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Year 3 > Week Seven - Case One > Flashcards

Week Seven - Case One Flashcards

1
Q

what are arrhythmias

A

abnormal heart rhythms

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2
Q

what are the shockable cardiac arrest rhythms

A

ventricular tachycardia
ventricular fibrillation

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3
Q

what are the non shockable cardiac arrest rhythms

A

pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)

asystole (no significant electrical activity)

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4
Q

what does narrow complex tachycardia refer to

A

a fast heart rate with a QRS complex duration of less than 0.12 seconds

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5
Q

on a normal 25mm/sec ECG, 0.12 seconds equals how many small squares?

A

3 small squares

therefore the QRS complex will fit within 3 small squares in narrow complex tachycardia

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6
Q

what are the four main differentials of a narrow complex tachycardia

A

Sinus tachycardia (treatment focuses on the underlying cause)

Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)

Atrial fibrillation (treated with rate control or rhythm control)

Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)

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7
Q

what are patients with syncope, heart muscle ischaemia (chest pain), shock or severe heart failure treated with

A

synchronised DC cardioversion under sedation or general anaesthesia

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8
Q

what is added if initial DC shocks are unsuccessful

A

intravenous amiodarone

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9
Q

what does broad complex tachycardia refer to

A

a fast heart rate with a QRS. complex duration of more than 0.12 seconds or 3 small squares on a ECG

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10
Q

what are the broad complex tachycardias

A

Ventricular tachycardia or unclear cause (treated with IV amiodarone)

Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)

Atrial fibrillation with bundle branch block (treated as AF)

Supraventricular tachycardia with bundle branch block (treated as SVT)

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11
Q

what is atrial fuller caused by

A

a re-entrant rhythm in either atrium

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12
Q

how does the electrical signal re-circulate in atrial flutter

A

in a self-perpetuating loop due to an extra electrical pathway in the atriaw

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13
Q

what is the usual atrial rate in atrial flutter

A

300 beats per minute

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14
Q

why does the signal not usually enter the ventricles on every lap

A

due to the long refractory period of the AV node

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15
Q

what does this result In, in terms of ratio of atrial and ventricular contractions

A

this often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute

there may be a 3:1 or a 4:1 variable conduction ratio

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16
Q

what is the appearance of atrial flutter on an ECG

A

sawtooth appearance on the ECG with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia

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17
Q

what is the treatment for atrial flutter

A

similar to AF, including anticoagulation based on the CHA2DS2-VASc score

radiofrequency ablation of the re-entrant rhythm can be a permanent solution

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18
Q

what is the QT interval

A

from the start of the QRS complex to the end of the. T wave

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19
Q

what does the QTc estimate the QT internal is if the heart rate was 60BPM

A

prolonged at:
More than 440 milliseconds in men
More than 460 milliseconds in women

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20
Q

what does a prolonged QT interval represent

A

represented prolonged repolarisation of the heart muscle cells (myocytes) after a contraction

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21
Q

what is depolarisation

A

the electrical process that leads to heart contraction

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22
Q

what is repolarisation

A

is a recovery period before the muscle cells are ready to depolarise again

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23
Q

what can waiting a long time for repolarisation result in

A

spontaneous depolarisation in some muscle cells

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24
Q

what are these abnormal spontaneous depolarisations before repolarisation known as

A

afterdepolarisations

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25
Q

what do these afterdepolarisations do

A

spread throughout the ventricles, causing a contraction before proper repolarisation.

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26
Q

when this leads to recurrent contractions without normal repolarisation, what is this called

A

torsades de pointes

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27
Q

what is tornadoes de pointes a type of

A

polymorphic ventricular tachycardia

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28
Q

what does torsades de pointes look like on an ECG

A

it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. the height of the QRS complex gets progressively smaller, then larger, then smaller and so on

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29
Q

how does torsades de pointes terminate and what does the lead to

A

terminates spontaneously and will revert to sinus rhythm or progress to ventricular tachycardia

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30
Q

what can this ventricular tachycardia lead to

A

cardiac arrest

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31
Q

what are the causes of prolonged QT

A

Long QT syndrome (an inherited condition)

Medications,

Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia

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32
Q

what medications can cause a prolonged QT

A

such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics

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33
Q

what is the management of a prolonged QT internal include

A

stopping and avoiding medications that prolong the QT interval

correcting electrolyte disturbances

beta blockers

pacemakers or implantable cardioverter defibrillations

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34
Q

what beta blocker is not used in the management of a prolonged QT internal

A

sotalol

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35
Q

what is the acute management of torsades de pointes

A

correcting the underlying cause

magnesium infusion (even if they have a normal serum magnesium)

defibrillation if ventricular tachycardia occurs

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36
Q

what are ventricular ecoptics

A

premature ventricular beats caused by random electrical discharges outside the atria

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37
Q

how do ventricular ectopics appear on an ECG

A

as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG

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38
Q

what does bigeminy refer to

A

when every other beat is a ventricular ectopic.

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39
Q

what would the ECG show in bigeminy

A

a normal beat, followed immediately by an ectopic beat, then a normal beat, then an ectopic and so on

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40
Q

what is the management of bigeminy

A

Reassurance and no treatment in otherwise healthy people with infrequent ectopics

Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death

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41
Q

what medication is sometimes used to manage symptoms of bigeminy

A

beta blockers

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42
Q

when does first degree heart block occur

A

where there is delayed conduction through the AV node.

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43
Q

what does first degree heart block look like on an ECG

A

despite the delated conduction, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex.

on an ECG , first degree heart block present as a PR interval greater than 0.2 seconds

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44
Q

what is second degree heart block

A

is where some atrial impulses do not make it through the AV node to the ventricles

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45
Q

what else are there instances of in second degree heart block

A

where P waves are not followed by QRS complexes.

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46
Q

what are the two types of second degree heart block

A

Mobitz type 1 (Wenckebach phenomenon)

Morbitz type 2

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47
Q

what is Mobitz type One

A

when the conduction through the AV node takes progressively longer until it finally fails, after which it resets and the cycle restarts

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48
Q

what is shown on an ECG in Mobitz type One

A

there is an increasing PR interval until a P wave is not followed by a QRS complex.

the PR interval then returns to normal, and the cycle repeats itself

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49
Q

what is Mobitz type 2

A

where there is intermittent failure of conduction through the AV node, with an absence of QRS complexes following P was vested

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50
Q

usually, what is there with Mobitz type two

A

usually a set ratio of P waves to QRS complexes

for example, three P waves for each QRS complex
the PR interval remains normal

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51
Q

what is there a risk of in Mobitz type two

A

asystole

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52
Q

what is a 2:1 block

A

is where there are two P waves for each QRS complex

every other P wave does not stimulate. a QRS complex.

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53
Q

what is third degree heart block also called

A

complete heart block

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54
Q

what sort of relationship between the P waves and QRS complexes is seen in third degree heart block

A

no observable relationship

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55
Q

what is there a significant risk of in third degree heart block

A

significant risk of asystole

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56
Q

what does bradycardia refer to

A

a slow heart rate, typically less than 60 beats per minute

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57
Q

what are the three main causes of bradycardia

A

medications
heart block
sick sinus syndrome

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58
Q

what medications can cause bradycardia

A

beta blockers

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59
Q

what does sick sinus syndrome encompass

A

many conditions that cause dysfunction in the SA node

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60
Q

what is sick sinus syndrome often caused by

A

idiopathic degenerative fibrosis of the SA node

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61
Q

what can sick sinus syndrome result in

A

sinus bradycardia, sinus arrhythmias, and prolonged pauses

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62
Q

what does asystole refer to

A

the absence of electrical activity in the heart - resulting in cardiac arrest

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63
Q

there is a risk of asystole in what conditions

A

Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds

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64
Q

what is the management of unstable patients and those at risk of asystole

A

Intravenous atropine (first line)

Inotropes (e.g., isoprenaline or adrenaline)

Temporary cardiac pacing

Permanent implantable pacemaker, when available

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65
Q

what are the two options for temporary cardiac pacing

A

Transcutaneous pacing, using pads on the patient’s chest

Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly

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66
Q

what is atropine

A

an antimuscarinic medication

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67
Q

how does atropine work

A

by inhibiting the parasympathetic nervous system, inhibiting the PNS leads to side effecting of pupil dilation, dry mouth, urinary retention and constipation

68
Q

what is Wolff-Parkinson-White Syndrome

A

a genetic disorder that allows abnormal conduction to occur in the heart, via an accessory pathway

69
Q

what is WPW sometimes called

A

a pre-excitation syndrome

70
Q

what are the other types of pre-excitation syndromes

A

Others include Lown-Ganong-Levine syndrome, and Mahaim-type pre-excitation.

71
Q

what can WPW lead to

A

atrial fibrillation, atrial flutter and a type of SVT known as Atrioventircular re-entry tachycardia (AVRT)

72
Q

what is V node re-entry tachycardia (AVNRT).

A

the tachycardia excite due to aberrant conduction through the AV node itself, and occurs in structurally normal hearts

73
Q

what is Atrioventricular re-entry tachycardia (AVRT)

A

the abnormal conduction occurs though an accessory pathway which is an anatomical abnormality

74
Q

what can AVRT pre-dispose to

A

VF and cardiac arrest

75
Q

what do all pre-excitation syndromes result in

A

faster conduction of impulses through an accessory pathway

76
Q

what does faster conduction of impulses through an accessory pathway lead to

A

a shorter PR interval on ECG. once this impulse reaches the ventricles, conduction does not occur via the normal conducting system route, which causes an altered QRS complex

77
Q

what is the altered QRS complex seen in WPW

A

sloping R wave - known as a delta wave

78
Q

what are the defining ECG changes of WPW

A

short PR interval
delta wave
non-specific t wave change

79
Q

what is the epidemiology and aetiology of WPW

A

incidence 0.3 per 1000

prevalence 0.1-0.3%

more common in men

congenital structural heart abnormality, although most often does not present until teenage years or early adulthood

80
Q

what is the presentation of WPW often

A

often asymptomatic and may be discovered incidentally on an ECG

81
Q

what do acute episodes of SVT present with

A

SOB, palpitations, dizziness, chest pain and syncope

may also present with AF or atrial flutter

82
Q

what may acute episodes be followed by

A

polyuria - SVT causes dilation of the atria, which releases atrial natuertic factor

83
Q

what can happen in severe cases of WPW

A

VF and cardiac arrest

84
Q

what does the accessory pathway allow for in most individuals and what is the exception

A

in most, the accessory pathway allows conduction in both directions, in 15% of cases, it allows only retrograde conduction

85
Q

what is orthodermic conduction

A

the accessory pathway allows the electrical signal to return to the atria from the ventricles. (usually the only route by which this ca occur is the AV node, and in a healthy individual the AV node only allows conduction in one direction, and thus this cannot occur

86
Q

what is the accessory pathway sometimes referred to as in WPW

A

Bundle of Kent

87
Q

in what percentage of patients with WPW does atrial flutter occur in

A

up to 7%

88
Q

in what percentage of patients with WPW does atrial fibrillation occur in

A

20%

89
Q

what can atrial flutter and atrial fibrillation lead to

A

VF or VT as the rapid atrial rate can be transferred directly to the ventricles via the accessory pathway without passing through the moderating effect of the AV node

90
Q

when is pre-excitation

A

not during an acute episod e

91
Q

what is a classical WPW sign which may be seen outside of the acute episode in an otherwise normal asymptomatic patient

A

delta wave

92
Q

what does the delta wave refer to

A

a slurred upstroke of the QRS complex, often in association with a short PR interval

93
Q

what may the delta wave do to the QRS complex

A

make the base of the QRS complex broad

94
Q

what are the usual ST changes seen in pre-excitation

A

usually discordant changes occur in the opposite direction to the QRS complex

95
Q

what are the two types of WPW

A

Type A

Type B

96
Q

what is Type A WPW

A

positive delta wave and QRS throughout. can look like right bundle branch block

97
Q

what is Type B WPW

A

negative delta wave in V1 and V2, positive in other precordial leads. can look like left bundle branch block

98
Q

what is orthodermic conduction

A

retrograde conduction through the accessory pathway

99
Q

what are the features of orthodermic conduction

A

Rate 200-300

Absent p waves (not visible behind fast QRS complexes)

Narrow QRS (<120ms) unless other abnormalities (e.g. Bundle branch block) are present

T wave inversion

wST segment depression

100
Q

what are the features of antidromic conduction

A

rate 200-300
wide QRS due to abnormal ventricular depolarisation through accessory pathway

101
Q

what are the features of atrial fibrillation

A

ratem>200
irregular
wide QRS complex as an abnormal ventricular conduction and depolarisation as signal bypasses AV node

102
Q

what is used to aid diagnosis of WPW

A

May involve the use of 24-hour Holter monitors to try to capture episodes of arrhythmia

Stress testing can help elicit arrhythmias

Routine bloods will likely be normal, but can rule out other causes of arrhythmias

Echo may be performed to rule out other visible structural heart abnormalities

Electrophysiology studies can show where the accessory pathway is to mark a site for ablation

103
Q

what is the treatment of choice for AVRT episodes / haemodynamically unstable patients

A

DC cardio version is the treatment of choice

104
Q

if haemodynamically stable:

A

Attempt vagal manoeuvres (e.g. ask patient to blow on 50ml syringe, carotid sinus massage)

If unsuccessful, give adenosine (6mg initially, followed by 12mg if required. Further 12mg dose can also be given)

Consider synchronised DC cardioversion if above unsuccessful

Avoid adenosine in AF as can paradoxically increase ventricular rate

105
Q

what do you treat as if there is any doubt as to the diagnosis

A

treat as VT

106
Q

what is the treatment for asymptomatic patients

A

may just have regular follow ups

Can have radio-frequency (RF) ablation therapy to destroy the accessory pathway
- 95% successful
- Usually done after electrophysiology studies have confirmed the site of the accessory pathway
- Has now largely replaced surgical ablation. Surgical may still be used in those in which RF ablation has failed, or who have other structural heart abnormalities

Drug treatment may be used in those unsuitable or unwilling to undergo ablation therapy

107
Q

after resolution of the acute episode, what is the treatment of symptomatic patients

A

May require drug therapy to prevent further episodes. Often amiodarone, flecainide or sotalol are used

An anti-arrythmic (usually calss IC or III) plus an AV node blocker should be used. AV node blocker alone is not enough to control the rapid rates seen in WPW involving the accessory pathway

108
Q

what is contraindicated in WPW

A

digoxin and is associated with increased risk of death

109
Q

what is the prognosis for WPW

A

prognosis is generally very good. radio frequency ablation is often curative

sudden death can occur but is rare - around 0.1%

110
Q

what does the risk of death correlate with

A

risk correlates with short R-R interval <250ms indicates highest risk

111
Q

what are the 3 features of heart failure

A

basal crepitations, ankle oedema, JVP

112
Q

what can anaemia result in as a physiological response to low haemoglobin

A

results in sinus tachycardia, the heart pumps faster to ensure oxygen reaches the organs

113
Q

what is the definition of palipitations

A

rapid pulsations or abnormal rapid or irregular beating of the heart.

114
Q

what are the causes of high output state palpitations

A

anaemia or pregnancy

115
Q

what are the structural cardiac causes of palpitations

A

valvular heart disease, ischaemic heart disease, hypertension

116
Q

what is Bradycardia

A

slow heartbeat

the resting heart rate is less than 60 beats in a minute in an adult

117
Q

what is tachycardia

A

fast heartbeat

the resting heart rate is greater than 100 beats a minute in an adult

118
Q

what is the pathophysiology of bradycardia

A

occur when depolarisation fails to initiate or conduct properly

119
Q

what are some examples of bradycardias

A

SA node disease

heart block (AV node, His bundle)

120
Q

what is the pathophysiology of tachycardias

A

occur when there is abnormal depolarisation occurring in the heart;

  • enhanced automaticity
  • reentry
121
Q

what is the pacemaker of the heart

A

the SA node

122
Q

what does sinus bradycardia look like on an ECG

A

when there is a normal upright P wave in lead II - sinus P wave - preceding every QRS complex with a ventricular rate of less than 60 beats per minute

123
Q

what is needed for treatment of permanent pathologic bradycardia

A

pacemaker

124
Q

what is sinus pause

A

describes a condition where the SA node fails to generate an electrical impulse for what is generally a brief period of time

125
Q

if a patient has sinus pause, what may they complain of

A

missed or skipped beats, flutters, palpitations, hard beats or may feel faint, dizzy or lightheaded or experience a synopal episode (passing out)

frequent pauses would heighten these symptoms. this is a result of the patient actually missing or dropping beats

126
Q

what is the treatment for sinus pause

A

may involve the use of medications or the use of a temporary to permanent pacemaker

127
Q

what happens during Sino-atrial exit block

A

the depolarisations that occur in the sinus node cannot leave the node towards the atria. they are blocked

128
Q

what is sinaltrial exit block (heart block) expressed as on ECG

A

a pause.

129
Q

how can SA exit block be distinguished from sinus arrest

A

because the pause in SA exit block is a multiple of the P-P interval that preceded the pause

130
Q

what is first degree heart block

A

slow conduction through the AV node

131
Q

what is 2nd degree heart block - Wenckebach or Morbitz type I

A

AV conduction becomes slower and slower until it misses a beat

132
Q

what is 2nd degree heart block - Mobitz type II

A

fixed block usually 2:!

133
Q

what is third degree heart block

A

complete heart block - no conduction to the ventricles

an escape pacemaker takes over from the His-bundle / bundle branch

134
Q

what is automaticity

A

an area of myocardial cells that depolarise faster than the SA node. this may be atrial or ventricular tissue

most occur at a single focal sight

135
Q

what is reentry

A

an electrical pathway that is not supposed to be there, connecting two areas that should not be connected

abnormal electrical connections can be congenital, or they can form because of heart disease.

if such a connection exists, it can form an electrical circuit

136
Q

what is supra ventricular tachycardia

A

is a heart condition where the heart suddenly beats much faster than normal.

137
Q

where does SVT originate from

A

faulty electrical impulses in the upper part of the heart, rather than from the ventricles

138
Q

what is ventricular tachycardia

A

defined as a sequence of three or more ventricular beats

the frequency must be higher than 100bpm

139
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

in atrial fibrillation

A
  • grossly irregular
  • 400-600 bpm
  • 75-175 bpm
  • absent
  • slows down rate; irregularity remains
140
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

in atrial flutter

A
  • regular (sometimes alternating block)
  • 250-350 bpm
  • 75-150bpm
  • negative sawtooth in lead II
  • temporary reduced conduction
141
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

AVNRT

A
  • regular
    -180-250 bpm
  • 180-250 bpm
  • in QRS complex (R’)
  • stops
142
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

atrial tachycardia

A
  • regular
  • 120-250bpm
  • 75-200 bpm
  • preceded QRS, p wave differs from sinus-p
  • temporary AV block
143
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

atrio-ventriclar reentry tachycardia (AVNT)

A
  • regular
  • 150-250bpm
  • 150-250bpm
  • RP<PR
  • stops
144
Q

what are the two types of VT

A

ventricular tachycardia
ventricular fibrillation

145
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

Ventricular tachycardia

A
  • regular (mostly)
  • 60-100 bpm
  • 110-250bpm
  • AV dissociation
  • no rate reduction (sometimes accelerates)
146
Q

what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine

ventricular fibrillation

A
  • irregular
  • 60-100 bpm
  • 400-600 bpm
  • AV dissociation
  • none
147
Q

what type of SVT is WPW syndrome an example of

A

AVRT

148
Q

what is the pattern of pre-excitation on an ECG

A

sinus rhythm with a short PR interval and clear delta waves

149
Q

what does pre-excitation indicate

A

conduction via an accessory pathway

150
Q

what is the trio used to diagnose WPW syndrome

A

The presence of pre-excitation on a 12 lead ECG, symptoms and SVT is called Wollf-Parkinson-White (WPW) syndrome.

151
Q

what is WPW syndrome

A

SVT that uses an AV accessory tract

the accessory pathway may also allow conduction during other supra ventricular arrhythmias such as atrial fibrillation or flutter

152
Q

what is type A WPW syndrome

A

the delta wave and QRS complex are predominantly upright in the precordial leads

the dominant R wave in lead V1 may be misinterpreted as right bundle branch block

153
Q

what is type B WPW syndrome

A

the delta wave and the QRS complex are predominantly negative in leads V1 and V2 and positive in the other precordial leads, resembling left bundle branch block

154
Q

how common is WPW syndrome

A

relatively common, and found in 1-3 per 1000 of the population

155
Q

what are vagal manoeuvres

A

physical actions that make your vagus nerve act on your hearts natural pacemaker, slowing down its electrical impulses

156
Q

what is the most common Vagal manoeuvre

A

valsalva maneourve

157
Q

how are vagal manoeuvres used diagnostically

A

can be used to distinguish between ventricular tachycardia and supraventircular tachycardia by slowing down the rate of conduction at the SA or AV nodes

158
Q

how are vagal maneouvres used therapeutically

A

Therapeutic: Vagal manoeuvres are the first-line treatment of hemodynamically stable supraventricular tachycardia, serving to slow down or terminate the arrhythmia. Vagal manoeuvres have a reported success rate of conversion to sinus rhythm for SVT around 20-40%, possibly being higher for AVNRT (an SVT associated with a bypass tract). Whereas the modified Valsalva manoeuvre is most effective in adults, cold water immersion may be preferred as a safe, effective, and non-invasive treatment for paediatric SVT.

159
Q

what is the Valsalva manoeuvre

A

While lying on your back, take a deep breath and act like you’re exhaling but with your nose and mouth closed for 10 to 30 seconds. It should feel like trying to breathe air out into a blocked straw.

160
Q

what is the Diving reflex

A

While sitting, take several deep breaths, hold your breath and then quickly put your whole face into a container of ice water. Keep your face submerged as long as you can. The alternative approach is putting a bag of ice water or an ice-cold, wet towel against your face.

161
Q

what is the carotid sinus massage

A

Carotid sinus massage - Lie on your back with your head turned to one side. The doctor will use their fingers to push on your carotid sinus for five to 10 seconds. If it doesn’t work, they can try again after a minute or try the other side of your neck.

162
Q

when should you not do vagal manoeuvres

A
  • Low blood pressure
  • Chest pain
  • Shortness of breath
  • A shortage of oxygen in their body
  • An inability to get enough blood to their organs
163
Q

if concerned about an arrhythmia, what steps should you take?

A

request a 24-48 hour ECG

164
Q

what are the DVLA guidelines regarding arrhythmias for Group One - cars and motorcycles

A

Group 1 (car or motorcycle):
- Must stop driving if the arrhythmia has caused or is likely to cause incapacity.
- Driving may be permitted when the underlying cause has been identified and the arrhythmia has been controlled for at least four weeks.

165
Q

what does the DVLA say regarding arrhythmias for Group 2: lorry or bus

A

Group 2 (lorry or bus):
- Disqualifies from driving if the arrhythmia has caused or is likely to cause incapacity. DVLA must be informed.
- Driving may be permitted when:
– The underlying cause has been identified.
– The arrhythmia is controlled for at least three months.
– The LV ejection fraction is ≥40%.
– There is no other disqualifying condition.

166
Q

if you are getting sinus tachycardia as a result of anxiety or stress, what can be prescribed

A

a beta blocker such as propranolol

167
Q
A

Year 3 (63 decks)

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