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cardiology > heart failure > Flashcards

heart failure Flashcards

1
Q

what is heart failure

A

when the heart i unable to pump blood at a rate that the body needs it to - cannot meet requirements of the tissues (or can only do so at high pressure)

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2
Q

impairment of left ventricular filling

A

in diastole, LV walls relax allowing for filling of the LV cavity
without proper LV relaxation, the volume of blood filling the cavity is reduced, thus reducing the stroke volume (the volume of blood ejected with each contraction)

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3
Q

impaired ejection of blood

A

due to LV wall damage the LV may have reduced ability to pump or eject the blood ie after an MI

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4
Q

importance of prompt diagnosis

A

super important !

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5
Q

diagnostic evaluation of new onset heart failure

A
  • can determine the type of HF
  • determine aetiology and treat potentially reversible causes
  • define prognosis
  • guide therapy
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6
Q

aetiology

A

-coronary heart disease (with or without myocardial infarction)
-hypertension/diabetes
-dilated cardiomyopathy (primary about 30% hereditary, secondary eg EtOH, adriamycin etc)
-valve disease
-tachycardic arrthymias
40% have HEFpEF (heart failure with preserved ejection fraction ie anything below 55%)

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7
Q

DCM - dilated cardiomyopathy

A

when the heart becomes enlarge and can’t pump blood as effectively

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8
Q

cardiovascular continuum

A

risk factors such as hypertension/hyperlipidaemia&raquo_space; atherosclerosis & LVH&raquo_space; MI&raquo_space; LV remodelling&raquo_space; ventricular dilation&raquo_space; congestive HF&raquo_space; end stage microvascular and heart disease&raquo_space; death

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9
Q

how does HF present

A
  • SOB
  • difficulty breathing at night when recumbent
    (orothpnoea ie SOB when lying down, paroxysmal nocturnal dyspnea ie SOB that wake up patient from sleep and is resolved usually in upright position)
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10
Q

how does HF present

A
  • SOB
  • difficulty breathing at night when recumbent
    (orothpnoea ie SOB when lying down, paroxysmal nocturnal dyspnea ie SOB that wake up patient from sleep and is resolved usually in upright position)
    -reduced exercise tolerance
    -fatigue
    -tiredness
    -ankle swelling
    »think NYHA functional class
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11
Q

what is another common physical finding of HF

A

volume overload !!
>neck exam = elevated JVP
>auscultation of the lungs = rales or crackles
>auscultation of the heart = 3rd or 4th heart sound sometimes called a gallop rhythm, murmur
>oedema in dependant areas = ie in the sacrum/feet/ankles/lower legs

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12
Q

diagnostic tests in HF

A

ECG -to identify potential causes of HF
ie arrhythmias, a past MI, LVH
CXR - to identify the size and shape of the cardiac silhouette and evidence of fluid accumulation in the lungs
**on a CXR, HF will present with perihilar congestion, fluid in inferior accessory fissure, Kerley B lines, and an enlarged cardiac silhouette

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13
Q

what else is a super useful diagnostic test ie after an ECG and CXR

A

an echocardiogram ! it is the gold standard
it reveals
chamber size
R & L ventricular function
regional wall motion abnormalities, and can calculate EF and loads more
>reveals structure and function
>LVEF - systolic dysfunction -diastolic dysfunction (TDI)
>may help define aetiology … valve, previous AMI
>however not easily accessible in primary care

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14
Q

what is EF - ejection fraction

A

it is the % if blood that is pumped out of the heart during each beat
normal EF = anything above and occluding 50%
HF with an EF of <40% is a known HF with reduced EF (HFrEF)
HF with normal EF is known as heart failure with preserved ejection fraction (HFpEF)

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15
Q

difference between HFrEF and HFpEF

A

> in reduced the LV is unable to eject an adequate amount of blood during systole
in preserved, less blood is able to fill the LV diastole due to myocardial stiffness thus the LV has less blood to eject during systole

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16
Q

blood tests : ANP / BNP (atrial and brain natriuretic peptide)

A

atrial hormone / ventricular hormone

17
Q

BNP from blood tests

A

if BNP is elevated it is likely there is HF
>can rule out HF in symptomatic patients
» NT-proBNP (n terminus)

18
Q

use BNP and full blood tests with SOB symptoms

A

if BNP is elevated it is likely there is HF
>can rule out HF in symptomatic patients
» NT-proBNP

19
Q

mitral regurgitation - MR

A

mitral valves don’t close tightly allowing back flow of blood

20
Q

viability imaging techniques

A

PET
dobutamine echo
cardiac MRI
angiogram

21
Q

late gadolinium enhanced cardiac MRI

A

shows the thickness of the scar tissue - ie if goes bright yellow then there is all thickness of the scar
>wall thickness viable rim thickness or total wall thickness
>infarct transmural extent by assessing myocardial cell wall integrity so you can see the viable tissue and the non-viable tissue

22
Q

treatment ! (1)

A 
lifestyle modification 
- more exercise ! if there is adherence to exercise the benefit to survival is seen 
>exercised based rehabilitation !!
>>water and salt intake restriction (1.5-2L daily of all fluids)(avoid salt)
>>encourage exercise 
>>keep vaccination up to date
>>manage mental health 
>>encourage good nutrition
23
Q

treatment ! (2)

A

pharmacological measures
>drugs that prolong survival
-RAS inhibition
ACE inhibitors and ARII antagonists (would push to the max. dose tolerated)
-beta blockers (sympathetic NS)
start at low dose and slowly build concentration to the highest dose tolerated
-aldosterone antagonists ie spironolactone and eplerenone
-vasodilators
hydralazine and nitrates combines (For those who cannot tolerate ACEI/ARB)
-sinus node blocker
ivabradine
>drugs that improve symptoms
-digoxin

24
Q

what are really effective drugs

A

ACE inhibitors and beta blockers

25
Q

CRT - cardiac resynchronisation therapy

A

> the presence of LBBB in HF
-abnormal contractile wave front across the LV
-the LV does not contract efficiently = dysnchronous contraction
-worseniing LV systolic function
pacing the LV from the left lateral wall
-increases synchronous contraction
-improves LV haemodynamics

26
Q

new treatment (2)

A

shift !
>ivabradine : If channel modulator
specifically binds to the funny current modulator and acts to slow HR down
however it does not work in AF
-does not alter
ventricular repolarisation, myocardial contractility or BP
>LCZ696 : is an angiotensin receptor blocker to block angiotensin aldosterone system (RAAS) , decreasing BP, sympathetic tone, aldosterone levels
-also it …
enhances the effects pf natriuretic peptides

27
Q

HFpEF

A

has a complex pathophysiology and so there are no current effective treatments
but exercise training could improve symptoms

28
Q

advanced HF therapy

A

> transplantation
left ventricular assist devices
-this is considered for patients with refractory end stage HF, repeat hospitalisations, resistance to diuretics, iv inotropics / vasodilators during decompensation …

29
Q

mechanical assist device - fake heart !!

A

LVADs !!

can keep patients alive with LVADs until they can get their transplant

30
Q

heart transplantation indications

A

if they have refractory cardiogenic shock, documented dependence on IV inotropic support to maintain adequate organ perfusion
peak VO2 <10 ml /kg/min
severe symptoms of ischaemia not amenable by revascularisation
recurrent symptomatic ventricular arrthymias refractory to all therapeutic modalities
contraindication = age and severe comorbidity

31
Q

treatment (3)

A

palliative care if too risky to undergo LVAD/transplant
>there to relieve suffering
>symptom control
>help family with disease and bereavement
>psychological and spiritual support

32
Q

fucntion of ANP/BNP

A

> assist the stretched atria and ventricle by increasing GFR and decreasing renal sodium absorption thereby reducing fluid load and by relaxing smooth muscle thereby decreasing preload
the heart secretes natriuretic peptides as a homeostatic signal to maintain stable blood pressure and plasma volume and to prevent excess salt and water retention

33
Q

when is ANP released

A

in response to atrial dysfunction (hypervolemic stress)

is a 28 amino acid peptide synthesised and stored by atrial muscle cells

34
Q

neurohormonal changes as a result of HF

A

activation of RAS.. the stimulants of RAS include ..

cardiology (22 decks)

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