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YEAR 3 TCD > WEEK 4 - acute-on-chronic breathlessness > Flashcards

WEEK 4 - acute-on-chronic breathlessness Flashcards

1
Q

what does the P wave represent?

A

atrial contraction

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2
Q

what represents ventricular contraction on an ECG?

A

QRS complex

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3
Q

what happens in the isoelectric line between the end of the T wave and the beginning of the next P wave?

A

passive atrial filling

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4
Q

what closes/opens in the QRS complex?

A
  • tricuspid and mitral valves close
  • aortic and pulmonary valves open
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5
Q

when on an ECG are the tricuspid and mitral valves open and the atria are relaxed?

A

isoelectric line between end of T wave and beginning of next P wave

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6
Q

what does diaphoretic mean?

A

sweating heavily

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7
Q

Ankle oedema, hepatomegaly and elevated JVP suggests _____________ and bibasal crepitations suggest ___________.

A
  • right heart failure
  • left heart failure
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8
Q

Although this is no longer routinely advised in acute heart failure, low dose _____________ can be very effective in acute pulmonary oedema due to its anxiolytic properties, alongside reduction in pre-load. However, it can lead to respiratory depression and therefore must be used with caution in patients who are already hypoxic

A

morphine

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9
Q

unless the patient has cardiac sounding chest pain, a history suspicious for myocarditis or ischaemic ECG changes, a _________ is unlikely to be helpful, and can often lead to more confusion regarding the diagnosis

A

troponin

Aimed to determine if patient has had myocardial injury which this is often linked to acute coronary syndrome, but is frequently elevated for other reasons (eg: infection, tachy or bradycardia, hypertension, decompensated heart failure, pulmonary embolism, myocarditis and therefore if raised, is not specific for acute coronary syndrome).

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10
Q

what is this describing:

This is a cardiac neurohormone biomarker which is secreted from the heart when it is under stress. This is a useful test to perform in a patient with shortness of breath, as a normal result will exclude acute heart failure. It is often used as a prognostic marker in chronic heart failure

A

BNP

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11
Q
A
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12
Q

What term is used to describe the condition where breathlessness is made worse by lying flat?

A

orthopnoea

often a symptom of left ventricular failure and/or pulmonary oedema but is also experienced by patients with chronic respiratory disorders

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13
Q

In heart failure, orthopnoea occurs because on lying flat, there is increased venous return to the heart from the ______ extremities of the body. This results in increased blood flow to the _________ circulation. In normal physiology, the left ventricular stroke volume will increase to compensate. However, in heart failure, the weakened heart isn’t strong enough to pump out this extra volume, leading to pooling of blood in the pulmonary circulation. Elevated intravascular pressure in the pulmonary circulation results in fluid leakage into the alveoli, and therefore _______________.

A
  • lower
  • pulmonary
  • pulmonary oedema
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14
Q

Why is the jugular venous pressure important and what does it show?

A

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

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15
Q

where can you apply pressure to make the JVP visible?

A

liver (this is the hepatojugular reflex)

(pressing on the liver does not alter the carotid pulse)

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16
Q

what are 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 (many reasons for this, congestive heart failure, renal failure, iatrogenic)
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17
Q

how are murmurs graded?

A

1 to 4

grade 1 : 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

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18
Q

the chance that blood flow will be turbulent in a situation is dependent on its what?

A

Reynold’s number

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19
Q

what can murmurs be produced by?

A
  • low viscosity of blood (eg. anaemia)
  • decreased radius of vessel or valve (eg. valvular stenosis, coarction of the aorta, ventricular septal defect)
  • increased velocity of blood through morphologically normal structures (hyper dynamic states eg. sepsis, hyperthyroidism)
  • regurgitation across an incompetent valve (valvular regurgitation)
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20
Q

what things cause systolic murmurs?

A

“flow murmurs”

  • aortic/pulmonic stenosis
  • mitral/tricuspid regurgitation
  • ventricular septal defect
  • aortic outflow tract obstruction
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21
Q

what things cause diastolic murmurs?

A
  • aortic/pulmonic regurgitation
  • mitral/tricuspid stenosis
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22
Q

what causes a continuous murmur?

A

patent ductus arteriosus

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23
Q

what are the 3 murmur shapes? when are they heard?

A
  1. crescendo-decrescendo
  2. decrescedno
  3. uniform (aka plateau or if in systole, holosystolic)

1 + 3 heard in systole
2 heard in diastole

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24
Q

what are 2 endocrine causes of HF?

A

thyrotoxicosis and phaeochromocytoma

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25
Q

describe the New York Heart Association classification of HF

A

1-4

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26
Q

other than breathlessness, what are some signs/symptoms of HF?

A
  • pulmonary oedema/pleural effusion
  • raised JVP
  • pulmonary crackles
  • pitting oedema
  • ascites
  • tachycardia
  • S3 Gallop
  • loss of energy/tiredness
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27
Q

normal levels of ____ rule out heart failure

A

BNP

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28
Q

what 2 groups are patients with heart failure divided into according to their ejection fraction?

A

(normal EF approx 60%)

HF with preserved LV function (EF > 45%)
HF with LV systolic dysfunction (EF < 45%)

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29
Q

what can be seen on ECG in HF?

A
  • presence of AF/other arrhythmias
  • presence of evidence of old AMI; aetiology
  • presence of LBBB; may guide therapy such as specialist device therapy
  • LVH; may indicate hypertension, aortic stenosis, HOCM
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30
Q

treatment of HF is dependent on what?

A

LV function

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31
Q

treatment of HF with preserved LV function

A
  • diuretics
  • treatment of co-morbidities (HTN, DM)
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32
Q

treatment of HF with impaired systolic function

A

EF < 45%

  • diuretics
  • ACEi
  • beta blockers
  • ARBs
  • devices : CRT / ICD
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33
Q

what beta blockers are/are not licensed for treatment of HF?

A
  • bisoprolol
  • carvedilol
  • nebivolol
  • metoprolol (modified release)

ATENOLOL is NOT LICENSED

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34
Q

in chest x rays, what are the ABCDE findings of heart failure?

A

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

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35
Q

the Frank Starling curve represents the relationship between what?

A

the preload and the stroke volume

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36
Q

effect of acidosis on heart contractility?

A

decreases it

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37
Q

ejection fraction in lay terms

A

‘This is the percentage of your heart’s resting blood volume in the main pumping chamber, that it can squeeze out to your body, each time it pumps.’

38
Q

what are 4 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 patient with endocarditis
  4. functional mitral valve regurgitation due to dilated left atrium or ventricle
39
Q

what are the 2 most common causes of HF in the UK?

A

coronary heart disease and HTN

40
Q

_________ 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.

A

digoxin

41
Q

Rate control with __________ are first line for most patients with symptomatic rapidly conducted AF. _________ initiation tends to be avoided in acute heart failure where there is pulmonary oedema until this has been stabilized and resolved.

A

beta blockers

42
Q

never cardioverting someone who has been in AF for more than ________ unless it’s going to be life-saving

A

48 hours

43
Q

what is used to predict the risk of stroke in patients with AF?

A

CHADS2-VASc score

44
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)

45
Q

Explore the statements “because the duration of atrial fibrillation is not clear, a rate control strategy using medical therapy would be preferred at this stage” and “never cardiovert someone who has been in AF for more than 48 hours unless it’s going to be life- saving” in greater detail.

A

In atrial fibrillation, atrial blood flow will be turbulent and uncoordinated, with possible areas of decreased flow or stasis of blood in the atria, particularly in the left atrial appendage (LAA)- which is a pocket-like structure, where blood clots are most likely to form. The risk is significantly greater after a patient has been in atrial fibrillation for longer than 48 hours. Therefore, if normal sinus rhythm was restored by cardioverting the patient, the clots could be dislodged and there is a risk of causing an embolic stroke. If the onset of atrial fibrillation is not known, or the patient has been in atrial fibrillation for longer than 48 hours, cardioversion (a “rhythm control” strategy) is not recommended. In these circumstances a safer approach would be to control the rate with appropriate medication and anti-coagulate the patient for 4 weeks. If appropriate, cardioversion can be attempted at a later date once the patient is fully anti coagulated and an echocardiogram has excluded the presence of thrombi.

Unfortunately, due to positioning of the left atrial appendage, this structure is usually not well seen on standard transthoracic echo. If a rhythm control strategy is the only option, then a transoesophageal echo or gated cardiac CT should be performed to ensure that there is no LAA thrombus prior to cardioversion

46
Q

In patients with heart failure with reduced ejection fraction (LVEF <___), the NICE acute and chronic heart failure guidelines recommend commencing an ACE inhibitor (or angiotensin receptor blocker [ARB] if ACE inhibitor not tolerated) and _________ as first line therapy to improve long term outcomes and reduce mortality. _____________________ are then added in patients who remain symptomatic. Sacubitril Valsartan (Entresto) is only indicated in patients with LVEF <___, who remain symptomatic with NYHA class II to IV heart failure despite taking a stable dose of ACE inhibitor or ARB.

Recently, NICE approved the use of Dapagliflozin (an ________) as an add-on therapy for patients with symptomatic heart failure with reduced ejection fraction despite optimal medical therapy, to reduce the risk of death, hospitalisation and urgent outpatient visit for heart failure.

A
  • 40%
  • beta blockers
  • Mineralocorticoid receptor antagonists
  • 35%
  • SGLT2 inhibitor
47
Q

chronic HF management summary

A
48
Q

are flow murmurs in anaemia systolic or diastolic?

A

systolic

49
Q

what should be a top differential in any patient with new heart failure signs and symptoms in the context of sepsis?

A

infective endocarditis

50
Q

what is infective endocarditis?

A

refers to infection of the endothelium (the inner surface) of the heart. Most commonly, it affects the heart valves. It can be acute, subacute or chronic, depending on how rapidly and acutely the symptoms present and the causative organism.

51
Q

what are risk factors for infective endocarditis?

A
  • Intravenous drug use
  • Structural heart pathology
  • Chronic kidney disease (particularly on dialysis)
  • Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
  • History of infective endocarditis

Structural pathology can increase the risk of endocarditis:

  • Valvular heart disease
  • Congenital heart disease
  • Hypertrophic cardiomyopathy
  • Prosthetic heart valves
  • Implantable cardiac devices (e.g., pacemakers)
52
Q

what is the most common cause of infective endocarditis? other causes?

A

most common = Staphylococcus aureus

Other causes include:

  • Streptococcus (notably the viridans group of streptococci)
  • Enterococcus (e.g., Enterococcus faecalis)
  • Rarer causes include Pseudomonas, HACEK organisms and fungi
53
Q

what are the presenting symptoms for infective endocarditis?

A

non-specific for an infection:

  • fever
  • fatigue
  • night sweats
  • muscle aches
  • anorexia (loss of appetite)
54
Q

what are key examination findings in infective endocarditis?

A
  • new or ‘changing’ heart murmur
  • splinter haemorrhages (thin red-brown lines along the fingernails)
  • petechiae on the trunk, limbs, oral mucosa or conjunctiva
  • Janeway lesions
  • Osler’s nodes
  • Roth spots
  • splenomegaly (in longstanding disease)
  • finger clubbing (in longstanding disease)
55
Q

what are petechiae?

A

small non-blanching red/brown spots

common but nonspecific finding

56
Q

what are Janeway lesions?

A

painless red flat macules on the palms of the hands and soles of the feet

57
Q

what are Osler’s nodes?

A

tender red/purple nodules on the pads of the fingers and toes

58
Q

what are Roth spots?

A

retinal haemorrhages with small, clear centres

rare and observed in only about 5% of patients

59
Q

Modified Duke criteria for diagnosis of infective endocarditis are the clinical criteria and requires what?

A

either of the following:

  • 2 major criteria
  • 1 major and 3 minor criteria
  • 5 minor criteria
60
Q

what is the major criteria for infective endocarditis?

A
61
Q

what is the minor criteria for infective endocarditis?

A
62
Q

what is blood culture-negative infective endocarditis (BCNIE)?

A

refers to Infective Endocarditis (IE) in which no causative micro-organism can be grown. BCNIE can occur in up to 31% of all cases of IE and most commonly arises as a consequence of previous antibiotic administration.

63
Q

what are the main focuses of endocarditis management?

A
  • Early identification
  • Blood cultures from 3 separate sites before antibiotic administration (unless the patient is septic)
  • Transthoracic echo (TTE) is first line imaging modality
  • Transoesophageal echo (TOE) is used where there is high suspicion of IE but TTE is not confirmatory
  • Referral to endocarditis MDT
  • Assessment of embolic complications
  • Timing of surgery (in case of need for valve repair or replacement)
64
Q

IE:

Antibiotics are typically continued for at least:

__ weeks for with native heart valves
__ weeks for patients with prosthetic heart valves

A
  • 4
  • 6
65
Q

a patient with severe aortic stenosis may present in what variety of ways?

A
  • symptomatic fluid overload (SOB/orthopneoa/peripheral oedema)
  • exertional syncope
  • chest pain

additionally, they may be picked up as an asymptomatic cardiac murmur

66
Q

where does an aortic stenosis murmur radiate to?

A

carotids

67
Q

pulse pressure in aortic stenosis?

A

narrow (small difference between systolic and diastolic BP)

68
Q

exertional _____ is common in aortic stenosis

A

syncope

69
Q

pulse pressure in aortic regurgitation?

A

wide

70
Q

pulse in aortic regurgitation?

A

collapsing/water hammer pulse (= a forcefully appearing and rapidly disappearing pulse. typically felt in the radial artery with the patients arm held straight upwards)

71
Q

what connective tissue disorders is aortic regurgitation associated with?

A

Ehlers-Danlos syndrome and Marfan syndrome

72
Q

what are signs of mitral stenosis?

A
  • diastolic murmur
  • tapping apex beat, prominent S1
  • malar flush
  • atrial fibrillation (irregularly irregular pulse)
73
Q

what causes malar flush in mitral stenosis?

A

Malar flush refers to red discolouration of the skin over the upper cheeks and nose. It is due to the back pressure of blood into the pulmonary system, causing a rise in CO2 and vasodilation.

74
Q

what are 2 causes of mitral stenosis?

A
  • rheumatic heart disease
  • infective endocarditis
75
Q

murmur in mitral regurgitation?

A

pansystolic, high pitched “whistling”

radiates to the left axilla

may hear a third heart sound

76
Q

mitral regurgitation: The leaking valve causes a reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart, resulting in ________________

A

congestive cardiac failure (CCF)

(signs of heart failure and pulmonary oedema common)

77
Q

signs of tricuspid regurgitation

A
  • pansystolic murmur
  • there is a split second heart sound due to the pulmonary valve closing earlier than the aortic valve, as the right ventricle empties faster than the left ventricle
  • thrill
  • raised JVP with giant C-V waves (Lancisi’s sign)
  • pulsatile liver
  • peripheral oedema
  • ascites
78
Q

Pulmonary stenosis causes an ________ ________ murmur loudest in the pulmonary area with _______ ___________. There is a ________ split second heart sound, as the left ventricle empties much faster than the right ventricle.

A

Pulmonary stenosis causes an ejection systolic murmur loudest in the pulmonary area with deep inspiration. There is a widely split second heart sound, as the left ventricle empties much faster than the right ventricle.

79
Q

Pulmonary stenosis is usually congenital and may be associated with what?

A
  • Noonan syndrome
  • Tetralogy of Fallot
80
Q

what is Tetralogy of Fallot?

A

= a congenital condition where there are four coexisting pathologies:

  • Ventricular septal defect (VSD)
  • Overriding aorta
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
81
Q

long QT syndrome::

an inherited condition associated with delayed ____________ of the ventricles. It is important to recognise as it may lead to ventricular _________/____________ and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the ______ subunit of the slow delayed rectifier ____________ channel. A normal corrected QT interval is less than 430 ms in ______ and 450 ms in _________.

A
  • repolarisation
  • tachycardia/torsade de pointes
  • alpha
  • potassium
  • males
  • females
82
Q

summarised causes of long QT syndrome

A
83
Q

management of long QT syndrome?

A
  • avoid drugs which prolong the QT interval and other precipitants if appropriate (eg. strenuous exercise)
  • beta blockers
  • ICDs in high risk cases
84
Q

what is the usual mechanism by which drugs prolong the QT interval?

A

blockage of potassium channels

85
Q

what beta blocker may actually exacerbate long QT syndrome?

A

sotalol

86
Q
A

Ivabradine

87
Q
A

synchronised DC cardio version

88
Q

what is amiodarone? MoA?

A

= anti-arrhythmic drug

  • blocks potassium currents that cause repolarisation of the heart muscle during the 3rd phase of the cardiac action potential. As a result amiodarone increases the duration of the action potential as well as the effective refractory period for cardiac cells (myocytes). Therefore, cardiac muscle cell excitability is reduced, preventing and treating abnormal heart rhythms
89
Q

indications for amiodarone

A
  • AF
  • supraventicular tachycardia (SVT)
  • recurrent ventricular fibrillation
  • recurrent hemodynamically unstable ventricular tachycardia (VT)
90
Q

what are indications for DC cardio version?

A
  • treatment of a tachyarrythmia that has been present for LESS than 24 hours with an aim to revert to sinus rhythm
  • treatment of a tachyarrhythmia that has been present for less than 24 hours when pharmacological measures have failed
  • treatment of a tachyarrythmia when the patient shows signs of decompensation —> chest pain, confusion, hypotension or signs of heart failure
91
Q
A

2

92
Q
A

single positive blood culture for Coxiella burnetti

YEAR 3 TCD (15 decks)

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