Heart failure Flashcards
Whcih side heart failure causes JVP raise?
Right
Which side heart failure causes pulmonary congestion?
left
How does Pulmonary hypertension cause cor pulmonale?
Increased pressure in pulmonary circulation -> R ventricle working harder -> hypertrophy -> failure
Bloods before start a statin:
Non fasting lipid profile
Liver function tests
Renal function - eGFR
HBA1c
Creatinine kinase if persistent muscle pain
TSH if dyslipidemia present
Which sputum is suggestive of HF?
Pink, frothy
Cardiac causes chronic HF
IHD
Arrhytmias
Valvular or congenital HD (ASD,VSD)
Myocarditis/pericarditis
Cardiomyopathy
Perciardial effusion, cardiac tamponade etc
What drugs can cause HF?
Negative inotropes eg beta blockers
Fluid retaining properties - steroids, NSAIDs
alcohol
Chemotherapy
What increases in metabolic demand can cause HF?
Pregnancy
hyperthyroidism/thryotoxicsosi
Anaemia
Liver failure
BeriBeri - thiamine deficiency
Pagets disease
What are the three features of Becks triad?
Jugular vein distension
Low BP
Muffled heart sounds
What does Becks triad indicate?
Cardiac tamponade
Signs of HF on CXR
Pulm oedema
Cardiomegaly
What positive test on bloods indicates HF?
Raised pro-Brain Naturietic peptide
When is BNP released? What does it do?
Released by myocardium when under tension, cleaved into BNP and pro. Increases diuresis and blocks RAS system
Indications for ECHO
Septal defects
Valve function
When its hard to visulaise eg tamponade, endocarditis, pericarditis
Heart function eg pre-op, before cardiotoxic chemo
Emergency - unstable nedocarditis, aortic dissection
What criteria is used to classify heart failure?
New York Heart Association classification
What does II stage NYHA mean?
Slight limitation physical activity, comfortable at rest. Ordinary physcial activity results in fatigue, palpitation, dyspnoea
What is the difference between III and IV NYHA HF classification?
Marked limitation of physical activity vs unable to carry on any physical activity without discomfort.
Comfy at rest vs symptoms HF at rest. Less than ordinary activity causes fatigue palpitation or dyspnoea in stage III, any physical activity increases discomfort in stage 4
Stage I of NYHA HF criteria
No limitation physical activity
Ordianry activity doesnt cause undue symptoms
Two other stagings of HF
Canadian CVS society grading of angina pectoris
European Heart Rhythm association score of AF
What levels of BNP rule out HF?
BNP less than 100ng/L
NT-proBNP < 300ng/litre
What investigation shouldbe done next with new suspected AF with raised BNP levels?
Transthoracic doppler 2D ECHO
Consider with people presenting with sus acute HF within 48 hours of admission
When should a HF patinet not be on beta blockers
HR under 50
2 or 3 degree Aventricular block
Sick sinus syndrome
Shock
When do you start a beta blocker in people with acute heart failure due to LV systolic dysfunction in hospital
When condition stabilised eg IV diuretics no longer needed 48 hours before
What to start in patients with acute HF and reduced LV ejection fraction in hopsital
ACE i and aldosterone antagonist
Immediate treatment for acute AF
IV diuretic with bolus or infusion
Higher dose if already taking
What important to monitor in diuretic therapt
Renal fucntion
Weight
Urine output
When are nitrates offered in acute HF?
Concomittant MI, severe HPTN, regurgitant aortic or mitral valve disease, monitor BP closely
When do you consider inotropes or vasopressors in acute HF?
Acute HF and potentially reversible cardiogenic shock
When to consider invasive ventialtion in acute heart failure?
Leading to or complicated by respiratory failure or reduced consciousness or physical exhaustion
When to refer 2 week pathway vs 6 week pathway for ECHO for suspected HF
2 week - above 2000 ng/litre NT-proBNP
6 week - 400-2000 ng/L
Because high levels of NTproBNP are associated with poor prognosis
What are other causes that could -> high BNP levels
Over 70
LVH
Ischaemia
Tachycarida
RV overload
Hypoxaemia (incl PE)
Renal dysfunction (eGFR <60)
Sepsis
COPD
Diabetes
Cirrhosis
What do ECHO to look for
Exclude valve disease, assess systolic and diastolic function of L ventricle and detect intracardiac shunts
What can reduce levels of serum natiuretic peptide?
Obesity
African /african-caribbean family background
Diuretic treatemtn
ACEis
Betablockers
ARBs
Mineralcorticoid receptor antagonists
What need to do for HF diagnosis
ECHO
CXR
Bloods:
-FBC
-U+Es
-Thyroid function profile
-LFTs
-Lipid profle
-HbA1c
Urinalysis
Peak flow or spirometry
If confirmed and unsure why,m investigate cause
First line treatment for chronic HF and reduced ejection fraction
ACEi (start low and tirate up)
and a beta blocker
Diuretics for fluid retention
2nd line for HF and reduced ejection fraction if still have symptoms after ACEi and beta blocker
Mineralcorticoid receptor antagonists
What to monitor with MRA
Serum sodium and potassium
Renal function
Before and after start and after each dose uncrement
Blood pressure
Monthly for 3 months then every 6 months
When is Ivabradine used in HF?
NYHA II to IV
AND
Sinus rhythm, HR 75BPM +
AND In combo with standard therapu - ACE is, beta blockers, aldosterone antafonists, or when beta blocker therapy contraindicated
AND with LV ejection fraction <35%
How long is the stabilisation period before ivabradine initiated?
4 weeks
When to use sacubitril valsartan
NYHA II to IV
AND LV ejection fraciton under 35%
Already taking ACEi or ARBs
What drug can be used for peope of afro caribbean family origin and mod to sev HF with reduced ejection fraction
Hydralazine + nitrate
When is digoxin initiated?
Worsening or severe HF with reduced ejection fraction despite first line treatment HF.
What are people with CKD and chronic HF may prone to on the first line medications?
Hyperkalemia
Other drugs used inHF
Amiodarone
Diuretics
What CCB should be avoided in HF with reduced ejection fraciton?
Verapamil, diltiazem, Short acting dihydropyridine agents
Lifestyle advice for HF
Cut out smoking and alcohol
DVLA
aIR TRAVEL
Fluid restriction for dilutational hyponatremia
Reduce if high intake of salt or fluids.
Cardiac rehabilitation unless unstable
What should chronic HF patients be monitored for?
6 monhtlya clinical assessment of functional capacity, fluid status, cardiac rhythm
(minimum of examining the pulse), cognitive status and nutritional status
* a review of medication, including need for changes and possible side effects
* an assessment of renal function.
Serum potassium esp important if on digoxin or MRA
Whenh is cardiac transplant considered?
Severe refractory symptoms or refractory cardiogenic shock
Symptoms of L sided HF
Breathlessness
Cough
Cardiac wheeze
Orthopnea + PND
Bilateral crepitations in lower zones
Pleural effusion
Gallop rhythm - S3
Pitting oedema
R sided HF symptoms
Peripheral oedema
Ascites
Raised JVP
Hepatomegaly
List as many causes of R sided HF as can
Sleep apnoea
COPD
Chronic TE puomonary disease
Cystic fibrosis
Interstitial lung disease
Kyphoscoliosis
Pneumoconicosis
Primary/secondary pulmonary HPTN
Pulmonary vascualr disease
signs of general Heat failure
Hypotension
Tachycardia
Gallop rhythm - presence S3,S4
Displaced apex
When is a heart failure considered to have reduced ejection fraction?
less than 40%
Is there systolic or diastolic dysfunction in HF with reduced ejection fraction
Systolic
What conditions cause increased metabolic demand that can lead to HF?
Pregnancy
Hyperthyroidism
Anaemia
Changes in CXR in HF
Cardiomegaly
Upper lobe diversion
Alveolar oedema
Kerley B lines
Pleural effusions
Why is there fluid accumulation in heart failure?
Neuro-hormonal activation -> impaired regulation of sodium excretion through kidneys
Sodium and fluid accumulation. Glycosaminoglycan networks become dysfunctional in buffering this, also organ dysfunction affecting kidneys
What neuro hormonal systems are affected in heart failure?
RAAS
Arginine-vasopressin system
Sympathetic nervous system
When does tissue oedema occur?
When the transudation from capillaries into the interstitium exceeds the maximal drainage of the lymphatic system due to increased transcapillary hydrostatic gradient, decreased oncotic pressure gradient and increased interstitial compliance
What cardiac complications arise from congestion?
S3, JVP, + hepatojugular reflux
Functional mitral and tricuspid regurgitiation
Elevated BNPs
What resp complications arise from congestion?
PLeural effusion
Dyspnoea, orthopnea, PND
Rales, crackles, wheeze, tachypoea, hypoxia
Congested lungs on ultrasound appearance
B-lines/comets
Complications for kidney from congestion
Decreased urine output
Elevated creatinine levels
Hyponatremia
Complications for liver from congestion
RUQ discomfort
Hepatomegaly
jaundice
Elevated parameters of cholestasis
Bowel complications from congestion
N+V
Abdo pain
Ascites
Increased abdominal pressure
Cachexia
Treatments chronic HF
- ACEi and B blockers
- SGLT2 inhibitors - dapagliflozin
- Aldosterone antagonists eg epleronone
- Control of risk factors - statins, smoking cessation, alcohol etc
Acute Heart failure stepwise management
Sit patient up
High flow oxygen
IV furosemide
Diamorphone + anti-emetic
BP stable then consider GTN spray
Catheterisation to monitor urine output
Treat underlying causes
Consider CPAP
If BP low consider ITU + inotropes eg IV dobutamine
Treatment for cardiogenic shock
inotropes eg IV dobutamine
Immunisation in HF
Annual flu and covid
Single pneumococcal vaccine
Which NYHA classes can fly without oxygen?
I + II
Drugs that reduce mortality vs symptomatic relief
Mortality -
-ACEis/ARBS
-Beta blockers
-Spirinolactone
-Hydralazine with nitrates
Symptomatic
-Loop or thiazide like diuretics
-Digoxin
-Ivabradine
Ivabradine indications
treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Lowers HR and therefore increase flow to myocardium
Why use ivabradine over CCBs and Beta blockers
Ivabradine acts directly on funny channels in the SA node to lower HR, but no negative ionotropic side effects
When are negative inotropes helpful?
keep your heart muscles from working too hard by beating with less force. This is helpful when you have high blood pressure, chest pain, an abnormal heart rhythm or a disease like hypertrophic cardiomyopathy.
What drugs are negative inotropes?
beta-blockers, calcium antagonists, and antiarrhythmics
Signs of HF on CXR
Alveolar oedema - bats wings
Kerley B lines - interstitial oedema
Pleural effusion
Prominent upper lobe vessels - Antlers sign
Cardiomegaly
Investgiations for HF
Bloods - FBC, U+Es, LFTs, TFTs, lipid profile, BNP or pro-BNP
Urinalysis
CXR
ECG
ECHO
Lung function tests
Cardiac MRI - gold standard for ventricular volumes, mass and wall motion
Resp causes of HF
COPD
Obstructive sleep anoea
PE
How is cardiac output maintatined inHF?
Increasing stroke volume, HR, ventricular remodelling -> increased wall thickness
How is MAP maintained in HF?
Activation of sympathetic, RAAS
How do compensatory mechanisms damage the heart?
Sodiy=um/water retention and vasoconstriction from SNS and RAAS activation cause increased preload and afterload, causing increased cardiac workload and myocyte damage -> decreased cardiac input, further activating those systems
Why do BNP before take for ECHO even though its not specific to HF?
Because its very sensitive so if there is a low level you can rule out HF
Cardiac terminology explanation
-
CO = SV x HR
- CO = blood pumped per min
- SV = ml blood per contraction pumped
- Preload = blood filling up ventricle. eg end diastolic volume. Affected by
- Venous return
- Fluid volume in body
- Atria contractility → ventricles
- Afterload - pressure required to pump blood into arteries
- BP
- Atherosclerosis
- Aortic stenosis
- Contractility - ability heart to contract and pump out blood during systole
- inotropes eg epinephrine increase
- inotropes eg beta blockers, CCBs decrease
- Ejection fraction - % ventricular blood pumped out per contraction
- Normal = 50-70%
Causes of reduced ejection fraction
Coronary HD
Muscle damage after MI
DCM
HPTN
Causes of HF w preservef EF
Anything that effects the filling of ventricle and the ability of the wall to stretch
Common -
- HPTN
- CAD
- Diabtets
Rare
- Hpertrophic CM
- Infiltrative diseases eg amyloidosis, sarcoidosis
Bloods for oedema
- U+Es + LFTs
- Albumin - reduced synthesis (liver) or increased excretion (kidney)
- FBC - anaemia
- Thyroid profile
- Hypothyroidism → oedema and fatigue
- Pro-BNP> 400 = HF
Signs of palleation with HF
Frequent hospital admissions for decompensations or comorbid conditions
Symptoms refractory to optimal med treatment
Poor QOL + dependent for all ADLs
Others:
- Poor response to treatment and severe breathlessness at rest (New York Heart Association class IV).
- Presence of cardiac cachexia.
- Low serum albumin.
- Progressive deterioration in estimated glomerular filtration rate (eGFR) and hypotension limiting the use of drug treatments.
- Acute deterioration and increasingly frequent hospital admissions from comorbid conditions (such as a chest infection).
- Poor quality of life and dependence on others for most activities of daily living.
- People who are clinically judged to be close to the end of life.
Symtpoms of end stage HF
- Pain
- SOB
- persistent cough
- fatigue
- Limited physical actiity
- Depression and anxiety
- Loos of appetite and nausea
- Oedema
- Insomnia
- Cognitive impairment
What do if proBNP >400
ECHO and specialist assessment within 6 weeks
What do if proBNP >2000
Urgent review within 2 weeks
NYHA scoring
Class I - no limitation of physical activity
II - slight reduction in physical activity -> faigue, palpitation, SOB
III - marked limitation of activity. Less than ordinary physical acitvity -> fatigue, palpitation or dyspnoea
IV - Unable to do any physical activity without discomfort. Symtpoms of HF at rest.
Lifestyle for chronic HF
- Salt reduction (reduce sodium and water retention)
- Strict fluid restrictions only neessary when acute decompesnation or sever dilutional hyponatremia
- Smoking cessation
- Annual flu and pneumonia vaccines
- Tracking weight
- Exercise
1st line for HF w preserved EF
Manage comorbidities eg HPTN, AF, IHD, DM
Exercise based cardiac rehab
If symptoms persist - hydralazine + nitrate
Digoxin for symptoms
1st line for HF w reduced EF
ACEi + BB + MRA
ARB if ACEi intolerant
Hydralazine and nitrate if intolerant to both
2nd line for HF w reduced EF
ACEi/ARB -> sacubitril valsartan if <35% EF
+ ivabradine for sinus rhtyhm if HR >75 and EF <35%
What is sacubatril valsartan
angiotensin receptor-neprilysin inhibitor - ARNI
Physiology of HF meds how worj
- ACEis → minimise RAS system (and therefore excess fuid and sodium retenrion), reduces preload and afterload
- Beta blockers - slow HR allow more ventricular filling and greater contractility
- Nitrates reduce vasocnstriction and therefpre afterload
- Diuretics and ladosterone antagonists - reduce sodium and water retention, therefore reduce preload
When use ICD in HF
LCSD and EF <35%
ICD detect fatal rhtyhms, pace and defib
When is ICD innapropriate HF
v severe disease or severe comorbidities, palleative in next year
What is cardiac resynchronisation therapy used in in HF
Poor ventricular contraction
>150ms and LBBB
Prolonged QRS
SystolicHF
Mod/sev symptoms
- to improve morbidity, mortality and reduce exacerbations.
- With or without a defib (CRT
Heart transplants in HF
- Low donor availability and high risk
- Strong immunosupression required
- LC assist device used to keep patient alive/optimise before transplant. Physically pumps blood from heart.
Medical anagement of acute HF
- Clearly identified trigger should be treated
- Oxygen if hypoxic
- Position sat upright
- Loop diuretics if fluid overload - IV furosemide _ monitor renal function
- Inotropes/vasopressors if unstable.hypovolaemix
Causes of HF decompensation
- ACS - MI
- Tachyarrhytmia eg AF
- PE
- Severe HPTN
- Infection
- Drugs eg NSAIDs, steroids
- Renal insufficiency
- Not taking meds or folloing dietary requirements
Signs of HF decompensation
- Bi basal coarse crackles
- Raised JVP (raised central venous pressure)
- Peripheral oedema
- Wheeze, S3 heart sound, ascites, poor perfusion
Warm/cold vs wet/dry HF
- Warm = normal perfusion
- Cold = cold peripheries, prolonged CRT, reduced urine output
- Wet - pulmonayr/peripheral oedema, raised JVP
- Dry - normal/not congested
- Warm and wet
- Perfused but congested
- Fluid overload
- Diuretics/vasodilators
- Warm and dry
- Compensated
- Optimise meds and treat triggers
- Cold and dry (least common)
- Poorly perfused but not congested
- Hypovolaemic shock
- Consider fluid bolus/inotropes
- Cold and wet
- Poorly perfused and congested
- Cardiogenic shock
- Consider diuretics if BP>90
- Vasopressors/inotropes
- Worst prognosis
Acute HF management
- ASSESS A to E
- Bedside:
- Obs
- ECG - Arrhytmias OR MI
- Bloods
- FBC
- U+Es
- LFTs
- NT-proBNP
- Troponin if sus ACS
- Consider d-dimer if sus PE
- Imaging
- CXR
- ECH0 - urgent if HF new of EF not known
