Heart Failure Flashcards
Define heart failure
- inability of the heart
- to generate sufficient CO
- to meet demands of body
- without increased filling pressure
- secondary to an underlying cause
Most common cause of HF
coronary artery disease
hypertension
Age group common HF
Over 70
Presentation of chronic HF
- breathlessness with impaired exercise tolerance
- slowly progressive
- periods of acute decompensation
- state of fluid retention and overload
Acute HF Presentation
- flash pulmonary oedema
- precipitating ischaemia, arrhythmia, intercurrent infection
- OR gradual deterioration = fluid accumulates, exercise tolerance falls, orthopnoea, PND
Systolic HF alternative name
HFrEF
HF with mildly rEF
Severities of systolic HF
- mild = 46-55% EF by Echo
- moderate = 36-45%
- severe = <35%
Diastolic HF alternative name
HFpEF
- stiffness of ventricular wall with impaired filling and reduced CO
Echo signs of diastolic HF
- LVH
- L atrial dilatation
- abnormal relaxation
Right HF features
- fluid overload
- secondary to L. heart disease, cor pulmonale, congenital heart disease, cardiomyopathy
Left HF Features
HFrEF
Low output HF
- common
High Output HF
- overworked heart
- physiological or pathophysiological
What does HF result in?
- decreased SV and CO
What is the neurohormonal response to HF?
- sympathetic system activated
- RAAS system activated
- both result in vasoconstriction and sodium and fluid retention
- further stress of ventricular wall and dilatation (remodelling)
- worsening ventricular function
- further HF
Explain the RAAS mechanism?
- liver, vessels and brain produce angiotensinogen
- renin produced by JGA in kidney when blood flow to kidney is low
- renin converts angiotensinogen to angiotensin I
- ACE from lungs converts angiotensin I to II
- angiotensin II = vasoconstriction and enhanced sympathetic activity as well as aldosterone release
- aldosterone = salt and water retention
What does the sympathetic nervous system do?
- RAAS
- vasoconstriction
- increased HR and contractility
- direct cardiotoxicity
What does direct cardiotoxicity result in?
- myocyte damage
What does increased HR and contractility result in?
- increased myocardial oxygen demand = decreased contractility
What does vasoconstriction and RAAS result in?
RAAS = fluid retention = increased wall stress = myocardial hypertrophy and decreased contractility as increased myocardial oxygen demand Vasoconstriction = increased wall stress = myocardial hypertrophy and decreased contractility
What does CO =?
SV x HR
HR increases via autonomic systemic
SV dependent on ventricular performance
What is Starling’s Law of the heart?
- contractile function depends on velocity of muscle contraction, load being moved and amount of stretch
- pre-stretch improves relationship
Main causes of HF?
- IHD
- Dilated cardiomyopathy
- hypertensive heart disease
Infectious causes of HF?
Viral mycoarditis
Right HF causes
COPD
Metabolic causes
Anaemia
Thyrotoxicosis
Haemochromatosis
Arrhthmic causes
AF
bradycardia
Drug causes of HF
EtOH
Chemo
Other cardiac causes
Valvular heart disease
Primary heart muscle disease
Symptoms
Breathlessness - on exertion or rest Orthopnoea PND Tiredness and falling exercise tolerance Peripheral oedema Palpitations Depression Gout
NYHA Classification of symptoms
1 = none 2= symptoms on exertion 3= symptoms on minimal exertion 4= symptoms at rest
Signs
Raised JVP 3rd heart sound pulmonary crepitations hepatomegaly peripheral or sacral oedema cachexia
Routine bloods
FBC Iron studies U&E Glucose Cholesterol LFTs TFTs BNP Uric acid Ferritin CK Immunoglobulins Autoimmune profile Viral titres Genetics
What diagnostic tests are done?
Routine bloods
ECG
CXR
Transthoracic echocardiography
Others = holter monitoring, lung function, cardiopulmonary exercise testing, cardiac catheterisation, perfusion imaging, cardiac MRI
Management of acute pulmonary oedema
- medical emergency
- high flow oxygen
- morphine and anti-emetic
- IV GTN
- furosemide if fluid overload
- ECG monitor
- ventilatory support
- find cause
Principles of chronic HF management
- prevent decompensation
- maintain or improve symptoms
- increase longevity
Types of management for chronic HF
- drug therapy start low dose then uptitrate
- device
- surgical
- exercise training through cardiac rehab
- palliation
- remove exacerbating factors
Drugs used in HFrEF
1) Symptomatic = ACEi or ARB and Beta blocker
2) MR antagonist add
3) still symptomatic and LVEF <35% = ARNI replace ACEi/HR>70 = ivabradine
4) resistant symptoms = digoxin, heart transplant, LVAD
Advanced Treatment
Implantable cardiac defibrillators
Cardiac Resynchronisation Therapy
LVAD
Extracorporeal Membrane Oxygenation
Surgical Options
Valve Surgery
Revascularisation
Stem Cells
Heart Transplants
