Heart failure Flashcards

1
Q

What is Heart failure ?

A

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
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2
Q

What is stroke volume ?

How do you calculate Cardiac output ?

What is the ejection fraction ?

  • normal ?
  • abnormal ?
A

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.

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3
Q

How does Systolic heart failure impact EF , EDV , EDP ?

A

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 )

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4
Q

Causes of systolic heart failure

A

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
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5
Q

How does Diastolic heart failure effect EF , EDV , ECF ?

A

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

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6
Q

Causes of Left sided HF - Diastolic heart failure ?

A

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

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7
Q

Symptoms of Left sided heart failure ?

A

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.

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8
Q

Symptoms of Right sided heart failure ?

A

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.

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9
Q

Most common cause of Right sided Heart failure ?

A

Left sided heart failure

LSHF ———————-> back of blood to lungs ———————–> increased pressure in pulmonary artery ————————> right ventricle has to pump harder against the pressure

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10
Q

Treatment of Heart failure ?

A

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
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11
Q

Causes of Right sided heart failure ?

A

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 .

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12
Q

Typical symptoms of HF - CKS

A

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.

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13
Q

Risk factors

A

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

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14
Q

What would you examine for if HF suspected

A

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.

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15
Q

Management of suspected HF ?

A

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

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16
Q

Test for Heart failure

A

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).

17
Q

Interpretation of natriuretic peptide levels ?

What does elevated or reduced levels suggest?

Who may have naturally elevated ore reduced levels ?

A

https://cks.nice.org.uk/topics/heart-failure-chronic/diagnosis/how-to-assess/

18
Q

Treatment of HF with reduced EF ?

above 16

A

Review drugs which may worsen HF - stop if appropriate

  1. Prescribe loop diuretic - titrate up or down according to symptoms + addition of other drugs
  2. Prescribe ACE inhibitor and Beta blocker - one after the other - not at the same time.
  3. Diabetes Mellitus or fluid overload signs - give ACE inhibitor first (Beta blocker may worsen symptoms of HF )
  4. 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.

19
Q

What is end-stage HF ?

A

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

20
Q

What is end-stage HF ?

A

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.

21
Q

What is Cachexia ?

A

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
22
Q

Underlying causes of Cachexia ?

A

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.

23
Q

Treatment of Cachexia?

A

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.

24
Q

What is peripartum cardiomyopathy ?

A

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.
25
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.
26
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.
27
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
28
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.
29
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.
30
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. 2. 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.
31
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.
32
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 ? 1. HEPTCIDIN - blocks ferroprotein channels in duodenum ------------> blocked absorption of iron from gut 2. 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 )
33
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) ------------------------------------------->
34
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.