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Med 1 Block > Palpitations > Flashcards

Palpitations Flashcards

1
Q

Define palpitations

A

Feeling of the heart racing, punding or fluttering or missed heart beats.
Last seconds, minutes or longer.
Felt in chest, neck or throat.
Are often common and harmless

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2
Q

What are some cardiac causes of palpitations?

A

Arrhythmia
Cardiomyopathy
Congenital heart disease
Heart failure
Heart valve disease

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3
Q

What are some non-cardiac causes of palpitations?

A

Alcohol
Caffeine
Ectopic beats
Recreational drugs
Smoking
Stress/anxiety
Hyperthyroidism

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4
Q

What are the S1 and S2 hearts sounds?

A

S1 - mitral and tricupside valves closing
S2 - aortic and pulmonary valves closing

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5
Q

How do the S1 and S2 heart sounds relate to systole/diastole?

A

S1 to S2 is systole
S2 to S1 is diastole

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6
Q

What is the brief electrical conduction system in the heart?

A
  1. Depolarisation begins at the SA node (sinus rhythm)
  2. Passes through the atrial walls to the AV node - temporaly held ensures all atria contracted and blood forced intro ventricle
  3. Electrical activity passes through AV node down the Bundle of His.
  4. Electrical activity dissipates through the purkinje fibres.
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7
Q

What is an arrhythmia?

A

An abnormal heart beat
Occurs due to a defect in the normal cardiac conduction, can happen at any point in the cardiac cycle.

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8
Q

How does atrial/ventricular systole/diastole relate to the different stages on an ECG?

A
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9
Q

What part of the ECG is abnormal in atrial fibrillation/flutter?

A

P wave

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10
Q

What part of the ECG is abnormal in a heart block?

A

PR interval

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11
Q

What part of the ECG is abnormal in a Bundle Branch Block?

A

QRS complex

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12
Q

What are the different types of heart block?

A

First degree - fixed prolonged PR interval (>0.2s)
Second degree Type 1/ Mobitz 1 - longer longer longer drop rest
Second degree type 2 - Constant PR interval with intermittently dropped QRS often 3;1 or 4:1
Third degree/complete - p waves and QRS complex have no relation to each other, ventricular rate is often slower 20-40bpm.

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13
Q

What are the key features of a Bundle Branch Block on a ECG?

A

Broad QRS
WiLLiaM MaRRoW
LBBB - W in V1 and M in V6
RBBB - M in V1 and W in V6

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14
Q

In MLA terms what are the proper annotation for what happens in a LBBB ECG?

A

V1 - small R followed by large S wave
Lateral leads/V5 - Large R waves and small S waves, may show inverted T waves or depressed ST
Lateral leads/V5 - L1, AvL, V5, V6 - within this the large R wave is M shaped, notched or RS complex

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15
Q

In MLA terms describe the changes in the ECG in a RBBB?

A

V1 = RSR (large second R gives an M shape) - may show invested T waves or depressed ST
Lateral leads - broad S wave.

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16
Q

What are the rules regarding SVT and driving?

A

DVLA should be informed if tachy cause sudden dizziness or fainting within the last 12 months
May NOT need to tell the DVLA about abnormal heart rhythm if underlying cause has been identified and treated, controlled for at least 4 weeks.

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17
Q

How does the prognosis of left and right bundle branch block compare?

A

Left poorer prognosis - more likely to be sign of underlying cardiovascular disease, can lead to HF, ACS, cardiomyopathy or HTN. Higher/earlier mortality in patients

RBBB - better prognosis, can occur in otherwise fit and health individuals, may be no apparent cause.

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18
Q

What is an SVT?

A

A tachydysrhytmia arising above the level of the Bundle of HIS
Includes regular atrial irregular atrial and regular atrioventricular tachycardia.

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19
Q

What are the three main types of SVT?

A

Classified by site or origin and regularity.
1. AV nodel reentrant tachycardia (AVNRT)
2. Atrioventricular reentrant tachycardia (AVRT)
3. Atrial tachycardia

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20
Q

What are the three ways to manage SVT?

A

Vagal maneuvers to try to stimulate the vagus nerve to slow down HR
Caortid sinus massage
Drugs - e.g adenosine

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21
Q

What is an AVNRT?

A

Is an SVT
Abnormal electrical activity around the AV nodal area.
Ectopic beat occurs whilst the fast pathway in the AVN is in refractory period resulting in impulse travelling only down the slow conduction pathway.
By the time this reaches the bottom of the loop the fast pathway has recovered allowing to travel back up the fast pathway and enter a circus like rhythm.
Alongisde sending signals to ventricles
Results in retrograde P waves that be by hidden within, just after or rarely just before the narrow QRS complex. (may have scooped out appreance to S wave)
This is due to near-simultaneous contraction of the atria and the ventricles.

22
Q

What is an AVRT?

A

Type of SVT
re-entrant of circus movement of electrical activity within the heart by a bypass tract - can enable antegrade early ventricular repolarisation or retrograde early atrial depolarisation

23
Q

What is an example of a AVRT syndrome?
What does it look like on an ECG?

A

Wolf Parkinson White syndrome
WPW - antegrade - results in short PR and delta wave or slurred rise QRS.

24
Q

What is an atrial tachycardia?

A

Is unifocal
A focus point outside the SAN fires off automatically at a rapid rate.
This normally occurs in patients with structural heart disease or following extensive ablation within atria.
Shows on an ECG with organised atrial activity with P wave morphology different from sinus rhythm (but same in all complexes) and PR is an isoelectrical line preceding QRS.

25
Q

Define atrial fibrillation.

A

Supraventricular cardia arrhythmia
Characterised by disorganised electrical activity within the atria resulting in ineffective atrial contraction and irregular ventricular contraction.

26
Q

What is the relevant epidemiology of atrial fibrillation?

A

Most common heart rhythm disorder
1% population
Particularly in the elderly - 5% over 65yrs, 10% over 80yrs.
Rare in young

27
Q

What is the basic pathophysiology of AF?

A
  1. Predisposing condition such as HTN or mitral regurg cause the atria to stretch which changes their electrical properties.
  2. Increased likelihood that an atrial ectopic will occur and the SAN will sustain it leading to AF
  3. resulting chaotic electrical activity is intermittently conducted through the AVN giving rise to irregularly irregular ventricular contraction.
  4. Ineffective movement of the blood into the ventricles from the atria reduced cardiac output leads to function consequences (often heart failure symptoms)
28
Q

What is the consequence of ineffective atrial contraction in atrial fibrillation?

A
  1. Blood stasis in the atria increased chances of thrombosis (Virchows triad) and subsequent embolic complications such as stroke.
  2. Ineffective blood movement into ventricles, reduced cardiac output - can exacerbate heart failure like symptoms.
29
Q

What type of Atrial fibrillation has the highest rate of complications?

A

Paroxysmal

30
Q

What are the three different types of atrial fibrillation?
How are they different?

A

Paroxysmal: ep >30s but less than <7d and self terminating but recurrent

Persistent episodes - can last longer than 7dys, or less if treated, always require electrical or chemical cardioversion

Permanent: Fail to terminate with cardioversion or terminated episode that replace within 24hrs, or long standing AF (>1yr) where cardioversion is not indicated or attempted.

31
Q

What is meant by fast and slow AF?
What is more common?

A

Fast AF is more common
Tachyarrhythmia

Slow AF - slow ventricular response - bradyarrhthmia and may cause syncope.

32
Q

What conditions/medical risk factors in AF most commonly associated with?

A

Hypertension
Obesity
Alcohol

33
Q

What is meant by AF as insidious disease?

A

Develops gradually and without obvious symptoms at first
Often due to chronic cardiac deterioration which makes the heart vulnerable to AF

Note can also occur acutely.

34
Q

What are some cardiac cause of acute AF?

A

Heart Failure (secondary to MI)
Structural pathology - valve stenosis or regurg
Pre-excitation syndromes - WPFS
Inflammatory conditions - pericarditis or myocarditis

35
Q

What are some non-cardiac causes of acute AF?

A

Acute infection
Electrolyte imbalance
Pulmonary embolism
Thyrotoxicosis or hypothyroidism.

36
Q

What are the key symptoms of atrial fibrillation?

A

Asymptomatic
Breathlessness
Chest discomfort
Palpitations
Light-headedness
Reduced exercise tolerance
Syncope: due to bradycardia (particularly in paroxysmal AF as when rhythm restored can take a few seconds for SAN to wake up)
Primary presenting feature is often a TIA or a stroke.

37
Q

What are the key examination findings in AF?

A

Irreguarly irregular pulse when palpating the radial or carotid arteries or auscultating at the apex.

May have co-exisiting heart failure:
Raised JVP
Added heart sounds on chest (gallop rhythm)
Crackles on chest ausculatation
Ankle swelling.

38
Q

What investigations should be done for a patient with suspected AF?

A

Bedside:
Obs (NEWS, hemodynamic instability), 12-lead ECG +/- ambulatory ECG
Bloods:
FBC (infection or low Hb), U&E (electrolyte abnormality trigger), TFT (thyroid disturbance as a cause), Coagulation screen (before starting treatment)
Imaging:
ECHO - structural cause
CXR - Heart failure features

39
Q

What are the different types of ambulatory ECG?

A

24hr tape
Holter (7 day monitoring)
Implantable loop recorder

40
Q

What clinical scoring system is used to calculate the risk of stroke in AF patients?

A

CHADS2-VASc score

41
Q

How to calculate and interpret a CHADS2-VASc Score?

A

Congestive heart failure -1
Hypertension 1
Age >= 75 2
DM 1
Stroke or TIA prior 2
Vascular disease (MI,aortic plaque)1
Age 65-74 1
Sex - female - 1
Higher score = higher risk of TIA/Stroke

42
Q

What clinical scoring system is used to calculate a bleeding risk in patients on anti-coagulation with AF?

A

HAS-BLED scoring system

43
Q

How to manage a haemodynamically stable patient with AF for >48hrs or unknown time frame?

A

Consider late cardioversion - must be on anticoagulant 4w pre and post. Patient profile should have high change of NSR persisting after shock - young, reversible cause that is now corrected.

Long term control:
Anticoagulation - warfarin, DOACs (apixaban)
Rate control - beta-blockers, rate limiting CCBs, digoxin

44
Q

What is the general management plan for AF patients?
Need to know the orange boxes

A
45
Q

What drugs tend to be used for long term anti-coagulation in AF patients?

A

Apixaban (DOAC) first line - does not require INR monitoring
Warfarin - after shared decision making, required if patient has a prosthetic valve as INR required is higher than what can be achieved with DOACs.

46
Q

What drugs can be used for rate control in patients with AF?

A

Beta blockers - bisoprolol
CCB - verapamil, diltiazem
Digoxin - for sedentary patients only.

47
Q

What are the risk factors for atrial fibrillation?

A
  1. valvular disease
  2. heart failure
    3, Ischemic heart disease
  3. Inflammation/infiltration of the heart - sarcoidosis, amyloidosis
  4. HTN
  5. Age
  6. secondary lifestyle, obestity
  7. Hyperthryoidism
48
Q

What are the different stages in the cardiac cycle?

A

Isovolumic ventricular contraction
Ejection
Isovolumic ventricular relaxation
Rapid inflow
Diastole
Atrial systole

49
Q

Cardiac history with new xxxx bundle branch block is considered a STEMI

A

Left

50
Q

Other than palpitations how can SVT present?

A

Tachycardia
Tachypnoea
Lightheadedness
Syncope /pre-syncope
Progressive Fatigue
Reduced exercise tolerance
Angina-like symptoms - chest pain or tightness
Pounding in the head or neck

51
Q

What are some risk factors for SVT?

A

Heart disease - congential, HF, coronary artery disease
Previous ablation of heart tissue
Obstructive sleep apnoea
Diabetes
Thyroid disease

Med 1 Block (39 decks)

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