CARDIOVASCULAR Flashcards

1
Q

What is absolute bradycardia?

A

HR is <40bpm

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2
Q

What is relative bradycardia?

A

Where HR is inappropriately slow for the haemodynamic state of the patient.

Oxford clinical handbook definition of bradycardia = <60bpm

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3
Q

Signs that may indicate haemodynamic instability?

A
Systolic BP < 90mmHg 
HR <40 
Poor perfusion 
Poor urine output 
Ventricular arrhythmias that need suppression 
Heart failure
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4
Q

How can bradycardia be classified?

A

Based on the pacemaker that is faulty:

  • sinus node e.g. sinus bradycardia
  • AV node
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5
Q

List some causes of bradycardia

A

Physiological:
- athletes

Cardiac:

  • degenerative changes/fibrosis of conduction pathways in elderly
  • post-MI (especially inferior MI (leads II, III, aVF)
  • sick sinus syndrome
  • iatrogenic —> ablation, surgery
  • aortic valve disease e.g. infective endocarditis (rheumatic fever)
  • myocarditis, cardiomyopathy, sarcoidosis, SLE

Non-cardiac origin:

  • vasovagal
  • endocrine = hypothyroidism, adrenal insufficiency
  • metabolic = hyperkalaemia, hypoxia
  • other = hypothermia, raised ICP (Cushing’s triad - bradycardia, hypertension and irregular breathing), pericarditis, haemochromatosis,

Drug induced:

  • Beta blockers
  • amiodarone
  • verapamil
  • diltiazem
  • digoxin
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6
Q

Main management for pt with symptomatic sinus node disease (e.g. a sinus bradycardia)?

A

Pacemaker is indicated

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7
Q

What are categories of sinus node dysfunction?

A

Sinus bradycardia
Sick sinus syndrome
Sinus arrest
Part of vasovagal syncope

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8
Q

How are AV node bradycardias classified?

A

According to the degree of nodal dysfunction:

  • First degree AV block
  • Second degree AV block Mobitz Type I aka Wenckebach
  • Second degree AV block Mobitz Type II
  • Complete/Third degree AV block
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9
Q

How is First degree AV block characterised?

A

PR interval >0.2s

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10
Q

Pt has bradycardia. What rate limiting drug should you check pt is on and why?

A

Digoxin. Why? Digoxin toxicity - can worsen conduction abnormalities and worsen heart block

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11
Q

How is Second degree AV block: Wenckebach/Mobitz Type I characterised?

A

Lengthening of PR interval. Followed by failure of atrial impulse to conduct to the ventricles.

i.e. QRS is dropped after progressive lengthening of PR interval.

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12
Q

Who is more likely to have Second degree AV block: Wenckebach/Mobitz Type I?

A
  • Young fit patients with a high vagal tone

- Patients after inferior MI

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13
Q

How is Second degree AV block: Mobitz Type II characterised?

A

Constant PR interval followed by sudden failure of a p wave to be conducted to the ventricles.

i.e. PR length constant, then drop of QRS. 2 p waves for every QRS

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14
Q

How is complete heart block/ Third degree AV block characterised?

A

No conduction from atria to the ventricles. No relationship between p waves and QRS complexes

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15
Q

What does complete/ third degree heart block look like on ECG?

A

Rate is slow. Broad complex QRS escape rhythm seen, with no linkage of p waves and QRS - they are both independent.
Sometimes can look intermittent - see trifascicular or bifascicular block (RBBB, with or without prolonged PR interval) and alternating LBBB and RBBB.

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16
Q

Where can complete/third degree block occur?

A

Either:

  • above AV node at the HIS region
  • beneath AV node
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17
Q

Causes of complete/third degree AV block?

A

Anti-arrhythmic drugs - especially digoxin toxicity!!
Post- inferior STEMI (will resolve in hrs-days)
Anterior MI
Severe hyperkalaemia

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18
Q

How to treat severe hyperkalaemia causing. complete/third degree AV heart block?

A

IV calcium chloride - 10ml of a 10% solution over 3-5mins

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19
Q

How to treat a haemodynamically unstable patient with complete/third degree AV heart block?

A

Atropine - 600micrograme to 3 mg.

Isoprenaline - at rate of 5micrograms/minute

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20
Q

Main management for complete/ third degree AV heart block?

A

Urgent permanent pacemaker. Within 24hrs unless they are likely to have a recovery of conduction (e.g post inferior STEMI)

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21
Q

Types of tachycardic arrhythmias?

A

Atrial fibrillation
Supraventricular tachycardia = in atria
Ventricular tachycardia

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22
Q

Presentation of AFib?

A
Asymptomatic 
Breathlessness 
Palpatations
Syncope/dizziness 
Chest discomfort 
Stroke or TIA
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23
Q

Complications of AFib?

A

Cardioembolic stroke
Cardiac instability
Death

Increase in healthcare costs

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24
Q

How to diagnose A fib?

A

Presence of symptoms - palpitations, dizziness/syncope, breathlessness, chest discomfort, stroke, TIA
ECG used to confirm if an irregular pulse is due to A fib.

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25
What to do before treating suspected AFib just from clinical picture?
Do an ECG to confirm. | Why? Irregular pulse may be due to other reasons
26
Pt has intermittent AFib. What is next step in investigation?
Short term cardiac monitoring with 24hr cardiac monitor
27
Disadvantage of 24hr cardiac monitor to identify arrhythmia?
Symptoms need to be very frequent to diagnose an arrhythmia - this is a short time period - delivers low yield results.
28
What are the different types of prolonged cardiac monitors?
Prolonged Holter monitor | Implantable loop recorder
29
When/ In what circumstances is an echocardiogram carried out for AFib ?
1. Suspected structural heart disease - from symptoms, murmer or signs of HF 2. When considering cardioversion to control rhythm 3. When a baseline is needed to inform long term management
30
How to manage AFib?
1. Anticoagulation to prevent stroke 2. Rate control 3. Rhythm control
31
Scoring tool to assess whether pt with AFib needs anticoagulation? State and explain
``` CHA2DS2-VASc Congestive heart failure Hypertension Age >75 = 2, 65-74 = 1 Diabetes Stroke or Tia = 2 Vascular disease Sex category (female) ``` Higher score = higher risk of stroke or embolism. - Score of 2+ = significant risk. Offer anticoagulant. - Score of 1 in men = intermediate risk, consider anticoagulant - Score of 0 = low risk, not offered anticoagulant
32
Scoring tool to assess risk of major bleeding when on anticoagulation?
``` HAS-BLED Hypertension Abnormal renal and liver function - 1 point for each Stroke Bleeding Labile INRs (poor INR control while on warfarin) Elderly (65 + ) Drugs or alcohol - 1 point each ```
33
Anticoagulant options for AFib?
DOACs - apixaban, rivaroxaban, edoxaban, dabigatran
34
How does the mechanism of action of dabigatran differ to other DOACs?
Apixaban, rivaroxaban, edoxaban = inhibit factor Xa directly so prevent conversion of prothrombin —> thrombin. Dabigatraan = direct thrombin inhibitor so prevents conversation of fibrinogen —> fibrin
35
Benefit of DOAC compared to warfarin?
Less monitoring (INR monitoring) No restrictions on food or alcohol Lower rates of bleeding to warfarin Better reduction in stroke
36
How are DOACs excreted and why is this important?
Via kidney. Need to monitor renal function yearly
37
Other management options available for AFib, other than anticoagulants?
Rate control Electrical cardioversion Drug therapy
38
Pathophysiology of supraventricular tachycardia (SVT)?
AV nodal re-entry tachycardia (a re-entry within the AV node) OR Atrio-ventricular re-entry tachycardia (an anatomical re-entry) Both of these depend on AV nodal conduction
39
First line treatment of supra ventricular tachycardia in haemodynamically stable patients?
Vagal manoeuvres e. g. breath holding, valsalva manoeuvre e. g. carotid massage (younger patients) These slow down conduction in AV node so can interrupt re-entrant circuit
40
What should you do before attempting carotid massage for treating supra ventricular tachycardia?
Auscultate for bruits before carotid massage manoeuvre | Why? Risk of stroke from emboli
41
Short term management options for SVT if vagal manoeuvres do not help?
IV adenosine | CCBs
42
Route of administration and dose of adenosine for SVT?
IV - rapid bolus Followed by saline flush immediately. Administered via three way stopcock. Give 6mg stat followed by 12mg if unsuccessful. Repeat 12mg if unsuccessful after first 12mg dose. In antecubital fossa
43
Describe half life of adenosine?
Very short half life
44
Why is it important that dose of adenosine is given IV and in antecubital fossa via large bore cannula?
Needs to reach heart quickly to minimise cellular uptake en route - so need large bore cannula and entry to be as proximal as possible.
45
ADRs of adenosine given for SVT?
Chest discomfort Transient hypotension Flushing
46
Contraindication for adenosine use in SVT management?
Pts with significant reversible airway disease e.g asthma or COPD - as can cause bronchospasm
47
Safety precautions to have in place before administering adenosine to a pt?
Crash trolley next to pt - as possibility of bradyarrhythmia or tachyarrhythmia
48
ECG findings of SVT?
A narrow-complex tachycardias with a QRS interval of 100 ms or less
49
When is verapamil contraindicated for SVT control?
Pts on B-blockers | Pts with LV dysfunction
50
If adenosine and verapamil are ineffective/contraindicated for SVT, what can be done for SVT?
Electrical cardioversion under GA or sedation
51
Second line drugs for SVT?
IV flecainide can be used if they don't have PMH of MI Sotalol Amiodarone
52
ECG findings of VT?
Regular broad QRS
53
Management for sustained VT in haemodynamically compromised pts?
* oxygen * IV access * exclude reversible factors - e.g. PA catheter in RV, hypokalaemia, hypomagnesia * synchronised DC shock - up to 3 attempts * if unsuccessful = Amiodarone 300 mg IV over 10–20 min. Repeat synchronised DC shock
54
Pharmacological options for VT?
B-blockers Amiodarone Lidocaine
55
Maximum dose of lidocaine that can be given in 1hr?
200-300mg
56
Presentation of stable angina?
Chest discomfort/ pain provoked by effort, emotion and relieved by rest
57
How may severe angina present?
Accompanied by autonomic features- fear, sweating and nausea
58
ddx for chest pain/discomfort
angina, GORD, MSK discomfort, pulmonary disease
59
What is Cardiac Tamponade? Mechanism of how it happens?
Accumulation of fluid, blood, purulent exudate or air in the pericardial space. This raises intra pericardial pressure. Diastolic filling is reduced, which reduces cardiac output. Life threatening emergency that requires prompt diagnosis with echocardiogram and treatment.
60
How would a pt with cardiac tamponade present?
``` Shortness of breath Tachycardia Confusion Chest pain Abdominal pain ```
61
What are the signs of cardiac tamponade. Hint a helpful ____ triad?
BECK'S Triad of signs: 1. Hypotension 2. Quiet heart sounds 3. Raised JVP Other signs: dyspnoea pulsus paradoxus - an abnormally large drop in BP during inspiration. an absent Y descent on the JVP - this is due to the limited right ventricular filling
62
What are RF for cardiac tamponade?
malignancy, purulent pericarditis, severe thoracic trauma.
63
RF for angina?
cigarette smoking, hypertension, DM, hypercholesterolaemia, Fhx of premature coronary artery disease presence of other acquired vascular disease
64
What drugs do you prescribe to someone with angina?
Aspirin 75mg OD Sublingual GTN Statin Beta blocker OR CCB- depending on contraindications, co-morbities and pt preference- first line. If using CCB monotherapy, use rate limiting one- verapamil or diltiazem. If pt is still symptomatic on CCB or Beta blocker monotherapy, add the other. Ensure CCB is now a is long-acting dihydropyridine one e.g modified release nifedipine. If patient on monotherapy cannot tolerate addition of a CCB or Beta blocker, consider long-acting nitrate, ivabradine ( when B blocker is not tolerated and not prescribed with verapamil or diltiazem), nicorandil or ranolazine if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
65
Hx for someone presenting with angina?
``` precipitants of anginal attacks relieving factors stability of symptoms risk factors (smoking history, high BP, lipids, diabetes, prior CV disease) • occupation assessment of the intensity, length and regularity of exercise basic dietary assessment alcohol intake drug history family history ```
66
Examination for someone presenting with angina?
weight and height (to allow calculation of BMI) or waist / hip ratio blood pressure presence of murmurs, especially that of aortic stenosis evidence of hyperlipidaemia evidence of peripheral vascular disease and carotid bruits (especially in diabetes).
67
Investigations for someone presenting with angina?
FBC and biochem screen incl glucose and HbA1c Full lipid profile Resting 12 lead ECG- provides info on rhythm, presence of heart block, previous MI, myocardial hypertrophy and iscahemia
68
What investigations for Cardiac tamponade?
ECG - low voltage QRS complexes or electrical alternans (alternating QRS amplitude) Chest x-ray - show a large globular heart ECHO - fluid around the heart and quantify the level of ventricular compromise. Pericardiocentesis - sampling of the fluid to find the underlying cause and treat the immediate problem.
69
What is first line management for cardiac tamponade in a haemodynamically unstable pt?
pericardiocentesis | using a needle and small catheter to drain excess fluid
70
In a pt with cardiac tamponade when would surgical drainage be indicated as first line management ?
In patients with haemopericardium, associated malignancy, traumatic/purulent effusion
71
What are some complications of pericardiocentesis?
pneumothorax (all patients should have a CXR post procedure to exclude this) Damage to the myocardium / coronary vessels Thrombus Arrhythmias/cardiac arrest Damage to the peritoneum.
72
Causes of non-cardiac chest pain?
``` Costo-chondritis Gastro-oesophageal PE Pneumonia Pneumothorax Psychogenic/psychosomatic ```
73
When do you offer invasive coronary angiography to a pt for angina?
If estimated likelihood of CAD is between 61-90%
74
When do you offer functional imaging as the first- line diagnostic investigation (stress MRI, echo or myoview) of angina?
If the estimated likelihood of CAD is 30 - 60%
75
When do you offer CT calcium scoring as the first- line diagnostic investigation in angina?
If the estimated likelihood of CAD is 10 - 29%
76
How do you interpret CT calcium scoring?
0- minimal likelihood there is significant coronary disease 1-400: Consider CTCA or stress perfusion imaging Above 400- coronary angiography should be seriously considered
77
What is top differencial for Cardiac tamponade?
Constrictive pericarditis
78
How would differentiate between cardiac tamponade and constrictive pericarditis?
CT - absent Y descent JVP - reduced RV filling - Pulsus paradoxus - (+ drop in BP w/inspiration) CP - Y+ X present in JVP - no Pulsus paradoxus - Kussmaul's sign +ve - Pericardial calcification seen on CXR
79
When should you NOT use exercise ECG to diagnose stable angina?
If they do NOT have known CAD
80
For men older than 70 with atypical or typical symptoms what risk do you assume of having CAD
>90%
81
For women older than 70, with typical or atypical symptoms, what risk do you assume of CAD?
61-90%
82
When do you assume women over 70 has a risk of CAD of >90%?
If she has high risk factors AND typical symptoms
83
What is the danger of leaving valvular heart disease untreated? What can it lead to?
Irreversible ventricular dysfunction and / or pulmonary HTN
84
What are the three classic symptoms of aortic stenosis?
Angina heart failure syncope
85
What is the most common INITIAL symptom of aortic stenosis? i.e. what pt might recognise and then seek help as change in normal
Exercise intolerance or dyspnoea on exertion
86
What are some causes of aortic stenosis?
Most common: AGE -senile/degenerative calcification congenital bicuspid valve CKD rheumatic fever william's syndrome
87
Where on the chest is best place to listen to murmur due to aortic stenosis?
Aortic area: | 2 ICS Right sternal border
88
How would you describe aortic stenosis murmur ?
Ejection systolic murmur radiating to the carotid / neck Tom says: ejection -systolic, high pitched murmur. crescendo - decrescendo character.
89
What are the indications for surgery in Aortic stenosis?
Symptoms (no matter severity) Asymptomatic severe - LV systolic dysfunction Asymptomatic severe - abnormal exercice test (drop in BP, ST elevation) Asymptomatic severe - at time of other cardiac surgery e..g CABG
90
What extra should you consider doing for older patients with aortic stenosis? How is this implanted?
especially with co-morbidities Transcatheter aortic valve implantation (TAVI) implanted via femoral artery
91
When doing a cardio exam (yay) what special manoeuvres would you do to listen for mitral stenosis or aortic regurgitation?
Mitral stenosis Listen with patient on left hand side Aortic regurgitation Pt sat up, leaning forward and holding exhalation
92
How does Aortic regurgitation ultimately lead to heart failure?
increased volume load on Left ventricle causes dilation of LV and ultimately HF
93
What is the most common initial symptom in aortic regurgitation?
exertional dyspnoea / reduction in exercise tolerance
94
What are the causes of aortic regurgitation ?
``` Many! Dilation of aorta (pulls the valve leaflets apart) congenital (e.g. bicuspid valves) Calcific degeneration rheumatic disease infective endocarditis Marfan's ```
95
Where is aortic regurgitation best heard on the chest?
Left sternal edge 3rd ICS
96
Where is aortic regurgitation best heard on the chest?
Left sternal edge Early diastolic blowing murmur (associated with collapsing pulse + headbobbing -De Musset's Sign)
97
What is the role of ACEi in aortic regurgitation?
Reduces afterload so can slow LV dilatation - standard therapy for pt with severe AR and LV dilation
98
Which 2 heart murmurs often have delayed presentation?
``` Mitral regurgitation (16 years from onset to diagnosis) Aortic regurgitation (many pt do not know they have it despite large LV dilation) ```
99
Most pt with Mitral regurgitation will never need surgical intervention - TRUE or FALSE
TRUE! | most pts have mild - moderate disease and wont need surgery
100
What are some causes of Mitral regurgitation?
``` Mitral valve prolapse - (Marfans) pts with pectus excavatum Rheumatic heart disease IHD Infective endocarditis drugs collagen vascular disease 2ndary to dilated annulus from LV dilatation ```
101
What are some of the few cases where mitral regurgitation may be acute and severe?
Ruptured chordae ruptured papillary muscle Infective endocarditis
102
Where is mitral regurgitation best heard? How would you characterise it?
Mitral area - 5th ICS in midclavicular line Pan-systolic blowing murmur radiates to axilla TOM: cause congestive heart failure -leaking valve = reduced ejection fraction + backlog of blood. May hear 3rd heart sound (stiff / weak ventricles + chordae "guitar string twang")
103
What are the indications for surgery in mitral regurgitation?
Symptomatic pts Asymptomatic w/ mild/mod LV dysfucntion (EF 30-60%) mitral valve replacement or repair
104
What is the drug treatment for mitral regurgitation?
Diuretics ACEI used in pt w/ dilated / ischaemic cardiomyopathy LV dysfunction ? Give: ACEi and B-blockers e.g. bisoprolol and CRT reduced severity pg MR
105
What are some causes of mitral stenosis?
Rheumatic heart disease | infective endocarditis
106
What kind murmur does mitral stenosis cause? Where should you listen to it?
Mid-diastolic low pitched rumbling murmur Large S1- thick valves need big systolic force to shut. Listen at apex Palpate a 'tapping' apex beat - due to loud SI
107
What other examination findings is mitral stenosis associated with and why?
Malar flush: back pressure of blood into pulmonary system causing increase in C02 and vasodilation Atrial fib: Left atrium struggling to push blood through stenosed valve - strain - electrical disruption - fibrillation
108
What are the acute coronary syndromes?
STEMI NSTEM Unstable angina
109
What is a STEMI ?
Cardiac sounding chest pain with: ST segment elevation >1mm in limb >2mm in chest or New LBBB on ECG hs-Tnl (Troponin I ) - >100ng/L CK usualluy > 400
110
What is an NSTEMI ?
Cardiac sounding chest pain with: ST depression, T wave inversion (can be normal) hs-Tnl (Troponin I ) - >100ng/L + previous ECG changes: old MI (pathological Q waves), LV hypertrophy / Afib may be present on ECG
111
What is unstable angina?
Cardiac sounding chest pain with ST depression, T wave inversion (can be normal) hs-Tnl (Troponin I ) - NORMAL RANGE
112
Apart from Troponin I (Tnl) levels what else should be measured in STEMI pts?
Creatinine Kinase
113
What levels of Tnl (troponin) in men and women suggest high likelihood of myocardial necrosis?
men: hs-Tnl levels >34 ng/L women: hs-Tnl levels >16 ng/L
114
if suspect ACS when should you take a Tnl (troponin)?
1 on admission and then 1 hour later | only 1 needed if onset of symptoms was >3 hours ago
115
What other conditions can cause a rise in Tnl (Troponin) and therefore give a false positive result when investigating for suspected ACS?
``` Non cardiac: sepsis Advanced renal failure (rhabdmyolysis - CTF) Large PE Congestive cardiac failure malignancy stroke ``` ``` Cardiac: Myocarditis - post tacchyarrythmias aortic dissection aortic stenosis hypertrophic cardiomyopathy ```
116
What ECG findings do you need for a STEMI diagnosis?
ST elevation on 2 or more leads from the same zones e.g. II, III , AVF (inferior) or presence of LBBB
117
What conditions can mimic STEMI on ECG?
Early repolarisation causes up-sloping ST elevation V1-V2 -Younger athletic / afro Caribbean pts. Pericarditis - concave ST elevation. Widespread changes
118
If there are raised troponins, and / or ECG changes such as ST depression, T wave inversion, pathological Q waves) what is diagnosis?
NSTEMI
119
If troponin is normal and ECG shows no pathological changes, what is diagnosis?
Unstable angina or musculoskeletal chest pain
120
If a pt presents with a STEMI within 12 hours of onset of symptoms what are the two treatment options that are time dependant ?
PCI - Percutaneous coronary intervention w/in 2 hours of presentation Thrombolysis - if PCI not available w/in 2 hours
121
How is PCI for STEMI performed?
catheter is fed through pts femoral / brachial artery up to the coronary arteries. A dye is injected so that the blockage can be visualised. Balloons to widen or devices to aspirate and remove the blockage are performed. Stent is then placed to keep the artery open
122
What does thrombolysis involve?
Fibrinolytic material is injected to rapidly break down clots e.g. alteplase streptokinase tenectplase
123
What is the management for an STEMI -? This is workbook one
1. IV access 2. Pain relief (morphine + antiemetic) 3. O2 (ONLY IF hypoxic aim >94%) 4. Aspirin (300mg loading dose) 4 a. Prasugrel (Ticagrelor if contra) 4 b. Clopidogrel 5. PCI 6. Biochem - lipid progile, glucose, HbA1c, FBC 7. Meds (Bblocker, statin, ACEi) 8. Diabetic control 9. HTN control 10. Smoking cessation 11. Triple therapy - AF pts 12. complication monitoring - HF diuretics etc.
124
What is the risk with pts who have AF and then get a STEMI in terms of their drug regimine?
AF taking anticoagulation (not anti-platelets such as asprin). They will be on 3 medications - increasing the risk of bleeding. SO - limit time on all 3 drugs and give a PPI
125
What is NSTEMI treatment? Dr Tom mnemonic
BATMAN B – Beta-blockers unless contraindicated A – Aspirin 300mg stat dose T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk) M – Morphine titrated to control pain A – Anticoagulant: Fondaparinux (unless high bleeding risk) N – Nitrates (e.g. GTN) to relieve coronary artery spasm Give oxygen only if their oxygen saturations are dropping (i.e. <95%). SANDILANDS PLUS: repeat ECG Grace score for elevated troponins
126
What are some complications of MI?
(Heart Failure DREAD) D – Death R – Rupture of the heart septum or papillary muscles E – “Edema” (Heart Failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome
127
Secondary Prevention Medical Management for Acute Coronary Syndromes / STEMI DR TOM
Aspirin 75mg once daily Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months Atorvastatin 80mg once daily ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily) Atenolol (or other beta blocker titrated as high as tolerated) Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
128
What is some secondary Prevetion lifestyle advice for ACS (acute coronary syndromes - STEMI/ NSTEM/UA)
Stop smoking Reduce alcohol consumption Mediterranean diet Cardiac rehabilitation (a specific exercise regime for patients post MI) Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
129
What is Grace score ? who is used for ?
gives a 6-month risk of death or repeat MI after having an NSTEMI: <5% Low Risk 5-10% Medium Risk >10% High Risk If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
130
Coronary arteries anatomy : The Left Coronary Artery becomes the _____1___and _____2_____
The Left Coronary Artery becomes the ___Circumflex___and __Left anterior descending (LAD)___
131
What part of the heart does the Right Coronary Artery (RCA) supply?
Curves around the right side and under the heart and supplies the: Right atrium Right ventricle Inferior aspect of left ventricle Posterior septal area
132
What part of the heart does the Circumflex Artery supply?
curves around the top, left and back of the heart and supplies the: Left atrium Posterior aspect of left ventricle
133
What part of the heart does the Left Anterior Descending (LAD) supply?
it travels down the middle of the heart and supplies the: Anterior aspect of left ventricle Anterior aspect of septum
134
What ECG leads correspond with Left Coronary Artery?
I, aVL, V3-6 Anterolateral
135
What ECG leads correspond with LAD Artery?
V1-4 Anterior
136
What ECG leads correspond with Circumflex Artery?
I, aVL, V5-6 Lateral
137
What ECG leads correspond with the Right Coronary Artery?
II, III, aVF Inferior
138
What is stage 1 HTN?
Clinical BP is 140/90 mmHg or higher. | Ambulatory BP monitor or home BP monitor averages out at 135/85 mmHg
139
What is stage 2 HTN?
Clinical BP is 160/100 mmHg or higher | ABPM or HBPM average is 150/95 mmHg or higher
140
What is severe HTN?
Clinical systolic BP is 180 mmHg or higher. | Clinical diastolic Bp is 110 mmHg or higher.
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When should ambulatory BP readings be offered?
If BP is >140/90.
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How to manage pt with severe HTN (S=>180mmHg or= 110mmHg)?
Consider treatment immediately. | No need to do ABPM or HBPM
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Signs and symptoms of pt with HTN?
Asymptomatic
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Main ddx of pt with HTN, sweating, headache, palpatations, anxiety?
Phaeochromocytoma
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Main ddx of pt with HTN, muscle weakness and tetany?
Hyperaldosteronism
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CVS RF that may lead to HTN?
TIA, stroke, DM, previous renal disease, smoking, cholesterol, NSAID excess
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Pt has HTN. What may be present in PMH?
Angina, CCF, palpatations, syncope, valvular heart disease
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Pt has HTN. What should you cover in FHx?
FHx of HTN? FHx of premature coronary disease FHx of polycystic kidney disease
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What are secondary causes of HTN?
``` Cushing's syndrome Polycystic kidney disease Renal bruits Radio-femoral delay (coarctation) Phaechromocytoma Hyperaldosteronism ```
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What investigations would you fo for pt with HTN?
Urinanalysis - albumin:creatinine ratio Urinanalysis - haematuria Blood glucose, U+Es = creatinine and eGFR Lipid profile - serum total cholesterol, HDL cholesterol U+Es for secondary cause too - low potassium and high sodium = hyperaldosteronism 12 lead ECG ECHO - if LVH, valve disease, LVSD, diastolic dysfunction
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How to do a CVS risk assessment?
Use Q risk calculator
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When should pts with stage 1 HTN (under age of 80) be offered treatment?
- if they have evidence of: target organ damage - if they have evidence of: established CVD - have renal impairment - have DM - have 10 year risk >20%
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When should pts with stage 2 HTN be offered treatment?
Always offer if have stage 2 HTN
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What is target BP in low-moderate risk pts with HTN?
<140 mmHg systolic
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What is target BP in pts who have HTN with a background of either DM, stroke, TIA, IHD, CKD?
<130/80 mmHg
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Elderly pt with systolic >160mmHg should have target BP of ?? (a) if under 80 (b) if over 80
(a) 140-150mmHg if under 80, ideally <140mmHg | (b) 140-150mmHg
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What is target diastolic BP in: 1) all pts with HTN? 2) diabetics specifically?
1) <90 mmHG | 2) <85mmHg
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What is target systolic BP in pt with CKD and overt proteinuria?
<130mmHg
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Non-pharmacological treatment for HTN?
- lose weight if BMI >25 kg/m2. (for every kg lost = reduce BP by 3/2 mmHg) - reduce salt intake (can reduce BP by 8/5mmHg) - minimise alcohol intake - exercise - smoking cessation
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Initial pharmacological treatment for HTN in pt under 55?
ACEi or ARB
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Initial pharmacological treatment for HTN in pt 55+, or black person of African or Carribean family origin of any age?
CCB
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Pt is already on ACEi for HTN. It isn't reducing BP. What to add next ?
ACEi + CCB
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Pt is already on CCB for HTN. It isn't reducing BP. What to add next ?
CCB + ACEi
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Pt is already on ACEi and CCB for HTN which is not helping. What to consider adding next?
Thiazide like diuretic
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Pharmacological treatment for resistant HTN?
ACEi, CCB, Thiazide like diuretic + one of the following: - spironolactone - higher dose of thiazide like diuretic - alpha or beta blocker if the above 2 do not work.
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What is a hypertensive crisis?
An increase in BP which if sustained over the next few hours, will lead to irreversible end-organ damage E.g. encephalopathy, LV failure, aortic dissection, unstable angina, renal failure.
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Distinguish between a hypertensive emergency and a hypertensive urgency
Hypertensive emergency: = high BP associated with a critical event (e.g. encephalopathy, pulm oedema, AKI, MI) Hypertensive urgency: = high BP without a critical illness but may include malignant hypertension.
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What is main target BP aim of treating a HTN emergency?
Reduce diastolic BP to 110mmHg in 3-12hrs
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What is main target BP aim of treating a HTN urgency?
Reduce diastolic BP to 110mmHg in 24hrs.
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What IV drugs should be started in hypertensive emergency?
1. Sodium nitroprusside 2. Labetalol 3. GTN (1-10mg/hr) 4. Esmolol
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Oral treatment options for hypertensive urgency?
Amlodipine - 5-10mg OD Diltiazem - 120-300mg daily Lisinopril - 5mg OD Note: ACEi and CCB is effective and well tolerated
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What is the safest and most effective oral treatment for hypertensive urgency (according to CVS booklet)?
Nifedipine 20mg BD + Amlodipine 10mg OD for 3 days. After 3 days, continue with amlodipine 10mg OD.
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Triad of symptoms in pheochromocytoma? | Most common sign?
The triad: Episodic headache sweating tachycardia most common sign: sustained or paroxysmal HTN
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Investigation for phaeochromocytoma?
24hr urine collection. Measure urinary metanephrines and catecholamines. Measure plasma fractionated metanephrines and catecholamines. CT scan or MRI of abdomen and pelvis - detect adrenal tumours. If these do not show, can do MIBG scan.
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Management of phaeochromocytoma?
Resection
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How to manage phaeochromocytoma before surgery?
Alpha adrenergic blockade and beta adrenergic blockade.
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Name of commonly used alpha adrenergic blockage used for phaeochromocytoma?
Phenoxybenzamine
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Which order are alpha adrenergic blockade and beta adrenergic blockades given to pt for phaeochromocytoma? Describe dosage.
Alpha first - ALWAYS. Phenoxybenzamine is used. Initial dose is 10mg OD/BD. Dose is increased every 2-3days to control BP. Final dose is 20-100mg daily. After use of alpha adrenergic blockade is achieved, can start beta-adrenergic blockade - usually 2-3 days pre-operatively.
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Investigations and findings for Cushing's syndrome with HTN?
Blood glucose = hyperglycaemia 24hr urine cortisol excretion = elevated by 3x Adrenal CT Low dose - dexamethasone suppression test. = Show high cortisol.
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Investigations for primary aldosteronism with HTN?
Aldosterone:renin - plasma renin will be low, aldosterone will be high Adrenal CT
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What are some cardiac RF for developing Infective endocarditis?
``` Mitral valve prolapse Prosthetic (valves + patches NOT stents) bicuspid aortic valve disease rheumatic heart disease congenital heart disease ```
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How are normal heart valves often involved in infective endocardiits?
previously normal heart valves can be infected due to a intravascular device e.g. central line?
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What are the most common organisms involved in native-valve Infective Endocarditis?
``` Strep viridans (50%) Staph aureus (20%) ```
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What is the most common organism for Infective Endocarditis in IV drug users?
Staph aureus (50-60%) of cases
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What is the organism most commonly involved in 'early' (up to 1 year) Infective Endocarditis, post prosthetic heat valve operation?
Peri-operative contamination- mainly staphylococci | especially coagulase - negative e.g. staph epidermis
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What is the organism most commonly involved in 'late' Infective Endocarditis, post prosthetic heat valve operation?
Viridans streptococci Staph aureus coagulase negatvie staph e.g. staph epidermis
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In Infective Endocarditis, what organisms might suggest concurrent disease of GU / GI tract?
Enterococcal infective carditis 10% of all cases e.g. Enterococcus feacalis
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Which groups of people at risk of contracting Infective Endocarditis due to Fungi (+ which types) ?
E.g. Candidas / Aspergillus sp. ``` Immunosuppression IV drug use cardiac surgery prolonged exposure to AB IV feeding ```
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Why might blood cultures be negative in cases of infective endocarditis?
5% of those with IE is negative often due to recent exposure to AB or Infection with slow growing / fastidious organisms e.g. streptococci, Coxiella Burnetii or Brucella
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What is the main causes of mortality in Infective Endocarditis?
Heart failure CNS emboli uncontrolled infection
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What features should make you immediately suspect Infective Endocarditis in a pt?
Unexplained fever Bacteraemia systemic illness and / or new murmur
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What initial investigations should be performed on a pt with suspected Infective Endocarditis you have just admitted to hospital?
Bloods: FBC ESR / CRP U&E LTF urine dip analysis and MSU for microscopy / culutre. BLOOD CULTURES - 3 SETS FROM 3 DIFFERENT SITES ** Imaging: CXR ECG ECHOCARDIOGRAM - TRANS OESOPHAGEAL ECHOCARDIOGRAM **
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How many blood cultures, over how long and where should you take in a pt with Infective Endocarditis?
at least 3 (ideally 6) from different sites over several hours. Sampling during temperature peak does not make cultures more sensitive
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In a pt who is STABLE and has Infective Endocarditis, is it reasonable to delay AB treatment to take blood cultures - TRUE / FALSE
TRUE once AB have been given harder to identify a causative organism
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What imaging modality should you use to visualise Infective Endocarditis?
Echocardiogram Transthoracic echo - 65% of vegetations Transoesophageal echo (TOE) - 95% of vegetations
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Which type of echocardiography is better for detecting mitral valve and prosthetic valve vegetations?
Transoesophageal echocardiography (TOE) Also better at detecting aortic root, septal abscesses and leaflet perforations
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Diagnostic criteria for Infective Endocarditis: How many of major / minor criteria do you need to make a diagnosis?
2 major or 1 major + 3 minor or 5 minor
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What are the major criteria for diagnosing Infective Endocarditis?
1. +ve blood cultures - typical org from 2 BC - +ve BCs >12 hrs apart - >3 +ve BCs >1hour 2. Endocardial involvement 3. +ve echo findings (abscess / vegetations) 4. New valvular regurgitation 5. dehiscence of prosthesis
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What are the minor criteria for diagnosing Infective Endocarditis?
1. Predisposing valvular or cardiac abnormality 2. IV drug user 3. Pyrexia > 38°C 4. Embolic phenomenon 5. Vasculitic phenomenon 6. Blood cultures suggestive (grown but not achieving major criteria) 7. Suggestive echo findings (but not meeting major criteria)
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In terms of the management of Infective Endocarditis, what is the general principal? (before organism specific)
AB therapy tunnelled central venous line good for prolonged IV AB (discuss regimens with duty microbiologist)
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What AB therapy is recommended for Infective Endocarditis caused by Viridans streptococci?
IV Benzylpenicillin (+ low dose IV gentamicin 80 mg BD) (Vancomycin if penicillin allergic)
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What AB therapy is recommended for Infective Endocarditis caused by Enterococci e.g. Enterococcus faecalis?
IV amoxicillin (+ low dose IV gentamicin 80 mg BD) (Vancomycin if penicillin allergic)
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What AB therapy is recommended for Infective Endocarditis caused by staphylocci, e.g. Staph aureus / Staph epidermis?
Flucloxacillin Vancomycin if penicillin allergic plus gentamicin / fusidic acid
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How would you recommend response to AB therapy in a pt with Infective Endocarditis? imaging, bloods etc
1. bedside reviews of clinical status 2. Echo 1 x weekly (vegetation size, complications e.g. abscess / valve destruction) 3. ECG 2 x weekly conduction disturbances- aortic root abscess / valve infection 4. Blood tests 2 x weekly ESR / CRP/ FBC / U&Es AB - 6 weeks depending on response
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Referral for surgery is indicated for pts with Infective Endocarditis who have .....
* Cardiac failure (valve compromise) * Valve dehiscence * Uncontrolled infection despite AB * Fungal / Coxiella burnetii infection * Relapse after medical therapy * Threatened / actual systemic embolism * Para-valvular infection (aortic root abscess) * Valve obstruction *Common exam question: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess*
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Examination findings in cardiac tamponade?
Becks triad present - raised JVP, Hypotension, muffled heart sounds Kussmaul’s sign - raised JVP with inspiration Pulsus paradoxus - reduced systolic BP with inspiration ECG - may show alternating heights of QRS
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What type of shock can you get from cardiac tamponde and why?
Mechanical shock Why? CTamponade is where there is a build up of fluid/blood in pericardial space. This restricts filling of heart. Get high central venous pressure and low arterial BP = mechanical shock.
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Causes of heart failure?
``` Ischaemic heart disease Hypertension Valvular heart disease AF Chronic lung disease Cardiomyopathy Previous cancer chemo drugs HIV ```
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What is heart failure with normal ejection fraction (HFNEF) ?
Pts with heart failure who have clinical picture of HF but have echo that shows mild impairment or even normal systolic function
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Who suffers from heart failure with normal ejection fraction?
They are usually more elderly, overweight and have hypertension and atrial fibrillation
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What is the HFNEF pathophysiology?
Expected that relates to impaired filling or diastolic dysfunction
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Worst prognostic indicators for HF?
``` Severe fluid overload very high NT-proBNP levels severe renal impairment advanced age multi- morbidity frequent admissions with heart failure ```
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Investigations for HF and why?
Renal function (baseline and for diuretic effect), FBC (anaemia should be treated as consequence of bone marrow issue) LFT’s hepatic congestion TFT’s Thyroid disease Ferritin and transferrin (Younger patients with possible haemochromatosis) Brain natriuretic peptide (NT-proBNP)- identification of LV dysfunction
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When should you measure NTproBNP
Only when there is doubt about the diagnosis of HF Above normal range does not equate to HF--> the levels will be increased in anything that causes cardiac strain e.g. AF or right heart strain
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CXR findings in HF?
1. Cardiomegaly 2. Could be pleural effusions 3. Perihilar shadowing/consolidations 4. Alveolar oedema 5. Air bronchograms 6. Increased width of vascular pedicle
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What investigations do you do in HF?
Echocardiography: THE KEY INVESTIGATION. It will confirm whether the diagnosis is correct. Cardiac MRI: May elaborate cause for heart failure as echo may miss right ventricle.
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What would you find on an echo in HF?
Possibly: dilated poorly contracting left ventricle (systolic dysfunction) ; stiff, poorly relaxing, often small diameter left ventricle(diastolic dysfunction); valvular heart disease; atrial myxoma; pericardial disease
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What lifestyle advice would you give to someone with HF?
Smoking cessation Restrict alcohol consumption Salt restriction Fluid restriction especially in the presence of hyponatraemia
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What would you prescribe to a pt with Chronic HF?
1st line treatment: ACE inhibitor and beta blocker (diuretics for symptomatic relief) 2nd line treatment: aldosterone antagonist 3rd line treatment: ivabradine: sinus rhythm > 75/min and a left ventricular fraction < 35% sacubitril-valsartan: left ventricular fraction < 35% Considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs Initiated following ACEi or ARB wash-out period Digoxin: not proven to reduce mortality may improve symptoms due to its inotropic properties strongly indicated if there is coexistent atrial fibrillation hydralazine in combination with nitrate this may be particularly indicated in Afro-Caribbean patients cardiac resynchronisation therapy indications include a widened QRS (e.g. left bundle branch block) complex on ECG
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What is the purpose of Implantable cardiac defibrillators in HF?
Not to improve symptoms, but to prevent sudden cardiac death by delivering electroshock if pt in VT/VF
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What is the acute management for HF? | SODIUM mnemonic
IV loop diuretics- symptoms relief Oxygen: 94-98% sats Vasodilators- nitrates, not to all patients but inconcomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease. If pt is hypotensive/ cardiogenic shock: Inotropic agents e.g. dobutamine Vasopressor agents e.g norepinephrine Mechanical circulatory assistance ## Footnote S – Sit up O – Oxygen D – Diuretics I – Intravenous fluids should be stopped U – Underlying causes need to be identified and treated (e.g., myocardial infarction) M – Monitor fluid balance
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How does GTN spray help alleviate symptoms of angina | CVS revision
1) Nitric oxide causes vascular smooth muscle relaxation. NO activates granulate cyclase which increases cGMP. this lowers intracellular calcium levels so causes relaxation of vascular smooth muscle. 2) It acts primarily on veins - ventilation will lower preload. So the heart will fill less so force of contraction is reduced. This lowers oxygen demand needed. 3) GTN also acts on coronary collateral arteries - so improves oxygen delivery to the ischaemic heart muscle.
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ECG findings in PE?
Sinus tachycardia "S1Q3T3” pattern of acute cor pulmonale is classic; this is termed the McGinn-White Sign. —> A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain
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Diagnostic investigations for infective endocarditis?
``` Blood cultures (3 different sites over several hours) Echocardiogram (transoesophageal) ```
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Symptoms of digoxin toxicity?
* abdo pain * nausea * vomitting * arrythmia * yellow-green tint to vision * diarrhoea * confusion * fatigue * palpitations
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RF for digoxin toxicity?
* hypokalaemia * hypomagnesia * hypercalcaemia * elderly
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ECG changes in digoxin toxicity?
* Downsloping ST depression - 'Reverse Tick' * T wave changes (inversion) * Biphasic/flattened and shortened QT interval * Slight PR interval prolongation
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Treatment for digoxin toxicity?
Stop digoxin Correct dyselectrolytaemia Administer digifab (digoxin specific antibody indicated in lifethreatening digoxin toxicity).
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What is dresslers syndrome?
central, pleuritic chest pain and fever 4 weeks following a myocardial infarction. The ESR is elevated - Dressler's syndrome
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What is acute pericarditis?
inflammation of the pericardial sac, lasting for less than 4-6 weeks.
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Causes of acute pericarditis?
* viral infections (Coxsackie) * tuberculosis * uraemia * post-myocardial infarction * early (1-3 days): fibrinous pericarditis * late (weeks to months): autoimmune pericarditis (Dressler's syndrome) * radiotherapy * connective tissue disease * systemic lupus erythematosus * rheumatoid arthritis * hypothyroidism * malignancy lung cancer breast cancer * trauma
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Features of pericarditis?
* chest pain: may be pleuritic. Is often relieved by sitting forwards * other symptoms include a non-productive cough, dyspnoea and flu-like symptoms * pericardial rub: heard as a scratching or creaking noise at the left lower sternal border.
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Inv for acute pericarditis?
Bedside: * ECG: widespread saddle shaped ST elevation, PR depression Bloods: * FBC- for WBCs * CRP * Troponins (may be elevated, this could be myocrditis) Imaging: * Transthoracic echocardiography
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Management of acute pericarditis?
* the majority of patients can be managed as outpatients patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient * treat any underlying cause most patients however will have pericarditis secondary to viral infection, meaning no specific treatment is indicated * strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers * a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis * until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over
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