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MBChB > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What bacteria is responsible for rheumatic valve disease?

A

Streptococcus pyogenes

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2
Q

What are the three leaflets of the aortic valve called?

A

Right
Left
Non-coronary

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3
Q

What are three causes of aortic stenosis?

A

Age (wear and tear –> calcification)
Rheumatic valve disease
Congenital

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4
Q

Describe the murmur associated with aortic stenosis

A

Ejection systolic murmur

Radiates to the right upper sternal edge, suprasternal notch and carotids

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5
Q

What is the progressive effects of aortic stenosis?

A

Increased LV cavity pressure –> pressure overload –> LV hypertrophy

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6
Q

What are the symptoms of aortic stenosis?

A 
SOB
Chest pain
Pre-syncope
Syncope
Reduced exercise capacity
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7
Q

What are the causes of aortic regurgitation?

A 
Degenerative
Rheumatic valve disease
Aortic root dilation
Systemic disease
Endocarditis
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8
Q

Give examples of systemic diseases that can result in aortic regurgitation

A

Marfan’s syndrome
Ehler Danlos syndrome
Ankylosing spondylitis
SLE

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9
Q

What is the effect of aortic regurgitation?

A 
Blood pushed into aorta 
In diastole, the valves are incompetent
Blood flows back into LV 
Volume overloaded 
LV dilation
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10
Q

What are the symptoms of aortic regurgitation?

A

SOB

Reduced exercise capacity

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11
Q

What is the prevalence of people having a bicuspid aortic valve rather than a tricuspid aortic valve?

A

1-2%

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12
Q

What are people with a bicuspid aortic valve prone to developing?

A

Premature dysfunction

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13
Q

Describe the mitral valve

A

Fibrous annulus - this can become dilated which pulls the valve leaflets apart

Anterior and posterior leaflets - anterior do the most work

Chordae tendinae and papillary muscles

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14
Q

What is the nomenclature of the anterior and posterior leaflets of the mitral valve?

A

A1, A2, A3

P1, P2, P3

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15
Q

What is the major cause of mitral stenosis?

A

Rheumatic valve disease

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16
Q

What is the effect of mitral stenosis?

A

Pressure overload
Dilated LA
AF

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17
Q

Other than AF, what are the two other potential effects of mitral stenosis?

A

Pulmonary hypertension

Secondary right heart dilatation

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18
Q

What are the symptoms of mitral stenosis?

A 
SOB
Palpitations
Chest pain
Haemoptysis
Right heart failure symptoms (pitted oedema, ascites etc)
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19
Q

What is the effect of mitral regurgitation?

A

Volume overload in both LA and LV
LA and LV dilation
Pulmonary hypertension and secondary right heart dilation
AF

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20
Q

What are the symptoms of mitral regurgitation?

A

SOB
Palpitations
RHF symptoms

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21
Q

Who is most likely to develop pathology of the pulmonary valve?

A

Children and young adults

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22
Q

What are the causes of tricuspid valve pathologies?

A

Pulmonary hypertension
IVDU
Endocarditis

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23
Q

How should valvular disease be assessed?

A 
History 
Examination - murmur 
BP
ECG
ECHO - valvular dysfunction
CT 
MRI 
Exercise tolerance test, CPET, Stress ECHO
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24
Q

What medical treatments can be used in the management of valvular disease?

A

Diuretics - reduce overload on heart

Mainly surveillance - watch and wait

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25
Q

What are the different surgical options for the management of valvular disease?

A

Valve repair
Valve replacement
Mechanical
Tissue

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26
Q

What type of valve replacement requires warfarin?

A

Mechanical

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27
Q

What are the two procedures that can be used in the management of valvular disease?

A

TAVI (transcatheter aortic valve intervention)

Valvuloplasty

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28
Q

When can valvuloplasty be used?

A

Role in mitral valve disease
Mainly young people with RVD
Buy time before valve replacement

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29
Q

What is the risk of stroke associated with AF?

A

5-fold increase compared to general population

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30
Q

What percentage of the population have AF?

A

1.5-2% (prevalence is increasing with the ageing population)

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31
Q

Give examples of conditions that predispose to or encourage the progression of AF

A 
HTN
Symptomatic HF 
Valvular heart disease
Cardiomyopathies
ASDs
Coronary artery disease
Thyroid dysfunction
Obesity
DM 
COPD 
Sleep apnoea
Chronic renal disease
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32
Q

What symptoms are associated with AF?

A

Asymptomatic
Palpitation
Dyspnoea

(rare: chest pain, syncope)

May present with the complications of AF (stroke/peripheral emboli)

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33
Q

What type of pulse is associated with AF?

A

Irregularly irregular

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34
Q

What are the three types of AF?

A

Paroxysmal
Persistent
Permanent

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35
Q

Describe paroxysmal AF

A

Intermittent
Starts and stops
Can last from 30s to over 24hrs at a time

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36
Q

Describe persistent AF

A

Requires intervention to terminate the arrhythmia (IV antiarrhythmic drug or DC cardioversion)

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37
Q

Describe permanent AF

A

Continually there, won’t try to restore sinus rhythm

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38
Q

What ECG changes are associated with AF?

A

Absence of P waves

Irregular QRS complex

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39
Q

Describe the ECG changes associated with AF

A

Atria aren’t contracting as a synctium
Different cells are contracting at different rates
There are multiple entry circuits
Ventricles have a variable rate dependent upon which impulses are able to pass through the AV node –> Bundle of His –> activate the ventricles

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40
Q

Describe atrial flutter

A

Re-entry around the tricuspid valve
Atria contracting at a rate of 250-300bpm
Saw-tooth pattern on ECG

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41
Q

On what ECG leads can a saw-tooth pattern be seen during atrial flutter?

A

Inferior leads II, III and aVF

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42
Q

What are the haemodynamic effects of AF and atrial flutter?

A

Loss of cardiac output
Atria are not beating in a coordinated fashion so blood clots may form in the atria –> break off –> thrombus can emboli to the brain, kidneys etc

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43
Q

What are the treatment aims in AF?

A 
Prevention of stroke
Symptom relief
Optimum management of concomitant cardiovascular disease
Rate control 
\+/- correction of rhythm disturbance
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44
Q

What are the essential investigations for a patient with AF?

A

ECG - confirm arrhythmia
ECHO - structural heart disease
Thyroid function tests
LFTs

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45
Q

What is the target HR for a patient with AF who is:

a) asymptomatic
b) symptomatic

A

Asymptomatic: <110 bpm
Symptomatic: <80 bpm

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46
Q

If a patient doesn’t have cardiac failure, how should their AF be managed?

A 
Beta blocker (bisoprolol 2-5-5mg OD or atenolol 25-50mg BD)
OR
Ca antagonist (verapamil 120-240mg BD)
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47
Q

What is the second line treatment for a patient with AF who does not have HF?

A

Digoxin

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48
Q

What scoring system can be used to ascertain a patient’s risk of having a stroke?

A

CHA2DS2-VASc

out of 9

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49
Q

What are the components of the CHA2DS2-VASc scoring system?

A 
Congestive heart failure/LV dysfunction
HTN
Age >/= 75 (2pts)
DM 
Stroke/TIA/thrombo-emobolism (2pts)
Valvular disease
Age 65-74
Female sex
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50
Q

What should the INR target be for a patient with AF?

A

2-3

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51
Q

What is the risk of an INR >3?

A

Increased risk of intracranial bleed

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52
Q

What is the risk of an INR <2?

A

Increased risk of stroke

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53
Q

What treatment for AF requires INR measurements?

A

Warfarin

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54
Q

What are the new oral anti-coagulants that can be used in the management of AF?

A

Dabigatran - thrombin inhibitor
Rivaroxaban - factor Xa inhibitor
Apixaban - factor Xa inhibitor
Edoxaban - factor Xa inhibitor

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55
Q

Who should be referred for specialist assessment?

A

Patients who are symptomatic despite adequate rate control

Younger patients <60

Inadequate rate control despite beta-blocker/Ca antagonists + digoxin

Structural heart disease on ECHO

Co-existing HF

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56
Q

How can rhythm control be managed in patients with AF?

A

Direct current cardioversion
Antiarrhythmic drugs
Catheter ablation

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57
Q

What are class 1 antiarrhythmic drugs?

A

Na channel blockers

(Flecainide 100mg bd
Propafenone 150-300mg bd)

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58
Q

What are class 3 antiarrhythmic drugs?

A

K channel blockers –> prolong action potential duration/QT interval

Sotalol 80mg bd
Amiodarone 200mg OD

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59
Q

Give an example of a multichannel blocker that can be used in the management of AF

A

Dronedarone 400mg bd

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60
Q

Which veins can be the trigger of paroxysmal AF?

A

Pulmonary veins

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61
Q

What are the two ways of performing catheter ablation?

A

Radiofrequency current (burning)

Cryo-ablation (freezing)

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62
Q

In what patient group is catheter ablation more effective?

A

Structurally normal hearts

Minimal heart disease

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63
Q

In what proportion of patients is catheter ablation curative in:

a) paroxysmal AF?
b) persistent AF?

A

Paroxysmal - 65-80%

Persistent - 50-60%

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64
Q

Define endocarditis

A

Inflammation of the endocardium which results in vegetation formation and ultimately damage to the cusps of the valves

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65
Q

What are the components of the endocarditis vegetation?

A 
Fibrin mesh 
Platelets
White blood cells
Red blood cell debris 
Organisms
66
Q

Give some example microorganisms that can cause endocarditis

A 
Staph. aureus
CoNS
Strept. viridans
HACEK
Coliforms
67
Q

Describe HACEK

A

5 gram negative bacteria which cause endocarditis
Relatively rare
Culture negative endocarditis

68
Q

What are the three classifications of endocarditis?

A
  1. Native valve endocarditis
  2. Endocarditis in IVDUs
  3. Prosthetic valve endocarditis
69
Q

What microorganisms commonly cause NVE?

A

S.viridans (oral flora –> transient bacteraemia caused by brushing teeth –> underlying valve disease)
Staphylococcus

70
Q

What microorganisms commonly cause Endocarditis in IVDUs?

A

S.aureus
E.coli
Pseudomonas
Fungal endocarditis

71
Q

What microorganisms commonly cause PVE?

A

Staphylococcus endocarditis eps CoNS
E.coli
Pseudomonas
Fungal endocarditis

72
Q

What risk factors are associated with NVE?

A

Underlying valve abnormalities
Aortic stenosis
Mitral valve prolapse

73
Q

Describe aortic stenosis

A

Narrowing of the aortic valve
Age-related calcification (50%)
Calcification of congenitally abnormal valve (30-40%)
Rheumatic fever (10%)

74
Q

Briefly describe how Rheumatic Fever can cause NVE

A

Group A Strept or Strept. progenes infection
Contains streptolysin O toxin
Infection from streptococcus pyogenes –> strept. throat
Partially or untreated liberates the streptolysin toxin
Toxin attracts ASO antibodies
Causes destruction of streptolysin toxin
Protein of heart valves is similar to that of streptolysin toxin
Ab attack the heart valves
Stenosis/regurgitation

75
Q

In IVDU endocarditis, what valve is most commonly affected?

76
Q

Describe the acute clinical features associated with endocarditis

A

Patient appears very sick
Progressive valve destruction and metastatic infection
S.aureus and gram negative bacteria

77
Q

Out of all congenital heart defects, what percentage are atrial septal defects?

78
Q

What type of atrial septal defect is the most common, and what does this result in?

A

Secundum (80%)

Patent foramen ovale

79
Q

What type of ASD results in an atroventricular septal defect?

80
Q

What is the physiological effect of an ASD?

A

Abnormal mixing of blood
Blood flows path of least resistance (LV –> RV = left-right shunt)
Increased volume in RV (blood from RA and from LV)
RV dilates to accommodate blood
Will eventually fail –> Right Ventricular Failure

81
Q

What symptoms are associated with ASD?

A

Often asymptomatic
Murmur –> ECHO –> diagnosis
Stretching of RA –> vulnerable to supraventricular arrhythmias such as AF/atrial flutter (palpitations, SOB, signs of peripheral heart failure)
May present with stroke (thrombus passes from RHS - LHS of heart –> carotid arteries –> stroke)

82
Q

If a young person has a stroke, what should they be investigated for?

83
Q

What are the O2 sats like in a patient with ASD?

84
Q

What is coarctation of the aorta?

A

Narrowing of the aorta generally at the site of the ductus arterioles insertion

85
Q

What is the physiological implication of coarctation of the aorta?

A

LV has to pump harder to force blood through the narrowing
LV hypertrophy
LVF
Collateral vessels may develop to bypass blood flow around the narrowing

86
Q

Describe the presentation of coarctation of the aorta

A

Severe narrowing –> poor peripheral perfusion (cold feet, claudication, abdominal angina)

Symptoms of pre-coarctation HTN (before coarctation, the BP is very high –> headaches and nose bleeds)

87
Q

When performing a CV examination on a patient with coarctation of the aorta, what signs would you expect to see?

A

Discrepancies in limb BP (lower limb BP is lower than upper limb BP - should. be the other way around)
Radio-femoral delay
Continuous murmur
Normal O2 sats

88
Q

Describe transposition of the great arteries

A

Aorta and pulmonary arteries switch

Aorta comes off RV
Pulmonary arteries come off LV

89
Q

What is the physiological effect of transposition of the great arteries?

A

Two separate circulations - incompatible with life

Systemic circulation:
Deoxygenated blood –> RA –> RV –> AORTA –> systemic circulation

Pulmonary circulation:
Oxygenated blood –> LA –> LV –> PULMONARY ARTERIES –> lungs

90
Q

Describe foetal circulation

A

Receives oxygenated blood from placenta –> IVC –> RA
Lungs under-developed therefore high pressure
Blood follows path of least resistance –> foramen ovale –> LHS of heart
(Some blood may pass into pulmonary circulation but most of this blood will pass into the aorta via the ductus arteriosus)

91
Q

Describe what happens at birth to the components of the foetal circulation

A

First breath
Change in pressure in heart and lungs
Within a few hours, foramen ovale and ductus arteriosus will close

92
Q

Neonates with transposition of the great arteries depend on what for survival?

A

Patent ductus arteriosus and foramen ovale

93
Q

In a neonate with transposition of the great arteries, what needs to be administered at the time of birth and why?

A

IV prostaglandins
Maintains patency of the foramen ovale and the ductus arteriosus - allows mixing of blood - allows time for surgical intervention

94
Q

Describe the surgical intervention for transposition of the great arteries

A

Historically - atrial switch (baffle connects SVC, IVC and mitral valve to LV –> remove atrial septum = O2 blood —> atrial septum –> RA –> RV –> aorta –> systemic circulation)

Now: arterial switch (cut aorta and pulmonary arteries –> switch them over and reconnect ie pulmonary arteries to RV; aorta to LV)

95
Q

What complications are associated with atrial switch?

A

RV dilates due to increased blood volume
RVF
+ Tricuspid regurgitation –> compounds RVF

96
Q

What complications are associated with arterial switch?

A

Pulmonary arteries supplies coronary arteries –> occlusion/stenosis –> MI/sudden death post op

97
Q

What are the components of Tetralogy of Fallot?

A
  1. VSD
  2. Overriding aorta
  3. Right outflow tract obstruction
  4. Right ventricular hypertrophy
98
Q

Tetralogy of Fallot is a _____ abnormality

99
Q

How is Tetralogy of Fallot treated?

A 
IV prostaglandins to maintain patency 
BT shunt (improves blood supply to lungs)
Complete repair
100
Q

What is associated with a patient who has had a BT shunt to treat Teratology of Fallot?

A

Unrecordable BP in that arm

101
Q

After a complete repair of Teratology of Fallot, what will happen eventually?

A

Pulmonary regurgitation (needs replacing)

Increased pressure in RV –> RV hypertrophy –> RVF

Increased pressure in RV is transmitted to RA –> dilatation of RA –> vulnerable to Arrhythmia (AF/atrial flutter)

102
Q

Describe univentricular heart

A

Only have one functional ventricle

103
Q

What is the most common cause of an univentricular heart?

A

Tricuspid atresia

104
Q

In treating an univentricular heart, if it is not feasible to produce two ventricles from the ventricle, what circulation needs to be created?

A

Fontan circulation

105
Q

Describe Fontan circulation

A

Ventricle is dedicated to systemic circulation

Venous blood supply directly supplies the pulmonary arteries (deoxygenated blood does not pass through the heart)

106
Q

What problems are associated with a Fontan circulation?

A

Pulmonary circulation is dependent upon sufficient pressure to supply the lungs
Univentricle needs to supply enough pressure in order to push the blood into the lungs
The lungs need to be at a low pressure (must have low vascular resistance)

107
Q

Describe an aortic stenosis murmur

A

Low pitch ejection systolic murmur

Aortic area and radiates up into neck

108
Q

Describe an aortic regurgitation murmur

A

High pitch early diastolic murmur

Left sternal edge with patient sat forward in expiration

109
Q

Describe a mitral stenosis murmur

A

Low pitch mid systolic murmur

Heard at apex with patient on left side

110
Q

Describe a mitral regurgitation murmur

A

High pitch pan-systolic murmur

Apex radiating to axilla

111
Q

Describe a tricuspid stenosis murmur

A

Rare

Diastolic murmur at left sternal edge

112
Q

Describe a tricuspid regurgitation murmur

A

Soft high pitch pan systolic murmur at left sternal edge

Increases during inspiration

113
Q

Describe a pulmonary stenosis murmur

A

Soft ejection murmur in pulmonary area

114
Q

Describe a pulmonary regurgitation murmur

A

Soft early diastolic murmur in pulmonary area

115
Q

Define heart failure

A

The inability of the heart to keep up to the demands of the body. This is due to inadequate cardiac function due to damage of the heart that prevents it from pumping effectively

116
Q

Give some causes of HF

A 
Coronary artery disease
HTN
Idiopathic
Toxins (alcohol, chemo)
Valve disease
117
Q

Define Ejection Fraction

A

EF = SV/Total left ventricle volume

118
Q

What are the two classifications of HF depending on EF?

A

HF-REF: EF = <40% (systolic HF)

HF-PEF: EF= >40% (diastolic HF)

119
Q

Describe HF-REF

A

Ventricles can’t pump blood hard enough during systole
More often seen in younger men
Associated with coronary aetiology

120
Q

Describe HF-PEF

A

Not enough blood fills into the ventricles during diastole
More often seen in older female patients
Associated with a HTN aetiology

121
Q

What are the two types of congestion associated with HF?

A

Acute (decompensated)

Chronic (congested)

122
Q

Describe Chronic HF

A

Present for a period of time

May have been acute or may become acute

123
Q

Describe Acute HF

A

Usually admitted to hospital
Worsening of chronic
Can be new onset ‘de novo’

124
Q

Describe the pathophysiology of HF

A

The body interprets the reduced cardiac function as a reducing circulating volume

Activation of SNS, RAAS, BNP to increase fluid retention

Fluid overload –> exacerbates the reduced cardiac function

125
Q

In LVHF, where does the fluid back up and what symptoms does this cause?

A

Fluid backs up into lungs –> pulmonary HTN and oedema

Dysnpnoea
Orthopnoea (lying flat –> more venous blood flow into heart –> worsens congestion)
Crackles on auscultation

126
Q

What type of pulse may be felt in severe LVHF? What is the mechanism behind this pulse?

A

Pulsus alternans (alternating strong and weak pulse in the periphery)

Reduced EF –> reduced SV –> more blood in ventricle
At next systole:
Increased myocardium stretch –> increased strength of myocardial contraction –> increased strength of systolic pulse

127
Q

Where does fluid back up into in RVHF and what are the symptoms?

A

Fluid backs up into body

Raised JVP
Hepatosplenomegaly
Ascites
Pitted oedema

128
Q

Why does a new S3 heart sound occur with chronic HF?

A

Dilation of the ventricles causes remodelling of the atria in order to accommodate the high filling pressure

S3 is heard (due to volume overload)

129
Q

What type of tachycardia occurs in advanced HF? And what are the results?

A

Resting sinus tachycardia (reduced tissue perfusion)

Patient is:
Cool
Pale
Cyanotic extremities
Diaphoresis (due to hypotension)
Narrow pulse pressure (reduced SV)
130
Q

Describe the classification of HF

A

New York Associated Functional Classification

Class 1: Symptoms only during extreme exertion
Class 2: Symptoms during moderate exertion
Class 3: Symptoms during mild exertion
Class 4: Symptoms at rest

131
Q

What investigations are required for all patients with HF?

A 
Bloods: FBCs, U&amp;Es, Cr, urea, LFTs, urate
Natriuretic peptides - BNP
ECG
ECHO
CXR
132
Q

Why is BNP important in the investigation of HF?

A

BNP low = exclude HF

BNP raised = HF possible diagnosis –> ECG + ECHO to confirm

133
Q

What further tests might be required in a patient with HF?

A 
Coronary angiography
Exercise test
Ambulatory ECG monitoring 
Myocardial biopsy
Genetic testing
134
Q

Describe the basic treatment algorithm for HF

A

Beta Blocker + ACEi (ARB if unable to tolerate ACEi) + mineralocorticoid receptor antagonist (spironolactone/epenelone)

135
Q

What specialist meds can a cardiologist start a patient with HF on?

A

Sacubitril/Valsartan + Beta blocker + mineralcorticoid receptor antagonist

136
Q

What is the aim of treatment in patients with HF?

A

Increase life expectancy

Reduce rate of hospital admissions

137
Q

Why are ARNI drugs useful in HF management?

A

Angiotensin receptor neprilysin inhibitor

Inhibits breakdown of neprilysin
Increases natriuretic peptide
Vasodilation, natiuresis, diuresis, inhibition of pathological growth/fibrosis
Inhibits AT1 receptor

138
Q

What are the two devices that can be used to increase survival in HF?

A

Defibs - shock out abnormal heart rhythms

CRT - synchronise the RHS and LHS of heart

139
Q

How is it decided if a patient should either get a Defibs or CRT fitted?

A

More severe symptoms + narrow QRS –> defib

More severe symptoms + broad QRS –> CRT

140
Q

Describe the MoA of Ivabradine

A

Inhibits depolarisation of SA node

Decreases rate of hospitalisation

141
Q

Define HTN

A

Persistent elevation in arterial BP of >140/90mmHg

142
Q

What is the optimum BP?

A

<120/<80mmHg

143
Q

What is normal BP?

A

120-129/80-84mmHg

144
Q

What is high-normal BP?

A

130-139/85-89mmHg

145
Q

What is grade I HTN?

A

140-159/90-99mmHg

146
Q

What is grade 2 HTN?

A

160-179/100-109mmHg

147
Q

What is grade 3 HTN?

A

> /=180 over >/= 100 mmHg

148
Q

What is isolated systemic HTN?

A

> /= 140/<90 mmHg

149
Q

Give some risk factors for the development of HTN

A 
Non-modifiable:
Age
Gender
Ethnicity
Genetic factors
Modifiable:
Diet
Physical activity
Obesity
Alcohol excess
Stress
150
Q

Give some secondary causes of HTN

A

Endocrine: phaechromocytoma, hyperaldosteronism, thyroid disorders

Vascular: coarctation of the aorta

Renal: renal artery stenosis

Drugs: NSAIDs, herbal remedies, cocaine, exogenous steroid use

Other: Obstructive Sleep Apnoea

151
Q

How is HTN diagnosed?

A

2 readings 5 mins apart/2 separate occasions

152
Q

What out of office BP measurements can be taken?

A

24hr ambulatory - night-time dippers/non-dippers (non-dippers increased CV risk)
Home BP monitoring - 2-3 readings, 2x a day, 4-7 days

153
Q

How does hyperthyroidism affect BP?

A

Increased SBP

154
Q

How does hypothyroidism affect BP?

A

Increased DBP

155
Q

How can CV risk be ascertained in patients with HTN?

A 
ASSIGN score (>20 = 20% CV risk in 10 years)
Q-risk
156
Q

What examinations are useful in a patient with HTN?

A 
Measure BP in both arms
Weight/BMI
Xanthelasma 
Pulses
Oedema
Rashes
Heart - murmur
Abdomen - renal masses
Vascular bruit - kidneys, carotids
Eyes
157
Q

What initial investigations should be organised in a patient with HTN?

A 
U&amp;Es
Glucose/HBA1c
Lipid profile
TFTs
LFTs
Urine dipstick ± ACR/PCR
12 lead ECG
158
Q

What additional investigations may be useful for a patient with HTN?

A 
Renin-aldosterone
24h catecholamines
ECHO
Renal US
MRA renal
159
Q

What lifestyle factors can be beneficial in reducing a patient’s BP?

A 
Increased exercise
Reduce Na intake
Reduce alcohol intake
Smoking cessation
DASH diet - more fruit and veg, more wholegrain, less processed food
160
Q

What is the target BP in the management of HTN?

A

<140/90

<130/80 - if tolerant

161
Q

Describe the treatment algorithm for HTN

A

<55: ACEi/ARB
>55 or black African/Caribbean: Ca channel blocker

ACEi/ARB + Ca channel blocker

ACEi/ARB + Ca channel blocker + thiazide diuretic

Resistent HTN:
ACEi/ARB + Ca channel blocker + thiazide diuretic + (diuretic/alpha blocker/beta blocker)

162
Q

What is a side effect of amlodipine?

A

Ankle swelling

MBChB (14 decks)

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