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YEAR 3 - SEMESTER 1 > CASE 1 - HEART FAILURE > Flashcards

CASE 1 - HEART FAILURE Flashcards

1
Q

List 5 DDx for a patient presenting with pink, frothy sputum

A
  • PE
  • CHF
  • Lung cancer
  • Tuberculosis
  • Bronchiectasis
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2
Q

List 3 DDx for acute dyspnoea presenting at 2am

A
  • PND
  • Orthopnoea
  • Sleep apnoea
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3
Q

TRUE OR FALSE? Most episodes of haemoptysis are non-life threatening

A

TRUE

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4
Q

List 2 chronic causes of haemoptysis

A
  • Lung cancer
  • Chronic bronchiectasis

These are the 2 most common causes of haemoptysis

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5
Q

TRUE OR FALSE? Haemoptysis is rare during the chronic phase of bronchitis.

A

TRUE

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6
Q

‘Streaky’ phlegm with minor amounts of blood mixed in suggests which condition?

A

Chronic bronchiectasis

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7
Q

Name 2 non-cardiac and non-pulmonary causes of dyspnoea

A
  • Panic attack and/or anxiety disorder

- Anaphylaxis

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8
Q

insert clinical reasoning question

A

.

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9
Q

Cardiac elevations in potassium become problematic beyond…?

A

5mmol/L

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10
Q

List the ECG / EKG changes in hyperkalemia (in ascending order)

A
  1. Tented T waves
  2. Loss of P waves
  3. Wide QRS
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11
Q

The SA Node fires off impulses at ___bpm?

A

60-100bpm

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12
Q

The AV Node fires off impulses at___bpm?

A

40-55bpm

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13
Q

The Purkinje fibres fire off impulses at ___bpm?

A

25-40bpm

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14
Q

The heart will beat at the rate of which pacemaker?

A

The heart will beat at the rate of the fastest pacemaker

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15
Q

Name the 2 causes of tachyarrhythmias

A
  1. Increased automaticity

2. Re-entry circuits

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16
Q

Give 2 examples of things that may cause the aforementioned tachyarrhythmias

A
  1. INCREASED AUTOMATICITY: myocardial ischaemia, hypokalemia, digoxin - changes the resting membrane potential of the cell and brings it closer to the threshold for depolarisation)
  2. RE-ENTRY CIRCUITS: e.g. AVNR, AFib, VT, VF
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17
Q

How does a re-entry circuit manifest?

A

Continuous repetitive propagation of an excitatory wave traveling in a circular path, returning to its site of origin to reactivate that site.

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18
Q

List 3 predisposing factors for tachyarrhythmias

A 
IHD (e.g. acute MI)
Hypertension (dilated atria)
Cardiomyopathy
Drugs (e.g. digoxin)
Metabolic
Genetic
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19
Q

Why is CO usually maintained in arrhythmias that start above the AV node?

A

For arrhythmias that start above the AV node, the ventricles are limited by the AV node because it will stop the conduction of rapid pulses above the AV node.

Therefore, CO is maintained and ventricular rate is usually <150bpm

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20
Q

Why is the origin of the tachyarrhythmia important?

A

It affects ECG appearance and treatment

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21
Q

What does the QRS complex look like when tachyarrhythmias occur ABOVE the AV Node?

A

Usually normal: ventricles are activated via the usual pathway

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22
Q

Describe the appearance of atrial flutter on an ECG

A

Multiple P waves before each QRS (saw-tooth pattern)

Narrow QRS

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23
Q

Describe the clinical

A

.

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24
Q

Describe the ECG appearance of atrial fibrillation.

A

P waves usually absent
Irregular rhythm
Narrow QRS

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25
Q

Why are ventricular arrhythmias more lethal?

A

There is no delay at the AV node, so the rate isn’t being controlled by anything

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26
Q

How are supraventricular tachyarrhythmias treated?

A
  1. Slow AV Node conduction / RATE CONTROL –> reduces ventricular rate, e.g. beta-blockers
  2. Revert to sinus rhythm / RHYTHM CONTROL: (if possible) by suppressing abnormal automaticity or altering conduction, e.g. amiodarone
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27
Q

Describe the appearance of ventricular TACHYCARDIA on an ECG

A

P Wave Hidden
Broad QRS

Looks like villi or something

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28
Q

Describe the appearance of ventricular FIBRILLATION on an ECG

A

P waves absent
Broad, disorganised QRS

Looks like lazy grass drawing

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29
Q

5 anti-arrhythmic drugs

A

CLASS I: Fast (Na+ channel blockers), e.g. lignocaine, phenytoin

CLASS II: beta-blockers, e.g. metoprolol, bisoprolol

CLASS III: (K+ channel blockers), e.g. Sotalol, amiodarone

CLASS IV: Slow (Ca++ channel blockers), e.g. verapamil

CLASS V: variable mechanisms (e.g. digoxin)

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30
Q

How are supraventricular tachyarrhythmias treated?

A
  1. Slow AV Node conduction –> reduces the ventricular rate, e.g. beta-blocker
  2. Revert to sinus rhythm (if possible) by suppressing abnormal automaticity or altering conduction, e.g. amiodarone

RATE & RHYTHM CONTROL

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31
Q

Name 2 drugs for ventricular arrhythmias

A
  1. Amiodarone (the best one for ventricular arrhythmias - but lots of adverse events if used long-term lol, e.g. ILD)
  2. Sotalol
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32
Q

For fast VT or VF, what is the immediate treatment?

A

Defibrillation

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33
Q

For fast VT or VF, what is the treatment once sinus rhythm has been restored?

A

Prevent recurrence: amiodarone, sotalol

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34
Q

something about ventricular ectopics???

A

.

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35
Q

something about ventricular ectopics???

A

.

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36
Q

What is the difference between a cardiac pacemaker and an implanted defibrillator?

A

The pacemaker provides frequent/ongoing and more subtle regulation of the heartbeat whereas a defibrillator provides a shock when the heart’s function is dangerously abnormal.

37
Q

List 3 symptoms of MI which are more common in women than men.

A 
Choking feeling
Diaphoresis
NV
Dizziness 
(much higher sympathetic drive)
38
Q

Name 4 factors that can exacerbate heart failure

A
  • Nonadherence to drug therapy for HF
  • Infection
  • Dietary lapse (e.g. excess fluid, salt, alcohol)
  • Tachyarrhythmias
  • Bradyarrhythmias
  • Anaemia

https://tgldcdp-tg-org-au.proxy.library.adelaide.edu.au/viewTopic?topicfile=heart-failure&guidelineName=Cardiovascular&topicNavigation=navigateTopic#toc_d1e161

39
Q

Briefly outline the pathophysiology behind PND

3 key points: FAB

A
  1. FLUID Peripheral fluid redistribution and increased venous return –> fluid settles in the lungs when the patient is recumbent –> causes SOB during the night
  2. ADRENALINE decreases at night, so the myocardium becomes more relaxed, decreasing cardiac function
  3. BRAIN: Respiratory centre becomes less responsive during the night, so the RR and effort does not change, despite there being decreased SpO2.
40
Q

List 4 causes of heart failure

A
  • Diabetes
  • Hypertension
  • Coronary heart disease
  • Valvular heart disease
  • Arrhythmias

*note: patients typically have multiple risk factors that lead to CHF

41
Q

Why can heart failure cause hyponatremia?

A

Due to fluid overload

42
Q

List 3 symptoms specific to LEFT-sided heart failure

A
  • Pulmonary oedema
  • Dyspnoea
  • PND
43
Q

List 3 symptoms specific to RIGHT-sided heart failure

A
  • Peripheral oedema
  • Hepatosplenomegaly
  • Signs of hepatic congestion (abdo pain, jaundice)
  • Elevated JVP
44
Q

How does biventricular heart failure manifest? (FNT)

A

Symptoms of RHF and LHF, in addition to:

  • Fatigue
  • Nocturia
  • Tachycardia
45
Q

What is Pulsus Alternans, and what is it caused by?

A

Alternating strong and weak pulses (at a regular rate) caused by variations in CO

46
Q

What conditions are Pulsus Alternans a sign of?

A
  • Cardiac tamponade

- Left ventricular failure

47
Q

When does the S3 heart sound occur?

A

During early diastole, when the ventricles are filling rapidly

48
Q

What is the pathophysiology behind the S3 heart sound?

A

Pathological S3 occurs due to rapid ventricular filling and tensing of the chordae tendinae. In older patients or patients with heart failure, the elastic limit of the chordae tendinae is reached much faster.

49
Q

When in S3 not pathological?

A

In young, healthy patients: the heart works so well that the ventricles fill rapidly. The heart is capable of taking volume and expanding.

50
Q

What is the immediate management for acute decompensated heart failure? (LMNOP)

A 
LOOP diuretics
MORPHINE (controversial)
NITRATES (e.g. GTN - for venodilation) 
OXYGEN 
POSITIONING & PRESSURE (CPAP)
51
Q

Heart failure with reduced left ventricular ejection fraction (HFrRF) is defined as having a left ventricular ejection fraction (LVEF) of…?

A

< or equal to 50%

52
Q

What is the purpose of a transthoracic echocardiogram?

A
  • Assesses LVEF
  • Assesses LV diastolic function (estimated filling pressure)
  • Assesses valvular function
53
Q

Name 4 drugs that are commonly used in HF

A
  • ACEi
  • Beta blocker
  • Angiotensin receptor antagonist/blocker (ARBs)
  • Loop diuretic
54
Q

What is fluid retention in HF initiated by?

A

Drop in CO

55
Q

S3 is associated with _______ heart failure.

S4 is associated with _______ heart failure.

A

S3 is associated with SYSTOLIC heart failure. Ventricular dilation.

S4 is associated with DIASTOLIC heart failure. Stiffened ventricle.

56
Q

How can GGT be used to monitor alcohol consumption?

A

Isolated GGT elevation can be a crude indicator of high alcohol consumption. You can use it as a marker in alcoholics to see if they are cutting down.

57
Q

Why does excessive alcohol consumption cause elevated GGT?

A

Induces the enzymes

58
Q

Use the ABCDE pneumonic to describe CXR findings in heart failure

A 
A - alveolar oedema (batwing opacities)
B - kerly B lines
C - cardiomegaly
D - dilated upper lobe vessels
E - pleural Effusions

LOOK @ CXR EXAMPLES

https: //www.youtube.com/watch?v=TvcU-WPrRkI
https: //www.radiologymasterclass.co.uk/tutorials/chest/chest_pathology/chest_pathology_page8

59
Q

What are ‘batwing opacities’ indicative of? Describe their appearance.

A

Alveolar oedema

Bilateral peri-hilar shadowing.

60
Q

What are Kerly B lines indicative of?

A

Fluid infiltrating the lung interstitium (between alveolus and capillary)

61
Q

Contrast the pathophysiology between S3 and S4 heart sounds.

A

S3 heart sounds occur in SYSTOLIC heart failure when there is a very COMPLIANT ventricle. It occurs during the rapid filling phase of early diastole due to the tensing of chordae tendinae when all that volume fills up the LV.

S4 heart sounds occur in DIASTOLIC heart failure when there is a thick, STIFFENED ventricle. You hear the left atrium contracting into a stiffened ventricle at the END of diastole.

62
Q

S3 is a ________ overload condition.

S4 is a ________ overload condition.

A

S3 is a VOLUME overload condition.

S4 is a PRESSURE overload condition.

63
Q

Explain the pathophysiology behind inspiratory crackles/rales.

A

Rapid entry of air into the distal airways (alveoli) causes airways to open abruptly.

64
Q

How does the pathophysiology behind rhonchi/wheeze differ from crackles/rales?

A

Crackles occur in the alveoli.

Rhonchi/wheeze occurs in the bronchi.

65
Q

List 3 non-pharmacological aspects of CHF management

A
  • Low-sodium diet
  • Fluid monitoring (weight changes, fluid restriction)
  • Exercise, when tolerated
  • Smoking and alcohol cessation
  • Immunisation
66
Q

What needs to be monitored in patients taking spironolactone and an ACE inhibitor?

A

Hyperkalemia

67
Q

What is PRELOAD?

A

Stretching of cardiac myocytes prior to contraction - relates to ventricular filling

68
Q

What is AFTERLOAD?

A

The pressure that the heart must work against to eject blood

69
Q

Why does a greater end-diastolic volume increase the contractile strength of ventricles and stroke volume?

A

Greater stretching of the myocardium increases sarcomere length and sensitivity to calcium.

Results in stronger contraction

70
Q

What is the ‘axis of evil’ and how is this counteracted in treatment/management? (RAN)

A

AXIS OF EVIL FOR CHF (RAN)

  • RAAS
  • Noradrenaline/SNS
  • Aldosterone

The axis is responsible for causing high blood pressure and increasing mortality.

  • RAAS –> ACEi
  • Noradrenaline/SNS –> beta blockers
  • Aldosterone –> aldosterone antagonist

These actively help reduce mortality rates by 56% when using all three. They act to: improve quality of life, reduce hospitalisation and reduce mortality

Whereas a medication such as furosemide is a symptom relief medication which does not reduce mortality

71
Q

List 5 symptoms of heart failure

A
  • Nocturia
  • Orthopnoea
  • PND
  • Tachycardia
  • Fatigue
72
Q

What is Kussmaul sign (distension of the jugular veins during inspiration) caused by?

A

Inspiration causes negative intrathoracic pressure, pulling blood towards the right heart.

Normally, the JVP falls during inspiration. BUT in RHF there is decreased compliance, resulting in an elevated JVP during inspiration)

73
Q

Name 3 complications of heart failure

A
  • Acute decompensated heart failure
  • Cardiorenal syndrome (can be due to renal hypoperfusion, renal venous congestion, and/or RAAS activation)
  • Arrhythmias
  • Venous stasis, leg ulcers
74
Q

What is the difference between ADHF and de novo heart failure?

A

ADHF = acute heart failure due to decompensation of preexisting disease/cardiomyopathy (most common)

De Novo Heart Failure = acute heart failure occurring for the first time in a patient without known cardiomyopathy (∼15% of cases)

75
Q

Name 3 common triggers for acute decompensated heart failure

A
  • Coronary artery disease: ACS or myocardial ischaemia
  • Myocarditis
  • Acute valvular pathology (e.g. aortic or mitral regurgitation secondary to IE)
  • Progressive valve disease
  • Uncontrolled HTN
  • Rhythm disturbances
  • Nonadherence to drugs and diet

https://tgldcdp-tg-org-au.proxy.library.adelaide.edu.au/viewTopic?topicfile=heart-failure&guidelineName=Cardiovascular&topicNavigation=navigateTopic#toc_d1e161

76
Q

Heart failure is most frequently seen in older people, and median survival following a diagnosis is around _ to _ years

A

Heart failure is most frequently seen in older people, and median survival following a diagnosis is around 3 to 5 years

77
Q

The classification of heart failure, which is usually based on LVEF, guides the management of heart failure.

What % of LVEF is required for a diagnosis of Heart Failure with Reduced Left Ventricular Ejection Fracture (HFrEF)?

A

Heart failure with LVEF of 50% or less

78
Q

Name the 4 drugs that improve outcomes in patients with HFrEF

A
  • ACEi
  • Beta-bockers
  • Angiotensin II receptor blockers (ARBs)
  • Aldosterone antagonists
79
Q

Why are diuretics used in heart failure?

A

To control congestive symptoms (due to retention of sodium and water)

80
Q

How is heart failure diagnosed?

A

An echocardiogram is the single most useful investigation.

HFrEF: symptoms with/without signs + LVEF <50%

HFpEF: symptoms with/without signs + LVEF > 50% AND objective evidence of relevant heart disease AND/OR diastolic dysfunction demonstrated by other investigations

Good summary: https://www.heartlungcirc.org/action/showFullTableHTML?isHtml=true&tableId=tbl0015&pii=S1443-9506%2818%2931777-3

81
Q

An echocardiogram is the single most useful investigation for diagnosing heart failure. If an echo is unavailable in a timely manner, what other investigations can be done to improve diagnostic accuracy?

A

Plasma B-type natriuretic peptide (BNP)

NT-proBNP

82
Q

List 7 CHF investigations and your reasons for ordering them

A
  1. TRANSTHORACIC Echocardiography (TTE): demonstrates structural changes, left ventricular ejection fraction, underlying causes (e.g. valvular pathology, hypertrophy)
  2. Natriuretic peptides (BNP, NT-proBNP): can provide added diagnostic value. Produced mainly in the LV; when the LV is stretched, concentrations of BNP and NT-proBNP in blood can increase markedly, indicating that the heart is working harder and having more trouble meeting the body’s demands. This may occur in heart failure (when your heart is not strong enough to pump blood and nutrients to meet your body’s needs)
  3. CBC: anaemia, infection (can precipitate or worsen CHF)
  4. CXR: look for classic HF changes
  5. Basic metabolic panel (BMP): creatinine can be normal or elevated, possible hyponatremia, glucose (if comorbid diabetes)
  6. LFTs: hepatic venous congestion can cause elevation of cholestatic enzymes (ALP, GGT, bilirubin)
  7. Fasted lipids: elevated cholesterol possible and common
83
Q

Pulmonary oedema manifests in two forms. Name them and describe their appearance on a CXR.

A

Pulmonary oedema manifests in 2 forms: interstitial oedema (early) and alveolar oedema (as the disease progresses).

Interstitial oedema appears as Kerley B lines: septal lines caused by thickening of the interlobular septa.

Alveolar oedema appears as batwing opacities: bilateral peri-hilar shadowing

https://www.radiologymasterclass.co.uk/tutorials/chest/chest_pathology/chest_pathology_page8

84
Q

Describe the RAAS system.

A
  1. JG cells in the kidneys release renin. The liver release angiotensinogen.
  2. Renin converts angiotensinogen into Angiotensin I
  3. ACE (angiotensin-converting-enzyme) converts Angiotensin I into angiotensin II
  4. Angiotensin II acts on various receptors in the adrenal glands, blood vessels, and kidneys.
85
Q

How do ACEi affect RAAS?

A

Prevents the conversion of angiotensin I into angiotensin II.

Angiotensin II is a potent vasoconstrictor. Blocking it will help decrease BP.

86
Q

How do angiotensin-II-receptor-antagonists (ARBs) affect RAAS?

A

Blocks the effect of angiotensin II on its receptors in various tissues (adrenal glands, blood vessels, kidneys), inhibiting its vasoconstrictive effects.

87
Q

What causes the heart sounds S1 and S2?

A

S1 - closing of the atrioventricular valves (tricuspid, mitral)

S2 - closing of the semilunar valves (aortic, pulmonary)

88
Q

How can mitral stenosis lead to atrial fibrillation?

A

Impaired emptying of the LA causes it to enlarge, stretching the atrial conduction fibres, resulting in:

(a) increased atrial conduction time
(b) decreased atrial refractory period

YEAR 3 - SEMESTER 1 (15 decks)

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