Week Four - Case One Flashcards
what is heart failure typically defined as;
the inability of the heart to pump adequate amounts of blood to meet the body’s metabolic demands
what is the classic presentation of heart failure
shortness of breath (especially on exertion and on lying flat), fatigue and ankle oedema
what are the classic signs of heart failure
Signs may include hepatomegaly, tachycardia, tachypnoea and raised JVP.
what are the two broad groups heart failure can sometimes be divided into
those with a normal ejection fraction (>50%), and those with a reduced ejection fraction (<50%), however, the management is similar
There is a correlation between ejection fraction and prognosis – the lower the ejection fraction, the worse the prognosis
what is the mainstay drug of treatment that has been shown to improve survival
ACE inhibitors
what is systolic HF
Systolic HF – inability of the heart to contract efficiently to eject adequate volumes of blood to meet the body metabolic demand [most common].
what is diastolic HF
Diastolic HF – reduction in the heart compliance resulting in compromised ventricular filling and therefore ejection [pericardial disease, restrictive cardiomyopathy, tamponade]. Increasingly recognised as an important cause of heart failure – it is often present in elderly patients with a normal CXR and otherwise unexplained SOBOE (shortness of breath on exertion)w
what is left HF
Left HF – inability of the left ventricle to pump adequate amount of blood leading to pulmonary circulation congestions and pulmonary edema. Usually results in RHF due to pulmonary hypertension. Defined as an ejection fraction of <40%.
what is right HF
Right HF – inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion, therefore peripheral edema and hepatic congestion and tenderness.
Most commonly the result of respiratory disease – especially COPD
The presence of raised JVP and peripheral oedema are suggestive of right HF in particular
what is congestive HF
failure of both the right and left ventricles, which is common
what is low-output HF
heart failure resulting from reduced cardiac output [most common type] – also referred to as HFrEF – Heart Failure reduced Ejection Fractions
what is high-output HF
High-output HF – heart failure that occurs in normal or high cardiac output due to metabolic demand and supply mismatch, either due to reduced blood oxygen carrying capacity [anaemia] or increase body metabolic demand [thyrotoxicosis] – also referred to as HFpEF – Heart Failure preserved Ejection Fraction
what is acute HF
acute onset of symptom presentation often, but not always due to an acute event [MI, persistent arrhythmia, Mechanical event (ruptured valve, ventricular aneurysm)]
Often an acute presentation to hospital
May be the first presentation, or may be “acute on chronic”
what is chronic HF
– slow symptoms presentation usually due to slow progressive underlying disease [CAD, HTN]
Typically a GP based diagnosis
what is acute-on-chronic HF
Acute-on-chronic – acute deterioration of a chronic condition, usually following an acute event [anaemia, infections, arrhythmias, MI
how many people does HF affect in the uK
920,000 people - about 1 in 70
what is the average age of diagnosis of HF
77
what are the ischaemic heart disease causes of HF
- myocardial ischaemia
- myocardial infarction
- in IHD infarction causes impaired ventricular function, therefore reduced contractility function and HF. IHD is the most common cause of HF along with HTN
how does hypertension cause HF
increases strain on the heart, since the heart has to pump blood against a high after load, leading to hypertrophy which increase the chances of arrhythmias.
the heart eventually gets too big for the coronary system to perfuse leading to IHD and compromised ventricular function
what valvular diseases lead to HF
Mitral Regurgitation [volume overload]
Aortic stenosis [Pressure overload] – particularly chronic excessive afterload
Tricuspid Regurgitation [volume overload]
VSD/ASD [volume overload] – excessive preload
what pericardial diseases lead to HF
pericarditis
pericardial effusion
what drugs are the most common cause of HF
- chemotherapeutic drugs; beta-blockers are the most common cause, but calcium channel blockers and ant-arrhythmatics are also implicated
- alcohol; acute heart failure, arrhythmias such as AF and dilated cardiomyopathy are more common in alcoholics. Alcohol also increases the risk of infection – infection can worsen chronic heart failure due to toxic effects of infection on heart itself along with vasodilation and tachycardia increase myocardial oxygen demand
- cocaine
how can thyrotoxicosis/myxedema cause heart failure
can cause HF due to direct effets on myocardium, bradycardia and peridcardial disease
how does bradycardia induce HF
Bradycardia – CO = HR X SV. Therefore reduced HR reduces CO
how does tachycardia induce HF
Tachycardia –Reduced ventricular filling duration, increased heart oxygen demand and ventricular dilatation
how does abnormal artial and ventricular contractions induce HF
Abnormal atrial and ventricular contractions – AF removes active ventricular filling leading to reduced EDV and CO. VT also causes reduced EDV due to reduced ventricular filling period.
what is congestive cardiomyopathy
weakening and dilation of ventricular walls leading to overstretching, therefore reduced contractile efficiency. most common cause of HF in the absence if IHD, valvular disease and HTN.
what is hypertrophic cardiomyopathy
thickening of the heart muscle wall leading to reduced compliance and therefore reduced CO. the thickening involves an increase in fibrous tissue of the heart, which increases the chances of arrhythmias such as ventricular fibrillation
which disease has strong familial links
hypertrophic cardiomyopathy
what is the most common cause of death in young adults
ventricular fibrillation
what is restrictive cardiomyopathy
reduced heart compliance without significant increase in muscle wall thickness leading to reduced EDV and CO. this can be caused by infiltrative disease such as sarcoidosis, amyloidosis, haemachromotosis and endocardial fibrosis
what is MAP
CO X TPR
what is CO
SV x HR
what is SV
EDV - ESV
what does MAP stand for
mean arterial pressure
what does HF cause a drop in
heart failure causes a drop in the mean arterial pressure that initially stimulates baroreceptors that feed back into the medullary cardiovascular centre
what does this centre then try to do
tries to increase and maintain the mean arterial pressure
how does the MCVC try to increase and maintain the MAP
by reducing vagal tone and increase sympathetic tone leading to increase heart contractility and rate therefore output
what does the sympathetic system also do
also increases the contraction of arteries (increasing TPR) and veins (increasing venous return) and the release of adrenaline from the adrenal medulla
what other system is stimulated in HF and why
the RAS system is also stimulated due to reduced kidney perfusion caused by reduced MAP and vasoconstriction and direct sympathetic stimulations
what does angiotensin II cause
vasoconstriction, aldosterone release and ADH release causing sodium and water retention by the kidneys
why are these mechanisms beneficial initially
because they increase blood volume, therefore venous return and SV, TPR, and HR - leading to a high maintained CO
how does increased TPR lead to a worse situation
increased after load therefore increasing workload and strain on the heart
tissue undwrperfusion leading to ischaemia
RAS system stimulation
how does increased HR lead to a worse situation
increased world and therefore oxygen demand of the heart
how does fluid retention lead to a worse situation
increase stretching of the heart eventually leading to dilation of ventricles which possess reduced contractility
fluid build up causes fluid transudation into interstitial tissue causing peripheral and pulmonary oedema
what does fluid retention cause
hyponatremia and hypokalaemia
what are the symptoms of HF
- dyspnea
especially on exertion and is due to pulmonary oedema and respiratory muscle weakness - orthopnoea breathlessness on lying flat
- paroxysmal nocturnal dyspnoea
dyspnea that occurs during lying down/sleeping forcing sudden awakening of the patient. this occurs due to blood redistribution during lying down causing increase venous blood in the lungs causing transudation of plasma into the alveolar spaces
how do you ask patient about paroxysmal nocturnal dyspnoea
ask how many pillows they use to sleep at night
why does exercise intolerance occur
due to inability of the heart to raise the CO during exercise - it is already at the limit of its cardiac output.
fatigue and lethargy occur due to compromised CO leading to tissue hypo perfusion. muscle tissues are one of the tissues that undergo atrophy and altered metabolism due to hypo perfusion, causing lethargy and fatigue, as well as exercise intolerance when it involves respiratory muscles
can you have a cough or wheeze with HF
yes, the cough is usually worse at night however, the classical pink frothy sputum is rarely seen
what are the signs of HF
fluid overload
Pulsus alternans
Hypotension
Tachycardia
Cardiac heave
Displaced Apex Beat
gallop (S3)
bilateral crepitations
cardiomegaly on CXR
cachexia
hepatic tenderness
what are the signs of fluid overload
peripheral oedema
ascites
elevated JVP
why does fluid overload occur
predominantly due to right heart failure causing blood congestion in systemic circulation, causing increased venous pressure, therefore fluid transudation into interstitial spaces.
these spaces can be the lungs, ankles, sacrum and liver
where is the apex beat normally felt and where is it felt in cardiomegaly
Normal apex beat is felt around the 5th intercostal space at the mid-clavicular line
In cardiomegaly it may be displaced lateral and / or distally (down and out)
what is the classic criteria used to diagnose HF
Framingham Criteria
what has this criteria been superseded by
the use of echocardiography
what test in the UK is used to stratify patients in primary care
the use of a blood test for BNP (brain (or “B-type”) natriuretic peptide) – particularly N-terminal pro-B-type natriuretic peptide (NT-proBNP) is used to stratify patients in primary care
how can an echocardiogram confirm diagnosis of HF
- showing a reduced ejection fraction
- showing a normal ejection fraction, but demonstrating other signs of heart failure, such as LV hypertrophy, left atrial enlargement or diastolic dysfunction
what does diagnosis of congestive HF using the Framingham criteria require
simultaneous presence of 2 Major or 1 Major and 2 Minor criteria, which provide for a 100% sensitivity (but 78% specificity) value when diagnosing the symptoms and signs of CHF
what is the pneumonic for major
SAW-PANIC
what does SAW stand for
- S3 heart sound present (gallop sound)
- Acute pulmonary oedema (left side of heart is unable to clear fluid from the lungs)
- Weight loss of more than 4.5kg in 5 days when treated (patients lose their retained fluids)
what does PANIC stand for
- paroxysmal nocturnal dyspnoea
- abdominojugular reflux
- neck vein distended (i.e elevated JVP at rest)
- increased cardiac shadow on X ray
- crackles heard in lungs
what is the pneumonic for minor
HEART-VINO
what does HEART stand for
- hepatomegaly
- effusion, pleural
- ankle oedema bilaterally
- exeritonal dyspnoea
- tachycardia
- vital capacity decreased by a third of maximum value
- nocturnal cough
when can minor criteria only be used
the minor criteria can only be used if they are not attributable to other medical conditions
what is the single most useful investigation
echocardiogram
what would an ECG show
Myocardial infarction/ischemia
Bundle Branch Block
Ventricular hypertrophy
Pericardial disease
Arrhythmias
what does a normal ECG indicate
that heart failure is unlikely as the sensitivity is 89%
what do you look for on a CXR
signs of pulmonary congestion, and rule out an alternative cause
what are the signs seen on CXR
Kerley B lines
upper lobe diversion
pleural effusions
fluid in fissures
cardiomegaly
does a normal CXR exclude the possibility of Heart Failure
no
what are BNPs
peptides that cause natriuresis, diuresis and vasodilation. they are the body’s natural defence against hypervolaemia
what are BNP levels been proven to correlate with
correlate with cardiac filling pressures
what are the other blood tests used in suspected HF
FEB – for anaemia
U+E for Hyponatremia [in severe disease due to dilution] and Hypokalemia / Hyperkalemia
LFT’s to detect extent of liver congestion/damage
TFT’s to rule out thyrotoxicosis or myxedema
HbA1c to check for co-existing T2DM
what can you calculate using an ECG
can calculate the ejection fraction, ventricular wall thickness and other cardiac kinetics
an ejection fraction of what strongly indicates heart failure
an ejection fraction of <40% indicates HF
an ejection fraction of 41-49% is not diagnostic, but suggestive of HF
what is the classification used for HF
the New York Heart Association Classification of Heart Failure
what is grade I of the NYHA
no limitation of function
what is grade II of the NYHA
slight limitation, moderate exertion causes symptoms, but no symptoms at rest
what is grade III of NYHA
marked limitation - mild exertion causes symptoms but no symptoms at rest
what is grade IV of the NYHA
severe limitation. any exertion causes symptoms. may also have symptoms at rest but not always the case
what does prognosis depend on
age, sex and severity of the disease
what is the most common arrhythmia that exists with HF
atrial fibrillation
what is common in advanced HF
ventricular tachycardia
what minimises VT and how is this complicated
beta blockers are used to minimise these VT, hence sudden death
what are the two most important dietary restrictions in HF treatment
reduction in salt intake
fluid restriction of usually 1.5L a day
what should sublingual GTN never be used in conjunction with
phosphodiesterase inhibitors
what is an example of a phosphodiesterase inhibitor
(e.g. sildenafil [viagra])
what will most patients with class I and II disease be treated with
an ACE inhibitor and a diuretic
what are examples of ACE inhibitors
ramipril, enalapril, lisinopril, captopril
ACE inhibitors should be used in what patients
should be used in all patients with an LVEF <40%
what are ACE inhibitors
strong vasodilators
reduce afterload and fluid retention therefore slowing down left ventricular disease progression
when are ACE inhibitors not indicated
if previous angioedema or renal artery stenosis
what is the side effect of ACE inhibitors, and in this case what do you use instead
Can cause dry cough, if intolerable use Angiotensin II inhibitors [e.g. candesartan, valsartan, losartan]
what, if used in combination with an ACE can cause hyperkalaemia
a potassium sparing diuretic such as spironolactone
what other vasodilators may be considered if patient is intolerant to ACE-inhibtors and ARB’s
hydralazine and nitrates
what are examples of beta-blockers
atenolol, bisoprolol, carvedilol
what do beta-blockers do
reduce after load and heart rate to prevent arrhythmias
who does beta-blockers be avoided in
patients with fluid overload
what are the contraindications for beta-blockers
Asthma
2nd or 3rd degree heart block
Sick sinus syndrome
Sinus bradycardia (<50bpm)
what are diuretics useful for
helping the fluid overload in the acute setting
what is an example of a loop diuretic
frusemide - commonly used first line
examples of thiazide diuretics
Examples include bendroflumethiazide, hydrochlorothiazide, chlorthalidone or Indapamide
examples of potassium sparing diuretics and what is the big side effect
[Amiloride, spironolactone] [SE: gynecomastia]
when is digoxin considered
in sinus rhythm patients that remain symptomatic even after other pharmacological interventions (third line after ACE-i and diuretics)
in patients with severely impaired left ventricular function
recurrent hospital admissions
treating AF in CHF
who is Amiodarone used in
arrhythmic patients
what is the recommended calcium channel blocker if they are to be used
amlodipine
what are ARNI’s
relatively new drugs in the treatment of heart failure
they are angiotensin receptor neprilysin inhibitors that are generally reserved for use by a specialist in cases with an EF <40% that does not respond to treatment
what is an example of a ARNI
sacubitril
what is the step wise approach in HF management
ACE inhibitors or ARB
ADD diuretic
ADD beta-blocker (once euvolaemia)
ADD aldosterone antagonist (spironolactone or amiloride)
then – increase all above to maximum tolerated doses
CONSIDER ARNI (and cease ACE-i) for patients who remain with an EF <40%
CONSIDER ivabridine
CONSIDER another vasodilator, e.g. isosorbide dinitrate or hydralazine
CONSIDER digoxin
CONSIDER implantable cardiac devices
what drugs improve prognosis
ACEi
Cardioselective β- blockers (β1)
E.g. atenolol, bisoprolol, carvedilol
Angiotensin-II receptor antagonists
Spironolactone
what drugs improve symptoms but not prognosis
Loop diuretics
Digoxin
Vasodilators – e.g. nitrates, hydralazine
what are the surgical interventions used
Revascularization in IHD [CABG or Angioplasty (PTA)]
Valvular replacement
Implanted Automatic cardiodefibrillator or pacemaker
Heart transplant may be considered in the end stages
what type of effect should you aim for in diastolic HF
inotropic effect
what are the common pitfalls in management of HF
Overuse of diuretics
Use of diuretics as a monotherapy – without use of an ACE-inhibitor
Failure to treat underlying causes
Failure to monitor electrolytes and renal function
how does acute HF present
usually clinical presentations are dyspnea, anxiety and tachycardia
how is chronic HF characterised
by a slow progressive onset of symptom development.
patients in a stable chronic HF have a compensated heart, which undergo decompensation by acute events such as myocardial ischaemia/infarction, infections, persistent arrhythmias, anaemia, electrolytes imbalance etc
the combination of what symptoms indicates HF
Heart failure is the most likely cause due to the combination presence of dyspnoea, oedema, elevated JVP, basal crepitations.
what is dyspnoea defined as
a state where the subject is uncomfortably aware of their breathing
what suggests right heart failure and what suggests left
Note: Ankle oedema, hepatomegaly and elevated JVP suggests right heart failure and bibasal crepitations suggest left heart failure.
what investigations should be done to aid in the diagnosis of HF
ABG
ECG
CRP
liver function tests
CXR
FBC
BNP
U+E
What term best describes the condition where breathlessness is made worse by lying flat
Orthopnoea is the sensation of breathlessness that occurs when lying flat causing the person to have to sleep propped up in bed or sitting in a chair. It is often a symptom of left ventricular failure and/or pulmonary oedema but is also experienced by patients with chronic respiratory disorders.
why does orthopnoea occur in HF
because on lying flat, there is increased venous return to the heart from the lower extremities of the body. this results in increased blood flow to the pulmonary circulation.
in normal physiology the left ventricular stroke volume will increase to compensate
however, in HF, the weakened heart isn’t strong enough to pump out. this extra volume, leading to pooling of blood in the pulmonary circulation
what does elevated intravascular pressure In the pulmonary circulation result in
fluid leakage into the alveoli and therefore pulmonary oedema
why is the JVP important and what does it show
is an indirect measurement of the central venous pressure and thus the pressure in the right atrium
look up a waveform of JVP
this is important for the next few questions
what does wave A show
pre-systolic contraction of the right atrium
what does wave C show
as the right ventricle contracts, the tricuspid valve closes and bulges into the right atrium
is also the point where the carotid pulse is palpable
what does wave V show
at the end of ventricular systole, venous return fills the right atrium passively against a closed tricuspid valve
how can the A and V waves be identified
by timing the double waveform with the adjacent carotid pulse
a A wave will occur just before the carotid pulse and the V wave occurs towards the end of the carotid pulse
what are the 5 causes of an elevated JVP
Right ventricular failure
Tricuspid regurgitation or stenosis
Pericardial effusion or constrictive pericarditis
Superior Venous Cava obstruction
Volume overload (there are many reasons for this, congestive heart failure,
renal failure, iatrogenic)
what are the different grades of a murmur
Grade 1: The murmur is heard only on listening intently for some time.
Grade 2: A faint murmur that is heard immediately on auscultation.
Grade 3: A loud murmur with no palpable thrill.
Grade 4: A loud murmur with a palpable thrill.
what kind of murmurs are always abnormal
diastolic murmurs and a loud murmur with a thrill
what is the ABCDE of heart failure findings
A: Alveolar oedema (bat-wing opacity)
B: kerley B lines
C: Cardiomegaly
D: Dilated upper lobe vessels
E: pleural Effusion (often bilateral)
what are Kerley B lines
interstitial oedema
explain the physiological processes of the Frank-Starling curve in a failing heart
The Frank Starling curve represents the relationship between the preload and the stroke volume. In normal physiology, as the venous return (preload) increases , the left ventricle increases the force of contraction, augmenting the stroke volume to compensate for the increased workload. Changes in afterload or inotropy, move the curve up or down. In heart failure, the curve is flattened, so that higher filling pressure and preload is required to increase contractility and stroke volume .
what does increased fluid retention in heart failure help to do
to normalise the stroke volume and maintain cardiac output, but at the cost of raised pulmonary venous and pulmonary capillary wedge patterns
what is meant by the term ejection fraction
The left ventricular ejection fraction is a measurement of how much blood is being pumped out of the heart with each beat. It is expressed as a percentage of the LV end diastolic volume (immediately before systole) that is ejected out of the ventricle and into the aorta.
what is the normal range of ejection fraction
55-70%
list four causes of mitral regurgitation
- Rheumatic heart disease
- Ischaemic heart disease – relating to leaflet tethering or papillary muscle dysfunction
- Valvular vegetations - as in patients with endocarditis
- Functional mitral valve regurgitation due to dilated left atrium or ventricle
what are the most common causes of HF in the UK
coronary heart disease and hypertension
how should atrial fibrillation be managed in a patient with acute heart failure first line
Digoxin 500 micrograms orally, immediately , followed by further 500 micrograms in 6 hours if heart rate remains elevated
Digoxin is weakly positively inotropic and can be given in both heart failure with reduced ejection fraction, and preserved ejection fraction. It does not lower the blood pressure and can be used in patients with acute pulmonary oedema. It does not have a rapid onset of action therefore is not useful in patients in whom rapid rate control is required. Use with caution in patients with renal failure due to risks of accumulation and toxicity.
go through the 1med and look at the tables for treatment plan for different underlying causes
what is the CHA2DS2-VASc score used to do
to predict the risk of stroke in patients with AF
what are the 7 risk factors for a CHADS2VASc score
C – Congestive heart failure
H – Hypertension
A – Age
D – Diabetes
S – Stroke/TIA/VTE
S - Sex
VASC – Vascular history (Previous Myocardial infarction, Peripheral vascular disease)
in AF, where in the heart is there most likely to be areas of decreased flow or stasis of blood
in the atria, particularly in the left atrial appendage which is a pocket like structure where blood clots are most likely to form
why is cardioversion not recommended if the onset of AF is not known or the patient has been in AF longer than 48 hour
because, blood clots form in the LAA.
therefore, if normal sinus rhythm is restored by cardioverting the patient, the clots could be dislodged and there is a risk of causing an embolic stroke.
what is the safer approach for these patients
control the rate with appropriate medication and anti-coagulate for 4 weeks.
what should be performed prior to cardioversion
a transoesophageal echo or gated cardiac CT should be performed to ensure that there is no LAA thrombus prior to cardioversion.
who is Sacubitril Valsartan indicated in
in patients with LVEF <35%, who remain symptomatic with NYHA class II to IV heart failure despite taking a stable dose of ACE inhibitor or ARB.
the urgency of referral and specialist assessment depends on the NT-proBNP result. what are the guidelines according to NICE?
From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks
What is the pneumonic used for first line medical treatment of chronic heart failure
ABAL
what does ABAL stand for
A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
L – Loop diuretics (e.g., furosemide or bumetanide)
what can be used instead of an ACE inhibitor if it is not tolerated
An angiotensin receptor blocker (ARB) (e.g., candesartan)
who should avoid using ACE inhibitors
patients with valvular heart disease until initiated by a specialist
what is the A wave of JVP
pre-systolic contraction of the right atrium
what is the C wave of JVP
as the right ventricle contracts, the tricuspid valve closes and bulges into the right atrium
what is the V wave in JVP
at the end of ventricular systole, venous return fills the right atrium passively against a closed tricuspid valve
how can the A and V waves be identified
by timing the double waveform with the adjacent carotid pulse
when will the A wave occur
just before the carotid pulse and the V wave occurs towards the end of the carotid pulse
what are the ABCDE of heart failure findings
A: Alveolar oedema (bat-wing opacity)
B: kerley B lines
C: Cardiomegaly
D: Dilated upper lobe vessels
E: pleural Effusion (often bilateral)
