Cardiology Flashcards
(296 cards)
1
Q
How does a pacemaker work?
A
Delivers controlled electrical impulses to specific areas of the heart to restore normal electrical activity and improve heart function
2
Q
How long do pacemakers last?
A
Battery lasts approx. 5y
3
Q
What are CI with pacemakers?
A
Diathermy in surgery, tens machines, mri scans
4
Q
List indications for a pacemaker
A
Symptomatic bradycardia, mobitz type 2 av block, 3rd degree heart block (risk of asystole), severe heart failure (use biventricular pacemakers), HCOM
5
Q
Describe single chamber pacemakers
A
Leads in a single chamber– In RA if av conduction normal and issue in sino atrial node
-In RV if AV conduction abnormal
6
Q
Describe dual chamber pacemakers
A
Leads in RA and RV– Synchronises conduction
7
Q
Describe biventricular/triple chamber/CRT pacemakers
A
Leads in RA, RV and LV
Used in HF
8
Q
Describe ICDs
A
Continuously monitor heart and can give shock to cardiovert patient if in VF/VT
9
Q
Describe ECG changes with pacemakers
A
Pacemaker intervention = Sharp vertical line on all leads on the trace
Line before each P wave = Lead in atria
Line before QRS complex = Lead in ventricles
10
Q
What is cor pulmonale?
A
Right sided HF Caused by respiratory disease
11
Q
What is the pathophysiology of cor pulmonale?
A
Increased pressure in arteries (pulmonary HTN) results in right heart not pumping blood out of ventricle into PA– Back pressure in RA, vena cava, and systemic venous system
12
Q
What are the causes of cor pulmonale?
A
COPD most common, PE, ILD, CF, primary pulmonary HTN
13
Q
Outline presentation of cor pulmonale
A
Early– Asymptomatic or SOB
Peripheral oedema, increased breathlessness on exertion, syncope, chest pain
14
Q
What are the signs of cor pulmonale on examination?
A
Hypoxia, cyanosis, raised JVP, peripheral oedema, 3rd heart sound, pansystolic murmur (tricuspid regurgitation), hepatomegaly (pulsatile in tricuspid regurgitation)
15
Q
Outline management of cor pulmonale
A
Treat symptoms and underlying cause
Long term oxygen therapy
16
Q
Outline prognosis of cor pulmonale
A
Poor unless reversible underlying cause
17
Q
What is an arrhythmia?
A
Abnormal heart rhythm resulting from interruption to normal electrical signal that coordinate contraction of heart muscle
18
Q
List the shockable rhythms
A
Ventricular tachycardia
Ventricular fibrillation
19
Q
List the non-shockable rhythms
A
PEA
Asystole
20
Q
How to manage unstable tachycardia
A
Consider 3 stacked shocks
Consider amiodarone infusion
21
Q
What are the types of stable tachycardia?
A
Narrow complex or broad complex
22
Q
What is a narrow complex tachycardia?
A
QRS complex less than 0.12s duration
Af, atrial flutter, SVT
23
Q
How do you manage AF?
A
Rate control– BB, CCB (Diltiazam)
Rhythm control
24
Q
How do you manage atrial flutter?
A
BB
25
How do you manage SVT?
Vagal manoeuvres
Adenosine
26
What is a broad complex tachycardia?
QRS complex greater than 0.12s
27
How do you manage ventricular tachycardia or a tachycardia trace you are unsure of?
Amiodarone infusion
28
How do you manage an SVT with bundle branch block?
Vagal manoeuvres and adenosine
29
What is atrial flutter?
Electrical activity passes through atrial flutter as re-entrant rhythm
Extra electrical pathway in atria
Atrial contraction at 300bpm
Signal goes into ventricles every second lap due to long refractory period of av node causing ventricular contraction of 150bpm
30
What is the ECG characteristic of atrial flutter?
Sawtooth appearance
P wave after p wave
31
Which conditions are associated with atrial flutter?
Hypertension
IHD
Cardiomyopathy
Thyrotoxicosis
32
What is the management of atrial flutter?
Rate control (BB)
Rhythm control (cardioversion)
Anticoagulation using CHA2DS2-VASc
Radio frequency ablation can be a permanent solution
33
What is a prolonged QT interval?
Start of QRS complex to end of t wave
Men— More than 440ms
Women— More than 460ms
34
What is the pathophysiology of a prolonged QT interval?
Represents prolonged repolarisation of the myocyte after a contraction
Results in spontaneous depolarisation in some muscle cells= Afterdepolarisations= Spread throughout the ventricles causing contraction before proper repolarisation
Torsades de pointes= When this leads to recurrent contractions without normal repolarisation
35
What is Torsades de pointes?
Polymorphic VT
Height of QRS complex gets progressively smaller then larger
36
What is the progression of TdP?
Terminates spontaneously and reverts to sinus rhythm
Or
Progresses to VT and potentially CA
37
What are the causes of prolonged QT?
Long QT syndrome (inherited)
Meds- Antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide ABs
Electrolytes- Hypokalaemia, hypomagnesaemia, hypocalcaemia
38
Outline management of prolonged QT interval
Stop meds that prolong QT interval
Correct electrolytes
BBs
Pacemakers/implantable cardioverter defibrillators
39
Outline Acute management of TdP
Correct underlying cause
Magnesium infusion
Defibrillation if VT
40
What are Ventricular ectopics?
Premature ventricular beats caused by random electrical discharges outside the atria
41
What is a key characteristic of Ventricular ectopics?
Patients complain of random extra or missed beat
Common at all ages and in healthy patients
More common if pre-existing heart conditions (IHD or HF)
42
What do Ventricular ectopics look like on ECG?
Isolated, random, abnormal, broad QRS complexes on otherwise normal ECG
43
What is bigeminy?
When every other beat is a Ventricular ectopic
44
What does a bigeminy ECG look like?
Normal beat, followed immediately by an ectopic beat, then normal beat, then ectopic, etc…
45
What is repolarisation?
Recovery period before muscle cells are ready to depolarise again
46
What is depolarisation?
Electrical process that leads to heart contraction
47
What is 1st degree heart block?
Delayed conduction through the AV node- Every P wave is followed by a QRS complex
PR interval >0.2s
48
Outline Mobitz type 1 (Wenckebach phenomenon) heart block
Conduction through AV node takes progressively longer until it finally fails, then resets and starts again
Increasing PR interval until a P wave not followed by QRS complex
PR interval returns to normal, cycle repeats
49
Outline Mobitz type 2 heart block
Intermittent failure of conduction through AV node, with absence of QRS complex
Absence of QRS complexes following P waves
Set ratio of p waves to QRS complexes
PR interval normal
Risk of asystole
50
Outline 3rd degree heart block
Complete heart block
No relationship between the P waves and QRS complexes
Significant risk of asystole
51
List causes of Bradycardia
BBs
Heart block
Sick sinus syndrome
52
What is sick sinus syndrome?
Conditions that cause dysfunction in sino Atrial node
Caused by- Idiopathic degenerative fibrosis of sinoatrial node
Results in- Sinus bradycardia, sinus arrhythmia, prolonged pauses
53
What is asystole?
Absence of electrical activity in heart
54
What increases risk of asystole?
Mobitz type 2
3rd degree heart block
Previous asystole
Ventricular pauses longer than 3s
55
Outline management of asystole
IV atropine
Inotropes (adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker
56
What are the options for temporary cardiac pacing?
Transcutaneous (pads on chest)
Transvenous (catheter through vein to stimulate heart directly)
57
How does atropine work?
Antimuscarinic
Inhibits parasympathetic nervous system
58
What are the side effects of antimuscarinic medication?
Pupil dilation
Dry mouth
Urinary retention
Constipation
59
What is supraventricular tachycardia?
Abnormal electrical signals from above the ventricles cause a fast heart rate
60
Outline the pathophysiology of SVT
Electrical signals start in sinoatrial node (hearts pacemaker)- Located between SVC and RA
Signal travels through right and left atrium causing atria to contract
Travels through AV node causing ventricles to contract
SVT- Electrical signal re-enters atria from the ventricles
Self-perpetuating electrical loop- Results in narrow complex tachycardia
61
What is paroxysmal SVT?
SVT reoccurs and remits in same patient over time
62
List the types of narrow complex tachycardia
Sinus tachycardia
SVT
AF
Atrial flutter
63
What are the characteristics of AF on an ECG?
Absent p waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm
64
What are the ECG characteristics of SVT?
QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, etc
P waves often buried in T waves so can’t see them
Regular rhythm
65
How do you distinguish SVT from sinus tachycardia?
SVT- Abrupt onset, very regular pattern w/o variability, can have no apparent cause
Sinus tachycardia- Gradual onset, more variability in rate, usually has an explanation (pain or fever)
66
Which differential is important to consider in patients with tachycardia and wide QRS complexes?
SVT with a bundle branch block
67
What are the 3 main types of SVT?
Atrioventricular nodal re-entrant tachycardia- Re-entrant point is back through AV node (most common)
Atrioventricular re-entrant tachycardia- Re-entrant point is accessory pathway between atria and ventricles (Wolff-Parkinson-White syndrome)
Atrial tachycardia- Electrical signal originates in atria somewhere other than the sino atrial node
68
What is Wolff-Parkinson-White syndrome?
Caused by extra electrical pathway connecting atria and ventricles
Pre-excitation syndrome
Additional pathway allows bypassing of AV node
Might not cause symptoms or may cause SVT
69
What are the ECG changes in Wolff-Parkinson White syndrome?
Short PR interval
Wide QRS complex
Delta wave
70
What is a delta wave?
Slurred upstroke in QRS complex caused by electricity prematurely entering ventricles through accessory pathway
71
What is the definitive treatment for Wolff-Parkinson-White syndrome?
Radiofrequency ablation of accessory pathway
72
What is a cause of a polymorphic wide complex tachycardia?
Combination of AF/Atrial flutter with WPW
Chaotic atrial electrical activity can pass through accessory pathway into ventricles
LIFE-THREATENING EMERGENCY- HR can raise >200bpm and progress to VF and cardiac arrest
73
What can increase the risk of VF and cardiac arrest in polymorphic wide complex tachycardia?
Anti-arrhythmic meds- BBs, CCBs, digoxin, adenosine)- Reduce conduction through AV node and promote conduction through accessory pathway- CI in WPW that develop AF or flutter
74
Outline Acute management of tachycardia without life-threatening features
Continuous ECG monitoring
1. Vagal manoeuvres
2. Adenosine
3. Verapamil or beta blocker
4. Synchronised DC cardioversion
75
What are the life-threatening features of tachycardia?
Loss of consciousness (syncope)
Heart muscle ischaemia (chest pain)
Shock or severe HF
76
Outline treatment of life-threatening tachycardia
Synchronised DC cardioversion under sedation or general anaesthesia
IV amiodarone added if initial DC shocks unsuccessful
77
What is the management of WPWs with atrial arrhythmias?
Procainamide or electrical cardioversion if unstable
78
Why should adenosine, verapamil and BBs not be used to treat WPWs with atrial arrhythmias?
Blocks the AV node, promoting conduction of atrial rhythm through accessory pathway into ventricles, causing potentially life threatening ventricular rhythms
79
Outline vagal manoeuvres
Used to treat tachycardias
Stimulate vagus nerve, increasing activity in parasympathetic nervous system
Slows conduction of electrical activity in heart, terminating SVT
80
How does the valsalva manoeuvre work?
Treat SVT
Increases intrathoracic pressure
Patients blows hard against resistance
81
How does a carotid sinus massage work?
Treats SVT
Stimulate baroreceptors in carotid sinus
Avoid in patients with carotid artery stenosis
82
What is the diving reflex?
Used to treat SVT
Briefly submerge patient’s face in cold water
83
Outline the MoA of adenosine
Slows cardiac conduction, primarily through AV node
Interrupts AV node or accessory pathway during SVT And resets it to sinus rhythm
84
How should you give adenosine for SVT?
Rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway for a short period
Often causes brief asystole/bradycardia
Short half life so metabolises quickly and stops having effect
85
Which patients should adenosine not be given to?
Asthma
COPD
HF
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation
86
Outline synchronised DC cardioversion
Used for SVT
Electric shock applied to heart to restore normal sinus rhythm
Synchronised with ventricular contraction at R wave
Used in patients with a pulse to avoid shocking the T wave which can result in VF and cardiac arrest
87
Outline management of paroxysmal SVT
Long term BBs, CCBs, or amiodarone
Radiofrequency ablation
88
What is Radiofrequency ablation?
Catheter ablation in a Cath lab
General anaesthetic or sedation
Catheter inserted into femoral vein and fed through venous system under xray guidance to heart
Catheter tests electrical signals in different areas of the heart and identifies abnormal patterns
Radiofrequency ablation burns abnormal areas and leaves scar tissue that doesn’t conduct electrical activity
89
What are the effects of AF?
Irregularly irregular ventricular contractions
Tachycardia
HF due to impaired filling of ventricles during diastole
Increased risk of stroke
90
Outline pathophysiology of AF
Sinoatrial node produces disorganised electrical activity
Causes contraction of atria to become uncoordinated, rapid and irregular
Chaotic electrical activity overrides regular activity from SA node
Passes through ventricles causing irregularly irregular ventricular contraction
91
How can AF increase risk of a stroke?
Uncoordinated atrial activity can cause blood to stagnate in atria, forming a thrombus
Thrombus in LA May travel to Brian NS cause Ischaemic stroke
92
What are the most common causes of AF?
S-epsis
M-itral valve pathology (stenosis or regurgitation)
I-schaemic heart disease
T-hyrotoxicosis
H-TN
Alcohol and caffeine
93
Outline presentation of AF
Asymptomatic
Palpitations
SOB
Dizziness or syncope
Symptoms of associated conditions- Stroke, sepsis, thyrotoxicosis
94
What are the differential diagnoses for an irregularly irregular pulse and how can you differentiate between them?
Atrial fibrillation
Ventricular ectopics- Disappear when HR above a certain threshold
95
Which investigations are done for AF?
ECG
Echo- Valvular heart disease, HF, planned cardioversion
96
What is paroxysmal AF and how is it managed?
AF that reoccurs and spontaneously resolves back to sinus rhythm
If normal ECG- 24h ambulatory ECG, cardiac event recorder lasting 1-2 wks
97
What is valvular AF?
AF with significant mitral stenosis or a mechanical heart valve
98
Outline rate control for AF
Aims to get the heart rate <100bpm and extend time during diastole for ventricles to fill with blood
99
When is rhythm control offered to patients?
Reversible cause
New onset AF (within last 48h)
HF caused by AF
Symptoms despite being affective key rate controlled
100
Which drugs are given for rate control in AF?
BBs (atenolol or bisoprolol)
CCB (Diltiazem or verapamil)- Not preferable in HF
Digoxin- Only in sedentary people with persistent AF, requires monitoring and risk of toxicity
101
What are the options for rhythm control of AF?
Cardioversion
Long-term rhythm control using medications
102
When is immediate cardioversion used?
If AF is either:
Present for <48h or causing life-threatening haemodynamic instability
103
What are the 2 options for immediate cardioversion?
Pharmacological- Flecainide, amiodarone
Electrical- Defib
104
When is delayed cardioversion used?
If AF has been present for >48h and they are stable
Patient should be anticoagulated for >3wks before delayed cardioversion
105
Outline long term rhythm control
1st line- BBs
2nd line- Dronedarone
Amiodarone if HF or left ventricular dysfunction
106
Outline management of paroxysmal AF
‘Pill in the pocket’- Flecainide
Must have infrequent episodes w/o structural heart disease
Increased risk of converting AF into atrial flutter
107
What are the ablation options for AF?
Left atrial ablation
Atrioventricular node ablation and a permanent pacemaker
108
Which anticoagulation should be offered to AF patients?
DOACs
Warfarin
109
What is the MoA of apixaban, edoxaban and rivaroxaban?
Direct factor Xa inhibitor
110
What is the MoA of dabigatran?
Direct thrombin inhibitor
111
What is the antidote to apixaban and rivaroxaban?
Andexanet alfa
112
What is the antidote to dabigatran?
Idarucizumab
113
What is the MoA of warfarin?
Vitamin K antagonist
Vit K is important for functioning of several clotting factors
Warfarin blocks Vit K and prolongs prothrombin time= Longer clotting time
114
What does INR measure?
Assesses how anticoagulated the patient is by warfarin
Calculates patient’s prothrombin time compared with PTT of average healthy adult
115
How do you interpret INR?
1= Normal PTT
2= PTT twice that of an average healthy adult
116
What is the target INR for an AF patient on warfarin?
2-3
117
What is the TTR in regards to INR?
Time in Therapeutic Range
Percentage of time that INR is in the target range
If too low- Increased stroke risk
If too high- Increased bleeding risk
118
What does INR stand for?
International normalised ratio
119
What does the metabolism of warfarin involve?
Cytochrome P450 system in the liver
Interacts with other drugs- Inc. ABs
120
Which foods affect INR?
Foods that contain Vit K- Leafy green veg
Foods that affect P450- Cranberry juice, alcohol
121
What is the reversing agent of warfarin?
Vit K
122
What is the CHA2DS2-VASc tool used for?
Whether a patient with AF should start anticoagulation
Higher score= Higher risk of stroke or TIA
123
Outline the CHA2DS2-VASc tool
C- Congestive HF
H- HTN
A2- Age>75 (scores 2)
D- Diabetes
S- Stroke/previous TIA (scores 2)
V- Vascular disease
A- Age 65-74
S- Sex (female)
0= No anticoagulation
1= Consider anticoagulation in men (women automatically score 1)
2+= Offer anticoagulation
124
What is the ORBIT score?
Used to assess major bleeding risk in patients with AF taking anticoagulation
125
Outline the scoring system of the ORBIT score
O- Older age (>75y)
R- Renal impairment (GFR<60)
B- Bleeding previously (history of GI or IC bleeding)
I- Iron (low Hb or haematocrit)
T- Taking antiplatelet meds
126
What is a left atrial appendage occlusion?
Option for patients with CIs to anticoagulation and high stroke risk
Left atrial appendage= Most common site for thrombus to form
Insert catheter into femoral vein into RA and puncturing septum between atria to access LA and place a plug
127
What is HCOM?
Hypertrophic obstructive cardiomyopathy
LV hypertrophic, with thickening of muscle
Asymmetrically affects septum of the heart, blocks flow of blood out of LV
128
What risks are associated with HCOM?
HF
MI
Arrhythmias
Sudden cardiac death
129
What is the inheritance of HCOM?
Autosomal dominant
130
Outline the presentation of HCOM
Mostly asymptomatic
SOB
Fatigue
Dizziness
Syncope
Chest pain
Palpitations
Severe- Symptoms of HF (cough, SOB, orthopnoea, paroxysmal noctural dyspnoea, oedema)
131
Outline examination findings of HCOM
Ejection systolic murmur at lower left sternal border
4th heart sound
Thrill at lower left sternal border
132
Outline investigations of HCOM
ECG- LV hypertrophy
Chest xray- Normal or may show signs of pulmonary oedema
ECHO or Cardiac MRI- Establish diagnosis
Genetic testing
133
Outline management of HCOM
BBs
Surgical myectomy (remove part of heart muscle to relieve obstruction)
Alcohol septal ablation
Implantable cardioverter defibrillator
Heart transplant
Avoid intense exercise/heavy lifting/dehydration
Avoid ACE-i and nitrates
134
What is dilated cardiomyopathy?
Heart muscle becomes thin and dilated
Can be genetic or secondary to other conditions (eg: Myocarditis)
135
What is alcohol-induced cardiomyopathy?
Type of dilated cardiomyopathy
136
What is restrictive cardiomyopathy?
Heart becomes rigid and stiff, causing impaired ventricular filling during diastole
137
What is arrhythmogenic cardiomyopathy?
Genetic
Heart muscle progressively replaced with fibrofatty tissue
Becomes prone to ventricular arrhythmias
Notable cause of sudden cardiac death in young people
138
What is Takotsubo cardiomyopathy?
Rapid onset of LV dysfunction and weakness
Follows severe emotional stress
Broken heart syndrome
Resolves spontaneously with time
139
What is infective endocarditis?
Infection of endothelium of the heart
Most commonly affects heart valves
140
List the risk factors for infective endocarditis
IV drug use
Structural heart pathology (valvular HD, CHD, HCOM, prosthetic heart valves, ICD)
CKD (particularly on dialysis)
Immunocompromised
History of infective endocarditis
141
What is the most common cause of infective endocarditis?
*Staph aureus
Strep viridans
Enterococcus
142
Outline presentation of infective endocarditis?
Non-specific symptoms of infection:
Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)
143
What are the examination findings of infective endocarditis?
New/changing heart murmur
Splinter haemorrhages
Petechiae (small, non-blanching red/brown spots) on trunk/limbs/or mucosa/conjunctiva
Janeway lesions (painless red flat macules on palms of hands and soles of feet)
Osler's nodes (tender red/purple nodules on pads of fingers and toes)
Roth spots (haemorrhages on retina)
Splenomegaly and finger clubbing in long standing disease
144
Outline investigations of infective endocarditis
Blood cultures before starting ABs
Echo (TOE is more sensitive)— Vegetations May be seen on the valves
145
How is a diagnosis of HF established?
Clinical assessment
NT-proBNP
ECG
ECHO
Bloods- Anaemia, renal function, thyroid, liver, lipids, diabetes
Chest X-ray and lung pathology
146
What is the Modified Duke Criteria?
Diagnosing of infective endocarditis
One major plus 3 minor criteria
Five minor criteria
147
What are the major modified duke criteria?
- Persistently positive blood cultures
- Specific imaging findings (vegetation seen o
148
What are the minor modified duke criteria?
- Predisposition (eg: IV drug use or heart valve pathology)
- Fever >38 degree C
- Vascular phenomena (eg: Splenic infarction, ICH, Janeway lesions)
- Immunological phenomena (eg: Osler’s nodes, Roth spots, glomerulonephritis)
- Microbiological phenomena (positive cultures not qualifying as major criteria)
149
Outline management of infective endocarditis
IV broad-spectrum ABs (eg: Amoxicillin and optional gentamicin)- Continue for 4wks with native heart valves or 6wks with prosthetic heart valves
150
What are the key complications of infective endocarditis?
Heart valve damage, causing regurgitation
Heart failure
Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
Glomerulonephritis, causing renal impairment
151
What is the prognosis of infective endocarditis?
High mortality rate
152
What is the difference between bio prosthetic versus mechanical?
Bioprosthetic- Lifespan of 10y
Mechanical- 20y but require lifelong warfarin with INR 2.5-3.5
153
List gram-positive cocci
Staph
Strep
Entero
154
What are the major complications of mechanical heart valves?
- Thrombus formation
- Infective endocarditis
- Haemolysis causing anaemia
155
What is a TAVI?
Transcatheter Aortic Valve Implantation
Treatment for severe aortic stenosis
Insert catheter into femoral artery and implant bioprosthetic valve
156
What is the 1st HS?
S1
Closing of AV valves (tricuspid and mitral) at start of systolic contraction of ventricles
157
What is the 2nd HS?
Closing of semilunar valves (pulmonary and aortic) once systolic contraction is complete
158
What is the 3rd HS?
Heard 0.1s after 2nd HS
Rapid ventricular filling causing chordae tendinae to pull to full length and twang
Gallop rhythm
Normal in 15-40y
Older = Can indicate HF as ventricles and chordae are stiff and weak
159
What is the 4th HS?
Heard directly before S1
Always abnormal and rare
Indicates stiff or hypertrophic ventricle
Caused by turbulent flow from atria contracting against non-compliant ventricle
160
What is Erb’s point?
3rd intercostal space on left sternal border
Best for listening to heart sounds (S1 and S2)
161
Which manoeuvres can be used to emphasise murmurs?
Mitral stenosis- Patient on left
Aortic regurgitation- Lean forward and hold exhalation
162
Outline the mneumonic used to assess murmurs
S- Site- Where is the murmur loudest?
C- Character- Soft/blowing/crescendo/decrescendo/crescendo-decrescedo
R- Radiation- Over carotids (aortic stenosis), over left axilla (mitral regurgitation)
I- Intensity- What grade is the murmur?
P- Pitch- High/low/rumbling
T- Timing- Systolic or diastolic
163
Outline grades of murmurs
1- Difficult to hear
2- Quiet
3- Easy to hear
4- Easy to hear with palpable thrill
5- Audible with stethoscope barely touching chest
6- Audible with stethoscope off chest
164
Which valvular heart diseases cause hypertrophy?
Mitral stenosis- LA hypertrophy
Aortic stenosis- LV hypertrophy
165
Which valvular heart diseases cause dilatation?
Mitral regurgitation- LA dilatation
Aortic regurgitation- LV dilatation
166
What are the signs of pulmonary stenosis?
Ejection systolic murmur loudest in pulmonary area with deep inspiration
Wide split 2nd HS (LV empties quicker than RV)
Thrill in pulmonary area on palpation
Raised JVP with giant a waves (RA contracts against hypertrophic RV)
Peripheral oedema
Ascites
167
What is the pathophysiology of pulmonary stenosis?
Congenital
168
What conditions is pulmonary stenosis linked with?
Noonan syndrome
ToF
169
What are the signs of tricuspid regurgitation?
Blood flows back from RV to RA during systolic contraction of RV
Pan systolic murmur
Split 2nd HS due to pulmonary valve closing earlier than aortic valve (RV empties quicker than LV)
Thrill in tricuspid area on palpation
Raise JVP with giant C-V waves
Pulsatile liver
Peripheral oedema
Ascites
170
What are the causes of tricuspid regurgitation?
Pressure due to L sided HF or pulmonary HTN
Infective endocarditis
Rheumatic heart disease
Carcinoid syndrome
Ebstein’s anomaly
Marfan syndrome
171
What are the signs of aortic stenosis?
Ejection systolic, high pitched murmur due to high velocity through aortic valve
Crescendo-decrescendo
Radiates to carotids
Thrill in aortic area on palpation
Slow rising pulse
Narrow pulse pressure
Exertional syncope
172
What are the causes of aortic stenosis?
Idiopathic age-related calcification
Bicuspid aortic valve
Rheumatic heart disease
173
What are the signs of aortic regurgitation?
Early diastolic, soft murmur
Heard at apex
Rumbling
Thrill in aortic area on palpation
Collapsing pulse
Wide pulse pressure
HF and pulmonary oedema
174
What are the causes of aortic regurgitation?
Idiopathic age-related weakness
Bicuspid aortic valve
Ehlers-Danlos syndrome and Marfan syndrome
175
What are the signs of mitral stenosis?
Mid-diastolic, low pitched rumbling
Loud S1 (thick valves require large systolic force to shut)
Tapping apex beat
Malar flush
AF
176
What is the physiology causing a malar flush?
Back pressure of blood into pulmonary system, causing a rise in CO2 and vasodilation
177
What are the causes of mitral stenosis?
Rheumatic heart disease
Infective endocarditis
178
What are the signs of mitral regurgitation?
Reduced ejection fraction
Congestive HF
Pan-systolic, high pitched whistling
Radiates to left axilla
Potential 3rd HS
Thrill in mitral area on palpation
HF and pulmonary oedema
AF
179
What are the causes of mitral regurgitation?
Idiopathic weakening of valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Ehlers-Danlos or Marfans
180
What causes impaired LV function?
Chronic backlog of blood waiting to flow through left side of heart
LA, pulmonary veins and lungs have increased volume and pressure of blood
Start to leak fluid and can’t reabsorb excess = Pulmonary oedema
181
What is ejection fraction?
Percentage of blood in LV squeezed out with each ventricular contraction
>50 = Normal
182
What is HF with reduced ejection fraction?
Ejection fraction <50%
183
What is HF with preserved ejection fraction?
Clinical features of HF with ejection fraction >50%
Result of diastolic dysfunction- Issue with LV filling with blood during diastole
184
What are the causes of HF?
Ischaemic heart disease
Valvular heart disease (aortic stenosis)
HTN
Arrhythmias (AF)
Cardiomyopathy
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Outline the presentation of HF
Breathlessness (worse on exertion)
Cough (frothy pink sputum)
Orthopnoea (ask about pillows)
Paroxysmal nocturnal Dyspnoea
Peripheral oedema
Fatigue
186
What are the signs of HF on examination?
Tachycardia
Tachypnoea
HTN
Murmurs
3rd heart sound
Bilateral basal crackles
Raised JVP
Peripheral oedema
187
What is paroxysmal nocturnal dyspnoa?
Sudden waking at night with severe attack of SOB, cough, and wheeze
188
What is the New York Heart Association Classification?
Assesses severity of HF:
Class 1- No limitation on activity
Class 2- Comfortable at rest but symptomatic with ordinary activities
Class 3- Comfortable at rest but symptomatic with activity
Class 4- Symptomatic at rest
189
What is the use of NT-proBNP in HF?
400-2000ng/l = Have ECHO within 6wks
>2000ng/l = Have ECHO within 2wks
190
Which vaccinations are required in HF patients?
Flu
Covid
Pneumococcal
191
What is the medical management of chronic HF?
A- ACE inhibitor (ramipril)
B- BB (bisoprolol)
A- Aldosterone antagonist if symptoms not controlled with A and B (spironolactone/eplerenone)
L- Loop diuretic (furosemide/bumetanide)
192
What can you use instead of an ACE-I if not tolerated?
ARB- Candesartan
Avoid ACE-is in valvular heart disease
193
When are aldosterone antagonists used in HF?
Reduced EF
Symptoms not controlled with ACE-I and BB
194
Which HF meds require monitoring of U&Es and why?
Diuretics
ACE-is
Aldosterone antagonists
All can cause electrolyte disturbances
ACE-is and aldosterone antagonists can cause hyperkalaemia
195
What are the additional specialist meds for HF?
SGLT2 inhibitor (dpagliflozin)
Sacubitril with Valsartan
Ivabradine
Hydralazine with nitrate
Digoxin
196
What surgical interventions can be used for HF?
ICD- Used if previous VT or VF
Cardiac resynchronisation therapy (CRT)- Used if EF<35%- Involves biventricular pacemakers
Heart transplant
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What is acute LV failure?
Acute event results in LV unable to more blood efficiently through left side of heart and into systemic circulation
198
What is cardiac output?
Volume of blood ejected by heart per minute
CO = SV x HR
199
What is stroke volume?
Volume of blood ejected each beat
200
What is the cardiac cause of pulmonary oedema?
Backlog of blood waiting in LA, pulmonary veins and lungs = Increased volume and pressure of blood= Leak fluid and can’t reabsorb excess from surrounding tissues
201
What is pulmonary oedema?
Lung tissue and alveoli filled with interstitial fluid
Interferes with normal gas exchange= SOB and reduced O2 sats
202
What are the triggers of acute LV failure?
Often result of decompensated chronic HF
Iatrogenic (aggressive IV fluids in frail elderly with impaired LV function)
MI
Arrhythmias
Sepsis
Hypertensive emergency (acute, severe increase in BP)
203
How do you treat an 85y patient with CKD and aortic stenosis who has been given 2l fluid over 4h and starts to drop O2 sats?
IV furosemide
204
Outline presentation of Acute LVF
Acute SOB exacerbated by lying flat and improves sitting up
Looking unwell
Cough with frothy white/pink sputum
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What are the signs of Acute LVF on examination?
Raised RR
Reduced O2 sats
Tachycardia
3rd heart sound
Bilateral basal crackles
Hypotension if severe- Cardiogenic shock
206
What are the signs of R sided HF?
Raised JVP
Peripheral oedema
207
What investigations are required for Acute LVF?
Clinical assessment
ECG
Bloods- Anaemia, infection, kidney function, BNP, troponin (if suspect MI)
ABG
Chest X-ray
ECHO
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What does a raised BNP suggest?
Hormone released from heart ventricles when myocardium stretched beyond normal range
Raised BNP indicates heart overloaded
Sensitive but not specific= Can be positive due to other causes
209
What is the role of BNP?
To relax smooth muscle in blood vessels to reduce systemic vascular resistance= Easier for heart to pump blood
Acts in kidneys as diuretic to promote water excretion in urine= Reduces circulating volume
210
What are the causes of raised BNP?
Tachycardia
Sepsis
PE
Renal impairment
Acute LVF
COPD
211
What may be seen on a chest X-ray of Acute LVF?
Cardiomegaly
Upper lobe venous diversion- When standing erect lower lobe veins usually contain more blood and upper remain small- In Acute LVF back pressure means upper lobes fill with blood and become engorged = Increased prominence and diameter of upper lobe vessels on CXR
Fluid leaking from oedematous lung tissue= Bilateral pleural effusions, fluid in interlobar fissures, fluid in septal (Kerley) lines
212
Outline basic management of Acute LVF
S- Sit up
O- Oxygen
D- Diuretics
I- IV fluids stopped
U- Underlying causes identified and treated
M- Monitor fluid balance
213
What are the specialist management options for Acute LVF?
IV opiates (morphine)- Vasodilator
IV nitrates- Vasodilator (consider in every HTN or ACS)
Inotropes (dobutamine)- Improves contractility and cardiac output
Vasopressors (noradrenaline)- Improves BP- Vasoconstricts= Increases SVR and MAP
NIV
Invasive ventilation
214
How do positive inotropes work?
Increase contractility of heart
Increase CO and Mean arterial pressure
Used in Acute HF, recent MI, or following heart surgery
215
How do vasopressors work?
Cause vasoconstriction
Increase SVR and MAP
216
What is pericarditis?
Inflammation of pericardium (membrane surrounding heart)
217
What are the most common causes of pericarditis?
Idiopathic
Viral
218
Outline the presentation of pericarditis
Chest pain- Sharp, central, worse on inspiration (pleuritic), worse lying down, better sitting forward
Low grade fever
219
What is pleuritic chest pain?
Worse on inspiration
220
Outline the pathophysiology of pericarditis
Membrane surrounds heart is pericardium or pericardial sac- Has 2 layers with <50mls fluid between providing lubrication allowing beat without too much friction
Potential space between 2 layers is pericardial cavity
221
What are the causes of pericarditis?
Idiopathic
Infection (TB, HIV, Coxsackie, EBV)
AI and inflammatory (SLE, RA)
Injury to pericardium (after MI/open heart surgery/trauma)
Uraemia secondary to renal impairment
Cancer
Medications (methotrexate)
222
What is a pericardial effusion?
Potential space of pericardial cavity fills with fluid
Creates inward pressure on heart= Difficult to expand during diastole (filling of heart)
223
What is a pericardial tamponade?
Pericardial effusion large enough to raise intra-pericardial pressure
Increased pressure squeezes heart and affects ability to function
Reduces heart filling during diastole, decreasing CO during systole
224
What is a key examination finding in pericarditis?
Pericardial friction rub on auscultation
Rubbing/scratching sound occurring alongside heart sounds
225
Outline investigations of pericarditis
Bloods- Riased inflammatory markers (WBC, CRP, ESR)
ECG- Saddle-shaped ST-elevation, PR depression
ECHO
226
Outline management of pericarditis
NSAIDs- Aspirin or ibuprofen
Colchicine long term (3mths)
2nd line- Steroids if associated with inflammatory conditions or recurrent
Pericardiocentesis if fluid around heart
227
What is the prognosis of pericarditis?
Most resolve within a month
Can be recurrent
Some cases chronic
228
What is atherosclerosis?
Fatty deposits in artery walls
Hardening or stiffening of blood vessel walls
Affects medium and large arteries
Caused by chronic inflammation and activation of immune system in artery wall
229
What can be the result of plaques in the arteries?
Stiffening
Stenosis
Rupture
230
What is the result of stiffening of the arteries in atherosclerosis?
HTN
Heart strain
231
What is the result of stenosis in atherosclerosis?
Reduced blood flow
232
What is the result of plaque rupture in atherosclerosis?
Creates thrombus that blocks distal vessel and causes ischaemia
233
What is acute coronary syndrome?
Coronary artery becomes blocked
234
What are the modifiable risk factors for cardiovascular disease?
Raised cholesterol
Smoking
Alcohol consumption
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress
235
What are the non-modifiable risk factors for cardiovascular disease?
Older age
Family history
Male
236
What are the complications of atherosclerosis?
Angina
MI
TIA
Strokes
Peripheral artery disease
Chronic mesenteric ischaemia
237
What is the dietary advice for cardiovascular disease?
Reduced sugar
Whole grain
5 a day
2 a week fish
4 and week of legumes/seeds/nuts
238
What is the exercise advise for cardiovascular disease?
Aerobic activity 150mins moderate or 75mins vigorous/wk
Strength training 2d a week
239
What is a QRISK3 score?
Estimate of % risk of stroke or MI in next 10y
When >10% offer a statin (20mg atorvastatin at night)
240
When is atorvastatin offered as primary prevention for cardiovascular disease?
CKD (eGFR <60ml/min/1.73m2)
T1D for >10y or over 40y
QRSIK3 >10%
241
What is the role of statins?
Reduce cholesterol production in liver by inhibiting HMG CoA reductase
242
What monitoring is required on statins?
Lipids at 3mths
LFTs at 3mths and 12mths
Statins can cause transient rise in ALT and AST in first few weeks
243
List some rare and significant SEs of statins
Myopathy (muscle weakness and pain)
Rhabdomyolysis (muscle damage- Check creatine kinase if muscle pain)
T2D
Haemorrhaging stroke
244
Which medications interact with statins?
Macrolide antibiotics- Stop taking statin whilst taking erythromycin or Clarithromycin
245
Which drugs apart from statins lower cholesterol?
Ezetimibe (inhibits absorption of cholesterol in intestine)
PCSK9 inhibitors (evolocumab or alirocumab)
246
Outline secondary prevention of CVD
A- Antiplatelet (aspirin, clopidogrel, ticagrelor)
A- Atorvastatin 80mg
A- Atenolol (or bisoprolol)
A- ACE-I
247
What is the medical prevention treatment following an MI?
Aspirin 75mg/d indefinitely
Clopidogrel/ticagrelor 12mths
248
What is the anti platelet of choice following peripheral arterial disease or an Ischaemic stroke?
Clopidogrel
249
What is the Inheritance of familial hypercholesterolaemia?
Autosomal dominant
250
What are the criteria used for a clinical diagnosis of familial hypercholesterolaemia?
FH premature CVD (<60y)
Very high cholesterol (>7.5mmol/L)
Tendon Xanthomata (hard nodules in tendons containing cholesterol on back of hand or Achilles)
251
What is the management of familial hypercholesterolaemia?
Genetic testing
Statins
252
What is angina caused by?
Atherosclerosis affecting coronary arteries, narrowing lumen and reducing blood flow to myocardium
253
What is stable angina?
Symptoms come on with exertion and are relieved by rest
High demand = Insufficient supply of blood = Symptoms of angina
254
What is unstable angina?
Type of ACS
Symptoms not relieved by rest
255
What investigations are required for angina?
Physical examination (heart sounds, signs of HF, BP and BMI)
ECG
FBC (anaemia)
U&Es (required before starting ACE-I
LFTs (required before starting statin)
Lipid profile
TFTs
HbA1c
Cardiac stress testing- Assess heart function during exertion
CT coronary angiogram
Invasive coronary angiography
256
Outline medical management for immediate symptomatic relief of stable angina
GTN when symptoms start (causes vasodilation)
2nd dose after 5mins if symptoms remain
3rd dose after 5mins if symptoms remain
Ambulance after further 5mins if symptoms remain
257
Outline medical management for long term symptomatic relief of stable angina
BB (bisoprolol)
CCB (Diltiazem or verapamil- Avoid both in HF with reduced ejection fraction)
Specialist- Long acting nitrates (isosorbide mononitrate), ivabradine, nicorandil, ranolazine
258
What are the side effects of GTN?
Headaches
Dizziness
259
What are the medications used for secondary prevention of stable angina?
A- Aspirin 75mg once/d
A- Atorvastatin 80mg once daily
A- ACE-I if diabetes/HTN/CKD/HF
A- Already on BB for symptomatic relief
260
Which surgical interventions are used for stable angina?
Percutaneous coronary intervention (PCI)- Insert catheter into brachial/femoral artery to coronary arteries, dilate a balloon and stent
Coronary artery bypass graft (CABG)- Offered in severe stenosis, midline sternotomy- Graft from saphenous vein, internal thoracic artery or radial artery
261
What are the pros and cons of PCI over CABG?
Faster recovery
Lower rate of strokes
Higher rate of revascularisation (further procedures)
262
What is Acute coronary syndrome?
Result of thrombus from atherosclerosic plaque blocking a coronary artery
If formed in fast flowing artery = Mainly formed of platelets
263
What are the 3 types of ACS?
Unstable angina
STEMI
NSTEMI
264
Which coronary arteries branch from the aorta?
Right coronary artery
Left coronary artery
265
What does the right coronary artery supply?
Curves around right side of heart
RA
RV
Inferior aspect of LV
Posterior septal area
266
What does the left coronary artery become?
Circumflex artery
Left anterior descending
267
What does the circumflex artery supply?
Curves around top, left and back of heart
LA
Posterior aspect of left ventricle
268
What does the left anterior descending artery supply?
Travels down middle of heart
Anterior aspect of LV
Anterior aspect of septum
269
Outline presentation of ACS
Central constricting chest pain
Pain radiating to jaw or arms
Nausea and vomiting
Sweating and clamminess
Feeling of impending doom
SOB
Palpitations
Symptoms continue at rest for >15mins
270
What is a silent MI?
Patient doesn’t experience typical chest pain during acute ACS
Patients with diabetes at greater risk
271
What are the ECG changes in an acute STEMI?
ST segment elevation
New LBBB
272
What are the ECG changes in a new NSTEMI?
ST segment depression
T wave inversion
273
What do pathological Q waves suggest in ACS?
Deep infarction involving full thickness of heart muscle and typically appear >6h after onset of symptoms
274
Which heart area does the LCA supply and which ECG leads does it correlate with?
Anterolateral
I, aVL, V3-V6
275
Which area of the heart does LAD correlate with and which ECG leads?
Anterior
V1-V4
276
Which area of the heart does circumflex correlate with and which ECG leads?
Lateral
I, aVL, V5-V6
277
Which area of the heart does RCA correlate with and which ECG leads?
Inferior
II, III, aVF
278
What is troponin?
Protein in cardiac muscle (myocardium) and skeletal muscle
Rise in troponin is consistent with myocardial ischaemia
279
When is troponin used to diagnose an MI?
In NSTEMI, not STEMI
280
How do you diagnose NSTEMI based of troponin?
High troponin/rising troponin in context of suspected ACS
281
What are the causes of raised troponin?
MI
CKD
Sepsis
Myocarditis
Aortic dissection
PE
282
What investigations are required to confirm ACS?
ECG
Troponin
Baseline bloods- FBC, U&Es, LFTs, lipids, glucose
Chest X-ray
ECHO- Assess LV function
283
When is unstable angina diagnosed if symptoms suggest ACS?
Normal ECG
Troponin normal
Other ECG changes (ST depression or T wave inversion)
284
What is the initial management of ACS?
Aspirin 300mg
IV morphine if required + Metoclopramide
Nitrate (GTN)
285
Outline management of a STEMI
PCI if available within 2h of presenting
Thrombolysis if PCI not available within 2h
286
Which medications are given in preparation for PCI?
Aspirin and prasugrel
287
What is thrombolysis?
Dissolving the clot using a fibrinolytic agent- Streptokinase, alteplase, tenecteplase
288
Outline medical management of NSTEMI
B- Base decision about angiography and PCI on GRACE score
A- Aspirin 300mg stat dose
T- Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if angiography)
M- Morphine
A- Antithrombin therapy with fondaparinux
N- Nitrate (GTN)
289
What is Dressler’s syndrome?
Post-MI syndrome
Occurs 2-3wks after acute MI
Caused by localised immune response resulting in inflammation of pericardium (pericarditis)
290
Outline presentation of Dressler’s syndrome
Pleuritic chest pain
Low grade fever
Pericardial rub on auscultation (rubbing/scratching sound alongside heart sounds)
Can cause pericardial effusion and rarely pericardial tamponade
291
How is Dressler’s syndrome diagnosed?
ECG- Global ST elevation and T wave inversion
ECHO- Pericardial effusion
Raised inflammatory markers (CRP and ESR)
292
How is Dressler’s syndrome managed?
NSAIDs (ibuprofen or aspirin)
Steroids if severe (prednisolone)
Pericardiocentesis if required
293
List the complications of MI
D- Death
R- Rupture of heart septum or papillary muscles
E- oEdema (HF)
A- Arrhythmia and Aneurysm
D- Dressler’s syndrome
294
What is the GRACE score?
Gives 6mth probability of death after NSTEMI
295
Outline secondary management of ACS
Aspirin once daily indefinitely
Antipalatelet (ticagrelor or clopidogrel) for 12mths
Atorvastatin 80mg once daily
ACE-is (ramipril)
Atenolol or Bisoprolol
Aldosterone antagonist if clinical HF (epleronone 50mg once daily)
296
What is the risk associated with ACE-is and aldosterone antagonists that needs to be monitored?
Renal function to monitor for Hyperkalaemia
