Heart Failure Flashcards

1
Q

what is heart failure

A
  • “A syndrome in which patients have typical symptoms & signs resulting from an abnormality of cardiac structure or function”
  • Heart failure is a syndrome not a diagnosis and an aetiology (diagnosis) should be sought
  • Physiological definition —inability of the heart to pump sufficient oxygenated blood to the metabolising tissues despite an adequate filling pressure.
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2
Q

what are some common causes of HF?

A
  • Drinking
  • MI causes yellow scar in heart
  • Dilated Cardiomyopathy causes enlargement (or “Big Baggy Ball”)
  • Many have genetic basis - e.g., Cardiotropic Myopathy
  • High blood pressure (Hypertension) leads to thickening of heart muscle
  • Ageing of valves (esp. Aortic) leads to HF - vise versa
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3
Q

what is HF trajectory?

A

HF is characterized by a progressive decline in cardiac function, interspersed with acute episodes of exacerbation. In chronic HF, a process of progressive ventricular remodelling leads to a gradual decline in clinical status often interspersed with episodes of acute decompensation.

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4
Q

what happens with each acute event of HF trajectory?

A

each acute event, there is a rapid drop in clinical status that may not be fully resolved following the event.
The clinical course of HF tends to feature an increasing frequency of acute HF episodes as the disease progresses.

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5
Q

what happens after each hospitalisation for acute HF?

A

each rehospitalization for acute HF contributes to progressive left ventricular or renal dysfunction, leading to an inevitable downward spiral of increasing frequency of acute events, each causing further residual cardiac damage, leading to high rates of hospitalization and increased risk of death.

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6
Q

what are the symptoms of heart failure?

A

breathlessness
ankle swelling
fatigue
triad of cardiac symptoms

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7
Q

what are some physical signs of poor CO?

A
  • Sinus tachycardia
  • Atrial fibrillation or other arrhythmia
  • Hypo/hyper/normotensive
  • Raised JVP
  • Ankle / sacral oedema- Pulmonary crackles
  • Pleural effusion
  • Displaced apex beat
  • Hepatomegaly
  • Ascites
  • S3
  • Murmurs
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8
Q

how do you look for peripheral oedema?

A
  • Shiny chin common
  • Pitting oedema (press finger and colour should return within second)
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9
Q

how do you look for JVP?

A
  • Jugular Venous Pressure pulsates and can be assessed by hydrometer
  • Can’t be palpitated
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10
Q

what is CO?

A
  • CO describes the volume of blood being pumped by the heart, by the left and right ventricle, per unit time
  • Stroke volume is the volume of blood pumped from the left ventricle per beat.
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11
Q

what neurons and hormones activate HF?

A

-natriuretic peptide system Good (Vasodilators, and make you pee salty water)
-sympathetic nervous system (mild)
-renin, angiotensin aldosterone- bad (inc. sypmathetic tone, bp, muscle hypertrophy, fibrosis, and speed up death due to inc. heart rate due to inc. in circulating adrenaline)

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12
Q

what factors need to be considered for a diagnosis of HF?

A

CXR
blood tests
VO2
ECHO
ECG
angiography
history
CMR
examination

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13
Q

what can be seen on a chest ray of HF?

A

ski jump on birder of LV, LV aneurism post MI

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14
Q

what can be seen on an ECHO in HF?

A

-regional wall motion abnormality
-dilated chambers
-valvular dysfunction

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15
Q

what are the colours on a cardiac MRI?

A

living heart - black
scarred heart - white

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16
Q

how do we manage cardiac function?

A

relief of symptoms
avoid admission or readmission
prevention of premature death

17
Q

what does a decline in left ventricular systolic function lead to?

A
  • activation of three major compensatory neurohormonal systems in an attempt to increase cardiac output (CO):
    • Sympathetic nervous system (SNS)
    • Renin-angiotensin-aldosterone system (RAAS)
    • Natriuretic peptide (NP) system
18
Q

how do we achieve SNS and RAAS suppression?

A

Long-term over-activation of the SNS and RAAS in HF are thought to be harmful and blockade of these pathways has been the focus of current HF therapies.

19
Q

how can we inhibit SNS?

A

sing β-blockers and the RAAS using RAAS inhibitors such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor antagonists (ARBs), and mineralocorticoid receptor antagonists (MRAs).

20
Q

how do we enhance Natriuretic peptide system

A

In contrast to the RAAS and SNS, the natriuretic peptide system is a potentially beneficial counter-regulatory system in HF.

21
Q

how can we augment the natriuretic peptide systeM?

A
  • Augmentation of this system is a new therapeutic strategy being considered for HF.
  • This can be achieved by blocking the enzyme neprilysin which is responsible for the breakdown of NPs.
  • Neprilysin inhibition may enhance the effects of natriuretic and other vasoactive peptides, which include vasodilation, diuresis and natriuresis, reduced sympathetic tone, reduced aldosterone, and antifibrotic and hypertrophic effects.
22
Q

what are some abbreviations?

A
  • ACEI=angiotensin-converting enzyme inhibitor
  • ARB=angiotensin receptor blocker
  • MRA=mineralocorticoid receptor antagonist
  • NP=natriuretic peptide
  • RAAS=renin-angiotensin-aldosterone system
  • SNS=sympathetic nervous system
23
Q

what is sacubitril/valsartan?

A

first agent to be approved in a new class of drugs called angiotensin receptor neprilysin inhibitor (ARNI). The medication is FDA-approved for the treatment of patients with chronic heart failure with reduced ejection fraction (HFrEF) with NYHA class II, III, or IV.

24
Q

what drugs worsen HF?

A
  • NSAIDs
  • Ca2+ antagonists
    (except amlodipine)
  • Anti-arrhythmics
    (except amiodarone)
  • Tricyclic antidepressants
  • Corticosteroids
25
Q

why do HF patients die?

A
  • Cardiovascular
    Progressive HF (“pump failure”)
    Myocardial infarction
    Arrhythmia (“sudden death”)
    Stroke
    PE
  • Non-cardiovascular
    Cancer
    Infection
26
Q

how can defibrillators save lives?

A
  • Implanted in body
  • Improve and quickly react to sinus
  • don’t improve symptoms or cardiac function
  • cost 23k for every piece and replacement
  • You cant drive certain vehicles
27
Q

what is cardiac resynchronisation therapy?

A
  • Inotropes have been associated with death so need to be used infrequently!
  • What is an Intra-aortic balloon pump?
    • Device used in hospital for
      HF- A useful bridge
  • 1st line for cardiogenic shock
  • Diastolic augmentation of aortic pressure
  • ↑ coronary perfusion
  • Reduces afterload
  • Improves cardiac output
28
Q

what is a short term LVAD?

A
  • LV by-passing device (From LA to Aorta)
  • Levitated impeller
  • Flows up to 9.9l/min
  • No seals or bearings
  • One moving part
  • Licensed for 30 days
  • Salvage devices as a bridge to decision (e.g. multiorgan failure, uncertain neurology, sepsis)
  • Or can also bridge to
    Long term VAD, Transplant, Recovery,
  • Very Very Expensive
29
Q

what are the newer LVADs?

A
  • The pumps are getting smaller. The next generation of Thoratec pumps is the HeartMate III, shown here next to a HeartMate II.
  • And HeartWare is developing the MVAD, shown here next to an HVAD. It’s not much bigger than a golf ball. You might think who cares – they are all tiny and all the patient can see is the cable.
  • But there are big attractions of smaller pumps – they easier to implant, avoiding sternotomy and the need for cardiopulmonary bypass.
  • This makes the implant safer.
  • And is also likely to make subsequent transplantation safer.
30
Q

what is a driveline infection?

A
  • Cant be eradicated without heart transplant
  • Can only be managed
  • This is a drive line infection and associated cellulitis in a patient with an implantable LVAD.
  • Patients told not to shower but do anyway which gets line soggy which promotes infection
  • Infections are a problem.
31
Q

when is a heart transplant an option?

A
  • Only as a last resort!
  • Mortality of 19% at 1yr
  • Mean survival of ~10 years
  • Increased risk of:
    Opportunistic infection
    Malignancy
    Renal failure
    Hypertension
    Coronary artery disease