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semester 1 ( 3rd year) > Case 4: Acute-on-chronic Breathlessness > Flashcards

Case 4: Acute-on-chronic Breathlessness Flashcards

1
Q

A Wave (Cardiac Cycle)

A

end diastole

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2
Q

V Wave (Cardiac Cycle)

A

late systole

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3
Q

V Wave (Cardiac Cycle)

A

early systole

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4
Q

diastole

A

relaxation of heart

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5
Q

systole

A

contraction of heart

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6
Q

p wave

A

atrial depolarisation

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7
Q

QRS complex

A

ventricular depolarisation and atrial repolarisation

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8
Q

t wave

A

ventricular repolarisation

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9
Q

Symptoms of heart failure

A

Tachycardia, decreased exercise tolerance, dyspnea, peripheral and pulmonary edema, cardiomegaly
Heart failure is the most likely cause due to the combination presence of dyspnoea, oedema, elevated JVP, basal crepitations.

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10
Q

Dyspnoea

A

by definition refers to a state where the subject is uncomfortably aware of his/her breathing. It is usually associated with either the increase in the work of breathing - associated with reduced lung compliance (stiff lungs) or increased respiratory rate. It is therefore a non-specific symptom and may occur in diseases pertaining to the cardiovascular, respiratory systems or in the presence of severe anaemia. Review the causes of dyspnoea in these systems.

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11
Q

diaphoretic

A

sweating

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12
Q

Furosemide

A

loop diuretic used in the treatment of congestive heart failure and oedema

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13
Q

Loop diuretics MOA

A

Act on ascending loop of Henle, inhibit sodium-potassium-chloride transporter; decrease renal vascular resistance

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14
Q

investigations for presentation of heart failure

A

BNP
FBC
ECG
LFT
CXR
ABG

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15
Q

action potential in the heart starts in the

A

sinoatrial node

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16
Q

rapid depolarization

A

massive influx of sodium ions

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17
Q

voltage dependant inactivation

A

The fast inactivation of voltage-dependent calcium channels is an important, intrinsic regulatory mechanism that helps to precisely control the amount of calcium entering excitable cells during membrane depolarizations.

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18
Q

His-Purkinje system

A

portion of the conduction system consisting of the bundle of His, bundle branches, and Purkinje fibers

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19
Q

pacemaker

A

A group of cells located in the right atrium that sends out signals that make the heart muscle contract and that regulates heart rate.

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20
Q

myogenic mechanism

A

based on the tendency of smooth muscle to contract when stretched

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21
Q

Abnormal Pacemaker Function

A

bradycardia
tachycardia
ectopic pacemaker

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22
Q

Triggered arrhythmias

A

Early afterdepolarizations (torsades de pointes) occur in phase 2 or 3, before cell has repolarized
Treat by shortening AP, or decrease dose of antiarrhythmic patient is already on

Delayed afterdepolarizations occur in phase 4, after cell has repolarized but before normal successive depolarization would occur
Treat by reducing Ca overload, decreasing digitalis dose

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23
Q

Early After Depolarization Causes

A

Decreased outward K current > prolonged APD

Can be genetic or acquired - problem with drug potential

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24
Q

APD

A

cardiac action potential duration

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25
Q

cellular calcium overload

A

heart failure
spontaneous ca release from SR
activates depolarising membrane currents

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26
Q

Reentrant arrhythmias

A

Arrhythmias of abnormal conduction; they involve the repetitive movement of an impulse through
tissue previously excited by the same impulse

might be due to an area of dead heart

  • unidirectional block
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27
Q

unidirectional block

A

a type of partial conduction block in which impulses travel in one direction but not in the opposite one

might be a mismatched refractory period

post infarction

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28
Q

excitation-contraction coupling

A

events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract

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29
Q

Lusitropic

A

affects cardiac relaxation

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30
Q

Lusitropic effect

A

more rapid relaxation (after contraction)
caused by catecholamines

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31
Q

catecholamines effect on heart

A

^ L type ca current - more trigger and loading
^ SERCA via phosphorylation of phospholamban

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32
Q

SERCA

A

Sarcoplasmic Endoplasmic Reticulum Calcium ATPase

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33
Q

L-type calcium channels

A

Slow, long acting channels that open during cardiac depolarization

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34
Q

T-type calcium channels

A

Fast, transient channels that are open during phase 0 and help create the depolarization upstroke of the myocyte action potential

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35
Q

Phospholamban

A

regulatory protein in contractile myocardium that alters Ca2+ ATPase activity in the sarcoplasmic reticulum

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36
Q

orthopnea

A

ability to breathe only in an upright position

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.

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37
Q

Orthopnea in heart failure

A

In heart failure, orthopnoea occurs 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 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 pulmonary oedema.

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38
Q

JVP (jugular venous pressure)

A

reflects the volume & pressure of venous blood in the right side of the heart
Kussmaul sign= JVP increases during inhalation

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39
Q

How do you differentiate between the jugular vein and the carotid pulse in the neck?

A

The jugular vein sits in between the two heads of the sternocleidomastoid muscle and the earlobe. It is not visible unless it is elevated or unless pressure is placed on the liver (called the hepatojugular reflex). The carotid artery lies just medial to the internal jugular vein and is palpated at the point of the C wave, (see below) which occurs between the A and V waves of the JVP. The carotid pulsation does not alter when pressing on the liver. Unlike the carotid pulse which has one pulsatile wave, the JVP has three waves

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40
Q

hepatojugular reflex

A

Sustained elevated jugular venous pressure that occurs during abdominal compression; indicates that hepatic venous congestion is present

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41
Q

waveforms of jvp

A

A - Pre-systolic: contraction of the right atrium
C - As the right ventricle contracts, the tricuspid valve closes and bulges into the right atrium (also the point at which the carotid pulse is palpable)
V - At the end of ventricular systole, venous return fills the right atrium passively against a closed tricuspid valve
The A and V waves can be identified by timing the double waveform with the adjacent carotid pulse. The A wave will occur just before the carotid pulse and the V wave occurs towards the end of the carotid pulse. check google for image

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42
Q

waveforms of jvp - descents

A

X - pressure drops as the right atrium relaxes
Y- the tricuspid valve opens and blood flows passively into the right ventricle (google image)

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43
Q

from where do you measure JVP

A

The JVP is measured with the patient sitting at a 45 degree angle and height is measured from the sternal notch. The normal JVP is 4cm in height from the sternal notch.

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44
Q

Causes of 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)

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45
Q

Grades of murmurs

A

A Grade 4 murmur is a loud murmur with a palpable thrill. Based on the intensity of a murmur it may be classified into the four following grades:
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.

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46
Q

murmurs

A

sounds created by abnormal, turbulent flow of blood in the heart

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47
Q

bruits

A

unusual sound, usually abnormal, heard in auscultation

is a murmu from outside the heart eg AAA

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48
Q

Reynolds number

A

The ratio of inertial forces to viscous forces.

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49
Q

Key murmur tips

A

A soft ejection murmur may not signify organic pathology
A new murmur is always significant
A loud murmur associated with a thrill is always abnormal
Diastolic murmurs are always abnormal

50
Q

decreased blood viscosity

A

anaemia

51
Q

characteristic of murmurs

A

Timing
Location and Radiation
Shape
Intensity
Pitch
Quality
Response to manouveres

52
Q

most common murmurs

A

systolic

53
Q

systolic murmur cause

A

flow murmurs
aortic or pulmonic stenosis
Mitral tricuspid regurgitation
ventricular septal defect
aortic outflow tract obstruction

54
Q

Diastolic murmurs

A

aortic or pulmonic regurgitation
Mitral tricuspid stenosis

55
Q

continuous murmurs

A

patent ductus arteriosis

56
Q

Intensity of murmurs

A

Grade 1: Very faint, heard only after the listener has “tuned in”; may not be heard in all positions
Grade 2: Quiet, but heard immediately on placing the stethoscope on the chest
Grade 3: Moderately loud
Grade 4: Loud
Grade 5: Very loud, may be heard with a stethoscope partly off the chest
Grade 6: May be heard with the stethoscope entirely off the chest

57
Q

shapes of murmurs

A

crescendo, decrescendo, crescendo-decrescendo, plateau

58
Q

Heart failure

A

a chronic condition in which the heart is unable to pump out all of the blood that it receives

59
Q

Causes of heart failure

A

Ischamia
Hypertension
Diabetes
Vavular
Tachycardia
Toxins
Infective
Endocrine (thyrotoxicodod)
Dilated cardiomyopathy
Genetic (HCOM)

60
Q

HCOM (hypertrophic cardiomyopathy)

A

AD
mutations in beta myosin heavy chain protein
loud S1
Systolic murmur - similar in appearance to aortic stenosis - radiates to suprasternal notch
haphazard arrangement of myocytes
decreased LV volume
LV outflow obstruction thereby increasing afterload

61
Q

symptoms of heart failure

A

shortness of breath, fatigue, exercise intolerance, edema, raised JVP, polmonary edema, S3 gallop, tachy, ascites

62
Q

NYHA classification

A

Functional classification of the severity of heart failure.

class 1: no limitation of activity.
class 2: slight limitation of activity.
class 3: moderate, marked limitations.
class 4: severe, symptoms at rest.

63
Q

diagnosis of heart failure

A

Symptoms + Signs + Cardiomegaly, S3 gallop, echo abnormality

64
Q

HF is a syndrome not a

A

diagnosis

65
Q

syndrome

A

a group of symptoms

66
Q

HF investigations

A

FBC (anemia, B12)
U+E (30% of CCF patients also have renal failure)
TFT (hypo or hyper thyroidism)
Glucose (Diabetes)
BNP (stretching of heart muscle cells)
CXR

67
Q

BNP

A

brain natriuretic peptide. 32 amino acids. quantitiy is predictive of outcome

68
Q

what is BNP produced by

A

produced by ventricular muscle cells

69
Q

CXR heart failure

A

cardiomegaly, bilateral or right sided pulmonary effusions, perivascular or interstitial edema (kerley b lines), venous dilation and cephalization and alveolar fluid, calcification

70
Q

echocardiogram

A

ultrasound of heart

71
Q

ejection fraction

A

measurement of the volume percentage of left ventricular contents ejected with each contraction

72
Q

normal ejection fraction

A

55-70%

73
Q

HF with preserved LV function

A

EF >45%

74
Q

HF with LV systolic dysfunction

A

EF <45%

75
Q

DCM

A

dilated cardiomyopathy

76
Q

Left Bundle Branch Block

A

“LBBB” a block in the electrical conduction through the left bundle; evidenced by a wide QRS in lead 1 and V6

77
Q

Treatment of Heart Failure

A

-treat underlying causes such as high BP, valve defects, etc
-diet therapy with salt restriction
-carefully planned exercise
appropriate medications

78
Q

decompensated heart failure

A

failing myocardium is no longer able to propel sufficient blood to meet the needs of the body, even at rest

79
Q

Treatment for HF patients with imparied systolic function

A

Diuretics, ACE inhibitors, B Blockers
Adolsterone Receptor antagonists

80
Q

Treatment of HF for patients with preserved LV function

A

Diuretics
Treatment of co morbs

81
Q

ACE inhibitors moa

A

Inhibit ACE–> decrease angiotensin II–> decrease GFR (prevent constriction of efferent arteriole)
Increasing levels of renin (loss of feedback)
ACE inhibition–> prevents inactivation of bradykinin (vasodilator)

82
Q

ACe inhibitors Heart failure

A

-lower arteriole tone and improve regional blood flow.
-increase cardiac output by decreasing afterload.
-reduce pulmonary congestion and peripheral edema.
-suppress aldosterone and angiotensin II effects on cardiac remodeling and fribrosis
- decrease water and salt retention
- inhibit vasoconstriction therefore lower arterial constriction and increase venous capacity

83
Q

ACE inhibitors for heart failure

A

Captopril
Cilazapril
Enalapril

84
Q

beta blockers for heart failure

A

bisoprolol
metoprolol - MR
carvedilol

decreased HF hospitalisation

85
Q

Aldosterone receptor antagonists

A

Block stimulation of mineralocorticoid receptors by aldosterone, thus reducing high blood pressure by preventing sodium reabsorption

Antifibrotic efects in HF

86
Q

Aldosterone receptor antagonists examples

A

Spironolactone
Eplerenone

87
Q

mechanical desynchrony

A

15% of HF patients

88
Q

CRT device

A

improve synchonicity between LV and RV
Improve cardiac function
Reduce mortality and morbitiy in HF patients

89
Q

ICD

A

implantable cardioverter-defibrillator

90
Q

ICD for HF

A

sudden cardiac death counts for 50% HF mortality
SCD most likely the result of arrythmia
previously managed with anti arrythmic drugs
used in patients with EF <35%
ICDs detect and treat ventricular arrythmia

91
Q

followin admission with HF, mortality after 1 year

A

20-30%

92
Q

CXR ABCDE heart failure

A

Remember: The ABCDE of heart failure findings are:
A: Alveolar oedema (bat-wing opacity)
B: kerley B lines
C: Cardiomegaly
D: Dilated upper lobe vessels
E: pleural Effusion (often bilateral)

93
Q

Increased fluid retention in heart failure helps to normalise the stroke volume and maintain cardiac output, but at the cost of

A

raised pulmonary venous and pulmonary capillary wedge pressures.

94
Q

The curve can be shifted left or right by various factors that can increase or decrease myocardial contractility.

A

Decreased contractility can result from acidosis and some negatively inotropic drugs such as some anaesthetic agents. Catecholamines (such as adrenaline, noradrenaline and dopamine) can increase the strength of contractility.

95
Q

As the heart fails, the end diastolic volume will increase

A

Initially the heart will try to respond by increasing the force of contraction. However a greater end diastolic volume is required to give the same force of contraction. The graph is shifted to the right. Eventually a critical point will be reached where the heart can no longer respond to increasing end diastolic volumes and it will decompensate- stroke volume will decrease with further increases in end diastolic volume. The increased venous pressure causes fluid to leak out of the blood into the alveolar interstitial fluid resulting in pulmonary oedema.

96
Q

Severe mitral regurgitation

A

This occurs due to papillary muscle rupture following a myocardial infarction. It’ll show with a new murmur and hemodynamic compromise.

97
Q

heart failure as a clinical syndrome

A

The term heart failure is an umbrella term which encompasses, the above signs and symptoms relating to:
a structural cardiac abnormality and/or
a functional cardiac abnormality,

98
Q

CHADS2VASc

A

Helps to determine risk of annual stroke in untreated pts with AF

99
Q

Steve is then seen by the heart failure consultant Dr Sharma, 6 weeks later. Despite his initial improvement, he continues to feel breathless on moderate exertion and his ankle oedema fails to resolve completely, which causes Steve some concern as he still isn’t able to cycle to work again yet. Dr Sharma notices that his blood pressure remains well controlled (125/80mmHg) on taking 10mg Ramipril, 10 mg Bisoprolol and 25mg Eplerenone. Dr Sharma decides to change his Ramipril to Sacubitril Valsartan (Entresto) and commences Dapagliflozin, an SGLT2 inhibitor

What is the rationale for changing Ramipril to Entresto and adding an SGLT2 inhibitor? Look at the NICE (2019) guidelines on managing chronic heart failure to help with this. The NICE interactive flow charts are a good way of looking at the guidelines.

A

In patients with heart failure with reduced ejection fraction (LVEF <40%), the NICE acute and chronic heart failure guidelines recommend commencing an ACE inhibitor (or angiotensin receptor blocker [ARB] if ACE inhibitor not tolerated) and beta-blockers as first line therapy to improve long term outcomes and reduce mortality. Mineralocorticoid receptor antagonists are then added in patients who remain symptomatic. Sacubitril Valsartan is only indicated 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.
Recently, NICE approved the use of Dapagliflozin (an SGLT2 inhibitor) 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.

100
Q

euvolaemia

A

=Maintain fluids

101
Q

Neuro questions following collapse

A

Were there any odd smells, tastes, auditory changes before the collapse?
Was there a severe headache before the collapse?
Was the collapse witnessed? If so, was there seizures? Was there tongue biting or incontinence?
Any weakness of limbs after the collapse?

102
Q

Amlodopine

A

Calcium channel blocker used for hypertension and angina

103
Q

amlodipine moa

A

Amlodipine is a long-acting dihydropyridine calcium-channel-blocking drug with potent arterial and coronary vasodilating properties.

104
Q

Gliclazide moa

A

Sulphonylurea which stimulates secretion of insulin from B cells. Works by mimicing indirect action of glucose on ATP-sensitive K+ channels which subsequently cause depolarisation allowing Ca2+ to enter and evoke insulin release.

105
Q

mitral regurgitation

A

mitral insufficiency; incompetent mitral valve allows regurgitation of blood back into left atrium during systole

106
Q

low albumin

A

Assess pt for edema
Low serum albumin means that they are not holding volume in their vascular space and its escaping to the interstitial tissues=edema

107
Q

infective endocarditis

A

inflammation of endothelium that lines heart and cardiac valves. most commonly damages mitral valve, then aortic and tricuspid valves. commonly caused by bacteria that are normally present in the body. can also occur after an invasive medical or dental procedure. symptoms: valvular dysfunction, may affect organ systems, chest pain, CHF, clubbing, meningitis, low back pain, arthralgia, arthritis

108
Q

risk factors for IE

A

Congenital heart defects, hx of endocarditis, damaged heart valves, rheumatic fever or infection, hx of IV illegal drug use TX amoxicillin or macrolide, dental work recently

109
Q

clinical signs of IE

A

Petechiae - Common but nonspecific finding (remember to look at the mucosa)
Subungual (splinter) haemorrhages - Dark red linear lesions in the nail beds
Osler nodes - Tender subcutaneous nodules usually found on the distal pads of the digits
Janeway lesions - Non-tender maculae on the palms and soles
Roth spots - Retinal haemorrhages with small, clear centres; rare and observed in only 5% of patients.

110
Q

roth spots

A

Round white spots on retina surrounded by hemorrhage

111
Q

janeaway lesions

A

Non-tender maculae on the palms and soles

112
Q

Osler nodes (infective endocarditis, immune complex deposition)

A

Tender subcutaneous nodules usually found on the distal pads of the digits

113
Q

Subungual haemorrhages

A

Dark red linear lesions in the nail beds

114
Q

petechiae

A

small, pinpoint hemorrhages

115
Q

Duke criteria

A

for endocarditis (need 2 major, 1 major + 3 minor, or 5 minor)
MAJOR:
1. Blood culture positive for IE:
A. Typical microorganisms consistent with IE from 2 separate blood cultures:
Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus;or
Community-acquired enterococci, in the absence of a primary focus; or
B. Microorganisms consistent with IE from persistently positive blood cultures, defined as follows:
At least 2 positive cultures of blood samples drawn >12h apart; or
All of 3 or a majority of >4 separate cultures of blood (with first and last sample drawn at least 1h apart); or
C. Single positive blood culture for Coxiella burnetii or phase I IgG antibody titre >1:800
2. Evidence of endocardial involvement
A. Echocardiogram positive for IE
Vegetation
Abscess, pseudoaneurysm, intracardiac fistula
Valvular perforation or aneurysm
New partial dehiscence of prosthetic valve
B. Abnormal activity around the site of prosthetic valve implantation detected by 18F-FDG PET/CT (only if the prosthesis was implanted for >3 months) or radiolabelled leukocytes SPECT/CT
C. Definite paravalvular lesions by cardiac CT

116
Q

Minor criteria for endocarditis

A
  1. Predisposition: predisposing heart condition, injection drug use2. Fever: temperature >38°C3. Vascular phenomena (including those detected only by imaging): major arterial emboli, septic pulmonary infarcts, infectious (mycotic) aneurysm, intracranial haemorrhage, conjunctival haemorrhages, and Janeway’s lesions4. Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor5. Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE
117
Q

duke criteria requirements

A

2 major criteria
1 major and 3 minor criteria
5 minor criteria.

118
Q

Blood culture-negative Infective Endocarditis

A

Blood culture-negative Infective Endocarditis (BCNIE) 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.

119
Q

Symptomatic aortic stenosis is the most common indication for cardiac valve surgery. A patient with severe aortic stenosis may present in a variety of ways

A

Symptomatic fluid overload (SOB/orthopnoea/peripheral oedema)
Exertional syncope
Chest pain

120
Q

aortic stenosis

A

narrowing of the aorta

121
Q

treatment for aortic valve stenosis

A

Treatment involves diuretics to improve symptoms and careful timing of either surgical aortic valve replacement or transcatheter aortic valve insertion (TAVI) depending in individual patient characteristics.

122
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semester 1 ( 3rd year) (12 decks)

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