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Cardiology > Congestive Cardiac Failure > Flashcards

Congestive Cardiac Failure Flashcards

1
Q

What five symptoms are suggestive of heart failure?

A
  • Dyspnoea
  • Oedema
  • Elevated JVP
  • Basal crepitations
  • Enlarged liver
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2
Q

What symptoms may indicate RIGHT sided heart failure specifically?

A
  • Ankle oedema
  • Hepatomegaly
  • Elevated JVP
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3
Q

What symptoms may indicate LEFT sided heart failure specifically?

A

Bibasal crepitation

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4
Q

What is orthopnoea?

A

Shortness of breath that occurs when lying flat
Patient sleeps better when propped up
- Often a symptoms of left ventricular failure/pulmonary oedema

Occurs because normal pooling of blood in the lungs when supine is added to a chronically congested vasculature
Increased venous return cannot be compensated for by the left ventricle

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5
Q

At what points do the different waves in a JVP occur?

A

Waves:
a - pre-systolic: produced by right atrial contraction
c - bulging of the tricuspid valvule into the right atrium during ventricular systole (isovolumic phase)

The a and v waves can be identified by timing the double waveform with the opposite carotid pulse (a comes just before and v comes at 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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6
Q

What are the grades of murmurs and what do they mean?

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
  • Grade 5: Very loud, can be heard with the stethoscope only partly in contact with chest wall
  • Grade 6: Audible without stethoscope
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7
Q

Why would you get a murmur in anaemia?

A

Decreased blood viscosity

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8
Q

What conditions cause decreased diameter of a blood vessel, valve, or orifice, resulting in a murmur?

A

Valvular stenosis
Coarctation of aorta
Ventricular septal defect

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9
Q

What could cause increased velocity of blood through normal structures?

A

Hyperdynamic states such as sepsis or hyperthyroidism

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10
Q

Why do we get murmurs across incompetent valves?

A

The regurgitation of the valve causes turbulent blood flow

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11
Q

What are some examples of systolic murmurs?

A

‘Flow murmurs’

  • Aortic/pulmonic stenosis
  • Mitral/tricuspid regurgitation
  • Ventricular septal defect
  • Aortic outflow tract obstruction
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12
Q

What are some examples of diastolic murmurs?

A
  • Aortic/pulmonic regurgitation

- Mitral/tricuspid stenosis

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13
Q

What are some examples of continuous murmurs?

A

Patient ductus arteriosus

only example

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14
Q

What are the 3 basic shapes of murmurs heard?

A
  • Crescendo-decrescendo
  • Decrescendo
  • Uniform

Generally determined by the pattern of the pressure gradient driving the turbulent flow

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15
Q

What should we consider when assessing the significance of a murmur?

A
  • A soft ejection murmur may not always signify organic pathology
  • A new murmur is always significant
  • A loud murmur associated with a thrill is always abnormal
  • Diastolic murmurs are always abnormal
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16
Q

What is heart failure?

A

Heart failure

  • Complex syndome
  • Results from any structural/functional cardiac disorder
  • Impairs ability of heart to function as a pump to support physiological circulation
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17
Q

What are some common heart failure aetiologies?

A
  • Ischaemic (coronary artery disease, MI)
  • Hypertension
  • Diabetes (diabetic cardiomyopathy or via CAD)
  • Valvular (AS, MR(
  • Tachycardia induced (uncontrolled AF)
  • Toxins/drugs (alcohol, doxorubicin)
  • Infective (viral myocarditis)
  • Endocrine (thyrotoxicosis, phaechromocytoma)
  • Dilated cardiomyopathy (idiopathic, perpartum)
  • Genetic (HOCM)
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18
Q

What are the symptoms of heart failure?

A 
Symptoms:
- Breathlessness
On exertion/ at rest
Orthopnoea
Paroxysmal nocturnal dyspnoea
- Loss of energy/tiredness
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19
Q

What are the New York Heart Association definitions?

A

NYHA 1: no symptoms and no limitation in ordinary physical activity
NYHA 2: Mild symptoms and slight limitation during ordinary activity
NYHA 3: Marked limitation in activity due to symptoms, even during less-than ordinary activity
NYHA 4: Severe limitations, experiences symptoms even whilst at rest

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20
Q

What clinical signs are seen in heart failure?

A

Signs:

  • Pulmonary oedema
  • Pleural effusion
  • Raised JVP
  • Pitting oedema
  • Ascites
  • Tachycardia
  • S3 gallop
21
Q

What investigations should be done when suspecting heart failure?

A

Bloods:

  • FBC
  • Haematinics
  • U&Es
  • TFTs
  • Glucose

Brain natruiretic peptide (BNP)

  • Indicates excessive stretching of heart muscle cells
  • Normal levels rule out heart failure
  • Provides prognostic information - high levels predict worse outcomes

CXR

22
Q

How is echocardiograpy used in investigating heart failure?

A
  • Provides information relating to ejection fraction of LV (normal approximately 60%)

Patients with heart failutre are subdivided into:

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

Helps define aetiology of HF

  • Assessment of valves
  • ?Previous AMI (akinetic/hypokinetic areas)
  • Provides information relating to cardiac chamber size/structure ie DSM, HOCM
23
Q

Why do we used ECGs in heart failure?

A

ECG provides diagnostic/therapeutic information

  • Presence of atrial fibrillation/other rhythms
  • 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
24
Q

What should heart failure treatment be focused upon?

A

Treatment of HF should be focused on treating underlying cause initially:

  • Rapid atrial fibrillation
  • Uncontrolled hypertension
  • Critical coronary artery disease
  • Significant valvular disease
  • Uncontrolled DM
  • Thyrotoxicosis
  • Etc
25
Q

How do we treat heart failure with impaired systolic function?

A

Ejection fraction <45%

  • Diuretics
  • ACEi
  • Beta blockers
  • Aldosterone receptor antagonists
  • Devices CRT/ICD
26
Q

How do we treat heart failure with preserved LV function

A

Ejection fraction >45%

  • Diuretics
  • Treatment of co-morbidities (HTN, DM)
27
Q

How are ACEi used in heart failure?

A

First line treatment, along with beta blockers
Decrease mortality and HF hospitalisation

ACEi:

  • Inhibit left ventricular hypertrophy and remodeling
  • Inhibit vasoconstriction, therefore lower arterial constriction and increase venous capacity
  • Decrease water and salt retention
28
Q

How are beta blockers used in heart failure?

A 
First line treatment, alongside ACEi
Decreaed HF mortality and hospitalisation
- Not all beta blockers licensed for heart failure
- Bisoprolol
- Carvedilol
- Nebivolol
- Metoprolol (modified release)
- ATENOLOL NOT LICENSED
29
Q

What are aldosterone receptor antagonists used for in heart failure?

A

Aldosterone receptor blockers )eplerenone and spironolactone) are used in treatment of severe LV dysfunction (EF <35%, NHYA II)

  • Anti-fibrotic effects
  • EMPHASIS and RALES trials
30
Q

Why do we used cardiac re-synchronisation therapy in heart failure?

A

CRT:

  • Patients with HF may have significant electrical/mechanical desynchrony (15%)
  • Mechanical desynchrony means that the heart does not contract as an efficient whole unit
  • L&R ventricles may contract at slightly different times
  • Left ventricle may contract in segments instead of as one unit

Devices:

  • Improve synchronicity
  • Improve cardiac function
  • Shown to reduce mortality and morbidity in HF patients with an ejection fraction <35% and QRS duration >120ms
31
Q

What are implantable cardiac defibrillators (ICD) used for?.

A

ICDs:

  • Sudden cardiac death accouns for 50% of HF mortality
  • Most likely the result of ventricular arrhytmias such as VT or VF
  • Previously managed with anti-arrhythmic drugs
  • ICD devices used in patients with HF with EF <35%
  • Mortality decreased
  • ICDs detect and treat ventricular arrhythmias
  • Can attempt to voerdrive pace VT
  • Deliver electrical shock to cardiovert VT/VF
32
Q

What investigations do you order for a patient with suspected heart failure?

A
  • CXR (looking for evidence of pulmonary oedema and/or consolidation)
  • ECG (looking for evidence of ACS as well as confirming fast atrial fibrillation)
  • ABG (level of oxygenation, CO2 and acid base balance)
  • FBC (elevated WCC? Hb low?)
  • U&E (this is important in relation to the treatment required)
  • Trop I (has there been a myocardial infarct?)
  • LFTs (pulmonary congestion - associated liver congestion)
  • BNP (to confirm the diagnosis of heart failure)
33
Q

How does pulmonary oedema occur in heart failure?

A
  • Failing heart has reduced contractility
  • End-diastolic volume increases
  • Initially the contraction force increases
  • Eventually the heart begins to decompensate as the EDV increases further and it annot keep up
  • Stroke volume decreases
  • Increased venous pressure causes fluid to leak out of the blood into the alveolar interstitial fluid -> pulmonary oedema
34
Q

What are the causes of heart failure?

A
  • Coronary heart disease
  • Hypertension
  • Structural: valvular diseases
  • Congenital: ASD, VSD, cardiomyopathies
  • Rate-related: uncontrolled AF, thyrotoxicosis, anaemia, heart block
  • Pulmonary: COPD, pulmonary fibrpsos, recurrent pulmonary emboli, priary pulmonary hypertension (RHF leading to congestive)
  • Alcohol and drugs: chemotherapy
  • Pericardial disease: chronic pericarditis caused by TB, lupus, viruses
  • Autoimmune: amyloidosis, sarcoidosis
  • Miscellaneous: pregnancy-induced cardiomyopathy, acute viral myocarditis
35
Q

What are some causes of mitral regurgitation?

A
  • Rheumatic heart disease
  • Ischaemic heart disease - associated with papillary muscle rupture
  • Valvular vegetations - as in patients with endocarditis
  • Physiological mitral valve regurgitation due to dilated left atrium
36
Q

What signs and symptoms are seen in atrial fibrillation?

A
  • Breathlessness/dyspnoea
  • Palpitations
  • Syncope/dizziness
  • Chest discomfort
  • Stroke/TIA
37
Q

What investigations are performed in suspected AF?

A
  • ECG in all patients with irregular pulse regardless of symptoms
  • If suspected paroxysmal AF, used ambulatory ECG

TTE:

  • Baseline echo is important for long term management
  • If a rhythm control strategy involving cardioversion is being considered
  • If patient has high risk/suspicion of structural/functional heart disease (HF, heart murmur) that influences management
  • For risk stratification for antithrombotic therapy is needed (stroke etc)
38
Q

When do we perform tranoesophageal ecocardiography?

A

In patients with AF:

  • When TTE demonstrates an abnormality (eg valvular heart disease) that warrants further assessment
  • If TTE is technically difficulty/of questionable quality, and need to rule out cardiac abnormalities
  • If TOW guided cardioversion is being considered
39
Q

When do we offer rate and rhythm control in AF?

A

Offer rate control as the first‑line strategy to people with atrial fibrillation, except in people:

  • whose atrial fibrillation has a reversible cause
  • who have heart failure thought to be primarily caused by atrial fibrillation
  • with new‑onset atrial fibrillation
  • with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
  • for whom a rhythm control strategy would be more suitable based on clinical judgement
40
Q

How do we control rate in AF?

A

As initial monotherapy:
- Standard beta blocker (NOT sotalol)
- Or rate limited calcium channel blocker
Bear in mind symptoms, heart rate, commodities and preferences

Digoxin:
- Consider monotherapy for patients with non-paroxysmal AF if they are sedentary

If monotherapy insufficient, and symptoms are due to rate control, consider combination of 2 of the following:

  • A beta blocker
  • Diltiazem
  • Digoxin
41
Q

How do we control rhythm in AF?

A
  • Consider pharmacological/electrical rhythm control for patients whose symptoms continue after rate control/if rate control unsuccessful

Cardioversion

  • Offer electrical if patient has had AF for more than 48 hours
  • Consider amiodarone for 4 weeks before and up to 1 year after electrical cardioversion to maintain sinus rhythm

For patients with AF for longer than 48 hours, and electrical cardioversion is indicated

  • Both TOE guided cardioversion and conventional cardioversion are equally effective
  • TOE-guided should be considered if staff and facilities are available, and there is a minimal period of precardioversion anticoagulation
42
Q

What drugs do we use for long term rhythm control in AF?

A
  • Assess the need for drug treatment for long‑term rhythm control, taking into account the person’s preferences, associated comorbidities, risks of treatment and likelihood of recurrence
  • Long‑term rhythm control: standard beta‑blocker (not sotalol) as first‑line treatment unless there are contraindications
  • If beta‑blockers contraindicated or unsuccessful: assess the suitability of alternative drugs for rhythm control, taking comorbidities into account

Dronedarone is recommended for maintenance of sinus rhythm after successful cardioversion in people with paroxysmal/persistent atrial fibrillation:

  • Whose atrial fibrillation is not controlled by first‑line therapy (usually beta‑blockers)
  • Or who have at least 1 of the following cardiovascular risk factors:
  • Hypertension requiring drugs of at least 2 different classes
  • Diabetes mellitus
  • Previous transient ischaemic attack, stroke or systemic embolism
  • Left atrial diameter of 50 mm or greater or
  • Age 70 years or older and
    do not have left ventricular systolic dysfunction/do not have a history of, or current, heart failure
43
Q

How would you explain ejection fraction to a patient?

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%

OFFER LEAFLET FROM AMERICAN HEART ASSOCIATION

44
Q

Why do we avoid cardioversion in patients who’ve had AF for more than 48 hours?

A
  • AF results in turbulent blood flow
  • Clots can form
  • Risk is greater when they’ve been in AF for more than 48 hours
  • If cardioverted, the clots could be dislodged and cause an embolic stroke
  • Hence veer to rate control if duration unknown, provide anticoagulation
  • Then cardiovert at later date if appropriate, exclude thrombi on echocardiogram
45
Q

What would we see in reentrant arrhythmias?

A

Needs:

  • Unidirect block
  • Sloe conduction
  • Short AP

Post infarction

46
Q

What causes delayed afterdepolarisations?

A
  • Due to cellular calcium overload (heart failure)
  • Spontanoues Ca release from sarcoplasmic reticulum
  • Activates depolarising membrane currents
47
Q

What peripheral signs are seen in infective endocarditis?

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
48
Q

What is the diagnostic criteria for infective endocarditis?

A

Modified Duke’s criteria

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

  • 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).

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 as noted above.
49
Q

What are the NICE guidelines for beta blocker and ACEi use in acute heart failure?

A

The Acute Heart Failure NICE guideline recommends stabilisation after initial treatment with beta-blocker and ACE inhibitor. The rationale is that in-hospital introduction of beta-blockers is associated with increased use of beta-blockers at follow-up and better long-term outcomes such as fewer adverse events and reduced mortality. Early initiation of ACE inhibitors and aldosterone antagonists for adults with acute heart failure is positively associated with improved outcomes such as lower mortality and readmission rates. If the ACE inhibitor has intolerable side effects, an angiotensin receptor blocker will be offered.

Cardiology (4 decks)

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