Heart failure Flashcards
What is Heart failure ?
Congestive heart failure
Inability of heart to pump blood to meet metabolic demand of the body.
2 types
Systolic heart failure
0 Ventricles cannot pump hard enough during systole
0 Diastolic heart failure - not enough filling of ventricles during diastole.
Can either be:
o left side
o right sided
o biventricular
left sided can cause right sided vice versa
as one side impacts the other - In this case it is whatever side came first.
O lefts sided most common
CONSQEUNCE
- Blood backs up into lungs causing fluid build up - pulmonary oedema
What is stroke volume ?
How do you calculate Cardiac output ?
What is the ejection fraction ?
- normal ?
- abnormal ?
SV - Volume of blood pump out of left ventricles per beat / systolic contraction
CO = SV X HR
Ejection fraction - measurement of the amount of blood leaving LV vs total volume in LV - expressed as a precentage
e.g total volume - 110 , SV - 70
EF = 70 / 110 ML = 64 %
Normal - 50 -70 %
40 - 50 % - borderline
Below 40 - systolic Heart failure - on pumping out a little blood each beat.
How does Systolic heart failure impact EF , EDV , EDP ?
SHF ————————-> LV cannot pump as hard ( decreased contractility - ability to contract ) ——————-> SV decreased ———————> Cardiac output decreased.
EF = SV / TV
(decreased EF - Top number decreased ) - Heart failure with reduced ejection fraction.
EDV - amount of blood in ventricle at the end of diastole. ( LEDV - Left ventricle - REDV - right V )
(LEDV = Leftover blood (which was not ejected ) + blood from lungs )
- high - more left over blood after systole ( so more in LV in diastole )
EDP - end diastolic pressure - HIGH
( Higher volume in ventricle - higher pressure )
Causes of systolic heart failure
or ischemic Heart disease due to Atherosclerosis - plaque build ( blocks blood supply , cells die )
Ischemia after MI (heart attack - BV completely blocked ———————> No blood ——————–> myocardium damaged ———————–> scar tissue —————–> cant contract with same force)
o Decreased
contractility
0 Hypertension ————– LV hypertrophy ——————> O2 demand increases (increased muscle ) + Reduced 02 demand (compression of cardiac vessels ) = weaker contractions
0 Dilated cardiomyopathy - chamber get bigger —————–> ventricle wall thin out (too thin ) —————-> weakened - cannot pump hard enough
( Frank starling - at first increased chamber size ————–> increased preload (more filling) ————–> increased volume = greater contraction strength ———–> but not sustainable
- Systolic heart failure - often the cause of Left sided heart failure
How does Diastolic heart failure effect EF , EDV , ECF ?
EF - normal
( even though stroke volume is low - Total volume is also low - because issue with not enough blood filling the ventricle ) -so fraction evens out
EX - SV - 70ml , TV - 110 ml
-normal 70 / 110 = 64 %
SHF - SV - 44 ml , TV - 110 ml = 40 %
DHF - SV - 44ml , 69 ml
44/69 = 64 % -HEART FAILURE WITH PRESERVED EJECTION FRACTION.
EDV - normal in beginning , then reduced by the end
EDP - is elevated
Causes of Left sided HF - Diastolic heart failure ?
Ventricular hypertrophy - ventricular wall gets thicker ( concentric hypertrophy - crowds into chamber space ) ——————-< ventricle less able to stretch ————–> fills less.
Long standing hypertension —————–> (concentric )V hypertrophy
Aortic Stenosis (narrowing of aortic valve )——————> Concentric Hypertrophy
Genetic - Hypertrophic cardiomyopathy —————————- > abnormal thickening of V wall
Restrictive cardiomyopathy —————-> Stiff ventricle wall (less stress )———-> reduced filling capacity
Symptoms of Left sided heart failure ?
0 Pulmonary oedema ( very important ) ———————-> Dyspnoea (trouble breathing )———————-> CRACKLES (heard on auscultation
Orthopnoea - difficulty breathing when lying down.
( lying down ———–> venous return increases ———> heart has to deal with more blood ———–> worsen SHF)
0 Orthopnoea ———————-> * Paroxysmal nocturnal dyspnoea ( not be able to breath wakes them up at night ————————> may sleep with more pillows to keep body elevated.
0 Fatigue
SHF ———-> reduced CO ———–> not enough blood to organs
o reduced blood flow to kidney —————> RAAS activation ——————–> aldosterone production ——————> increased reabsorption of NA / h20 ——————–> Fluid retention ————–> worsens pulmonary oedema & causes peripheral oedema ( legs etc )
0 Pitting oedema
0 sympathetic nervous system activation ——————— reduced CO ————–> SNV activation ————— >Activates RAAS (worsens fluid retention )
S3 /S4 extra heart sound.
Symptoms of Right sided heart failure ?
0 Chronic lung disease -
Chronic lung disease ——————> difficult gas exchange / 02 exchange——————–> Hypoxia ———————> vasoconstriction of arteries in lung—————————> pulmonary blood pressure rise ——————> harder for right side of heart to pump against ————————–> Hypertrophy ——————> reduced filling capacity —————-> cant contract as well ——————> failure
(Dyspnea )
FLUID RETENTION
0 congestion in veins
- blood backs up to body ———————–> IJV distention/ enlarged ———————> hepatomegaly ( congestive hepatopathy - in this case ) ——————– cardiac cirrhosis & liver failure
2. Splenomegaly
3. Ascities
( Liver - nutmeg liver - dark spots where veins enlarged )
0 Pitting oedema
0 blood sample - Haemosiderin laden macrophages / heart failure cells ———–> blood leaks into alveoli ———————-> macrophages digest these —————–> turn brown colour (iron build up )
0 Arrhythmia ( can happen in both L & R ) - heart cells get irritated by thinning or thickening of V wall.
Most common cause of Right sided Heart failure ?
Left sided heart failure
LSHF ———————-> back of blood to lungs ———————–> increased pressure in pulmonary artery ————————> right ventricle has to pump harder against the pressure
Treatment of Heart failure ?
ACE
ARB
Aldosterone receptor antagonists
Spironolactone
Beta blockers - beware in decompensated HF - rapidly worsens (BB decrease HR ,a
Carvedilol , bisoprolol
Metoprolol
Neprilysin inhibitors - neprilysin - enzymes - breaks down peptides which promote urine sodium excretion & vasodilation.
0 Thiazide / loop diuretics
0 Hydralazine & Nitrates
- VAD - ventricular assist device
Heart transplant - end stage - nothing worked.
- Cardiac resynchronisation therapy
Causes of Right sided heart failure ?
Atrial / ventricular septal defect - shunt form left atrium/ ventricle to right————————–> increased right fluid volume ——————-> Hypertrophy —————–> prone to ischemia —————–> (SHF ) or smaller V chamber size (DHF )
0 Chronic lung diseases -COR POLMONAE - when lung conditions cause RSHF .
Typical symptoms of HF - CKS
0 Breathlessness — on exertion, at rest, on lying flat (orthopnoea), nocturnal cough, or waking from sleep (paroxysmal nocturnal dyspnoea).
0 Fluid retention (ankle swelling, bloated feeling, abdominal swelling, or weight gain).
0 Fatigue, decreased exercise tolerance, or increased recovery time after exercise.
0 Light headedness or history of syncope.
Risk factors
0 Coronary heart disease
0 previous history of MI , Hypertension , atrial Fib , Diabetes
0 Family history of HF or sudden cardiac death
0 Drugs & alcohol
What would you examine for if HF suspected
0 Tachycardia (heart rate over 100 beats per minute) and pulse rhythm.
0 A laterally displaced apex beat,
o heart murmurs
o third or fourth heart sounds (gallop rhythm).
0 Hypertension.
0 Raised jugular venous pressure.
0 Enlarged liver (due to engorgement).
0 Respiratory signs
o
tachypnoea,
o basal
crepitations,
o pleural
effusions.
0 Dependent oedema (legs, sacrum), ascites.
0 Obesity.
Management of suspected HF ?
0 Review medication - reduce /stop any that could worsen HF
Sufficiently severe symptoms - give loop diuretic
o Furosemide 20–40 mg daily.
o Bumetanide 0.5–1.0 mg daily.
o Torasemide 5–10 mg daily.
if higher dose needed - check adherence - check alternative causes
Test for Heart failure
ESSENTIAL
N-terminal pro-B-type natriuretic peptide level test
Natriuretic peptides - made by the heart.
2 types
o brain natriuretic peptide (BNP) o N-terminal pro b-type natriuretic peptide (NT-proBNP
high levels indicate heart is not pumping as much blood as it needs too.
above 2000pg/mL (236 pmol /L ) - refer urgenlty - within 2 weeks
400pg/mL - 2000 (47–236 pmol/L), pmol /mL - referal within 6 weeks
referral for specialist assessment & echocardiography
under 400pmol/mL (47pmol / L ) - HF less likely
12 lead ECG
CAN DO THESE
0 Chest X-ray.
0 Blood tests - urea and electrolytes,
0 eGFR
FBC
0 TFT
0 LFT
0 HbA1c, and fasting lipids.
0 Urine dipstick for blood and protein.
0 Lung function tests (peak flow and/or spirometry).
Interpretation of natriuretic peptide levels ?
What does elevated or reduced levels suggest?
Who may have naturally elevated ore reduced levels ?
https://cks.nice.org.uk/topics/heart-failure-chronic/diagnosis/how-to-assess/
Treatment of HF with reduced EF ?
above 16
Review drugs which may worsen HF - stop if appropriate
- Prescribe loop diuretic - titrate up or down according to symptoms + addition of other drugs
- Prescribe ACE inhibitor and Beta blocker - one after the other - not at the same time.
- Diabetes Mellitus or fluid overload signs - give ACE inhibitor first (Beta blocker may worsen symptoms of HF )
- Angina - beta blocker first
still not working - refer to specialist
DO NOT USE ACE INHIBITOR IF SUSPICION OF HAEMODYNAMICALLY SIGNIFICANT VALVE DISEASE.
other stuff:
statin therapy , antiplatelet if indicated
manage co-morbidities
screen for anxiety & depression.
exercise - based group referral - if suitable
nutrional status assessment.
What is end-stage HF ?
High risk of dying within 6-12 months .
normal symptoms of HF
- can also be:
depressed
anxious
have :
cognitive impairment
loss of appetite & nausea
Often frequently admitted to hospital
progressive deterioration of eGFR & hypotension limiting use of drugs.
poor quality of life
low serum albumin
presence cardiac cachexia
What is end-stage HF ?
High risk of dying within 6-12 months .
normal symptoms of HF
- can also be:
depressed
anxious
have :
cognitive impairment
loss of appetite & nausea
Often frequently admitted to hospital - because of HF & co-morbid conditions e.g chest infection
0 progressive deterioration of eGFR & hypotension limiting use of drugs.
0 poor quality of life
0 low serum albumin
0 presence cardiac cachexia - muscle wasting -weight loss as a result of heart disease.
What is Cachexia ?
Common in
Muscle wasting - high risk of death - chronic
o Cancer (especially )
o Celiac disease
o COPD
o Crohns
o CHF -
o chronic /
o congestive o heart failure
Begin with C
Also Aids (next letter in cachexia)
Symptoms
- Weight loss
- Muscle loss
- Adipose loss
- Anorexia
- Weakness
Underlying causes of Cachexia ?
Elevated level of Leptin in the body
Increased Leptin ——————–> Inhibits neuropeptin Y ——————> does not act on the hypothamulus ————————–> feeding urge not stimulated ———————————-> makes you thin.
Treatment of Cachexia?
No specific pharmaceutical treatment - mostly focuses on nutrition
increased calorie intake
Appetite stimulus
weight bearing exercises - to build muscle
( this is dependent on the cause - if they are able too )
Treat underlying causes.
What is peripartum cardiomyopathy ?
Heart failure with no identifiable cause
0 last month of pregnancy and 6 months postpartum in patients without a previous heart disorder.
(most commonly develops right after birth )
0 rare - with mild or severe symptoms .
Risk factors.
0 Multiparity - has given birth more than once.
0 Age ≥ 30
0 Multifetal pregnancy
0 Preeclampsia
SYMPTOMS
- Shortness of breath
- Swelling in feet & legs
- echocardiogram can detect cardiomyopathy.
- Often undiagnosed as symptoms similar to third trimester.
What is cardiorenal syndrome ?
Acute / chronic dysfunction of heart can cause acute / chronic dysfunction of the heart and vise versa.
( dysfunction in one can cause dysfunction in the other ) - impair each other.
5 types
TYPE 1 - Acute heart failure causing chronic kidney injury
TYPE 2 -Chronic heart failure causing progressive/ chronic kidney disease.
TYPE 3 Acute Kidney Injury causing acute cardiac dysfunction ( e.g heart failure )
TYPE 4- Chronic kidney disease causing cardiovascular disease.
TYPE 5- Systemic disease (e.g sepsis / diabetes ) causing either kidney or heart dysfunction.
What is the relationship between the heart & the kidneys ?
0 Reduced Cardiac Output (CO) ————————-> sympatehtic activation ———————————–> - cause release of renin from kidneys - activating RAAS.
0 Reduced CO ————————-> reduce bloodflow / O2 to kidney ——————————> acute kidney injury ———————————> RAAS also activated in response to less perfusion.
- just a note = Reduced CO ———————————-> sympathetic activation ———————————-> HR increased & SV to increase CO
(CO = HR X SV)
PROBLEM
in normal cases activation of RAAS causing increase in BV and blood pressure as anti -diuertic hormone in H20 retention.
NA is also absorbed.
0 RAAS ————————–> cause vasoconstriction ———————————-. further lessen perfusion to kidneys
0 Right sided heart failure ———————————–> back of blood to the body —————————-> increase in pressur in veins e.g. IVC - backs up to other veins ( central venous pressure increases - average blood pressure in the venous compartment) e.g renal vein - contribute to acute Kidney injury
Increased presure in renal vein ———– ( renal vein hypertension )———————————————-> increased afferent pressure (in efferent vessel - coming in ) in glomerulus ————————————–> pressure gradient created by smaller diameter of efferent vessel reduced (now more similar in pressure )——————————————> reduced GFR
- we rely on arterial pressure being higher than venous pressure to keep blood flowing
0 RAAS system unchecked by by vasodilators such as NO (NITRIC OXCIDE ) , Prostaglandins ,
bradykinin relseased by heart and vessels. Usually mediate RAAS ———– but reduced CO compounded by AKI - stop having effect.
0 Inflammatory component.
How can chronic kidney disease cause cardiovascular dysfunction ?
Chronic kidney disease ( LOW -reduced GFR )
low GFR ——————–> RAAS activation ——————————> systemic vasoconstriction ( long run causing Hypertension ) —————————————> also causes NA & H20 retention ————————both leads to cardiac remodelling & left ventricular hypertrophy
( hypertension - left ventricular hypertrophy heart having to pump against a higher pressure & H20 retention increases BV - more blood to pump ) —————————————–> Mean aterial pressure increases ———————————————————–> afterload increases (pressure at which the heart must pump against - higher MAP - more resistance to bloodflow so heart works harder)———————————————-> cardiac output reduced .
Chronic KD ———————> reduced ethropoetin production —————————> anaemia ————————— > risk of ischemic events in heart.
0 CKD ———————> 1 alpha hydroxylase in kidneys ———————————> reduced vitamin D ———————> elevated PTH ——————————————> increased calcium & phosphate in blood ————————————-> increased coronary calcification ——————————–> increased risk of ischemic events
0 CKI ————————-> electrolyte imbalance ————————————– > e.g increased CA can cause arrhythmias
Treatment
Difficult - as drugs target heart issues may worsen kidney issues .
- Type 1 or 2 e.g acute / chronic heart failure causing acute ./ chronic KI
Diuretics - if fluid overload present
0 ACE I , ARB - treat HF - but dont really improve renal fucntion - actually nephrotoxic.
0 Ultrafiltration - mechanical fluid removal procedure – if the person is diuretic resistant.
0 Intravenous dilators
0 Ionotropic drugs.
What are the functions of Angiotensin II ?
0 Stimulates sympatehtic nervous s ———————-> Increases SV thus CO
0 Increases vasocontriction
0 Increased aldosterone biosynthesis from adrenal gland ————————-> increased H20 & NA reabsorption
0 Also directly increases NA & H20 absorption
0 cause secretion of ADH from piturary gland —————————–> H20 reabsorption.
0 inhibit formation of bradykinin (vasodilator )
Collectively increase Peripheral resistance , CO & Fluid volume.
Inflammation & MI ?
Acute inflammation ( inflammatory cell migrate to damage , necrosis & apoptosis————————————- > continued inflammation - healing phase - reparative fibrosis of infarct zone—————————————————> LATE PHASE- Remodelling phase - Scar formation , LV dilation , Reactive fibrosis and hypertrophy of non- infarct zone (THIS IS THE PROBLEM AREA - chronic inflammation persist after healing phase )
If inflammation persist after this period – chronic inflammation ————— non infract zone impacted and more areas affected ———————–> heart failure.
WHY ?
cause excessive replacement of cardiac parenchyma e.g cardiomyocytes with fibrous tissue .
MCP -1 ( MONOCYTE CHEMOATTRACTANT PROTEIN 1) released due to chronic inflammation - cytokine ————————–> it attracts a protein than attracts monocytes which become macrophages ——————–> macrophages release TNF - alpha , interleukins , TGF -B etc ———————————> these recruit fibroblast ————————————–> fibroblasts differentiate into myofibroblasts ————————————–> fibrosis occurs.
- Splenocytes also present (WBC recruited from spleen )————————————————-> secrete DAMPs ( damage associated molecular patterns ) in areas of damage ——————————————> cause necrotic stress in cardiomyocyte ——————————————> increased fibrosis ——————————> can cause heart failure.
What co-morbidities are associated with increasing prevalence of heart failure ?
0 renal failure
0 arterial hypertension
0 COPD
0 Diabetes mellitus
0 metabolic syndrome.
these promote systemic inflammation ——————————-> increases reactive oxygen species (these attract free radicals which cause damage) & preoxynitrite levels in cardiac endothelial cells.
( bottom line - systemic inflam causes cellular damage) also other factors cause signalling chages ———————> all this causes adverse LV remodelling & impaired LV relaxation.
What anaemia of chronic disease ?
Always linked some sort of inflammatory process in the body
Type of microcytic anaemia -difficulty producing HB
hepcidin is released to any inflammatory condition e.g infection , cancer , autoimmune conditions etc. (PATHOLGICAL ) ———————————> cytokines released ———————> increased hepcidin production ———————-. decreased serum iron ————————————–> decreased HB production ———————————> anaemia
WHY ?
0 body hiding iron from bacteria, cancer cells , inflammatory cells so they don’t use it to grow.
linked with hepcidin - major iron regulator
High LEVEL OF IRON - increased hepcidin production———————> decreases serum iron by blocking:
o intestinal iron absorption
o
macrophage
iron recycling
LOW LEVELS OF IRON - low hepcidin production by liver.
HOW ?
- HEPTCIDIN - blocks ferroprotein channels in duodenum ————> blocked absorption of iron from gut
- 120 days blood cells die ————————–> degraded by macrophages————————–>HEPTCIDIN - prevents degradation of RBC to stop recycling of iron (usually done to
and stored to make new RBC )
Anemia in chronic kideny disease ?
Normocytic
common in stage 3 and 4 of CKD - stage dependent on level of GFR
CAUSES
CKD -
causes reduced ethropoetin ———————————— > reduced RBC
0 increased hepcidin due to pathological -maybe linked with inflammation ————————————> reduced serum iron ———————> iron restricted ethropoiesis. (development of resistance to EPO) ——————————————->
Treatment of anaemia of CKD ?
Exogenous EPO or EPO stimulating agents (ESAs )
- pulsatile erythropoiesis - occurs when receive a dose of this drug.
0 Iron -
can overcome hepcidin blockade & decrease resistance to EPO
0 HIF -PHD (Hypoxia inducible factor prolyl hydroxylase enzyme) inhibitors
- increase uptake of iron
- increased EPO release from kidneys - inhibits downstream effects of hepcidin.
