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Cardiology Flashcards

1
Q

Management of hyperkalaemia

A

Stabilisation of the cardiac membrane
IV calcium gluconate
(does NOT lower serum potassium levels)

Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF) compartment
combined insulin/dextrose infusion
nebulised salbutamol

Removal of potassium from the body->
calcium resonium (orally or enema)
enemas are more effective than oral as potassium is secreted by the rectum
loop diuretics
dialysis
haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia

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2
Q

ECG changes in hyperkalaemia

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

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3
Q

Three layers of the aorta

A

Intima
Media
adventitia

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4
Q

With an aortic dissection blood enters which of the layers

A

blood enters between the intima and media layers

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5
Q

Stanford system of classification of aortic dissections

A

Type A - affects ascending aorta before the brachiocephalic artery
Type B - affects descending aorta after left subclavian artery

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6
Q

How to diagnose an aortic dissection

A

CT angiogram

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7
Q

Management of aortic dissection

A

surgical emergency
analgesia - morphine
BP and heart rate controlled (to reduce stress on aortic walls) - beta blockers

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8
Q

Strongest risk factor for IE

A

having a previous episode

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9
Q

Most common cause of IE

A

Staphylococcus aureus

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10
Q

Most common organism of IE in dental plaques

A

Streptococcus viridans

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11
Q

Non infective causes of IE

A

SLE
Malignancy

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12
Q

Indications for surgery in IE

A
  • Severe valvular incompetence
  • Aortic abscess
  • infections resistant to antibiotics/fungal infections
  • cardiac failurerefractory to standard medical treatment
  • recurrent emboli after antibiotic therapy
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13
Q

What is the DUKE criteria for

A

diagnosing IE

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14
Q

Features of acute pericarditis

A

CP - may be pleuritic and relieved when leaning forward
Non productive cough, dyspnoea
pericardial rub
Tachypnoea
Tachycardia

— | — | — |

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15
Q

Causes of pericarditis

A

Viral infection - coxsackie
TB
Uraemia
trauma
post MI - dressler’s syndrome
connective tissue disease
Hypothyroidism
Malignancy

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16
Q

Investigations for pericarditis

A

ECG changes - often global and widespread changes; saddle shaped ST elevation; PR depression (most characteristic finding

All patients presenting with acute pericarditis should have a TTE

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17
Q

Difference between pericarditis and constrictive pericarditis

A

Constrictive has a positive Kussmual’s sign and calcification seen on CXR

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18
Q

Secondary causes of hypertension

A

ROPE
R - renal disease
O- obesity
P - pregnancy/ pre-eclampsia
E - endocrine (Conn’s syndrome - hyperaldosteronism)

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19
Q

How often does NICE recommend screening for hypertension

A

Every 5 years
Should be more for borderline patients and every year for patients with T2DM

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20
Q

Stage 1 HTN

A

clinic reading >140/90
ambulatory reading >135/85

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21
Q

Stage 2 HTN

A

> 160/100 clinic
150/95 ambulatory

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22
Q

Stage 3 HTN

A

> 180/120 clinic

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23
Q

Investigations for end organ damage due to HTN

A

Urine albumin:creatinine ratio for proteinuria and dipstick for NVH
Bloods for HbA1c
Fundus examination - Hypertensive retinopathy
ECG - cardiac abnormalities

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24
Q

When would you medically manage HTN

A

All patients with stage 2 HTN
Patients <80 with stage 1 HTN and QRISK

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25
aged <55, non black patient htn first line management
A - ACE inhibitor (ramipril)
26
If HTN in diabetic patient what do you start as first line management
ACE or ARB regardless of age
27
Signs and symptoms of malignant hypertension
Papilloedema retinal bleeding increased cranial pressure causing headache CP - increased workload of the heart Haematuria due to kidney failure Epistaxis difficult to stop
28
How to diagnose malignant hypertension
systolic >180 or diastolic >120 evidence of end organ damage
29
Presentation of heart failure
SoB worsened on exertion Cough - may produce frothy/white/pink sputum Orthopnoea PND Peripheral oedema
30
How to diagnose heart failure
Clinical presentation BNP Echocardiogram ECG
31
Causes of heart failure
IHD Valvular heart disease - commonly aortic stenosis Essential/secondary HTN Arrhythmias
32
Management of heart failure
Medical management surgical treatment in aortic stenosis/mitral regurgitation Yearly flu and pneumococcal vaccine stop smoking
33
First line treatment for heart failure
ABAL A - ACE inhibitor (ramipril titrated up to 10mg a day) - avoid in patients with valvular heart disease B - beta blockers (bisoprolol titrated up to 10mg a day) A- aldosterone antagonist when symptoms not controlled by A+B (spirinolactone) L - loop diuretics (furesomide 40mg once daily)
34
What does the left coronary artery become
left circumflex and left anterior descending
35
cardiac territories for RCA
I, III, and aVF inferior
36
LCx cardiac territories
I, V5 and V6 Lateral
37
LAD cardiac territories
V1-V4 Anterior
38
NSTEMI ECG changes
ST segment depression in a region Deep T wave inversion Pathological Q waves (suggesting a deep infarct - late sign)
39
Causes of a raised troponin
MI Chronic renal failure Sepsis Myocarditis Aortic dissection PE
40
Ix for MI
physical exam ECG FBC - anaemia U&E - prior to ACEi and other meds LFTs - prior to statins Lipid profile Thyroid function tests HbA1c and fasting glucose CXR Echo CT coronary angiogram
41
Acute STEMI management - presenting within 12 hours of onset
Primary PCI if available within 2 hours of onset: thrombolysis if PCI not available within 2 hours - streptokinase, alteplase, tenectplase
42
Acute NSTEMI management
BATMAN B - beta blocker unless CI A - aspirin 300mg stat T - ticagrelor 180mg stat M - morphine analgesia A - anticoagulant - fondaparinux N - nitrates (GTN)
43
GRACE score is for?
6 month risk of death or repeat MI after having NSTEMI: PCI in NSTEMI if medium or high risk
44
Complications of MI
DREAD D - death R - rupture of heart septum or papillary muscles E - Edema (HF) A - arrhythmia and aneurysm D - Dressler's syndrome
45
What is Dressler's syndrome
usually 2-3 weeks post MI Caused by localised immune response and causes pericarditis presents with pleuritic CP, low grade fever and pericardial rub Diagnosis made with ECG (global ST elevation and T wave inversion), echo (pericardial effusion) and raised inflammatory markers (CRP and ESR) Management with NSAIDs (aspirin and ibuprofen) and in severe cases steroids (prednisolone) ; may need pericardiocentesis to remove fluid around heart
46
Secondary prevention medical management of MI
6As Aspirin 75mg once daily Another antiplatelet e.g. clopidogrel or ticagrelor for up to 12 months Atorvastatin 80mg once daily ACE inhibitor (ramipril titrated as tolerated up to 10mg OD) Atenolol (or another beta blocker) Aldosterone antagonist for those with clinical heart failure (eplerenone titrated to 50mg once daily
47
What is AF
Atrial fibrillation - Contraction of the atria is uncoordinated, rapid and irregular - Due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node
48
AF presentation
Palpitations SoB Syncope Symptoms of associated conditions (stroke, sepsis, or thyrotoxicosis)
49
Valvular AF
- Moderate or severe mitral stenosis or a mechanical heart valve - Assumption is valvular pathology itself has lead to AF
50
Non valvular AF
AF without valvular pathology such as mitral regurgitation or aortic stenosis
51
Causes of AF
AF affects mrs SMITH S - sepsis M - mitral valve pathology I - IHD T - thyrotoxicosis H - HTN
52
Treatment for AF
Rate or rhythm control - Anticoagulation to prevent stroke - The following DOACs are recommended by NICE for reducing stroke risk in AF: - apixaban - dabigatran - edoxaban - rivaroxaban - Warfarin is now used second-line, in patients where a DOAC is contraindicated or not tolerated
53
Who doesnt have rate control as first line management in AF
- Reversible cause of AF - AF is of new onset (within last 48hrs) - AF is causing HF - Remain symptomatic despite being effectively rate controlled
54
Options for rate control in AF
- Beta blocker → first line (atenolol 50-100mg OD) - Calcium channel blocker → diltiazem (not preferable in HF) - Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
55
Rhythm control for AF
- Pharmacological cardioversion: - Flecanide - Amiodarone (drug of choice in patients with structural heart disease) - Electrical cardioversion - Rapidly shock heart back into sinus rhythm - involves sedation or a GA and using a cardiac defibrillator machine to deliver controlled shocks in attempt to restore sinus rhythm - Long term rhythm control - Beta blockers - Dronedarone→ second line for maintaining normal rhythm where patients have had successful cardioversion - Amiodarone → useful in patients with HF or left ventricular dysfunction
56
Paroxysmal AF
Where AF comes and goes in episodes usually doesnt last longer than 48hrs should be anticoagulated based on CHADVASc score pill in pocket method - flecanide (have to have frequent episodes without underlying structural changes
57
What is rheumatic fever
Autoimmune condition triggered by streptococcus bacteria. Caused by antibodies created against the Streptococcus bacteria that also target tissues in the body.
58
Pathophysiology of rheumatic fever
- Caused by **group A beta-haemolytic streptococcus** - Typically **streptococcus pyogenes** causing tonsillitis - Immune system creates antibodies to fight the infection - Antibodies do not just target bacteria but also the antigens of the body, such as the myocardium of the heart - Results in type II hypersensitivity reaction - Where immune system attacks cells throughout the body - Process is delayed by 2-4weeks after the infection
59
Presentation of rheumatic fever
presents 2-4 weeks after a strep infection such as tonsillitis Fever joint pain rash SoB Chorea Nodules
60
Skin involvement in rheumatic fever
- Subcutaneous nodules - Occur over extensor surfaces such as the joints - Erythema marginatum rash - pink rings of varying sizes affecting the torso and proximal limbs
61
What antibodies would you send for if youre suspecting rheumatic fever
Antistreptococcal antibodies titre - Rise over 2-4 weeks - Peak around 3-6 weeks - Gradually falls over 3-12 months - ASO levels are usually repeated over 2 weeks to: - Confirm a negative test - Assess whether levels are rising or falling
62
What criteria do you use to diagnose rheumatic fever
Jones criteria need two major or one major plus two minor JONES - FEAR major criteria J - J → joint arthritis O → organ inflammation, such as carditis N → Nodules E → Erythema marginatum rash S → Syndenham chorea Minor criteria: F→ Fever E→ ECG changes (prolonged PR interval) without carditis A → Arthralgia without arthritis R → Raised inflammatory markers (CRP and ESR)
63
Difference between a thrombus and an embolus
A thrombus is a blood clot that forms within a blood vessel. If a thrombus breaks free and travels through the bloodstream, it has become an embolus.

Year 3 (14 decks)

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