Atrial Fibrillation and Heart Failure Flashcards

1
Q

What is AF

A

A heart condition caused by irregular atrial fibrillations superimposed on ventricular beats. this is caused by multiple ectopic foci developing and discharging asynchronously

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2
Q

What is ectopic foci?

A

abnormal pacemaker cells that sit outside the pacemaker node

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3
Q

How does AF differ from normal sinus rhythm?

A

In normal sinus rhythm, on electric impulse is caused by one point, the sinus node, in the right atrium. While in AF, multiple electric impulses are caused by several areas of both atrium.

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4
Q

Outline the prevalence of AF

A

PREVALENCE IS ABOUT 1.6% BUT OVER 10% IN ELDERLY.
increases risk of stoke x5 than those without AF

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5
Q

What are the risk factors of AF?

A

Age

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6
Q

Describe the five domains of integrated AF management? and what is the desired outcome of each one

A

Acute rate and rhythm control - haemodynamic stability (stable blood flow)
Manage precipitating factors - Reduce risk of cardiovascular problems

Assess stroke risk - stroke improvement
Assess heart rate - symptom improvement and preservation of left ventricular function
Assess symptoms -symptom improvement

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7
Q

What is the patient benefit of each domain?

A

Improved life expectancy:
- Acute rate and rhythm control
- manage precipitating factors

Assess stroke risk - improved life expectancy and improved quality of life, autonomy and social functioning

Improved quality of life, autonomy and social functioning
- Assess heart rate
- Assess symptoms

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8
Q

What are the cardiovascular morbidity and mortality risks associated with AF?

A

Death
stroke
Hospitalisation
Reduced quality of life
LVD and HF
Cognitive decline and vascular dementia

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9
Q

Why does AF increase stroke risk?

A

AF can cause blood clots because the blood may not be properly pumped out of the heart, results in pooling & clot forming (usually in the left atrial appendage). The Clot lodges in the cerebral vasculature (resulting in a stroke).

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10
Q

What are the 3 main contributors to Thrombosis according to Virchow’s triad?

A
  1. Endothelial injury -a type of nonobstructive coronary artery disease, which means that there is no blockage in the arteries. Instead, the arteries are not working properly.
  2. Abnormal blood flow
  3. Hypercoagulability

remember to learn the triangle chart

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11
Q

What is thrombosis?

A

Thrombosis occurs when blood clots block your blood vessels.

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12
Q

What is hypercoagulability?

A

increased tendency of blood to thrombose (increased tendency to form blood clots). A healthy response to bleeding is to form a blood cloth but hypercoagulability is when someone forms blood clots too often.

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13
Q

What types of AF are included in Atrial Fibrillation stroke prevention?

A
  • Persistent AF (> 7 days) your heart beats in an irregular pattern and often beats faster than usual. persists for more than 7 days or that has required cardioversion for termination of the rhythm
  • Permanent AF (cardioversion ineffective ) most common Your heart beats in an irregular pattern and often beats faster than usual. It cannot get back to its regular rhythm on its own.
  • Paroxysmal AF (<7 days duration) occurs from a few seconds to a few days before returning to normal sinus rhythm
  • Atrial Flutter - It occurs when a short circuit in the heart causes the upper chambers (atria) to pump very rapidly.
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14
Q

Give examples of stroke & bleeding risk calculators used to diagnose AF?

A
  1. CHA ₂ DS₂ Score for Atrial Fibrillation Stroke Risk
  2. HAS-BLED Score for Major Bleeding Risk **
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15
Q

Give examples of clinical risk factors for stroke, transient ischaemic attack and systemic embolism (CHA2DS2-VASc)?

A

Congestive heart failure
75 years or older
hypertension
previous stroke, transient ischaemic attack
Sex female
age 65-74
vascular disease
Diabetes mellitus

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16
Q

What are the HAS-BLED Bleeding risks?

A
  • t are the HAS-BLED Bleeding risks?
    1. Hypertension (uncontrolled >160mmHg diast) *(1 point)
    2. Abnormal Renal disease/Liver disease (1+1)
    3. Stroke history (1)
    4. Bleeding: prior major episodes (1)
    5. Labile INRs <60% time in therapeutic range* (1)
    6. Elderly>65 years old (1)
    7. Drugs or Alcohol consumption* (antiplatelets,NSAIDS)
    💡 Score > 3 =HIGH RISK then..Offer modification and monitoring of modifiable risk factors
17
Q

What are the 3 Thromboembolism risks in AF

A
  • High risk→ Previous thromboembolic event, Age over 75 with Diabetes, Hypertension or Vascular Disease. Anticoagulant treatment required
  • Moderate risk→ Age over 65 with no risk factors & Age less than 75 with risk factors. Anticoagulant treatment required
  • Low risk→ Age less than 65 with no risk factors. No treatment
18
Q

Give examples of Orally active anticoagulants

A
  1. Warfarin (Vit K inhibitor; VKORC1 enzyme inhibitor) → Drawback: Requires monthly INR test for coagulation (ensures correct dose via titration) but is quite cheap to produce
  2. Apixaban (Factor Xa inhibitor)
  3. Dabigatran Etexilate (Thrombin Inhibitor)
  4. Rivaroxaban (Factor Xa inhibitor)
  5. Edoxaban (Factor Xa inhibitor)
19
Q

Outline the coagulation cascade? Where do these anticoagulants work?

A

The coagulation cascade, or secondary hemostasis, is a series of steps in response to bleeding caused by tissue injury, where each step activates the next and ultimately produces a blood clot.

20
Q

What is the latest NICE draft 2020 treatment advice for AF?

A

When all outcomes were combined in the cost-effectiveness analysis, apixaban was the clinically most effective option followed by rivaroxaban & dabigatran

When costs were also considered apixaban & dabigatran emerged as the most cost effective options

21
Q

MOA of anticoagulants

A

Anticoagulants derive their effect by acting at different sites of the coagulation cascade.Some act directly by enzyme inhibition, while others indirectly, by binding to antithrombin or by preventing their synthesis from the liver (vitamin K dependent factors).

22
Q

Anti-arrhythmic drugs

A
  • Most of these drugs have multiple mechanisms of action
  • Classification indicates the main pharmacological action (e.g. verapamil blocks Ca, Na and K channels)
  • These are not simple drugs to prescribe → cardiologists
23
Q

Outline the Vaughan Williams Classification for the drug treatment of arrhythmias

A

Class I (Na+ channel blockade – phase 0)

Class II (blockade of sympathetic drive to heart)→ mostly beta blockers

Class III ( effect on repolarisation phase 3) → Potassium channel blockers

Class IV (blockade of calcium phase 2) → Calcium channel blockers
See PTH1 Lecture from 2nd year

24
Q

How do we treat AF Rate?

A
  • Offer rate control as the first-line strategy to patients with AF
  • Rate control is simpler, more cost effective and may result in fewer admissions
  • Beta Blockers are first line (not sotalol) → Alternatively Ca antagonists (Diltiazem, not a DHP(Dihydropyridine) as it has vascular effects) → Rarely Digoxin (only effective on resting rate) → Beta Blocker + Diltiazem if monotherapy fails.
25
Q

Definition of HF

A

A complex clinical syndrome of symptoms and signs that suggest impairment of the heart as a pump supporting physiological circulation

26
Q

Signs in HF is due to?

A
  1. Pulmonary and Systemic congestion
  2. Structural Abnormalities causing HF
  3. Structural Abnormalities resulting in HF
  4. Complications in therapy
27
Q

What are the common symptoms of HF?

A

Fatigue, Ankle Swelling, breathlessness

28
Q

How is HF Classified?

A
  • Class I → No symptoms with normal physical activity
  • Class II→ Slight limitation and shortness of breath on moderate to severe exertion
  • Class III→ Marked limitation of activity, less than ordinary activity causes SOB
  • Class IV→ Severe disability, dyspnoea at rest, no physical activity possible without discomfort
29
Q

How is HF diagnosed?

A

There is no single diagnosis, you need to look for structural changes of the heart.

  • B-type natriuretic peptide [BNP] > 100ng/l or…
  • N-terminal pro-B-type natriuretic peptide [NT-proBNP]>300ng/l

Then confirm with…

  • Transthoracic Doppler 2D echocardiography (measures size of chambers and flow)
30
Q

What can be provided as Initial treatment for HF?

A

Deal with congestion by providing Diuretics as iv. or bolus. Increase the dose if patient is already on diuretics. This will stabilise the patient and bring fluid levels back to normal.

31
Q

What medications are not routinely offered for initial treatment of HF?

A

Opiates (pain relief), Nitrates, Sodium nitroprusside, Inotropes and Vasopressors

32
Q

Give examples of drug treatments given after stabilisation

A

If ventricular systolic dysfunction provide: Beta blockers & Ace inhibitors (& aldosterone antagonists).

33
Q

Why/How do Beta Blockers & Ace inhibitors (& aldosterone antagonists) improve HF symptoms?

A

Beta Blockers block the release of the stress hormones adrenaline and noradrenaline

34
Q

Heart failure compensation

A

?

35
Q

What is the Prognosis of CHF?

A

Heart failure has a poor prognosis: 30–40% of patients diagnosed with heart failure die within a year – but thereafter the mortality is less than 10% per year

On average, a GP will look after 30 patients with heart failure, and suspect a new diagnosis of heart failure in perhaps ten patients annually

36
Q

How do GP’s diagnose CHF?

A
  • Refer patients with suspected HF & previous MI (Myocardial Infraction) refer urgently → transthoracic Doppler 2D echocardiography and specialist assessment within 2weeks.
  • If no previous MI, measure serum natriuretic peptides, high levels have poor prognosis
    1. BNP level above 400pg/ml or an NTproBNPlevel above 2000pg/ml

then

  1. refer immediately (within 2 weeks) If moderately raised (100pg/l, 400pg/l )NTproBNPlevel 400-2000pg/ml

then refer less urgently (within 6 weeks)

37
Q

Give examples of pre-existing treatments that can effect BNP tests?

A
  • Diuretics
  • Angiotensin-converting enzyme inhibitors
  • Angiotensin II receptor antagonists (ARBs)
  • Aldosterone antagonists

All these reduce levels of serum natriuretic peptides as can obesity hence could cofound diagnosis