left ventricle ( – function)
pump blood
rate
metabolic demands
venticuallar filling
ventricular ejection
pump
Heart failure – Classification: — or — Ejection Fraction
* NB – Pathologists often use — /— classifications e.g.
* —- failure V — Failure
* Lobar pneumonia V Bronchopneumonia
* Small cell carcinoma V Non-small cell carcinoma
* Clinicians often use — classifications e.g.
* — Ejection Fraction failure V — EF failure
* Community acquired V Hospital acquired pneumonia
* Primary lung carcinoma V Metastatic lung carcinoma
reduced or persevered
anatomical/ morphological
left ventricle vs right ventricle
clinical
reduced vs preserved
Types of Heart Failure
* Left ventricular failure (LVF): — ejection fraction (HFrEF) ( — HF) Vs — ejection fraction (HFpEF) ( — HF) reduced – during — period
* Right ventricular failure (RVF):
Cor — / Pulmonary —
* — &–
reduced
systolic
preserved
diastolic
filling
resting period
cor pulmonale
pulmonary hypertension
acute vs chronic
Cardiac Physiology:
* Cardiac Output [CO] = —- [L/min]
* Stroke Volume [SV] = —
– Factors include Preload / Afterload /
Contractility
* Ejection Fraction = — e.g
70/120 ~ 58% [n >/= 50%]
– HF with reduced or preserved EF
* HF(r)EF [ — HF] :
– index event
* — Contractility
– – ESV – SV – CO —EF
– – ESV – EDV — Pul Cap Wedge Pressure
* HF(p)EF [ — HF]
– Index event –
* – LV Wall thickness
– – LV compliance – wall is stiff
– — LV Filling - – EDV - — SV
– But Contractility –
– ∴ small amount of blood is
emptied from chamber i.e EF — BUT CO is —
HR x SV
End diastolic
Volume [EDV] – End systolic Volume [ESV]
SV / EDV
systolic
low
high
low
low
low
high
high
high
diastolic
high
low compliance
low
low
low
maintained
preserved
low
In heart failure— is insufficient
*Cardiac output dependant on:
– — & —
*Heart rate = —
–Autonomic influences on —
*Stroke volume = amount of blood — by — during each cardiac — and is
dependent on :-
* —
* — activity
* Pumping ability of —
cardiac output
heart rate and stroke volume
beats per min
sinoatrial node
pumped
ventricles
cardiac contraction
venous return, sympathetic , left ventricle
Compensation
Frank-Starling Mechanism : — stroke volume
– venous return
— ventricular filling (—) and – preload (initial — of cardiac myocyte prior to contraction)
– force of contraction and – stroke volume
More volume, — pump…up to a certain point
increase
increase
increase ( (end diastolic volume)
increase ( stretching)
increase
increase
better pump
Compensation
Other ways to increase stroke volume [1] :
* Increase – activity to the heart
– ↑ — of heart (better pump action)
– — (which increases venous return
* Both ↑ stroke volume
* — salt and water [RAAT *]
– — blood volume
* ↑ stroke volume
( Inotropes deployed in
severe pump failure)
Compensation
Other ways to increase stroke volume [2]:
* Release —
– Increases heart rate, augments myocardial contractility &
vascular resistance
* Release — (ANP & BNP)
– — levels are a good serum marker of heart failure in clinical practice
– ANP & BNP have — ; Natriuretic & — effects
– Also Inhibit — & –
– Vasodilatory peptide that may offset peripheral—
sympathetic
contractility
vasocotrcition
retain
expand
noradrenaline
Atrial Natriuretic Peptide
ANP
diuretic and vasodilatory
renine ad aldosterone
peripheral vasoconstriction
Summary
* In heart failure the body compensates by:
– Increasing —
* Increased – of blood in circulation
– Increasing ventricular —
– Increasing effective intravascular volume by —
– RAT (renin angiotensin system) system activated increasing fluid — and increasing —
* Increased Heart Rate:
– —
– —
stroke volume
volume
contractility
vasoconstriction
fluid retention
venous return
nor adrenaline
atrial natruiertic peptide
Types of Heart Failure
Reduced or Preserved Ejection Fraction
* Left-sided or right-sided heart failure:
– Can occur —
– Failure of one side can produce – in the
other causing global heart failure
* Acute or chronic (Discussed in MI lecture)
independently
strain
Left Heart Failure – Causes of The Index Event
Reduced or (Preserved) Ejection Fraction:
1- * — heart disease
– — failure and therefore – failure
2- * —
–Increased — to pump against [remember BP = CO x PR]
3- * — & — diseases
– Aortic Stenosis: Increased —- to pump against
–Aortic & Mitral regurgitation: Increased — to pump
–Mitral Stenosis : decreased —
*Other Cardiac muscle diseases
–eg — or —
* —
–Rate too fast to empty ventricle at each beat or to slow [remember CO = SV x HR)
Remember Heart failure can be present in High Output state
ishcemic
muscle failure –> pump failure
hypertension
increased pressure
aortic and mitral valve disease
pressure
volume
filling
cardiomyopathy or myocarditis
arrhythmia
Left Heart Failure – Effects:
* “— ” of the pulmonary – circulation → — & —
* — of systemic tissue → — dysfunction e.g. mesenteric — or —
What are the main manifestations of
left heart failure?:
* — : which may limit exercise tolerance
* (pulmonary oedema - orthopnoea / nocturnal cough /paroxysmal nocturnal dyspnoea)
* — : Low output from left ventricle with peripheral —
* – ventricular failure due to pulmonary venous
hypertension – peripheral —
Why does the patient have dyspnoea?:
* — in — heart causes pulmonary venous — , which may lead to— & reduced
ability to – lung alveoli → consequent — oxygenation of
blood
congestion
venous
pulmonary oedema and dysponea
hop perfusion
organ dysfunction
ischemia or renal failure
dysponea
fatigue
peripheral hypo perfusion
right
hypertension
peripheral stasis
fluid retention
left heart
hypertension
pulmonary oedema
aerate
reduced
Macro & Micro Heart Findings in LVF:
* Gross Examination of heart:
– Findings reflect the underlying disease – / — (e.g. Infarction; valve abnormality)
* Left ventricle is often — or — .
* — may be dilated eg — - risk of – and – .
* Microscopy of the heart:
– — [ — ] due to previous —
– Non-specific myocyte — ; diffuse —
– — of myocardium
* e.g. if the heart is failing due to viral myocarditis
process / index event
hypertrophied or dilated
left atrium
mitral stenosis
atrial fibrillation and thrombus
fibrosis ( localised)
infraction
myocyte hypertrophy
diffuse fibrosis
inflammation
Macro & Micro Heart Findings in LVF:
* — & — produces – , – lungs.
– Accumulation of oedema fluid in — spaces
– — air entry into alveolar spaces
– Reduced — transfer into pulmonary capillaries
– — on exertion, later at rest
– Wet lungs are prone to –
pulmonary odema and congestion
heavy and wet lungs
alveolar
reduced
oxygen
dyspnoea
infection
Decreased Peripheral Perfusion:
* Kidney
– Decreased renal perfusion activates — system with — of blood Volume
Can contribute to—
* Brain:
– – encephalopathy in – heart failure
* Mesenteric or hepatic –
renin angiotensin
expansion
pulmonary oedema
hypoxic
advanced
ischemia
Acute V Chronic LVF
symptoms differ:
* Acute eg —
– — and severe —
– Systemic – failure due to — eg
* Renal failure
* Hepatic failure
– Hypoxic cerebral damage/encephalopathy
* Chronic eg —
– Pulmonary — and often mild – and –
acute MI
pulmonary oedema
breathlessness
organ failure
cariogenic shock
chronic angina
congestion
mild dysponea and oedema
PURE* Right Heart Failure – Causes
* — diseases of the —
*e.g. cor pulmonale [pulmonary heart disease]
* Diseases of —
–> primary pulmonary hypertension, recurrent pulmonary
thromboembolism
*Left Heart failure will cause— when the — is severe
( high Pulmonary artery pressure [pulmonary vascular bed]- high RV afterload– RV remodelling )
parenchymal
lung
pulmonary vasculature
2ndary right heart failure
former
PURE Right Heart Failure – Symptoms:
* — oedema ( — swelling)
* Pleural –
* —
* —
peripheral pedal oedema ( ankle)
pleaural effusion
ascite
Hepatosplenomegaly
PURE Right Heart Failure – Pathology Findings:
* Right atrial dilatation
* Right ventricular dilatation + /- hypertrophy; AV Ring
stretching – Tricuspid Incompetence
* Hepatic congestion & –> — [cardiac sclerosis cirrhosis]
– Congestion around central vein portal vein etc.
* Pleural effusions
* Pericardial effusions
* Ascites
* Pedal & lower limb & subcutaneous oedema
cirrhosis
check slide 27,28
Oedema : Abnormal increase in extracellular - interstitial fluid
Non-inflammatory causes
* Increased — pressure (fluid leaves vessels)
* — plasma [ protein ] oncotic pressure (fluid leaves
vessels)
* Sodium & water –
* – obstruction
Oedema in Heart Failure:
Site of oedema: —
- Left heart failure → —
- Right heart failure → — extremities and — .
hydrostatic pressure
reduced
retention
lymphatic
pulmonary oedema
lower and ascites
Management of cardiac failure
Extremely Complex
Index event - Stage - HFpEF – HFrEF - Acute - Chronic etc:
*Lifestyle
–Salt and fluid restriction decreases intra vascular —
*Pharmacologic approaches:
–Relieve fluid overload → —
–Block renin-angiotensin-aldosterone axis → —
–Lower adrenergic tone → —
*Non-pharmacologic: - for end stage cardiac failure
– Implantable —
– Left ventricular — device
– —
volume
diuretics
ACE inhibitors
b blockers
defibrillator
assist
transplantation
Left Ventricular Hypertrophy and failure:
1. Initial insult causing — .
2. Pathologic — causing left ventricular hypertrophy +/- dilatation.
3. Compensatory adaptations initially maintain— , however ultimately result in cellular
changes, — and —
4. Reduced cardiac output causes organ — and pulmonary venous — and—
myocardial injury
remodelling
cardiac output
fibrosis and pump failure
hypo perfusion , pulmonary venous congestion and pulmonary oedema
Pattern of hypertrophy reflects the nature of the stimulus:
* Pressure - overload —
– e.g. — / —
- Concentric increase in wall –
* Volume - overload — &—
* – dilatation
- Wall – increased, normal or decreased
New — in series with existing sarcomeres
hypertrophy
hypertension/aortic stenosis
thickness
dilatation and hypertrophy
ventricular
thickness
sarcomeres
check slide 34
summary:
- Must understand physiology of the heart
– CO = SV x HR
– SV = EDV - ESV
– EF = SV / EDV
– BP = CO x Total Peripheral Resistance
( for the reduced EF: - low contracting high end systolic pressure since more blood is left behind and isn’t pumped which means the stroke volume will decrease and since stroke volume is down the CO will go down too , the problem here is the dilated ventricles )
( while the preserved EF: - the problem here is the thickened ventricles so the ventricles cant stretch leading to low end diastolic , low CO , low stroke volume , low LV filling )
