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Medicine year 3 ANNA > Congestive Cardiac Failure > Flashcards

Congestive Cardiac Failure Flashcards

1
Q

What are the signs and symptoms of CCF?

A
  1. Breathing
    • dyspnoea
    • orthopnoea
    • tachypnoea
    • cough with frothy sputum
    • paroxismal nocturnal dyspnoea (LHF)
  2. Fluid O/E
    • peripheral oedema
    • sacral oedema
    • fine basal lung crackles
  3. Auscultation/palpation O/E
    • third heart sound (ventricular gallop)
    • displaced apex beat
  4. Raised JVP O/E
  5. Enlarged liver / spleen O/E
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2
Q

What is the definition of dyspnoea?

A

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.

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3
Q

What are the signs of LHF?

A

Left Heart Failure

→ causes ↓CO:

  • ↓exercise tolerance / fatigue / exercise-induced dyspnoea
  • poor tissue perfusion

→ pulmonary congestion:

  • pulmonary oedema
    • fine basal crackles
    • orthopnoea
    • dyspnoea
    • tachypnoea
    • wheeze
    • cough with frothy sputum (blood tinged)
    • paroxysmal nocturnal dyspnea
  • cyanosis / hypoxia → fatigue
  • Restlessness / confusion
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4
Q

What are the signs of RHF?

A

Right Heart Failure:

Congestion of peripheral tissues

  • Peripheral, gravity-dependent oedema
  • Ascites
  • Enlarged liver and spleen / liver failure signs
  • Raised JVP
  • Anorexia / GI distress / W/L
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5
Q

What is the difference between RHF and LHF?

A
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6
Q

What are the grades of murmurs?

A
  1. Faint, barely audible, in one position
  2. Soft, heard in all positions
  3. Moderately loud, no thrill
  4. Loud and with palpable thrill
  5. Very loud, with thrill, heard with stethoscope partly off the chest
  6. Very loud, with thrill, heard with stethoscope completely off the chest!
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7
Q

What are the 2 most common systolic murmurs?

Where would you hear them best?

A

Aortic stenosis

  • ejection systolic murmur
  • crescendo/decrescendo
  • right sternal edge
  • expiration
  • radiates to carotid

Mitral regurgitation

  • pansystolic
  • opening snap
  • left 5th intercostal space mid-clavicular line
  • expiration
  • radiates to axilla
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8
Q

Why does orthopnoea occur?

A

because the normal pooling of blood in the lungs in the supine position is added to a chronically congested pulmonary vasculature;

the increased venous return cannot be compensated for by the left ventricle.

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9
Q

What are the jugular waveforms caused by?

A

Waves:

  • A = pre-systolic: produced by right atrial contraction
  • C = bulging of the tricuspid valve into the right atrium during ventricular systole (isovolumic phase)
  • V = occurs in late systole; increased blood in the right atrium from venous return

(The a and v waves can be identified by timing the double waveform with the opposite carotid pulse. The a wave will occur just before the pulse and the v wave occurs towards the end of the pulse).

Descents:

  • X = a combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole
  • Y = the tricuspid valve opens and blood flows into the right ventricle
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10
Q

Name the mumurs

A
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11
Q

Describe the murmurs

A
  1. Aortic stenosis - ejection systolic, loudest on expiration, radiates to carotids
  2. Mitral regurgitation - Pansystolic, apex, loudest on expiration, radiates to axilla
  3. Aortic regurgitation - early diastolic (sounds like a breath), loudest on expiration
  4. Mitral stenosis - low rumbling mid diastolic with opening snap, loudest on expiration, bell of stethoscope
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12
Q

What are the New York Heart Failure Association criteria?

A
  1. NYHA 1: No symptoms and no limitation in ordinary physical activity
  2. NYHA 2: Mild symptoms and slight limitation during ordinary activity
  3. NYHA 3: Marked limitation in activity due to symptoms, even during less-than-ordinary activity
  4. NYHA 4: Severe limitations. Experiences symptoms even while at rest.
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13
Q

What investigations are important in heart failure?

A

Bedside:

  • ECG (arrythmias, prev ACS, LBBB; all help guide aetiology and so treatment)

Bloods:

  • FBC (anaemia)
  • U+Es (elecrolytes)
  • LFTs (RSHF → liver failure)
  • Glucose (DM)
  • ABG (CO2 levels, hypoxia)
  • Troponins (rule out MI)
  • BNP (Normal levels (<100mg/litre) rule out heart failure, also provides prognostic information, i.e. high levels predict worse outcomes)

Imaging:

  • CXR (cardiomegaly, pulmonary oedema, effusion = transudate)
  • Echocardiogram → need to measure ejection fraction for further sudivisions of heart failure
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14
Q

Patients with heart failure are subdivided into what 2 categories based on echo?

Why is this division helpful?

A
  1. Heart Failure with preserved LV function (EF >45%)
  2. Heart Failure with LV systolic dysfunction (EF <45%)

This division is helpful because those with impaired function need medications to manage this as well as diuretics:

  1. ACE-I
  2. ß-blockers
  3. Aldosterone Receptor Antagonists
  4. Devices e.g. CRT/ICD
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15
Q

What are some common underlying causes of HF? Why are they important?

A

Treatment of HF should be focused on treating underlying cause initially, e.g. :

  • Rapid atrial fibrillation
  • Uncontrolled hypertension
  • Critical coronary artery disease
  • Significant valvular disease
  • Uncontrolled DM
  • Thyrotoxicosis
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16
Q

What is first line treatment for heart failure with impaired LV function?

A
  1. ACE-I e.g. ramipril 2.5mg OD, increase to 10 OD
  2. ß-blockers e.g. bisoprolol 1.25 mg, increase to 10
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17
Q

Why are ACE-I effective in heart failure?

A
  • Inhibit left ventricular hypertrophy and remodeling
  • Inhibit vasoconstriction therefore lower arterial constriction and increase venous capacity
  • Decrease water and salt retention
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18
Q

What is the drug management of Heart Failure?

A
  1. first-line treatment for all patients is both an ACE-inhibitor (e.g. ramipril) and a beta-blocker (e.g. bisoprolol)
  2. second-line treatment is either an aldosterone antagonist (e.g. spironolactone), angiotensin II receptor blocker (e.g. candesartan ) or a hydralazine in combination with a nitrate
  3. if symptoms persist cardiac resynchronisation therapy or digoxin should be considered
  4. diuretics should be given for fluid overload
  5. offer annual influenza vaccine / one-off pneumococcal vaccine
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19
Q

What does a “cannon wave” in the JVP signify?

A
  • This is a large, positive venous pulse during A wave.
  • It occurs when the atrium contracts against a closed tricuspid valve.
  • This is becuase there is AV node dissociation, e.g. complete heart block.
20
Q

What are the 2 cardiac causes of pulmonary oedema?

A
  1. Left ventricular failure
  2. Mitral regurgitation
21
Q

What is atrial fibrillation? What is the pathophysiology?

A
  • Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia.
  • The pulse is irregularly irregular:
    • Atrial fibrillation causes an irregular atrial rhythm between 300-600bpm.
    • The AV node is unable to transmit beats as quickly as this, and thus does so intermittently, resulting in an irregular ventricular rhythm.
    • This irregular stimulation of the ventricles reduces cardiac output by up to 20%, as well as allowing stasis of blood in the heart chambers.
22
Q

What are the ECG findings in atrial fibrillation?

A
  • No p waves – just an irregular baseline
  • Irregular QRS – between 75-190bpm
  • Normal shape QRS – because conduction through the AV node is normal
  • In V1 the trace resembles atrial flutter
  • Normal T waves
23
Q

What investigations are needed in atrial fibrillation?

A

Bedside:

  • ECG

Bloods:

  • TFTs (hyperthyroidism can → AF)
  • U+Es (electrolyte imbalance; high or low K+, low Mg2+)
  • Troponins

Imaging:

  • Echocardiogram
    • TOE is necessary in patients presenting with new-onset AF, where the exact onset of AF is unclear, and cardioversion is necessary to restore sinus rhythm.
    • look for mitral valve disease, left ventricular dysfunction, left atrial enlargement.
24
Q

How is AF managed acutely?

A

Cardioversion? - only in:

  • Young patients
  • 1st episode of AF
  • Coexistent heart failure
  • Obvious reversible cause

Chronic AF - Rate control and stroke risk

(Rate control is as good as rhythm control in chronic AF – i.e. generally you don’t need to cardiovert – as the outcomes are the same as if the rate only is well controlled)

  • Rate control is acheived with either:
    • ß blocker OR
    • Ca2+ channel blocker (never both together)
    • 2nd line: add digoxin or amiodarone
  • Stroke Risk
    • ​Anticoagulate based on CHA2DS2-VASc Score - if 2 or above - vs HASBLED
    • Offer warfarin or NOACs
25
Q

What are the signs and symptoms of AF?

A
  • Most often, AF is asymptomatic and is picked up incidentally throught other investigations
  • Symptoms include:
    • palpitations
    • dyspnoea
    • chest pain
    • dizziness/syncope
  • Sign is an irregularly irregular pulse
26
Q

Name some causes of AF

A

Cardiac

  • Heart failure
  • Heart ischaemia (MI)
  • Hypertension
  • (Mitral) valve disease
  • Congenital heart disease (rare)

Pulmonary

  • PE
  • Pneumonia
  • Bronchocarcinoma

Other

  • Hyperthyroidism (fast AF) – Sometimes hypothyroidism can also cause slow AF
  • Alcohol
  • Post-operatively
  • Sepsis
  • High caffeine intake
  • Antiarrhythmic drugs!
  • ↓K+
  • ↑Mg2+
27
Q

What are the CHADSVASC criteria?

A
28
Q

What is the ejection fraction?

A
  • Ejection fraction is a measurement of how much blood is being pumped out of the heart with each contraction.
  • It is expressed as a percentage. (i.e. stroke volume/end diastolic volume).
  • A normal ejection fraction is 50 – 70%.
29
Q

What is the normal value of ejection fraction?

When is it borderline?

When is it reduced?

A
  1. Normal value 70-50%
  2. Borderline 41-49% (may notice symptoms on exertion)
  3. Reduced = 40% (Symptoms may become noticeable even during rest)
30
Q

Why should you never cardiovert someone who has been in AF for more than 48 hours unless it’s going to be life-saving?

A
  • In atrial fibrillation, blood flow will be turbulent, with possible areas of decreased flow or stasis of blood in the atria.
  • This can cause clots to form, and 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.
    • Therefore, 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.
    • 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.
31
Q

List 4 causes of mitral regurgitation

A
  1. Rheumatic heart disease
  2. Ischaemic heart disease - associated with papillary muscle rupture e.g. post-MI
  3. Valvular vegetations - as in patients with endocarditis
  4. Physiological mitral valve regurgitation due to dilated left atrium e.g. Marfan’s, congenital, dilated cardiomyopathy
32
Q

List 4 causes of aortic stenosis

A
  1. Age - calcification
  2. Bicuspid aortic valve (e.g. Turner’s syndrome [one X chromosome])
  3. Congenital
  4. Strep-associated (rheumatic heart disease)
33
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease

34
Q

Name 2 acute and 4 chronic causes of aortic regurgitation

A

Acute:

  1. Infective endocarditis
  2. Aortic dissection

Chronic:

  1. Connective tissue disorder (e.g. Marfa’s, AS)
  2. Rheumatic heart disease
  3. Longstanding HTN
  4. Syphilis
35
Q

What symptoms might you experience with a severe grade murmur?

A
  • dyspnoea - usually exertional
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • fatigue
  • palpatations
  • chest pain - angina (AS) / MS
  • haemoptysis (MS)
  • syncope (AS)
36
Q

What questions might you inlcude in a collapse history? e.g.

36year old lady who has collapsed at home. The triage note states that she has been unwell for the past couple of days with fever and breathlessness. She has been taking paracetamol because she thinks she developed a chest infection after having her tooth removed the previous week.

A
  • What were the exact circumstances of the collapse this morning?
  • Was there loss of consciousness?
    • How long did it last for?
    • What were you doing at the time of the collapse?
    • Was it witnessed?
    • Was there any change in skin colour?
    • Was there any seizure activity?
    • Is there a family history of sudden death?
  • Preceding dizziness in the past few days? Describe it
  • Duration of period of being unwell
  • Fevers - ?measured. ?pattern
  • Breathlessness – since when? Trigger? Any previous problems with breathing or respiratory conditions
  • Associated cough? Haemoptysis?
  • Associated chest pain?
  • Exactly what type of dental work did you have done? Were you given antibiotics at the time or since?
  • Any previous heart conditions?
  • Foreign travel?
  • IVDU (Intravenous Drug User)?
  • Could she be pregnant? LMP?
37
Q

Case continued:

She had a tooth removed just over a week ago. It was done with local anaesthetic and took a little longer than usual because “there was a lot of digging around” to get the tooth out. She was not given antibiotics at the time.

What is now in your differential?

A

Infective endocarditis secondary to dental infection.

38
Q

What are the signs of infective endocarditis on examination?

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.
39
Q

What are the major Duke’s criteria for diagnosis of infective endocarditis?

A

Major criteria (need 2 or 1 +3minor)

  • Positive blood culture for IE: typical micro-organism consistent with IE from two separate blood cultures.
  • Evidence of endocardial involvement:
    • Positive echocardiogram for IE:
      • Oscillating intra-cardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation; or
      • Abscess; or
      • New partial dehiscence of prosthetic valve); or
      • New valvular regurgitation (worsening or changing of pre-existing murmur not sufficient).
40
Q

What are the minor Duke’s criteria for diagnosing infective endocarditis?

A

Minor criteria

  • Predisposition: predisposing heart condition or intravenous drug use.
  • Fever: temperature >38°C.
  • Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages and Janeway’s lesions.
  • Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots and rheumatoid factor.
  • Microbiological phenomena: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE.
  • PCR: broad-range PCR of 16S (polymerase chain reaction using broad-range primers targeting the bacterial DNA that codes for the 16S ribosomal subunit).
  • Echocardiographic findings consistent with IE but do not meet a major criterion.
41
Q

What is the strongest risk factor for developing infective endocarditis?

What types of patients are affected?

A
  1. The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis.
  2. The following types of patients are affected:
  • previously normal valves (50%, typically acute presentation)
  • rheumatic valve disease (30%)
  • prosthetic valves
  • congenital heart defects
  • intravenous drug users (IVDUs, e.g. typically causing tricuspid lesion)
42
Q

Historically and now in developing countries, what is the organism most commonly resposible for infective endocarditis?

What is it now?

A

Then: Streptococcus viridans, a class which includes:

  • Streptococcus mitis*
  • Streptococcus sanguinis*

= Both commonly found in the mouth (hence why dental procedures / poor hygeine is often responisble for IE).

Now: Staphylococcus aureus

43
Q

What investigations are essential in diagnosing infective endocarditis?

A

Bedside

  • ECG (Progression of the infection may lead to conduction system disease, ie. prolonged PR interval; non-specific ST/T wave abnormalities; AV block)
  • Urinalysis (Septic emboli are common complications of IE, and urinalysis may demonstrate active sediment assisting in the clinical diagnosis)

Bloods

  • Cultures: 3 sets of blood cultures should be obtained 1 hour apart prior to initiating antibiotic therapy to ensure greatest yield. The most common cause of culture-negative endocarditis is antibiotic therapy preceding blood cultures
  • FBC (Most patients have a normocytic, normochromic anaemia. Leukocytosis is seen in about one third of cases often with neutrophilia)
  • U+Es w glucose (baseline)

Imaging

  • Echo - as early as possible to confirm or rule out the diagnosis / alter prognosis / management
44
Q

What is blood culture-negative infective endocarditis?

A

Blood culture-negative IE (BCNIE) refers to IE in which no causative micro-organism can be grown using the usual blood culture methods.

BCNIE can occur in up to 31% of all cases of IE and most commonly arises as a consequence of previous antibiotic administration.

45
Q

What is a CRT device? What types are there?

A

CRT: cardiac resynchronisation therapy

There are two types of CRT Devices:

  1. Cardiac Resynchronization Therapy Pacemaker (CRT-P)
  2. Cardiac Resynchronization Therapy Defibrillator (CRT-D)

Medicine year 3 ANNA (30 decks)

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