CV Flashcards
1
Q
Why do we have to see the same waveform 12 times on a standard ECG?
A
The 12 leads provide important spatial information about the heart
They all view the electrical activity of the heart from a different position
allows you to localise pathology to a particular heart region
2
Q
What is the normal cardiac axis?
A
-30 to +90
(2pm - 6pm)
Most positive deflection in lead II
most negative deflection in aVR
If leads I and II are positive, the axis is normal
3
Q
What can left axis deviation suggest?
A
conduction abnormality
4
Q
What can right axis deviation suggest?
A
pulmonary embolus/congenital heart defect
If the right ventricle becomes hypertrophied, it has more effect on the QRS complex than the left ventricle, and the average depolarization wave – the axis – will swing towards the right
5
Q
What would you see in left axis deviation?
A
overall electrical activity becomes distorted to the left
between -30° and -90°
positive lead I and aVL
negative lead II and III
6
Q
What would you see in right axis deviation?
A
overall direction of electrical activity is distorted to the right
between +90º and +180º
Negative QRS in lead I, positive in aVF
7
Q
What is the ECG paper speed?
A
25 mm/s
8
Q
How many large squares would you find in a second on ECG?
A
5 (one square = 0.2s)
9
Q
First degree heart block
A
slowing in AV nodal conduction
prolonged PR interval
10
Q
second degree heart block
A
intermittent failure of AV nodal conduction
two types:
1) Mobitz I: PR interval steadily increases until a QRS complex is missed. the pattern resets
2) Mobitz II: regular skipping of QRS. e.g. P – QRS – P – P – QRS (this is 2:1). Most beats are normal but there is occasionally atrial depolarisation without ventricular depolarisation.
11
Q
third degree heart block
A
complete failure of AV nodal conduction
No impulse conduction from atria to ventricles. No relationship between P:QRS.
ventricles are excited by a slow ‘escape rhythm’, from a depolarizing focus below the AV node
12
Q
Which ECG leads are inferior?
A
II, III and aVF
13
Q
Which ECG leads are anterior?
A
V1-V4
14
Q
Which ECG leads are lateral?
A
I, aVL, V5, V6
15
Q
What is an ECG lead?
A
imaginary line between 2 ECG electrodes.
Each lead provides a different view of the electrical activity of the heart
16
Q
Which plane are the limb leads in?
A
Coronal
17
Q
Which plane are the chest leads in?
A
Transverse
18
Q
Which lead usually provides the rhythm strip on an ECG?
A
Lead II
19
Q
What’s the normal range of the PR interval?
A
<1 large square
<200ms
20
Q
What’s the normal range of the QRS complexl?
A
< 3 small squares
< 120ms
21
Q
sinus rhythm
A
normal heart rhythm, starts in the sinoatrial node
Rhythm = activation sequence of the heart
22
Q
What does a narrow QRS indicate?
A
that the rhythm is arising from the AVN or above
i.e. the rhythm is using the specialized conducting system (His-Purkinje system) to depolarize the ventricles (the fast route to depolarize all ventricular muscle in a short period of time)
23
Q
What is heart failure?
A
failure of cardiac output to meet the physiological demands of the body
24
Q
Name 4 causes of heart failure
A
MI
hypertension
toxins (alcohol, chemotherapy)
valve disease
25
what is systolic heart failure?
heart failure with reduced ejection fraction. inability of the ventricle to contract normally
Usually has a coronary cause
Affects younger male patients
26
what is diastolic heart failure?
heart failure with preserved ejection fraction
Inability of the ventricle to relax and fill normally, causing increased filling pressures
older
more often female
hypertensive aetiology
27
How do compensatory changes lead to heart failure?
haemodynamic changes cause compensatory changes in the heart and cardiovascular system
these physiological changes occur to maintain cardiac output and peripheral perfusion
chronic activation increases cardiac workload, causing progressive damage
as heart failure progresses, these mechanisms are overwhelmed and become pathological
28
What neurohumoral adjustments are seen in heart failure?
ischaemic injury causes decreased efficiency of the heart --> perceived hypotension
neurohumoral adjustments act to maintain arterial pressure and perfusion of vital organs
Noradrenaline increases cardiac contractility and peripheral vasoconstriction
RAAS (activated by reduced renal perfusion) increases blood volume -> fluid overload
29
What is the significance of BNP in heart failure?
distinguishes HF from other forms of dyspnoea
secreted by the ventricles in response to myocardial wall stress
Levels are increased in patients with heart failure, and levels correlate with the severity of heart failure
Low BNP excludes heart failure
30
Treatment of hear failure (reduced ejection fraction)
1) start with a beta blocker/ACEi (ARB if intolerant)
2) with ongoing symptoms, add a MR antagonist
3) sacubitril/valsartan (stop ACEi)
4) devices/ivabradine
5) digoxin
6) LVAD or transplant
31
What is the most evidence-based therapy in heart failure?
Beta-blockers
32
Mechanism of action: sacubitril
inhibits neprilysin, an enzyme that breaks down natriuretic peptides
this increases the number of natriuretic peptides in the body
this increases natriuresis
33
LCZ696
contains bothan ARB (valsartan) and a neprilysin inhibitor
blocks the unwanted effects of ANG-II and upregulates the beneficial system (natriuretic peptides)
34
What is an implantable cardioverter-defibrillator (ICD)
a device implantable inside the body
able to perform cardioversion, defibrillation, and pacing of the heart
35
ivabradine
selectively inhibits the pacemaker If current
Blocking this channel reduces cardiac pacemaker activity
This slows heart rate at the SAN
36
How would you manage inadequately perfused patients?
give them positive inotropes
e.g. adrenaline/dopamine
37
How would you manage congested patients?
treat the fluid overload with diuretics
38
NYHF classification
I - No symptoms and no limitation in ordinary physical activity
II - dyspnoea during normal activities but comfortable at rest
III- dyspnoea limits normal activities
IV - dyspnoea at rest, essentially bedbound
39
CXR signs in LV failure
remember: ABCDE
```
A = alveolar oedema (perihilar - bat's wings)
B = kerley B lines (interstitial oedema)
C = cardiomegaly
D = dilated upper lobe vessels
E = pleural Effusion
```
40
Infective endocarditis
Infection of endocardium
Results in formation of a vegetation - a mass of platelets, fibrin, microorganisms, and inflammatory cells
Results in damage to cusp of valves
41
Which valve is most commonly affected by infective endocarditis?
mitral valve
42
Which valve is most commonly affected by IE in PWIDs?
tricuspid
causes:
(1) particulate-induced endothelial damage to right-sided valves
(2) increased bacterial loads in these patients
(3) direct physiologic effects of the injected drugs
(4) deficient immune response caused by IVDU
43
Classification of infective endocarditis
1) Native valve endocarditis (NVE) = most common type
2) Endocarditis in PWIDs
3) Prosthetic valve endocarditis (PVE)
44
What is the most common cause of infective endocarditis in PWIDs?
staph aureus
45
What is the most common cause of infective endocarditis in native valve endocarditis?
Strep viridans
presents more indolently, causing Subacute disease
46
What is the most common cause of infective endocarditis in prosthetic valve endocarditis?
CoNS
remember: CoNS because a prosthetic valve is a con
47
List some risk factors for infective endocarditis
underlying valve abnormalities (aortic stenosis/mitral valve prolapse)
IVDU
Rheumatic heart disease
Dental work
48
Acute infective endocarditis
patient presents very unwell
progressive valve destruction
metastatic infection developing rapidly → i.e. septic emboli
commonly caused by S. aureus
49
Subacute infective endocarditis
presents indolently over weeks to months in an insidious manner
rarely leads to metastatic infection
commonly caused by Strep. viridans
50
What is the most common cause of IE
Strep. viridans
51
What should you be worried about in a patient who has Fever + murmur?
Fever + murmur = IE until proven otherwise
52
what embolic events can occur in infective endocarditis?
Small emboli:
- Petechiae
- Splinter haemorrhages
- Haematuria
Large emboli:
- CVA
- Renal infarction
Right sided endocarditis (in PWID)
-Septic pulmonary emboli
53
What are possible long term effects of infective endocarditis?
can be categorised into immunological damage and direct tissue damage
Immunological reaction:
- Splenomegaly
- Nephritis
- Vasculitic lesions of skin & eye
- Clubbing
Tissue damage:
- Valve destruction
- Valve abscess
54
What are 3 cases in which you should be suspicious of infective endocarditis?
1) patients with S.aureus bacteraemia
2) Any PWID with a positive blood culture
3) patients with prosthetic valves and positive blood cultures
55
How should you investigate infective endocarditis?
1) blood culture
| 2) echocardiography (transthoracic)
56
What are the guidelines for blood cultures in suspected infective endocarditis?
- 3 sets of blood cultures of 10ml in each bottle (20ml total)
- different peripheral sites
- before antibiotic administration
- aseptic technique crucial
57
What are the Duke criteria?
used to diagnose infective endocarditis
Major criteria:
- Typical organism in 2 separate blood cultures
- Positive echocardiogram or new valve regurgitation
Minor: FIIVE
- Fever >38 ̊C
- IVDU or other predisposition (heart condition)
- Immunological phenomena (eg. oslers nodes)
- Vascular phenomena (eg. septic emboli)
- positive blood culture
58
How many of the Duke criteria do you need to be diagnosed with IE?
Definite IE is defined as:
- 2 major
- 1 major + 3 minor
- 5 minor
59
What are 3 Indications for surgical intervention in IE?
1) Heart Failure
2) Uncontrolled Infection
3) prevention of embolism
60
How long will antimicrobial therapy be given for in IE?
4 weeks for NVE
| 6 weeks for PVE
61
What antibiotics would you use to treat IE caused by streptococcus species?
high doses of benzyl penicillin plus gentamicin
give IV
62
What antibiotics would you use to treat IE caused by enterococcus species?
amoxicillin or vancomycin +/- gentamicin
give IV
63
should you avoid beta blockers in patients with AF?
no
beta blockers work at the AV node to slow conduction
they are first line for rate management in AF
64
What do blunted costophrenic angles indicate?
pleural effusion
65
What is the difference between transudate and exudate?
Transudate is fluid pushed through the capillary due to high pressure within the capillary.
Exudate is fluid that leaks around the cells of the capillaries caused by inflammation. (Higher protein content)
66
Name three causes of transudate
LVF, Cirrhosis, Nephrotic syndrome
67
Name three causes of exudate
PE, Bacterial Infection, Bronchial Cancer
68
What is the difference between interstitial oedema and alveolar oedema?
interstitial oedema - occurs at lower pulmonary venous pressures. Fluid collects in interlobar fissures and septa (Kerley B lines)
alveolar oedema - occurs at higher pressures (>30 mm Hg). Causes areas of consolidation and mottling of the lung fields, and pleural effusion.
Continued fluid leakage into the interstitium, which cannot be compensated by lymphatic drainage.
Interstitium is overloaded and the fluid has nowhere else to go
Causes spill of fluid from interstitium into alveoli (alveolar oedema) and leakage into the pleural space (pleural effusion).
69
symptoms of MI
```
Crushing central chest pain
Back pain
Jaw pain – lower jaw
Indigestion
Sweatiness, clamminess
Shortness of breath
```
70
Possible signs of MI
```
Tachycardia (HR > 100bpm)
Distressed patient
crackles/ raised JVP
Low BP
Sweaty, clammy
Arrhythmia
```
71
What is troponin?
marker of cardiac necrosis
72
definition of MI
Any elevation in troponin in clinical setting consistent with myocardial ischaemia.
E.g. chest pain, breathlessness, etc.
73
Type 1 Spontaneous MI
due to a primary coronary event
e.g. coronary artery plaque rupture and formation of thrombus
Chest pain, ECG changes, raised troponin
74
Type 2 MI
Increased oxygen demand or decreased oxygen supply
Not a primary problem in the coronary arteries
Troponin increases due to another cause of heart stress
e.g. PE, Heart failure, sepsis, anaemia, arrhythmias, hypertension, or hypotension
75
Type 3 MI
sudden cardiac death
76
Type 4 MI
Iatrogenic
4a MI associated with percutaneous coronary intervention
4b MI Stent thrombosis
77
Type 5 MI
Iatrogenic
associated with CABG
78
What should you suspect in a patient who is Breathless with high troponin levels?
PE
79
Name 3 causes of Chronic elevation of troponin
renal failure (reduced excretion)
infiltrative cardiomyopathies, e.g. sarcoidosis
chronic heart failure
80
What is unstable angina?
An acute coronary event without a rise in troponin
81
What ECG findings do you expect in a Posterior infarct?
Location of the infarct means that an ST elevation is not seen
There are no ECG leads directly over the back of the heart
Can be diagnosed by looking for reciprocal ST elevation
82
What is the significance of Left bundle branch block in MI?
NEw - can indicate infarction
old - can obscure ST elevation on ECG
83
What is the general pattern of ECG manifestation of ischaemia?
1) ST elevation
2) pathological Q wave
3) T wave inversion
4) normalisation with persistent Q wave
other factors
- change in heart axis
- broad QRS complex
- ST depression
84
Which artery is likely to be blocked with ST elevation in the anterior leads?
LAD
85
Which artery is likely to be blocked with ST elevation in the lateral leads?
left circumflex artery
86
Which artery is likely to be blocked with ST elevation in the inferior leads?
right coronary artery
87
Which leads will show reciprocal ST depression when there is ST elevation in anterior leads?
reciprocal ST depression in inferior leads
88
What does ST elevation in aVR indicate?
occlusion of the left main coronary artery
89
Which leads will show reciprocal ST depression when there is ST elevation in lateral leads?
reciprocal ST depression in inferior leads
90
Which leads will show reciprocal ST depression when there is ST elevation in the inferior leads?
‘Reciprocal’ ST depression in high lateral leads (I and aVL)
91
Which leads will show a STEMI with right coronary artery occlusion?
inferior leads (II, III, and aVF)
92
What kind of STEMI doesn’t cause ST elevation?
posterior wall infarction
you would see anterior ST depression
93
Immediate Management of STEMI (common exam Q!)
ABCD
“CRITICAL TRANSFER PATHWAY”
Emergency transfer to heart centre. Put patient in an ambulance attached to defibrillator
Aspirin 300mg PO
Unfractionated heparin 5000U intravenously
Morphine 5-10mg intravenously
give anti-emetics to counter the nausea from morphine
Clopidogrel (in ambulance)
600mg if for PPCI
300mg if for Thrombolysis (75mg if aged > 75)
```
Ticagrelor 180mg (in hospital)
given with aspirin
```
Activate PPCI team at GJNH
94
Advantages of PCI over thrombolysis
```
Improves survival
Reduces strokes (thrombolytic drugs significantly increase the risk)
Reduces the chance of further MI
Reduces the chance of further angina
Speeds up recovery
Shortens the time spent in hospital
```
95
Difference between Primary angioplasty and rescue angioplasty
Primary angioplasty = straight to cath lab without thrombolysis.
Rescue angioplasty = angioplasty following failed thrombolysis
96
Subsequent management of STEMI (EXAM QUESTION)
Monitor in Coronary Care Unit for complications of MI
Drugs for secondary prevention (ABCDE)
- ACE inhibitors
- Beta blocker
- Cholesterol - Statin
- Dual antiplatelet (Aspirin + Ticagrelor)
- Eplerenone – only for diabetes/ LVSD/ clinical HF
- MR antagonist
Echocardiogram
Cardiac rehabilitation
If LVSD at >9 months post MI consider primary prevention ICD
defibrillator
97
Complications of MI (COMMON EXAM QUESTION)
```
Arrhythmias
Heart Failure
Cardiogenic shock
Myocardial rupture (papillary rupture causes mitral regurg. Free wall rupture causes tamponade)
Psychological
```
98
GRACE Score
Used to risk stratify NSTEMI patients
What is the risk of the person with the NSTEMI dying in hospital and over the first 6 months?
Used to decide who to send for angiogram
Low risk - discharge on medical treatment
Intermediate risk - discharge to be readmitted for angiogram within 1-2 weeks
High risk (GRACE>140): urgent inpatient angiogram
99
ticagrelor
P2Y12 receptor inhibitor
platelet aggregation inhibitor
recommended as dual antiplatelet therapy following MI in addition to aspirin for 12 months unless there are contraindications
100
What ECG findings do you expect with Pericarditis?
```
Clinical history not consistent with MI
Concave ST elevation
No specific territory (often global)
No reciprocal change
PR depression
```
101
Systemic Hypertension
persistent elevation in arterial blood pressure >140/90mmHg
This is the BP level that increases the vascular risk in patients sufficiently to require intervention
This is the threshold at which benefits of action (i.e. therapeutic intervention’) exceed those of inaction
diagnosis should not be made on a single elevated BP reading
at least two readings, five minutes between readings over at least two visits
102
Causes of Hypertension
complex and multifactorial
genetic factors - family history
lifestyle - obesity, physical inactivity, diet
RAAS overactivity - increase in salt/water retention
Sympathetic overdrive - vasoconstriction
103
Grade 1 hypertension
systolic: 140-159
diastolic: 90-99
104
Grade 2 hypertension
systolic: 160-179
diastolic: 100-109
105
Grade 3 hypertension
systolic: 180+
diastolic: 110+
106
isolated systolic hypertension
systolic: 140+
diastolic: below 90
Occurs in older patients as vessels become stiffer and less compliant with age
107
Primary Hypertension
no identifiable cause
108
Risk factors for Primary Hypertension
```
Non-modifiable:
• Age
• Gender
• Ethnicity
• Genetic factors
```
```
Modifiable:
• Diet – high salt, low fruit and veg
• Physical activity
• Obesity
• Alcohol in excess
• Stress
```
109
Secondary Hypertension
an identifiable cause of the raised BP
5-10% of cases
5 categories:
1) endocrine - hyperaldosteronism, phaeochromocytoma
2) renal - renal artery stenosis
3) drugs - NSAIDs, cocaine
4) vascular - coarctation of aorta
5) other - OSA
110
Examples of HTN end organ damage
```
stroke
retinopathy
renal failure
peripheral vascular disease
heart failure
```
111
Effect of beta blockers on HTN
Decrease blood pressure via blockade of b1 sympathetic tone on heart and reduction in renin release from kidney
Results in a decrease in heart rate and stroke volume = overall decrease in cardiac output
112
adverse Effects of beta blockers
(a) Exacerbate asthma (block b2 adrenoceptors in the lungs, blocks effectiveness of salbutamol = absolute contraindication)
(b) Intolerance to exercise because of limited capacity to increase CO
(c) Hypoglycaemia – problematic for diabetics
113
Name 2 ACEi
captopril and enalapril
114
NAme 2 ARB
Losartan and candesartan
115
Effect of Ca channel blockers on HTN
Reduce peripheral resistance
o Block of Ca2+ entry into vascular smooth muscle causes vasodilation
Reduce cardiac output
o Block of Ca2+ entry into cardiac muscle causes a reduction in heart rate and stroke volume
116
Resistant HTN
patients who are on 3 drugs including a diuretic and their blood pressure still fails to respond
117
HTN management under 55y
ACEi/ARB
ACEi/ARB + Ca channel blocker
ACEi/ARB + Ca channel blocker + thiazide-like diuretic
ACEi/ARB + Ca channel blocker + thiazide-like diuretic + other therapy (beta/alpha blocker)
118
HTN management >55y or Black
Ca channel blocker
ACEi/ARB + Ca channel blocker
ACEi/ARB + Ca channel blocker + thiazide-like diuretic
ACEi/ARB + Ca channel blocker + thiazide-like diuretic + other therapy (beta/alpha blocker)
119
atrial fibrillation
commonest sustained cardiac arrhythmia
causes an irregularly irregular pulse
irregular pattern persists when the pulse quickens in response to exercise
120
symptoms of AF
* May be asymptomatic
* Palpitation
* Dyspnoea – breathlessness
Rarely:
o chest pain
o syncope (collapse, transient loss of consciousness)
121
Conditions predisposing to AF
```
o Rheumatic heart disease
o Alcohol intoxication
o Thyrotoxicosis
o Hypertension
o Heart failure
o diabetes
o COPD/OSA
```
122
types of AF
1) Paroxysmal (intermittent, starting & stopping)
o most episodes last less than 24 hours
o stops spontaneously within 7 days
2) Persistent
o Episodes of AF that last more than 7 days and may require either pharmacologic or electrical intervention to terminate
3) Permanent
o both patient and clinician have decided to abort any further strategies to try and restore sinus rhythm
123
What would you see on ECG with AF?
* Irregular baseline between the QRS complexes
* No distinct P waves
* QRS complexes are narrow but at irregular intervals
ventricles will have a variable rate depending on how many impulses are getting through the AV node and bundle branches
124
Atrial Flutter
arrhythmia due to re-entry around the tricuspid valve on the right side of the heart
Not the same as AF but similar
Often associated with AF
125
AF vs Atrial flutter
* both abnormal heart rhythms.
* In AF the atria beat irregularly.
* In atrial flutter, the atria beat regularly but faster than usual and more often than the ventricles
126
What can cause saw tooth pattern on ECG?
atrial flutter
seen in leads II, III, aVF
127
what is the Haemodynamic Significance of AF/atrial flutter?
both cause a loss of cardiac output
Because the atria are not beating in a coordinated fashion, both predispose to thrombosis within the atria
128
What are the objectives of AF treatment?
1) Prevention of stroke
2) Symptom relief
3) Optimum management of cardiovascular disease
4) Rate control
5) +/- Correction of rhythm disturbance (if appropriate)
NB: if there is an obvious underlying condition (e.g. thyrotoxicosis), treat that
129
What are Essential investigations in AF?
* ECG – confirm arrhythmia
* Echocardiogram – look for structural heart disease
* Thyroid Function Tests – rule out thyrotoxicosis
* Liver Function Tests
130
What is the target HR n AF?
under 110 bpm
131
How is rate control achieved in AF?
by drugs that block the AV node plus administration of oral anticoagulants
first line: bisoprolol or verapamil (BB/CCB)
second line: digoxin
Heart failure: amiodarone
132
How would you achieve rate control in AF patients with heart failure?
amiodarone
don't use calcium channel blockers
133
CHA2DS2VASc score
used to assess the risk of stroke in AF patients. Maximum score of 9
```
CHF
HTN
Age >75 (2)
Diabetes
Stroke (2)
Vascular disease
Age >65
Sex (F)
```
Do not give anticoagulant to patients with CHADSVASc score of 0. (risk>benefit)
o 2 or more -> treat with NOAC
o 1 -> consider anticoagulant therapy
134
Which DOAC should be avoided in renal failure?
dabigatran
135
“Rhythm control” for patients with AF
Particularly used for younger patients, and patients with ongoing symptoms despite good rate control
Options:
o Direct current cardioversion (for persistent AF)
o Anti-arrhythmic drugs – E.g. amiodarone
o Catheter ablation
136
congenital heart disease
abnormality of foetal heart development
also encompasses the great vessels
137
Atrial Septal Defect
Acyanotic heart lesion – does not affect saturation because blood shunts from left to right
Different types:
1) Secundum - Found in the same region where you would normally find the foramen ovale (but not the same as a patent FO!)
2) Primum - often affects the ventricles
138
What kind of heart failure will you see with an ASD?
right ventricular HF
this is because blood shunts from left to right (path of least resistance), cause volume overload in the right heart.
The right ventricle dilates in compensation, but becomes overwhelmed
139
Why does an ASD predispose to arrhythmias?
volume overload causes dilation of the RA
Because of this stretching, the RA becomes vulnerable to arrhythmias -> AF/atrial flutter
140
What are possible consequences of ASD?
* RV failure
* Atrial arrhythmias
* Pulmonary hypertension
* Eisenmenger syndrome
Tricuspid regurgitation:
- RV dilates, this stretches the valve, so the leaflets no longer touch each other properly --> regurgitation
141
what is Eisenmenger syndrome?
process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect causes pulmonary hypertension
This results in eventual reversal of the shunt into a cyanotic right-to-left shunt
142
What are methods of ASD correction?
* Surgical - sternotomy
| * Transcatheter – through the groin
143
Coarctation of the Aorta
* congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.
* Acyanotic heart lesion – does not affect saturation
144
What kind of heart failure may be seen with coarctation of the aorta?
LV hypertrophy occurs because the heart has to pump harder to overcome the increased afterload
If this is not corrected, it leads to LV failure over time
Blood will try and find alternative ways to bypass the narrowing (as it follows the path of least resistance), leading to the development of collateral circulation
145
Symptoms of coarctation of the aorta
Symptoms of poor peripheral perfusion:
• Cold feet
• Claudication of the legs
• Abdominal angina (pain on eating)
• Upper body hypertension, Berry aneurysms, claudication and renal insufficiency may ensue
* Pre-coarctation hypertension – blood pressure will be very high before the coarctation, causing:
* Headaches
* Nose bleeds
146
What examination findings would you expect with coarctation of the aorta?
Discrepancies in the limb blood pressures:
• Normally, BP is higher in the legs than in the arms
• This is reversed in aortic coarctation
Radiofemoral delay:
• Delay between the radial pulse and femoral pulse
Continuous murmur:
• Because the narrowing causes turbulent blood flow
• Heard on both the front and the back of the chest
147
Which valve defect is associated with coarctation of the aorta?
bicuspid aortic valve
148
Treatment of coarctation of the aorta?
* Simple follow up for mild cases
* Transcatheter approach – balloon angioplasty
Surgical repair via thoracotomy:
• resection and end to end anastomosis
• Jump graft
149
Name 2 congenital cyanotic heart defects
1) tetralogy of fallot
| 2) transposition of the great arteries
150
Transposition of the great arteries
aorta and pulmonary artery switch
males more commonly affected
This creates 2 separate circulation systems. Without mixing of the oxgenated and deoxygenated blood there is profound cyanosis
The foetus is able to survive this condition because of the connections (ductus arteriosus and foramen ovale) that allow it to bypass the normal circulation
151
Management of transposition of the great arteries
Immediate administration of IV prostaglandins at birth
These maintain the patency of the foetal connections, allowing mixing of the blood
This buys time to perform corrective surgery
152
Methods of surgical correction in transposition of the great arteries
1) arterial switch (better method) -> gives more anatomically correct result but coronary arteries have to be reattached -> complications
2) atrial switch. RV has to pump blood to systemic circulation -> leads to RV failure
153
Tetralogy of Fallot
1) Ventricular septal defect
2) Overriding aorta
3) Obstruction of the right ventricular outflow tract
4) Right ventricular hypertrophy
• This is the net effect of all the other factors
154
Why does Tetralogy of Fallot result in low oxygenation of blood?
mixing of oxygenated and deoxygenated blood in the left ventricle via the ventricular septal defect (VSD)
preferential flow of the mixed blood from both ventricles through the aorta because of the obstruction to flow through the pulmonary valve.
155
Tetralogy of Fallot – operative strategy
give IV prostaglandins at birth to maintain the patency of the ductus arteriosus
BT shunt - redirect blood flow to the lungs
Complete repair:
- Close VSD using a patch
- Cut away extra muscle causing obstruction of the RVOT
- Use a patch to enlarge pulmonary artery
156
Univentricular Heart
congenital heart condition which results in only one effective pumping ventricle
heart relies on a PFO and PDA for mixing of the blood
• Tricuspid atresia
157
Fontan circulation
single functional ventricle is used to support the systemic circulation by disconnecting it from the pulmonary valve and artery.
The IVC and SVC are redirected and plumbed straight into the pulmonary arteries, bypassing the heart altogether
158
Problems with Fontan circulation
Without a RV the to pump blood into the pulmonary circulation, the heart relies on a sufficiently high systemic venous pressure to drive blood directly into the pulmonary arteries.
And the pulmonary vascular resistance needs to be low for optimal flow into the lungs.
This balance is very vulnerable and any change is difficult to adapt to -> can lead to haemodynamic collapse
159
commonest causes of haemodynamic collapse in Fontan patients
PE - increases pulmonary vascular resistance
arrhythmia - reduces your systemic circulation and therefore reduces systemic venous pressure (preload)
dehydration - reduced venous pressures
160
What does Acute Coronary Syndromes encompass?
STEMI
NSTEMI
unstable angina
share a common mechanism –rupture or erosion of the fibrous cap of a coronary artery plaque.
161
Left-Ventricular Ejection Fraction
Measurement of how much blood is being pumped out of the left ventricle of the heart with each contraction
Most commonly used objective measure of LV function
Normal ejection fraction is >50%
162
What imaging modality would you use to detect valve abnormality?
echocardiogram
| doppler
163
Which heart valves can be assessed using TTE?
LV, RV and aortic valve can easily be viewed with this method
164
Which imaging modality is best for visualising the mitral valve?
transoesophageal echocardiography
165
What is the purpose of Functional Stress Testing?
Aim is to compare the heart at rest and under stress.
Often used to determine if there is coronary artery narrowing.
Ischaemia is observed under stress because the blocked coronary artery loses its ability to vasodilate
166
Percutaneous Coronary Intervention
o Coronary revascularisation technique
| o Non-surgical widening of the coronary artery, using a balloon catheter to dilate the artery from within
167
What is the gold standard test for assessing coronary arteries?
CT angiography
168
Which form of imaging provides most accurate assessment of ejection fraction?
MRI
169
what does pink frothy sputum on coughing suggest?
pulmonary oedema (transudate)
170
What are the two types of systolic murmur?
ejection systolic murmur - aortic stenosis, pulmonary stenosis
pansystolic murmur - mitral regurgitation, tricuspid regurg, VSD
171
What are the types of diastolic murmurs?
early diastolic - aortic/pulmonary regurgitation
mid-diastolic - mitral/tricuspid stenosis
172
Annulus
base of a heart valve that supports the valve's leaflet
173
Rheumatic valve disease
cardiac inflammation and scarring triggered by an autoimmune reaction to infection with group A streptococci (strep pyogenes)
Antibody cross reactivity
174
Aortic stenosis
obstruction of blood flow across the aortic valve due to pathological narrowing.
175
Aortic stenosis symptoms
long subclinical period
* Shortness of breath
* Presyncope
* Syncope
* Chest pain
* Reduced exercise capacity
176
Aortic stenosis: murmur characteristics
systolic ejection murmur
crescendo decrescendo
radiates to carotids
177
Aortic stenosis causes
* Thickening
* Calcification (due to degenerative changes)
* Rheumatic valve disease
* Congenital (unicuspid or bicuspid valve)
178
Aortic regurgitation
diastolic flow of blood from the aorta into the left ventricle
Regurgitation is due to incompetence of the aortic valve or any disturbance of the valvular apparatus (eg, leaflets, annulus of the aorta)
179
Aortic regurgitation causes
* Degeneration
* Rheumatic valve disease
* Aortic root dilatation
```
Systemic disease
o Marfan’s syndrome
o Ehlers Danlos syndrome
o Ankylosing Spondylitis
o SLE
```
180
Aortic regurgitation symptoms
* Shortness of breath
| * Reduced exercise capacity
181
Mitral stenosis
obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve apparatus
left atrial pressure increases. This leads to transudation of fluid into the lung interstitium and dyspnea
182
Mitral stenosis causes
* Rheumatic valve disease - most common cause
| * Pressure overload
183
Mitral stenosis symptoms
```
o Shortness of breath
o Palpitation
o Chest pain
o Haemoptysis - if the bronchial veins rupture
o Right heart failure symptoms
```
184
Mitral regurgitation
abnormal reversal of blood flow from the left ventricle to the left atrium.
caused by disruption in any part of the mitral valve apparatus
185
Mitral regurgitation causes
rheumatic fever
ruptured chordae tendinea
186
Mitral regurgitation symptoms
* Shortness of breath
* Palpitation
* Right heart failure symptoms
187
The absence of P-waves and an irregular rhythm would suggest a diagnosis of
AF
In atrial fibrillation the atria no longer conduct electricity from the SA in an orderly fashion. Therefore P-waves are lost. As a result of disordered atrial activity only occasional waves of depolarisation pass through to the AV node and cause ventricular activation. This causes the typical irregular rhythm.
188
What view of the heart do leads I, aVL, V5 and V6 represent?
Lateral
189
What would it suggest if lead I became negative and lead III became more positive than lead II?
Right axis deviation
190
The duration of the PR interval is noted to be increasingly prolonged. In addition QRS complexes appear to be dropped at regular intervals. What diagnosis would this suggest?
Second degree heart block
Mobitz type I
191
If a rhythm is described as sinus, what does this indicate?
that a P-wave precedes each QRS-complex.
192
What is often the earliest ECG change seen during myocardial infarction?
Tall P-waves
Tall peaked T-waves
ST-depression
ST elevation
Tall peaked T-waves
193
What kind of ECG changes should you look for in suspected MI?
```
ST elevation/depression
QRS broadening
Inverted T wave
Arrhythmia
Bradycardia/Tachycardia
```
194
What tests would you perform on a patient who presents with suspected MI?
ECG
CXR - rule out other causes of chest pain
Troponin (rises 6-12 hours after onset of chest pain)
195
Percutaneous Coronary Intervention
invasive procedure to open the blocked artery and treat the underlying atheromatous plaque by balloon angioplasty and stent placement
treatment of choice for MI if the patient can receive treatment within 90 minutes
196
What is administered during thrombolysis?
Tenectaplase - fibrinolytic therapy to break-up thrombus in coronary artery
Heparin - anticoagulation to prevent further thrombosis
NB: patient should be immediately transferred to the Intervention Centre, to allow prompt “Rescue Angioplasty” if necessary, should reperfusion not occur with thrombolysis.
197
Treatment of bradycardia
Atropine
competitive antagonist of the muscarinic acetylcholine receptors. i.e. anticholinergic drug
increases heart rate and improves atrioventricular conduction by blocking parasympathetic influences on the heart
198
How would you manage a patient with bradycardia who is not responding to atropine?
temporary pacing, either trans-cutaneous or transvenous
199
ectopic rhythm
an irregular heart rhythm due to a premature heartbeat
200
What do Q waves represent?
transmural infarction
201
What further tests should be done following PCI?
```
Troponin
Cholesterol
Glucose
ECG
CXR
```
202
What is the role of Beta-blockers in the secondary prevention of MI?
cardio-selective beta-blocker = bisoprolol
Blocks the action of endogenous catecholamines, adrenaline and noradrenaline, on β-adrenergic receptors
Blunts any increase in the rate and force of the heartbeat, particularly during exertion → protective effect on the heart muscle, which may reduce the risk of developing complications
203
Which drugs would you prescribe to a patient for secondary prevention of MI?
ramipril (ACEi)
bisoprolol (beta blocker)
simvastatin (cholesterol)
aspirin (long term) and ticagrelor (6/12) = dual antiplatelet therapy
204
What are troponins?
regulatory proteins for contraction that are released from ischaemic and dying myocytes
function as a cardiac marker
NB: will not increase until 6-12 hours after onset of chest pain
The amount by which troponin rises correlates with outcome (higher troponin = greater mortality)
205
Unstable Angina
history of acute coronary syndrome (e.g. rest pain) but with no detectable troponin rise
should be investigated with exercise testing and coronary angiography
206
Absolute Contraindications to thrombolytic therapy
History of intracranial bleed or neoplasm, or recent (<4 weeks) head trauma.
Recent (<3 weeks) surgery (including dental surgery) and major trauma.
Ischaemic stroke (<6 months).
Active internal bleeding (<1 month).
Suspected aortic dissection.
Acute pancreatitis.
Bleeding disorder
Refractory hypertension (SBP >160 or DBP >100)
NB: Diabetic retinopathy is not a contraindication to fibrinolysis
207
Atherosclerosis
1) CV risk factors cause endothelial damage. This triggers leucocyte infiltration -> oxidative stress
2) LDL is deposited in tunica intima and oxidised -> fatty streak
3) macrophages engulf the oxidised lipid -> foam cells. Release pro-inflammatory cytokines -> VSMC proliferation and formation of a fibrous cap
4) lumen gradually narrows and plaque may rupture
208
What happens when a plaque ruptures?
As the plaque grows, pressure increases, and the plaque may rupture
Rupture leads to thrombosis → coagulation occurs to stop the plaque from spilling its contents into the lumen
This forms a thrombus, which can impede blood flow and cause serious complications → acute clinical events (e.g. MI)
209
What are the possible causes of acute arterial occlusion in a limb?
Thrombosis – pre-existing plaque disease. History of intermittent claudication
Embolism - more likely diagnosis in the absence of a previous history of PVD
210
long-term management of peripheral vascular disease
aspirin
antihypertensive - not beta blockers! lowering systemic BP will impair blood flow to limbs
statin
lifestyle changes
211
Resins
bind cholesterol-containing bile salts in the gut & prevent reabsorption
212
Intermittent claudication (IC)
pain in the leg brought on by walking and relieved by rest.
most common in the calf muscles but can affect the thigh or buttock
local manifestation of a systemic disorder - atheroma. indicator of widespread vascular disease
Pain at rest is a later symptom. This pain is experienced in the toes (most distal).
213
What are the features of critical ischaemia in the imminently non-viable limb?
"six Ps":
```
Pain
pale
paralysis
pulse deficit
paresthesia
Perishingly cold
```
214
Describe how to investigate and treat acute limb ischaemia
priority is imaging to demonstrate vascular disease and site of obstruction = MRI/CTA/arteriogram
majority can be treated by treating HTN, avoiding beta-blockers, stopping smoking, reducing weight and exercise
Patients can be treated by angioplasty/stenting or surgical bypass
215
What do forceful/displaced apex beats suggest?
o Forceful = hypertrophy of left ventricle to overcome the pressure gradient
o Displacement would suggest more of an overload problem
216
classic triad of symptoms in patients with aortic stenosis
Angina: precipitated by exertion and relieved by rest
dyspnoea on exertion, and shortness of breath
Syncope: Often occurs upon exertion when systemic vasodilatation in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline
217
What will cause a murmur that radiates to the carotid arteries?
Aortic stenosis
218
What will cause a murmur that radiates to the axilla?
Mitral regurgitation
219
Which are Ejection systolic murmurs?
Aortic and pulmonary stenosis
220
Which are Pansystolic murmurs?
Mitral and tricuspid regurgitation
This is because systole occurs during ventricular contraction
Or VSD
221
what type of murmurs are heard louder while sitting forward?
Aortic valve
Sitting forward brings the aortic valve closer to the chest wall, thus aortic murmurs are heard louder while sitting forward
222
what type of murmurs are heard louder in the left lateral decubitus position?
Mitral valve
Left lateral decubitus position brings the apex closer to the chest wall, thus mitral valve murmurs are heard loudest in this position
223
what type of murmurs are heard louder on inspiration?
Right-sided valve lesions (pulmonary and tricuspid valves) are heard loudest during inspiration
Intrathoracic pressure reduces, so more blood flows into the right heart chambers
224
what type of murmurs are heard louder on expiration?
Left-sided heart valve lesions (aortic and mitral valves) are heard loudest during expiration
Intrathoracic pressure increases, forcing pulmonary vessels to constrict, so blood is forced from pulmonary veins into the left atrium and through the left side of the heart
225
Aortic stenosis causes
age-related calcification (commonest cause)
Bicuspid aortic valve
226
Aortic regurgitation causes
Prosthetic aortic valve failure
Connective tissue disease
Infective endocarditis
NB: Heard loudest at left sternal edge
227
Treatment of atrial fibrillation
Both rate control and rhythm control must be considered
Rate control - digoxin, amiodarone
Rhythm control - amiodarone. NB dangerous drug and very toxic to veins -> thrombophlebitis. Use large cannula. Amiodarone is slow to work. Use direct electric cardioversion if necessary
Anticoagulant therapy - heparin - to manage the stroke risk
228
Treatment of heart failure
1) oral diuretic - FURESOMIDE - symptom control only.
2) ACEi - RAMIPRIL
3) Beta blocker - CARVERDILOL
4) Aldosterone antagonist - SPIRONOLACTONE
229
Treatment of atrial fibrillation
Anticoagulation - Apixaban for CHA2DS2-VASc score 2+
Rate and rhythm control - Amiodarone
230
Assessment of valve dysfunction
● History
● Examination
● Blood pressure
● ECG
● Exercise Tolerance Test
● Cardiopulmonary Exercise Testing (CPET)
● Stress echo
● Echo
● CT
● MRI
● Left heart catheterisation
● Right heart catheterisation
231
What antibiotics would you use to treat IE caused by CoNS?
high doses of vancomycin plus gentamicin
+/- rifampicin
give IV
232
What antibiotics would you use to treat IE caused by S. aureus?
high doses of flucloxacillin (vancomycin for MRSA) plus gentamicin
give IV
