Ward 9 Flashcards

1
Q

What can be used for stroke risk predictions

A

CHA2DS2VASc tool for stroke risk prediction in patients with atrial fibrillation

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2
Q

CHA2DS2VASc interpretation

A
  • Congestive heart failure (1 point), Hypertension (1), Age
    65–74y (1), Age >74y (2), Diabetes (1), previous Stroke/TIA/thromboembolism (2), Vascular disease (1), Sex Category (1 if female).
  • A score of 2 or more is considered high risk and anticoagulation should be offered, unless there is a contraindication (guidelines)
  • If the patient receives a 0 score, it is considered “low-risk,” and anticoagulation is not recommended in such cases. If the patient receives a score of 1, it falls in the “low-moderate” risk category; the providers should consider anticoagulant or antiplatelet therapy. If the patient receives a score of greater than 2, they are in the “moderate-high” risk category, and anticoagulation therapy is indicated
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3
Q

What is the most common type of arrhythmia?

A

Atrial fibrillation

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4
Q

What is atrial fibrillation due to?

A

It is due to abnormal electrical activity within the atria of the heart, causing them to fibrillate

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5
Q

What is atrial fibrillation classified as and into?

A
  • It is characterized as a tachyarrhythmia, which means that the heart rate is often fast
  • This arrhythmia may be paroxysmal (spontaneously resolves in less than seven days) or persistent (more than seven days)
  • Long standing persistent AF occurs when AF has been present for at least a year, either due to failure of initiation of pharmacological intervention or failure of cardioversion
  • Permanent AF: It is the type where a decision has been made to abort all therapies because the rhythm is unresponsive
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6
Q

Dangers of atrial fibrillation

A

Overall, atrial fibrillation leads to a turbulent and abnormal flow of blood through the heart chamber, decreasing the heart’s effectiveness in pumping blood while increasing the likelihood of thrombus formation within the atria, most commonly the left atrial appendage, which can ultimately dislodge and cause a stroke. Atrial fibrillation is the leading cardiac cause of stroke.

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7
Q

Causes of atrial fibrillation

A

There are many causes of atrial fibrillation (AF), but it shares a strong association with other cardiovascular diseases. The commonly encountered causes include:
Advanced age
Congenital heart disease
Hemodynamic stress
Underlying heart disease - valvular disease, coronary artery disease, structural heart disease, atrial ischemia
Increased alcohol consumption
Hypertension - systemic or pulmonary
Endocrine disorders - diabetes, pheochromocytoma, and hyperthyroidism
Genetic factors
Neurologic disorders - subarachnoid hemorrhage or stroke
Hemodynamic stress - mitral or tricuspid valve disease, left ventricular dysfunction, pulmonary embolism
Obstructive sleep apnea
Inflammation - myocarditis and pericarditis

Any condition that leads to inflammation, stress, damage, or ischemia affecting the anatomy of the heart can result in the development of atrial fibrillation. In some cases, the cause is iatrogenic

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8
Q

When is atrial fibrillation referred to as recurrent?

A

When a patient has two or more episodes

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9
Q

Paroxysmal AF in younger individuals

A

In younger patients, paroxysmal AF has been commonly found to be secondary to electrically active foci within the pulmonary veins. Elimination of these foci is found to be effective in treating this type of AF since it eliminates the trigger for such episodes

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10
Q

Consequences of persistent AF

A

if it is associated with a rapid and uncontrolled ventricular rate, it may lead to electrical remodeling in the cardiac myocytes causing dilated cardiomyopathy.
This type of AF may present as the first episode or as a result of recurrent episodes of paroxysmal AF

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11
Q

Most common age group for atrial fibrillation

A

Although the worldwide prevalence of atrial fibrillation is approximately 1%, it is found in approximately 9% of individuals over the age of 75. At the age of 80, the lifetime risk of developing atrial fibrillation jumps to 22%

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12
Q

Pathophysiology of AF

A
  • Variety of mechanisms, however it is cardiac remodelling that accounts for most of them
  • Cardiac remodeling, particularly of atria, results in structural and electrical changes that eventually become the cause of deranged rhythm in AF. Structural remodeling is caused by the changes in myocytes and the extracellular matrix, and fibrous tissue deposition also plays a major role in some etiologies. On the other hand, tachycardia and shortening of the refractory period lead to electrical remodeling
  • Most commonly, hypertension, structural, valvular, and ischemic heart disease illicit the paroxysmal and persistent forms of atrial fibrillation
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13
Q

Is AF genetic?

A

Most cases of atrial fibrillation are non-genetic and relate to underlying cardiovascular disease. Typically, an initiating trigger excites an ectopic focus in the atria, most commonly around the area of the pulmonary veins, and allows for an unsynchronized firing of electrical impulses leading to fibrillation of the atria

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14
Q

Presentation of AF

A
  • The presentation of AF can range from asymptomatic to devastating complications such as cardiogenic shock and ischemic stroke
  • Symptoms include palpitations, chest pain, shortness of breath, increased lower extremity swelling, dyspnea on exertion, presyncope/syncope, hypotension, pulmonary edema, and dizziness.
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15
Q

Important patient history relating to AF and questions to ask

A
  • Identifying risk factors such as hypertension, history of valvular, structural, or ischemic heart disease, obstructive sleep apnea, obesity hypoventilation syndrome, smoking, alcohol intake, illicit drug use, history of rheumatic fever/heart disease, history of pericarditis, and hyperlipidemia
  • Assessment of patients with existing AF includes questions regarding:
    Duration and frequency of symptoms
    History of triggers
    Previously successful modes of termination
    The use of anti-arrhythmic drugs
    Antecedent cardiac diseases
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16
Q

Evaluating circulation in AF. What is the usual heart rate of AF patients?

A

On general physical examination, patients may be tachycardic with an irregularly irregular pulse. The heart rate usually ranges from 110/min to 140/min. Extremities should be evaluated for edema, peripheral pulses in both upper and lower extremities, and integumentary signs of peripheral vascular disease (PVD), such as hair loss and skin breakdown.

17
Q

What should the physical exam focus on?

A
  • The physical exam should focus on identifying the cause of AF
  • should always begin with the assessment of airway breathing and circulation as it is going to affect the decision-making regarding management
18
Q

Examples of what to look for as a cause of AF during physical examination

A
  • Examining the neck of the patient may give some clues regarding carotid artery disease or thyroid problems. The pulmonary examination may reveal signs of heart failure in the form of rales, and the presence of wheezing may indicate antecedent pulmonary diseases such as asthma and chronic obstructive pulmonary disease (COPD). A cardiovascular exam should consist of careful auscultation of all four cardiac posts and palpation of apical impulse, as this would be crucial in diagnosing an underlying valvular pathology. An abdominal exam should consist of palpating the aorta and listening for abdominal bruits. Moreover, hepatomegaly and abdominal distension may indicate heart failure. Subsequently, a careful examination of the central and peripheral nervous system may reveal signs of transient ischemic attack or cerebrovascular accident.
19
Q

Main points in evaluating patients with AF

A
  • History
  • Physical evaluation
  • Instrumental and laboratory testing
20
Q

Instrumental testing in AF

A
  • ECG is crucial, Echo could also be done
  • It is imperative to evaluate the patient for pulmonary embolism (with the d-dimers test or spiral CT scan) because the right heart strain can lead to atrial malfunctioning and atrial fibrillation
21
Q

ECG findings in atrial fibrillation

A
  • On ECG, atrial fibrillation presents with the typical narrow complex “irregularly irregular” pattern with no distinguishable p-waves.
  • Fibrillatory waves may be seen, or they may be absent. The ventricular rate usually ranges between 80 and 180/min.
22
Q

Laboratory testing in atrial fibrillation

A
  • Laboratory work is required to evaluate for the causes of atrial fibrillation, for example, a complete blood count (CBC) for infection, basic metabolic panel (BMP) for electrolyte abnormalities, Mg2+, Ca2+, K+, thyroid function tests to evaluate for hyperthyroidism, and a chest x-ray to evaluate the thorax for any abnormality.
  • Several cardiac diseases are associated with AF; therefore, it is essential to send cardiac biomarkers and B-type natriuretic peptide (BNP) to preclude the underlying cardiac disorder. Interventions such as cardiac catheterization may also be needed in certain cases if the history and physical findings are suggestive
23
Q

Non-cardiac causes of arrythmias

A

Caffeine; smoking; alcohol;
pneumonia; drugs (2-agonists, digoxin, L-dopa, tricyclics, doxorubicin); metabolic imbalance (K+, Ca2+, Mg2+, hypoxia, hypercapnia, metabolic acidosis, thyroid disease);
and phaeochromocytoma

24
Q

Echo use in arrythmias

A

To look for structural heart disease, eg mitral stenosis

25
Q

Continuous ECG monitoring options

A
  • Telemetry
  • Exercise ECGs
  • Holter monitors
  • Loop recorders
  • Pacemakers and ICDs (implantable cardioverter-defibrillator
26
Q

Normal conduction pathway in the heart

A

Normal conduction: initiated by the
sinoatrial node (SAN), electrical activity
spreads around the atria. The
atrioventricular node (AVN) receives
this activity, pauses, then passes it
on, down the bundle of His which
splits into left and right bundle
branches. These cause depolarization
of the ventricular myocardium
from bottom (apex) to top (outflow
tracts).

27
Q

What is a score that can be used to assess a patient’s risk of major hemorrhage?

A

HAS-BLED (for atrial fibrilliation patients) score which assesses the 1-year risk for major bleeding (intracranial, hospitalization, hemoglobin decrease >2 g/L, and/or transfusion) associated with oral anticoagulation
Orbit score can also be used

28
Q

What is used to stratify the risk of a patient developing PE

A

Wells score

29
Q

Interpretation of Wells score

A

Wells’ Score
≤0 Low/unlikely 5% (prevelance)
1-2 Moderate 17%
≥3 High/likely 17-53%

30
Q

Treatment / Management of AF

A
  • Anticoagulation if high stroke risk
  • Rate control as first line treatment
  • Indications for rhythm control include new-onset AF within the past 48 hours, AF with haemodynamic instability, or persistent symptoms despite adequate rate control
  • Immediate cardioversion if patient is hemodynamically unstable
  • Most studies comparing rate versus rhythm control have reported no significant difference in outcomes
  • Rhythm control if symptoms continue after has been controlled or for whom a rate-control strategy has not been successful
  • Emergency electrical cardioversion, without delaying to achieve anticoagulation, in people with life-threatening hemodynamic instability caused by new-onset atrial fibrillation
31
Q

Orbit score interpretation

A

0-2: Low risk of bleeding (2.5 bleeds per 100 patient years)
3 Medium risk (4.7 bleeds per 100 patient-years)
4 or more high risk (8.1 bleeds per 100 patient-years)

32
Q

Anticoagulation choice for AF

A

DOACs in preference of vit K antagonists because lower stroke risk and major hemorrhage in studies

33
Q

Which patients with AF shouldn’t use DOACs

A

Key exclusions for DOAC treatment specific to AF include moderate-to-severe mitral valve disease and rheumatic valve disease and metallic valves, in part because these patients have largely been excluded from clinical trials of DOACs to date

34
Q

What to use for rate control in AF

A
  • Using either a beta-blocker or rate-limiting calcium channel blocker (Ca2+ blockers to be avoided in patients with HF)
  • Digoxin can be considered for rate control but is not advised as a first-line agent pertaining to its adverse effects and tolerance
  • Dual therapy with either beta-blocker, diltiazem, digoxin
35
Q

What should be done before initiating DOACs?

A

Obtain renal and liver function before initiating non-vitamin K oral anticoagulants

36
Q

When should rate control not be offered as a treatment in AF patients?

A

Patients:
* 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.

37
Q

When should digoxin or dual therapy be considered in AF patients?

A

Consider digoxin monotherapy for initial rate control for people with
non-paroxysmal atrial fibrillation if:
* the person does no or very little physical exercise or
* other rate-limiting drug options are ruled out because of comorbidities or the person’s preferences. [2021]
1.7.5 If monotherapy does not control the person’s symptoms, and if continuing
symptoms are thought to be caused by poor ventricular rate control, consider
combination therapy with any 2 of the following:
* a beta-blocker
* diltiazem
* digoxin

38
Q

Pharmacological cardioversion choice of drugs and when its needed

A

If pharmacological cardioversion has been agreed on clinical and resource
grounds for new-onset atrial fibrillation, offer:
* a choice of flecainide or amiodarone to people with no evidence of structural
or ischaemic heart disease or
* amiodarone to people with evidence of structural heart disease.

In people with atrial fibrillation in whom the duration of the arrhythmia is greater
than 48 hours or uncertain and considered for long-term rhythm control, delay
cardioversion until they have been maintained on therapeutic anticoagulation for
a minimum of 3 weeks. During this period offer rate control as appropriate