Cardiology Flashcards
1
Q
How should arrhythmias be investigated?
A
- bloods: (TFTs, U&Es, glucose, FBC)
- baseline ECG without symptoms
- Echo (not diagnostic)
- 24 hr ECG
- implantable loop recorders
2
Q
When do you worry about ectopic beats on a 24hr ecg?
A
when they occur >20% of the time, it may lead to heart failure
3
Q
Describe how regular narrow complex (SVT) regular tacharrhythmias are treated if the pt is haemodynamicaly stable? (4 steps)
A
1st: Valsalver maneouvre
2nd: carotid sinus massage
3rd: adenosine 6mg IV then 12mg x2
4th: IV verapamil or betablockers(last resort// in asthma)
5th: electrocardioversion (do this 1st if haemodynamically unstable)
4
Q
How should narrow complex irregular tachycardias be treated initially?
(if haemodynamically unstable, if new onset within 48hrs, if been present for >48hrs and if infrequent episodes)
A
Treat as AF- by far most likely diagnosis
DC if haemodynamically unstable
If presents acutely (within 48hrs)-> chemical rhythm control with amiodarone or 300mg PO flecainide then DC and if urgent rate control needed use CSM, VSM, bisoprolol then verapamil
If old: anticoagulate and offer bisoprolol for rate control/ digoxin in HF. Then bring back in two weeks for cardioversion. Flecainide PRN can be used in infrequent symptomatic AF.
5
Q
What are the criteria on the CHA2DS2 VASc score?
A
Congestive heart failure/ LVSD Hypertension Age >75 Diabetes Stroke/ TIA/ VTE Vascular disease Age 65-75 Sex -female
6
Q
What are the criteria on the HAS BLED score?
A
Hypertension Abnormal liver or renal function Stroke Bleeding Labile INR Elderly (>65) Drugs or alcohol abuse
7
Q
What can be done in AF if anticoagulants are not tolerated or contraindicated?
A
left atrial appendage occlusion
8
Q
Give 5 causes of AF
A
- hypertension
- valvular disease
- heart failure
- IHD
- chest infection
- PE
- lung cancer
- alcohol
- hyperthyroid
- electrolyte disturbance
- infections
- diabetes
- age
9
Q
How are unstable bradycardia treated?
A
- 500micrograms atropine IV every 3-5 mins (upto 6 times)
- Then give Iv adrenaline 2-20 micrograms/ min IVI while you try to get someone todo transcutaneous pacing
- find and treat cause (eg electrolyte disturbance)
10
Q
How should pulseless VT and V fib be treated?
A
defibrillation +/- lidocaine
adrenaline every 3-5 mins and amiodarone after 3 shocks
11
Q
How should unstable and stable sustained VT with a pulse be treated?
A
unstable: sedate and do DC cardioversion x 3 then amiodarone 300mg over 20 mins whilst doing more DC shocks, check and correct electrolytes
stable: amiodarone, then flecainide then lidocaine then cardioverision or pacing
12
Q
How can non sustained VT be treated?
A
beta blockers- may also need implantable defibrillator
13
Q
What is torsade de pointes
A
A very regular broad complex tachy with pointed QRS complexes.
Associated with long QT.
14
Q
How is torsade de pointes treated?
A
IV magnesium sulphate 2mg- if unsucessful then sedate for DC cardioversion
Look for cause of long QT (drugs, hypokalaemia, bradycardia, genetics)
Other anti arrhythmics cant be used as they prolong QT
15
Q
How would you calculate the heart rate from an ECG strip?
A
Each strip is 10 seconds long
Count the amount of QRS and then multiply by 6
16
Q
Bradycardia can be caused by SA or AV node dysfunction. Give 4 causes of SA node dysfunction
A
Hypothyroidism
Hypothermia
Rheumatic Fever
Haemachromatosis
17
Q
What is Sick Sinus?
A
Sinus Node Fibrosis
Presents as Tachy Brady
18
Q
Complete HB occurs when there is no relationship between P and QRS. How does the ECG change depending on where the block is?
A
Occurring at Bundle of His - Narrow Escape Complex
Occurring below Bundle of His - Broad Escape Complex
19
Q
Give 3 causes of Complete HB
A
Digoxin toxicity
Inferior STEMI
Severe Hyperkalaemia
20
Q
What is a Junctional Rhythm
A
Abnormal rhythm arising from AV node
21
Q
How would you manage ACUTE AF (<48hrs ago)? What do you need to consider?
A
Give Heparin and aim to DC cardiovert
Generally cardiovert young patients due to stroke risk (always listen for carotid bruits first)
22
Q
AVRTs are Narrow Complex Tachycardias, describe their pathway
A
Impulse starts in AV node, travels to ventricles and then back up into atria via accessory pathway (ORTHODROMIC)
23
Q
AVNRTs are Narrow Complex Tachycardias, describe their pathway
A
Re-entrant loops form within the AV node itself
24
Q
What is diagnostic on an ECG about AVRT/AVNRTs?
A
No P Waves
25
Describe the managements of AVRT/AVNRT
Aim to transiently block the AVN (also helps differentiate it from AF)
1 - Vagal Manouvres
2 - IV Adenosine (6mg, then 12g, then 12mg with long flush)
26
Describe 3 side effects of Adenosine
Chest Discomfort
Transient Hypotension
Flushing
27
Describe the 2 types of VT
Monomorphic - Appearance of all beats match eachother, common post MI scarring
Polymorphic - Beat to beat variation, includes Torsades de Pointes
28
Ventricular Tachycardia can be managed medically (lidocaine), but when would you cardiovert?
If haemodynamically compromised
29
What are fusion beats?
Sinus and ventricular beats fuse
30
What are capture beats?
Normal conduction of SVT beats
| Appears normal
31
What is SVT with Aberrancy?
Aberrancy is a functional BBB with increased HR
| Won't be able to tell the different between SVT with BBB until back in sinus rhythm
32
What is Antidromic WPW?
AVRT that conducts the opposite way
Conducts down through accessory pathway and up through AV node
Delta waves form as the impulse passes through accessory pathway
Treated the same as NCT
33
what are some cardiac and non cardiac causes of arrhythmias
Cardiac
- ischaemic heart disease (IHD)
- structural changes eg left atrial dilation secondary to mitral regurgitation
- cardiomyopathy
- pericarditis, myo-carditis
- aberrant conduction pathways
Non cardiac-
- caffeine, smoking, alcohol
- pneumonia
drugs (B2 agonists, digoxin, L-dopa, tricyclics, doxorubicin)
- metabolic imbalance (K, Ca, Mg, hypoxia, hypercapnia, metabolic acidosis, thyroid disease)
- phaeochromocytoma.
34
how do arrhythmias generally present
Palpitations, chest pain, syncope/pre syncope, hypotension or pulmonary oedema. Some arrhythmias may be asymptomatic incidental findings eg AF.
35
what are the different types of continuous egg monitoring and describe them and their uses
* Telemetry- an inpt wears ECG leads and the signals are shown on screens being watched by staff thus if a dangerous arrhythmia occurs, help is immediately available. Reserved for those at high risk of dangerous arrhythmias eg immediately post-STEMI.
* Excersise ECGs- the pt excersises, the BP and ECG are monitored, looking for ischameic changes, arrhythmias and features suggestive of arrhythmia risks such as delta waves
* Holter monitors- the pt wears an ECG monitor which records their rhythm for 24h-7d, this is later analysed. These can also be used to pick up ST changes of suggestive ischaemia.
* Loop recorders- These record only when activated by the pt and they record a small amount of ECG data before the event. Useful of the arrhythmia causes loss of consciousness/ infrequent epidoseed
* Pacemakers and ICDs- these record details of cardiac electrical activity and device activity. This information can be useful for establishing an arrhythmic origin for symptoms
36
what is the definition of bradycardia
Heart rates of less than 60bpm are considered to be bradycardia.
However, it is more helpful to classify a bradycardia as absolute (<40bpm) or relative when the heart is innapropriately slow for the haemodynamic state of the pt.
37
what are the signs of haemodynamic instability
- Systolic bp<90mmHg
- HR<40bpm
- Poor perfusion and urine output
- Ventricular arrhythmias requiring suppression
- Heart failure
38
what are some causes of sinus node disease? when is pacing required as the treatment?
- sinus bradycardia may be due to medications
- Hypothyroidism, hypothermia and sleep apnoea should be considered
- Less commonly sinus bradycardia can be the result of rheumatic fever, viral myocarditis, amyloidosis, haemochromatosis and pericarditis.
- common in the elderly as it is fibrosis of the sinus node
Pacing is rarely required in an acute setting. not all pt will be symptomatic, in pt with symptomatic sinus node disease a pacemaker is indicated.
39
how may a sick sinus syndrome patient present and how would you treat?
Symptoms: syncope and pre-syncope, light headedness, palpitations, breathlessness
Management: thromboembolism prophylaxis if episodes of AF are detected, permanent pacemakers for pt with symptomatic bradycardia or sinus pauses
• Some pt develop a 'tachy Brady syndrome' suffering from alternating tachycardia and bradycardic rhythms. This can prove difficult to treat medically as treating one circumstance (eg tachycardia) increases the risk from the other
• Pacing for bradycardic episodes in combination with rate slowing medications for tachycardia episodes may be required if the pt is symptomatic or usntable.
40
what is first degree heart block and how would you treat
- characterised by a PR interval>0.2secs. Every atrial depolarisation is followed by conduction to the ventricles but with delay
- no specific treatment is indicated.
- For pt on digoxin, check for toxicity.
- Also take care with other rate limiting drugs. If there are symptoms of dizziness or syncope cardiac monitoring should be considered to identify higher degrees of block.
41
what is 2nd degree type 1 heart block and how would you treat
- this is characterised by progressive lengthening of the PR interval, followed by failure of the atrial impulse to conduct to the ventricles giving P wave conduction failiure (dropped QRS).
- Progressive fatigue of AV nodal cells- due to functional suppression of AV conduction (eg drugs, reversible ischaemia).
- It can occur in fit young pt with high vagal tone so can be seen during the night if monitored. It can occur quite frequently following inferior MI and rarely proceeds to complete heart block.
- No specific therapy is indicated. Higher degrees of AV block should be looked for if pt present with syncope or dizziness. Does not require pacing unless poorly tolerated.
42
what is 2nd degree type 2 heart block and how would you treat
- characterised by a constant PR interval followed by a sudden failure of a P wave to be conducted to the ventricles, this is less common, but indicates more serious involvement of the conduction system.
- Much more likely to have haemodynacmic compromise, severe bradycardia and progression to third degree heart block
- In the absence of a recent acute coronary event, permanent pacing should be arranged (if drugs have been excluded).
43
what is 3rd degree (complete) heart block and how would you treat
- characterised by no conduction from the atria to the ventricles and thus AV dissociation.
- There is no relationship between the P waves and QRS completes.
- This block can occur above the AV node at the His region (narrow complex escape and usually well tolerated such as congenital complete heart block) or beneath the AVN with broad complex escape (not well tolerated).
- Causes include various anti-arrhythmic drugs but more notably digoxin toxicity. It can occur following inferior STEMI (<10% cases) and in this context can resolve in hours to days. It is a more ominous finding following anterior MI (infranodal). Another important cause is severe hyperkalaemia ( can be treated with IV calcium chloride- 10ml of 10% solution over 3-5 mins). In the haemodynamically unstable pt, atropine can be administered (600μg to a maximum of 3mg). Isoprenaline is administered ar a rate of 5μg/min and can be tried.
- Urgent permanent pacing is indicated and should be considered within 24hr is all pt except those with a reasonable likelihood of recovery of conduction- such as in pt w a recent coronary event.
44
what is the commenest cardiac arrhythmia
Atrial fibrillation
45
what are some signs and symptoms of AF? what is the main risk of AF
Symtoms: may be asymptomatic or cause chest pain, palpitations, dyspnoea, or faintness.
Signs: irregularly irregular pulse, the apical pulse rate is greater than the radial rate, and the first heart sound is of variable intensity; signs of LVF. Remember to examine the pt as AF is often associated with non cardiac disease
main risk is embolic stroke. Warfarin reduces this
46
what are the principles of AF management
There are two key parts of managing pt with AF:
1. Rate/ rhythm control
2. Reducing stroke risk
NICE advocate using a rate control strategy except in a number of specific situations such as coexistent heart failure, younger than 65, first onset AF or where there is an obvious reversible cause
• <48hr rate or rhythm, >48/ time unclear then usually rate control but if rhythm anticoagulant for 3wks!
47
what is the rate control management of AF
* 1st Bisoptolol or CCB eg verapamil
* 2nd Digoxin (preferred if concurrent heart failiure) then amiodarone
* If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following: a b blocker, diltiazem or digoxin.
* With rate control you have to accept that the pulse will be irregular but slow the rate down to avoid the negative effects on cardiac function
48
what are some contraindications of Bisoprolol and verapamil in AF patients
Bisoptolol (CI: asthma, COPD, heart block)
CCB eg verapamil (CI: heart block, hypotension, pulmonary oedema)
49
when should immediate vs delayed cardioversion be used in an AF patient
- There are a subgroup of pt for whom a rhythm control strategy should be tried first (coexistent heart failure, younger than 65, first onset AF or where there is an obvious reversible cause, <48hr rate)
- other pt may have had a rate control strategy initially but switch to rhythm control if symtoms/ HR fails to settle
- There is a choice between immediate cardioversion or delayed cardioversion:
- Immediate- if the AF has been present for less than 48hr or they are severely haemodynamically unstable.
- Delayed- if the AF has been present for more than 48 hrs and they are stable. If delayed cardioversion is chosen the pt must be anti coagulated for >3wks first. This is due to the fact that the moment a pt switches from AF to sinus rhythm presents the highest risk for embolism leading to stoke
50
what is atrial flutter and how do you treat
a regular atrial rhythm of approximately 300bpm. It conducts to the ventricles at a a rate of 2:1 (thus 150 ventricular bpm). It is characterised by a ‘saw tooth’ like baseline.
Anti AF drugs may not work but try anyway
- Cardioversion (anticoagulate first)
- IV amiodarone to restore sinus rhythm
- Amiodarone or sotalol to maintain it
- Aim to control rate as above (bisoprolol or verapamil)
- Cavotricuspid isthmus ablation (rarely)
51
what criteria may help differentiate SVT from VT
The Brugada criteria
52
What investigations are needed for angina
- ECG: pathological q waves, LBBB, ST segment changes, T flattening or inversion
- Bloods: (FBC (anaemia), U&E (renal function), glucose and cholesterol (RFs), LFTs (statins), Troponin if ECG changes or unstable
- Echo to asses function or if HCM or valve disease is suspected
53
How should stable angina be treated
- all need referral to cardio via rapid access chest pain clinic
- GTN spray for symptom relief
- aspirin (75-300mg) or clopidogrel for anticoagulant taking into account bleeding risk
- statins and other CVS risk reduction (HTN treatment, stop smoking etc)
- BB or CCB for hypertension to reduce risk factors
- ACEi if also got diabetes
- cardiac rehab (exercise)
- coronary revascularisation if high risk or medical therapy fails
54
How is an MI investigated?
- ECG
- Bloods: FBC, U&E, glucose, lipids, crp, troponin T and I and cardiac enzymes
- CXR
- pulse oxymetry
- cardiac catheterisation and angiography
- Echo
- MI perfusion scan / CTCA
55
How should a STEMI be treated? short and long term (inc drug doses)
- Aspirin (300mg) and ticagrelor (180mg) (or clopidogrel)
- Morphine (5-10mg)
- metaclopamide (anti emetic) 10mg
- GTN sublingual or IV (50mg in 50 ml NS at 2-10ml/hr)
- Oxygen if sats are low
- call cathlab for primary PCI or CABG if multi vessel disease, if no PCI available then thrombolysis
- long term continue dual antiplatelet for 12 months (add PPI for stomach protection)
- B blockers or CCB
- ACEi
- high dose statin
- Echo also needed to asses for HF
- long term treatment is for NSTEMI
56
What do you need to think about when assessing NSTEMI risk and need for angiography/ PCI?
- rise in troponin
- dynamic st or t wave changes
- diabetes
- CKD
- LVF
- recent PCI or prior CABG
57
What lead is normally the most positive? What would be the most positive in LBBB and RBBB respectively?
Lead II is normally the most positive
LBBB - aVL
RBBB- Lead III
58
State the normal parameters for the PR interval, the QRS interval and the QT interval
PR - 120-200ms
QRS - <120ms
QT - 2 large squares
59
RBBB can be present without heart disease, however name three common causes of LBBB
Anterior MI
CHF
Left Ventricular Hypertrophy
60
Describe the diagnostic features of a STEMI
Cardiac Chest Pain
ECG changes (persistent ST elevation or new LBBB)
Raised Troponin I (greater than 100 nanograms)
61
What are the parameters for ECG changes in a STEMI?
ST elevation in atleast 2 leads
Elevation greater than 1mm in limb leads and 2mm in chest leads
- ST elevation over mins- hrs
- T wave inversion, Q wave development and ST elevation persisting over hrs to days
- Q wave and T wave inversion can persist for a week as ST elevation goes down
- Q wave can persist for months, T wave inversion reverses
62
Describe the ECG changes in an NSTEMI
ST segment depression
| T wave inversion
63
When might an STEMI be mistaken for an NSTEMI?
If you have ST segment depression in V1-V4, it may be the reciprocal changes of a posterior STEMI
64
Describe the pathophysiology of ACS
Plaque rupture
Thrombosis to varying degrees
Inflammation
Artery occlusion and reduced blood supply to myocardium
65
Describe 5 of the classical presentations of ACS
```
Central crushing chest pain lasting >20 mins
Nausea
Sweating
Breathlessness
Palpitations
```
66
Some ACS can be 'Silent', what groups of people can this occur in? How would they present?
Elderly and Diabetics
Syncope
Epigastric Pain
67
What is the S4 heart sound?
Blood striking against a non compliant ventricle
68
What happens to Troponin I in an MI
Begin to rise 3-4hrs post MI
| Remain elevated for up to two weeks
69
When should Troponin I be sampled?
One sample on admission
| If onset of the symptoms was less than 3 hours ago, take another sample one hour after the original
70
Give 4 false positives of Troponin I
Advanced renal failure
Large PE
Severe CCF
Aortic Dissection
71
Give 3 possible features of an MI on a CXR
Cardiomegaly
Pulmonary Oedema
Widened Mediastinum
72
In four steps describe the medical management of a STEMI
1) Morphine and Antiemetic
2) Oxygen (Sats>94%)
3) Asparin (initially 300mg then 75mg lifelong)
4) Further anticoagulation (ideally Prasugrel, if req not met then Clopidogrel/Ticagrelor)
73
What are the four requirements for Prasugrel in an MI?
Undergoing PCI
Less than 75 y/o
Weight >60kg
No prior TIA/Stroke
74
Give 3 long term medications that could be considered post ACS
Bisoprolol
ACEI/ARB
Statin (80mg OD nightly - aim for total cholesterol<4mmol/l)
75
Describe the 4 step management of ACS
1) Morphine and Anti-Emetic
2) Asparin 300mg (75mg lifelong)
3) Enoxaparin for 48h (assuming no other anticoags)
4) Grace Score
76
What is the Grace Score?
Used on ACS patients to estimate their inpatient and 3 year mortality
77
Give 3 complications of an MI
Pericarditis
Cardiac Tamponade
Cardiac Arrest
78
Name four STEMI mimics
Early repolarisation in young & fit
Pericarditis (saddle shaped)
Brugada Syndrome (Sodium Channelopathy)
Takotsubo Cardiomyopathy (temporary and brought on by stress - broken heart syndrome)
79
What is stable angina?
Chest discomfort provoked by effort/emotion and relieved by rest
80
Describe four potential symptoms of Stable Angina
Chest Pain
Throat tightness
Arm Heaviness
Exertional Breathlessness
81
Describe four main pharmacological managements of Stable Angina
Asparin (75mg)
GTN Spray
Beta Blockers
Long term nitrates (Isosorbide Mononitrate)
82
When would you prescribe Ranolazine in Stable Angina?
If intolerant to all the other drugs
Commenced by consultants
eGFR>30
(reduces sodium and hence calcium - relaxes muscle)
83
Other than Stable/Unstable, describe two other types of Angina
Decubitus Angina - precipitated by lying flat
| Vasospastic Angina - spasm of coronary artery
84
What leads would be affected by an inferior MI and which vessel is affected
II, III, AVF
| RCA and/or LCx depending on which one is dominant in that area
85
What leads are affected in a lateral MI and which vessel is affected?
I, aVL, V5-6
| Lateral circumflex or diagonal of LAD
86
What leads are affected in a anterior MI and which vessel is affected?
V1-4
| left anterior descending
87
What reciprocal changes are seen on ECG of anterior MI
ST depression in II, III and aVF
88
Where is the occlusion of V3-6, II, III and AvF are affected by ST elevation?
Left main stem (takes out circumflex and LAD)
89
ST elevation is often seen normally in LBBB, what criteria are used to determine if it is truly an MI?
sgarbossa criteria
90
what are some complications of ACS
DARTH VADER pneumonic
* Death: usually from VF
* Arrhythmia (Tavhyarrhythmias- VT/VF, Bradyarrhythmias- AV block is more common following inferior MI that infarcts nodal tissue)
* Rupture: septum (VSD pan-systolic + RVF), papillary muscles (MR pan-systolic + pulmonary oedema)
* Tamponade: Beck’s Triad (low BP, JVP, muffled HS) + pulsus paradoxus + Kussmaul sign
* Heart failure: right-sided = fluid + avoid diuretics; left-sided = diuretics + avoid fluids
* Valve disease: MR commonest
* Aneurysm: 4 weeks after MI persistent ST elevation + LVF + thrombus ( anticoagulate)
* Dressler’s syndrome: post-MI pericarditis (myocardial neo-antigens formed post-MI)
* Embolism (mural thrombus)
* Recurrence
91
what is the pathophysiology of a STEMI vs NSTEMI
STEMI- complete occlusion of a coronary artery
NSTEMI- partial occlusion of a coronary artery and therefore less dangerous as less of the heart may be damaged
92
four causes of Aortic STENOSIS
Senile Calcification
Congenital (Bicuspid Valves)
CKD
Rheumatic Fever
93
Describe the triad of symptoms for Aortic STENOSIS
Angina
Heart Failure
Syncope
94
Give four features of the murmur heard in Aortic STENOSIS
Ejection Systolic
Aortic Area
Radiates to carotids
Crescendo Decrescendo
95
What instances would you consider a valve replacement in Aortic Stenosis
Symptomatic
| Asymptomatic with abnormal LV function, abnormal exercise test, other cardiac surgeries
96
What valve procedure would you consider if elderly/comorbidities?
via what artery?
TAVI
Transcatheter Aortic Valve Insertion
via Femoral
97
Give two acute and two chronic causes of Aortic REGURGITATION
Acute - Chest Trauma, Infective Endocarditis
| Chronic - Congenital, Rheumatic Fever
98
Describe three features of Aortic REGURGITATION
Exertional Dyspnoea
Orthopnea
PND
99
Other than the murmur, describe two signs of Aortic REGURGITATION
Corrigan's Pulse - Collapsing pulse
| De Musset's Sign - Head bobbing with heartbeat
100
Describe two managements of Aortic REGURGITATION
```
Afterload reduction (ACEI/ARB)
Valve replacement
```
101
what are the indications for surgery in aortic regurgitation
Indications for surgery incl:
• Increasing symptoms
• Enlarging heart on CXR/ECHO
• ECG deterioration (T wave inversion in lateral leads)
• Infective endocarditis refractory to medical therapy
• Replace valve before significant LV dysfunction occurs
102
State three causes of Mitral STENOSIS
Rheumatic Fever
Congenital
Infective Endocarditis
103
Describe two ways in which Mitral STENOSIS can present
```
Pulmonary Hypertension (Dyspnoea, Haemoptysis, Malar Flush)
LA Compression (Hoarseness, Dysphagia)
```
104
Describe three features of the murmur of Aortic REGURGITATION
Early Diastolic
Left Sternal Edge
Best heard sat forward in expiration
105
Describe two features of the murmur of Mitral STENOSIS
Mid Diastolic murmur
| Best heard on expiration with patient on left
106
Describe four possible managements of Mitral STENOSIS
AF - Rate control and anticoagulate
Diuretics
Balloon Valvuloplasty
Valve Replacement
107
Describe four causes of Mitral REGURGITATION
Rheumatic Fever
Mitral Valve Prolapse (APCKD, Marfans)
IHD
Infective Endocarditis
108
Give 5 features of Mitral REGURGITATION
```
Dyspnoea
Fatigue
Palpitations
Displaced Apex
AF
```
109
State 3 features of the Mitral REGURGITATION murmur
Pan Systolic Murmur
Heard in Mitral Area
Radiates to Axilla
110
What two features indicate Infective Endocarditis unless proven otherwise
Fever
| New Murmur
111
Give 4 risk factors of Infective Endocarditis
Mitral Valve Prolapse
Prosthetic Material (not stent)
Rheumatic Heart Disease
Poor Dental Hygiene + Procedure
112
Describe four features of Infective Endocarditis
Sepsis
Cardiac Lesions - New Murmur
Immune Complex Deposition - Vasculitis, Splinter Haemorrhages
Emboli - Janeway Lesions (lesion on palms)
roth spots on retina
osler nodes (nodes on fingers)
113
State the two most effective diagnostic methods for Infective Endocarditis
blood culture and echo
Blood Cultures - Atleast 3 from different sites over a few hours
Transthoracic echocardiography (TTE)
114
Describe the criteria of MAJOR Infective Endcarditis (dukes criteria)
Positive Blood Cultures
Endocardial Involvement
Positive Echo
Valvular Regurg
115
Describe the criteria of MINOR Infective Endcarditis (dukes criteria)
```
Predisposing factors
Pyrexia
Embolic/Vasculitis Signs
Suggestive blood cultures (not meeting criteria)
Suggestive Echo
```
116
Antibiotics are given via a central line in Infective Endocarditis. Give the abc for Empirical, Strep, Enterococci and Staph
Empirical - Amoxicillin & Gentamicin
Strep - Benzylpenicillin & Gentamicin
Enterococci - Amoxicillin & Gentamicin
Staph - Flucloxacillin (+ Gentamicin and rifampicin if prosthetic)
117
How would you monitor Infective Endocarditis?
Echo Weekly
ECG Twice Weekly
Bloods Twice Weekly
118
What can cause infective endocarditis? (5)
- valve trauma (catheters, pacing wires)
- dental procedures
- valve replacement
- valve pathology
- thrombus formation
- CKD
- SLE
- neoplasia
- malnutrition
- cuts
- IV drug use (tricuspid)
- nothing at all
119
Which valves are most commonly affected by infective endocarditis?
Mitral> aortic > both mitral and aortic > tricuspid> pulmonary
120
Which organisms most commonly cause infective endocarditis? (3)
staph a, strep viridans, enterococcus
121
what are the HACEK bacteria that may cause infective endocarditis
and how would you treat
```
• HACEK* (Gram –ve bacteria)
◦ Haemophilus
◦ Actinobacillus
◦ Cardiobacterium
◦ Eikenella
◦ Kingella
```
ceftrioxone or amoxicillin (broad spec to cover gram -ve bacteria)
122
Describe the classes of HTN in terms of clinic readings
Class 1 - 140/90
Class 2 - 160/100
Severe - 180/110
123
Describe the classes of HTN in terms of home readings
Class 1 - 135/85
| Class 2 - 150/95
124
Give 4 broad causes of Secondary HTN
Renal (Renal Artery Stenosis, PCKD)
Pregnancy
Drugs (Steroids, COCP, Cocaine)
Endocrine (Cushings, Conns)
125
What is Malignant Hypertension?
Rapid rise in blood pressure to over 200/130, leading to vascular and organ damage
Can causes bilateral retinal haemorrhages, headache, visual disturbances
126
How does Hypertension present?
Generally asymptomatic
If sweating/palpitations - Phaeochromocytoma
If muscle tetany/weakness - Hyperaldosteronism
127
Describe 5 investigations (apart from BP) necessary for HTN
```
Full range of bloods (inc cholesterol)
Urinalysis (A:Cr, Protienuria, Haematuria)
ECG
Fundoscopy
Cardiac Echo
```
128
You should aim to reduce blood pressure slowly in Hypertensive patients. What is the BP goal in treated patients?
Normal <140/90
| Diabetic <130/80
129
Describe the four step (up) management of Hypertension
```
1) Under 55 - ACEI/ARB
Over 55/AfroCaribbean - CCB
2) ACEI/ARB + CCB
3) ACEI/ARB + CCB + Thiazide
4) Add another diuretic/doxazosin/bisoprolol
```
130
Describe the 3 classes of CCBs, an example of each and their actions
Dihydropyridine - acts on peripheral vasculature (eg Amlodipine, Nifedipine)
Phenylalkamine - acts on cardiac vasculature (eg Verapamil)
Benzothiazepine - acts on cardiac and peripheral vasculature (eg Diltiazem)
131
Describe the difference between a Hypertensive Emergency and a Hypertensive Urgency
Emergency - High BP with critical illness (AKI,MI, Encephalopathy)
Urgency - High BP without critical illness at the moment, often accompanied by retinal damage
132
Describe the management of a Hypertensive EMERGENCY
```
The aim of therapy is to reduce the diastolic bp to 110mmHg in 3-12 hrs (emergency) or 24hrs (urgency. IV to start
◦ Sodium nitroprusside
◦ Labetalol
◦ GNT (1-10mh/hr)
◦ Esmolol
```
133
Describe the management of a Hypertensive URGENCY
Reduce diastolic to 100mmHg in 48-72hrs
| Usually use Nifedipine AND Amlodipine for 3 days and then continue Amlodipine alone
134
what is the non pharmacological management of hypertension
1. Weight reduction if BMI >25kg/m2. Each kg weight loss yields a BP reduction of 3/2mmHg
2. Moderate salt intake (can reduce bp by 8/5mmHg). Minimise alcohol intake. Aerobic exercise. Smoking cessation (to reduce cardiovascular risk)
135
what is the triad of symptoms in a patient with pheochromocytoma
episodic headache, sweating and tachycardia although most pt will not have all 3.
136
what is the most common sign of phaechromocytoma
sustained or paroxysmal hypertension
137
how do you diagnose and treat phaeochromocytoma
diagnosis is typically confirmed by measurements of urinary and plasma fractionated metanephrines and catecholamines. A 24hr urine collection is the main test. A CT or MRI scan of the abdomen and pelvis may detect adrenal tumors. A MIBG scan can detect tumors not detected by CT or MRI but where the diagnosis is still considered likely.
Once phaeochromocytoma is diagnosed all pt should undergo a resection. Pending surgery control of hypertension is combined alpha and beta adrenergic blockade. Phenoxybenzamine is most commonly used
138
what is heart failure
cardiac output is inadequate for the body requirements
139
what are a few causes of heart failure
Causes
1. Ischaemic heart disease (most common)
2. Hypertension
3. Vascular heart disease (rheumatic fever in elderly)
4. Atrial fibrillation
5. Chronic lung disease
6. Cardiomyopathy (hypertrophic, dilated and right ventricular, post-viral, postpartum)
7. Previous cancer chemo drugs
8. HIV
140
what criteria is used to diagnose heat failure
which is used for severity of heart failure
Framingham criteria- diagnosis of CCF requires simultaneous and presence of at least 2 major criteria, or 1 major and 2 minor criteria
Severity of heart failure can be classified using the NYHA (New York classification of heart failure) classification
141
Describe the features of SYSTOLIC Heart Failure
Inability of the heart to contract, EF<40%
| Caused by IHD/MI/Cardiomyopathies
142
Describe the features of DIASTOLIC Heart Failure
Inability of the heart to relax, EF>50% (HFpEF)
| Caused by Ventricular Hypertrophy/Tamponade
143
Right Ventricular Failure is caused by LVF or Chronic Lung Disease, give 3 features
Peripheral Oedema
Ascites
Facial Engorgement
144
State 3 causes of ACUTE Heart Failure
Infections
Anaphylaxis
PE
145
Describe the use of BNP
BNP can be used to rule out Heart Failure if it is less than 100ng/l
Not diagnostic as BNP can be raised by anything that causes chamber stress (AF etc)
146
Using the A-E mnemonic describe the 5 features of a CXR of Heart Failure
```
A - Alveolar Oedema (Bat Wings)
B - Kerley B Lines (Interstitial Oedema)
C - Cardiomegaly
D - Dilated Veins
E - Effusions
```
147
Give 5 features of Heart Failure
```
Cyanosis
Low BP
Narrow Pulse Pressure
Apex Displacement
RV Heave
```
148
Describe the New York Classification of Heart Failure
I - Heart Disease present but no limitations
II - Comfortable at rest but dyspnoea in normal activities
III - Less than ordinary activity causes dyspnoea
IV - Dyspnoea at rest
149
There are many medications that can be given for Heart Failure, but what device could patients have fitted?
Cardiac Resynchronisation Therapy
Adds pacing to septal and lateral walls will reduce QRS width
Considered if signs of LBBB
Can combine with Defib device
150
Describe the clinical features of right sided heart failure
- peripheral odema and associated weight gain
- ascites
- increased JVP
- anoerxia and GI complaints
- most have PND, orthopnoea, dyspnoea etc as most right sided heart failure is caused by left sided heart failure
151
what is the management of acute heart failure
- sit patient up right
- O2
- ecg and other investigations
- furosemide
- GTN spray
- if systolic BP >100 start nitrate infusion
if patient worsening
- consider increasing nitrate and furosemide
- also consider CPAP
152
management of chronic heart failure
Chronic heart failure
• Lifestyle modification:
• Treat the cause
• Treat exacerbating factors
• Avoid exacerbating factors
• Annual flu vaccine, one off pneumococcal vaccine
• Drugs:
1. Diuretics- give loop diuretics to relive symptoms eg furosemide 40mg/24hr
2. ACE-i: consider in all this ew left ventricular systolic dysfunction (LVSD);
3. B blockers (eg carvedilol). Reduces mortality in hf- benefit additional to those of ACE-i in pt with systolic dysfunction. Use with caution: start low an ego slow; wait 2 or more weeks between each dose increment.
4. Mineralocorticoid receptor antagonists: spironolactone (25mg/24h PO) reduces mortality when added to conventional therapy. Use in those still symptomatic despite optimal thrapy a listed previously and in post MI pt with LVSD.
5. Digoxin: Helps symptoms even in those with sinus rhythm and should be considered for pt w LVSD who have signs or symptoms of hf while receiving standard therapy incl ACE-i and B blockers or in pt w AF.
6. Vasodilators: the combo of hydralazine (SE: drug induced lupus) and isosorbide dinitrate should be used if intolerant of ACE-i and ARBs as it reduces mortaluty.
