Week Four - Case One Flashcards

1
Q

what is heart failure typically defined as;

A

the inability of the heart to pump adequate amounts of blood to meet the body’s metabolic demands

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2
Q

what is the classic presentation of heart failure

A

shortness of breath (especially on exertion and on lying flat), fatigue and ankle oedema

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3
Q

what are the classic signs of heart failure

A

Signs may include hepatomegaly, tachycardia, tachypnoea and raised JVP.

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4
Q

what are the two broad groups heart failure can sometimes be divided into

A

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

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5
Q

what is the mainstay drug of treatment that has been shown to improve survival

A

ACE inhibitors

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6
Q

what is systolic HF

A

Systolic HF – inability of the heart to contract efficiently to eject adequate volumes of blood to meet the body metabolic demand [most common].

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7
Q

what is diastolic HF

A

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

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8
Q

what is left HF

A

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%.

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9
Q

what is right HF

A

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

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10
Q

what is congestive HF

A

failure of both the right and left ventricles, which is common

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11
Q

what is low-output HF

A

heart failure resulting from reduced cardiac output [most common type] – also referred to as HFrEF – Heart Failure reduced Ejection Fractions

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12
Q

what is high-output HF

A

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

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13
Q

what is acute HF

A

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”

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14
Q

what is chronic HF

A

– slow symptoms presentation usually due to slow progressive underlying disease [CAD, HTN]

Typically a GP based diagnosis

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15
Q

what is acute-on-chronic HF

A

Acute-on-chronic – acute deterioration of a chronic condition, usually following an acute event [anaemia, infections, arrhythmias, MI

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16
Q

how many people does HF affect in the uK

A

920,000 people - about 1 in 70

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17
Q

what is the average age of diagnosis of HF

A

77

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18
Q

what are the ischaemic heart disease causes of HF

A
  • 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
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19
Q

how does hypertension cause HF

A

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

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20
Q

what valvular diseases lead to HF

A

Mitral Regurgitation [volume overload]

Aortic stenosis [Pressure overload] – particularly chronic excessive afterload

Tricuspid Regurgitation [volume overload]

VSD/ASD [volume overload] – excessive preload

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21
Q

what pericardial diseases lead to HF

A

pericarditis
pericardial effusion

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22
Q

what drugs are the most common cause of HF

A
  • 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
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23
Q

how can thyrotoxicosis/myxedema cause heart failure

A

can cause HF due to direct effets on myocardium, bradycardia and peridcardial disease

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24
Q

how does bradycardia induce HF

A

Bradycardia – CO = HR X SV. Therefore reduced HR reduces CO

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25
Q

how does tachycardia induce HF

A

Tachycardia –Reduced ventricular filling duration, increased heart oxygen demand and ventricular dilatation

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26
Q

how does abnormal artial and ventricular contractions induce HF

A

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.

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27
Q

what is congestive cardiomyopathy

A

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.

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28
Q

what is hypertrophic cardiomyopathy

A

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

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29
Q

which disease has strong familial links

A

hypertrophic cardiomyopathy

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30
Q

what is the most common cause of death in young adults

A

ventricular fibrillation

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31
Q

what is restrictive cardiomyopathy

A

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

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32
Q

what is MAP

A

CO X TPR

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33
Q

what is CO

A

SV x HR

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34
Q

what is SV

A

EDV - ESV

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35
Q

what does MAP stand for

A

mean arterial pressure

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36
Q

what does HF cause a drop in

A

heart failure causes a drop in the mean arterial pressure that initially stimulates baroreceptors that feed back into the medullary cardiovascular centre

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37
Q

what does this centre then try to do

A

tries to increase and maintain the mean arterial pressure

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38
Q

how does the MCVC try to increase and maintain the MAP

A

by reducing vagal tone and increase sympathetic tone leading to increase heart contractility and rate therefore output

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39
Q

what does the sympathetic system also do

A

also increases the contraction of arteries (increasing TPR) and veins (increasing venous return) and the release of adrenaline from the adrenal medulla

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40
Q

what other system is stimulated in HF and why

A

the RAS system is also stimulated due to reduced kidney perfusion caused by reduced MAP and vasoconstriction and direct sympathetic stimulations

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41
Q

what does angiotensin II cause

A

vasoconstriction, aldosterone release and ADH release causing sodium and water retention by the kidneys

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42
Q

why are these mechanisms beneficial initially

A

because they increase blood volume, therefore venous return and SV, TPR, and HR - leading to a high maintained CO

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43
Q

how does increased TPR lead to a worse situation

A

increased after load therefore increasing workload and strain on the heart

tissue undwrperfusion leading to ischaemia

RAS system stimulation

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44
Q

how does increased HR lead to a worse situation

A

increased world and therefore oxygen demand of the heart

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45
Q

how does fluid retention lead to a worse situation

A

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

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46
Q

what does fluid retention cause

A

hyponatremia and hypokalaemia

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47
Q

what are the symptoms of HF

A
  • 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
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48
Q

how do you ask patient about paroxysmal nocturnal dyspnoea

A

ask how many pillows they use to sleep at night

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49
Q

why does exercise intolerance occur

A

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

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50
Q

can you have a cough or wheeze with HF

A

yes, the cough is usually worse at night however, the classical pink frothy sputum is rarely seen

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51
Q

what are the signs of HF

A

fluid overload
Pulsus alternans
Hypotension
Tachycardia
Cardiac heave
Displaced Apex Beat
gallop (S3)
bilateral crepitations
cardiomegaly on CXR
cachexia
hepatic tenderness

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52
Q

what are the signs of fluid overload

A

peripheral oedema
ascites
elevated JVP

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53
Q

why does fluid overload occur

A

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

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54
Q

where is the apex beat normally felt and where is it felt in cardiomegaly

A

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)

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55
Q

what is the classic criteria used to diagnose HF

A

Framingham Criteria

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56
Q

what has this criteria been superseded by

A

the use of echocardiography

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57
Q

what test in the UK is used to stratify patients in primary care

A

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

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58
Q

how can an echocardiogram confirm diagnosis of HF

A
  • 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
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59
Q

what does diagnosis of congestive HF using the Framingham criteria require

A

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

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60
Q

what is the pneumonic for major

A

SAW-PANIC

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61
Q

what does SAW stand for

A
  • 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)
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62
Q

what does PANIC stand for

A
  • paroxysmal nocturnal dyspnoea
  • abdominojugular reflux
  • neck vein distended (i.e elevated JVP at rest)
  • increased cardiac shadow on X ray
  • crackles heard in lungs
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63
Q

what is the pneumonic for minor

A

HEART-VINO

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64
Q

what does HEART stand for

A
  • hepatomegaly
  • effusion, pleural
  • ankle oedema bilaterally
  • exeritonal dyspnoea
  • tachycardia
  • vital capacity decreased by a third of maximum value
  • nocturnal cough
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65
Q

when can minor criteria only be used

A

the minor criteria can only be used if they are not attributable to other medical conditions

66
Q

what is the single most useful investigation

A

echocardiogram

67
Q

what would an ECG show

A

Myocardial infarction/ischemia

Bundle Branch Block

Ventricular hypertrophy

Pericardial disease

Arrhythmias

68
Q

what does a normal ECG indicate

A

that heart failure is unlikely as the sensitivity is 89%

69
Q

what do you look for on a CXR

A

signs of pulmonary congestion, and rule out an alternative cause

70
Q

what are the signs seen on CXR

A

Kerley B lines
upper lobe diversion
pleural effusions
fluid in fissures
cardiomegaly

71
Q

does a normal CXR exclude the possibility of Heart Failure

A

no

72
Q

what are BNPs

A

peptides that cause natriuresis, diuresis and vasodilation. they are the body’s natural defence against hypervolaemia

73
Q

what are BNP levels been proven to correlate with

A

correlate with cardiac filling pressures

74
Q

what are the other blood tests used in suspected HF

A

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

75
Q

what can you calculate using an ECG

A

can calculate the ejection fraction, ventricular wall thickness and other cardiac kinetics

76
Q

an ejection fraction of what strongly indicates heart failure

A

an ejection fraction of <40% indicates HF

an ejection fraction of 41-49% is not diagnostic, but suggestive of HF

77
Q

what is the classification used for HF

A

the New York Heart Association Classification of Heart Failure

78
Q

what is grade I of the NYHA

A

no limitation of function

79
Q

what is grade II of the NYHA

A

slight limitation, moderate exertion causes symptoms, but no symptoms at rest

80
Q

what is grade III of NYHA

A

marked limitation - mild exertion causes symptoms but no symptoms at rest

81
Q

what is grade IV of the NYHA

A

severe limitation. any exertion causes symptoms. may also have symptoms at rest but not always the case

82
Q

what does prognosis depend on

A

age, sex and severity of the disease

83
Q

what is the most common arrhythmia that exists with HF

A

atrial fibrillation

84
Q

what is common in advanced HF

A

ventricular tachycardia

85
Q

what minimises VT and how is this complicated

A

beta blockers are used to minimise these VT, hence sudden death

86
Q

what are the two most important dietary restrictions in HF treatment

A

reduction in salt intake

fluid restriction of usually 1.5L a day

87
Q

what should sublingual GTN never be used in conjunction with

A

phosphodiesterase inhibitors

88
Q

what is an example of a phosphodiesterase inhibitor

A

(e.g. sildenafil [viagra])

89
Q

what will most patients with class I and II disease be treated with

A

an ACE inhibitor and a diuretic

90
Q

what are examples of ACE inhibitors

A

ramipril, enalapril, lisinopril, captopril

91
Q

ACE inhibitors should be used in what patients

A

should be used in all patients with an LVEF <40%

92
Q

what are ACE inhibitors

A

strong vasodilators

reduce afterload and fluid retention therefore slowing down left ventricular disease progression

93
Q

when are ACE inhibitors not indicated

A

if previous angioedema or renal artery stenosis

94
Q

what is the side effect of ACE inhibitors, and in this case what do you use instead

A

Can cause dry cough, if intolerable use Angiotensin II inhibitors [e.g. candesartan, valsartan, losartan]

95
Q

what, if used in combination with an ACE can cause hyperkalaemia

A

a potassium sparing diuretic such as spironolactone

96
Q

what other vasodilators may be considered if patient is intolerant to ACE-inhibtors and ARB’s

A

hydralazine and nitrates

97
Q

what are examples of beta-blockers

A

atenolol, bisoprolol, carvedilol

98
Q

what do beta-blockers do

A

reduce after load and heart rate to prevent arrhythmias

99
Q

who does beta-blockers be avoided in

A

patients with fluid overload

100
Q

what are the contraindications for beta-blockers

A

Asthma
2nd or 3rd degree heart block
Sick sinus syndrome
Sinus bradycardia (<50bpm)

101
Q

what are diuretics useful for

A

helping the fluid overload in the acute setting

102
Q

what is an example of a loop diuretic

A

frusemide - commonly used first line

103
Q

examples of thiazide diuretics

A

Examples include bendroflumethiazide, hydrochlorothiazide, chlorthalidone or Indapamide

104
Q

examples of potassium sparing diuretics and what is the big side effect

A

[Amiloride, spironolactone] [SE: gynecomastia]

105
Q

when is digoxin considered

A

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

106
Q

who is Amiodarone used in

A

arrhythmic patients

107
Q

what is the recommended calcium channel blocker if they are to be used

A

amlodipine

108
Q

what are ARNI’s

A

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

109
Q

what is an example of a ARNI

A

sacubitril

110
Q

what is the step wise approach in HF management

A

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

111
Q

what drugs improve prognosis

A

ACEi
Cardioselective β- blockers (β1)
E.g. atenolol, bisoprolol, carvedilol
Angiotensin-II receptor antagonists
Spironolactone

112
Q

what drugs improve symptoms but not prognosis

A

Loop diuretics
Digoxin
Vasodilators – e.g. nitrates, hydralazine

113
Q

what are the surgical interventions used

A

Revascularization in IHD [CABG or Angioplasty (PTA)]
Valvular replacement
Implanted Automatic cardiodefibrillator or pacemaker
Heart transplant may be considered in the end stages

114
Q

what type of effect should you aim for in diastolic HF

A

inotropic effect

115
Q

what are the common pitfalls in management of HF

A

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

116
Q

how does acute HF present

A

usually clinical presentations are dyspnea, anxiety and tachycardia

117
Q

how is chronic HF characterised

A

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

118
Q

the combination of what symptoms indicates HF

A

Heart failure is the most likely cause due to the combination presence of dyspnoea, oedema, elevated JVP, basal crepitations.

119
Q

what is dyspnoea defined as

A

a state where the subject is uncomfortably aware of their breathing

120
Q

what suggests right heart failure and what suggests left

A

Note: Ankle oedema, hepatomegaly and elevated JVP suggests right heart failure and bibasal crepitations suggest left heart failure.

121
Q

what investigations should be done to aid in the diagnosis of HF

A

ABG
ECG
CRP
liver function tests
CXR
FBC
BNP
U+E

122
Q

What term best describes the condition where breathlessness is made worse by lying flat

A

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.

123
Q

why does orthopnoea occur in HF

A

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

124
Q

what does elevated intravascular pressure In the pulmonary circulation result in

A

fluid leakage into the alveoli and therefore pulmonary oedema

125
Q

why is the JVP important and what does it show

A

is an indirect measurement of the central venous pressure and thus the pressure in the right atrium

126
Q

look up a waveform of JVP

A

this is important for the next few questions

127
Q

what does wave A show

A

pre-systolic contraction of the right atrium

128
Q

what does wave C show

A

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

129
Q

what does wave V show

A

at the end of ventricular systole, venous return fills the right atrium passively against a closed tricuspid valve

130
Q

how can the A and V waves be identified

A

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

131
Q

what are the 5 causes of an elevated JVP

A

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)

132
Q

what are the different grades of a murmur

A

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.

133
Q

what kind of murmurs are always abnormal

A

diastolic murmurs and a loud murmur with a thrill

134
Q

what is the ABCDE of heart failure findings

A

A: Alveolar oedema (bat-wing opacity)
B: kerley B lines
C: Cardiomegaly
D: Dilated upper lobe vessels
E: pleural Effusion (often bilateral)

135
Q

what are Kerley B lines

A

interstitial oedema

136
Q

explain the physiological processes of the Frank-Starling curve in a failing heart

A

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 .

137
Q

what does increased fluid retention in heart failure help to do

A

to normalise the stroke volume and maintain cardiac output, but at the cost of raised pulmonary venous and pulmonary capillary wedge patterns

138
Q

what is meant by the term ejection fraction

A

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.

139
Q

what is the normal range of ejection fraction

A

55-70%

140
Q

list four causes of mitral regurgitation

A
  1. Rheumatic heart disease
  2. Ischaemic heart disease – relating to leaflet tethering or papillary muscle dysfunction
  3. Valvular vegetations - as in patients with endocarditis
  4. Functional mitral valve regurgitation due to dilated left atrium or ventricle
141
Q

what are the most common causes of HF in the UK

A

coronary heart disease and hypertension

142
Q

how should atrial fibrillation be managed in a patient with acute heart failure first line

A

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.

143
Q

go through the 1med and look at the tables for treatment plan for different underlying causes

A
144
Q

what is the CHA2DS2-VASc score used to do

A

to predict the risk of stroke in patients with AF

145
Q

what are the 7 risk factors for a CHADS2VASc score

A

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)

146
Q

in AF, where in the heart is there most likely to be areas of decreased flow or stasis of blood

A

in the atria, particularly in the left atrial appendage which is a pocket like structure where blood clots are most likely to form

147
Q

why is cardioversion not recommended if the onset of AF is not known or the patient has been in AF longer than 48 hour

A

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.

148
Q

what is the safer approach for these patients

A

control the rate with appropriate medication and anti-coagulate for 4 weeks.

149
Q

what should be performed prior to cardioversion

A

a transoesophageal echo or gated cardiac CT should be performed to ensure that there is no LAA thrombus prior to cardioversion.

150
Q

who is Sacubitril Valsartan indicated in

A

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.

151
Q

the urgency of referral and specialist assessment depends on the NT-proBNP result. what are the guidelines according to NICE?

A

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

152
Q

What is the pneumonic used for first line medical treatment of chronic heart failure

A

ABAL

153
Q

what does ABAL stand for

A

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)

154
Q

what can be used instead of an ACE inhibitor if it is not tolerated

A

An angiotensin receptor blocker (ARB) (e.g., candesartan)

155
Q

who should avoid using ACE inhibitors

A

patients with valvular heart disease until initiated by a specialist

156
Q

what is the A wave of JVP

A

pre-systolic contraction of the right atrium

157
Q

what is the C wave of JVP

A

as the right ventricle contracts, the tricuspid valve closes and bulges into the right atrium

158
Q

what is the V wave in JVP

A

at the end of ventricular systole, venous return fills the right atrium passively against a closed tricuspid valve

159
Q

how can the A and V waves be identified

A

by timing the double waveform with the adjacent carotid pulse

160
Q

when will the A wave occur

A

just before the carotid pulse and the V wave occurs towards the end of the carotid pulse

161
Q

what are the ABCDE of heart failure findings

A

A: Alveolar oedema (bat-wing opacity)
B: kerley B lines
C: Cardiomegaly
D: Dilated upper lobe vessels
E: pleural Effusion (often bilateral)

162
Q
A