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Cardio Yr 3 > Conditions > Flashcards

Conditions Flashcards

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1
Q

What is the drug management in chronic heart failure?

A

1st line - both an ACE-inhibitor and a beta-blocker, start one drug at a time

2nd line - aldosterone antagonist e.g. spironolactone
an increasing role for SGLT-2 inhibitors

3rd line - specialist, include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy

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2
Q

What vaccines should be offered to patients with heart failure?

A

Annual influenza vaccine

One-off pneumococcal vaccine

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3
Q

What should be measured before starting ACEi?

A

Serum sodium, potassium and assess renal function

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4
Q

What are some features of mitral stenosis?

A

dyspnoea
↑ left atrial pressure → pulmonary venous hypertension

haemoptysis - due to pulmonary pressures and vascular congestion

mid-late diastolic murmur (best heard in expiration)

loud S1

opening snap
- indicates mitral valve leaflets are still mobile

low volume pulse

malar flush

atrial fibrillation
- secondary to ↑ left atrial pressure → left atrial enlargement

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5
Q

What drug can be given to terminate SVT?

A

Adenosine

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6
Q

What is a contraindication of adenosine?

A

Asthma - risk of bronchospasm

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7
Q

What are some adverse effects of adenosine?

A

Chest pain

Bronchospasm

Transient flushing

can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

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8
Q

What is the MOA of adenosine?

A

causes transient heart block in the AV node

agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux

adenosine has a very short half-life of about 8-10 seconds

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9
Q

What are some features of aortic regurgitation?

A

early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre

collapsing pulse

wide pulse pressure

Quincke’s sign (nailbed pulsation)

De Musset’s sign (head bobbing)

mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

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10
Q

What are some causes of acute and chronic aortic regurgitation due to valvular disease?

A

Acute:
-infective endocarditis

Chronic:
-rheumatic fever
-calcified valve disease
-connective tissue disorders
-bicuspid aortic valve

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11
Q

What are some acute and chronic causes of aourtic regurgitation due to aortic root disease?

A

Acute:
-aortic dissection

Chronic:
-bicuspid aortic valve
-spondylarthropathies
-HTN
-syphilis
-Marfan’s, Ehler-Danlos

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12
Q

What are some contraindications for statins?

A

Pregnancy

Macrolides - erythromycin, clarithromycin

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13
Q

What are some features of complete heart block?

A

syncope

heart failure

regular bradycardia (30-50 bpm)

wide pulse pressure

JVP: cannon waves in neck

variable intensity of S1

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14
Q

What are some cautions and contraindications for using ACEi?

A

Pregnancy and breastfeeding
Renovascular disease
Aortic stenosis
hereditary idiopathic angioedema
Hyperkalaemia - specialist advice

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15
Q

What are some adverse effects of ACEi?

A

Dry cough
Angioedema
Hyperkalaemia
1st dose hypotension

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16
Q

What are some risk factors for developing AF?

A

HTN
Ischaemic heart disease
Diabetes
Obesity
Thyrotoxicosis
Caffeine
Alcohol
CKD
Increasing age
Inherited RF
Smoking
OSA

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17
Q

What are some risk factors for developing chronic heart failure?

A

Coronary artery disease
HTN
Valvular heart disease
Cardiomyopathies
Diabetes
CKD
Obesity
Aging
Tobacco
Alcohol
Sedentary lifestyle

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18
Q

How is heart failure classified by symptom severity?

A

New York Heart Association (NYHA) Functional Classification:

Class I: No limitation of physical activity; ordinary activity does not cause undue breathlessness, fatigue, or palpitations.

Class II: Mild limitation of physical activity; comfortable at rest, but ordinary activities result in symptoms.

Class III: Marked limitation of physical activity; comfortable at rest, but less than ordinary activities cause symptoms such as breathlessness or fatigue.

Class IV: Unable to carry out any physical activity without discomfort; symptoms may be present even at rest.

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19
Q

How is heart failure investigated?

A

NT-proBNP
BNP
Echocardiogram
ECG

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20
Q

How is chronic heart failure managed pharmacologically?

A

ACEi or ARBs 1st line
Beta blockers

Mineralocorticoid Receptor Antagonists (MRAs): Can be added if symptoms persist despite optimal ACEI and beta-blocker therapy

SGLT-2 inhibitors

If symptoms still persist, consider adding a combination of sacubitril/valsartan or ivabradine

Diuretics to manage symptoms of fluid overload

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21
Q

What are some complications of chronic heart failure?

A

Cardiac arrhythmias
Ventricular remodelling
Pulmonary oedema
Anaemia
Renal dysfunction
Hepatic congestion
Thromboembolism

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22
Q

What are the classic clinical features of cardiac tamponade?

A

Beck’s triad:
Hypotension
Raised JVP
Muffled heart sounds

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23
Q

What are some other features of cardiac tamponade?

A

Dyspnoea
Tachycardia
Absent Y descent on JVP
Pulsus paradoxus
Electrical alternans on ECG

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24
Q

What is atherosclerosis?

A

Combination of atheromas (fatty deposits in artery walls) and sclerosis of blood vessel walls

Affects medium and large arteries

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25
What can atherosclerosis lead to?
Chronic inflammation and activation of immune system -> deposition of lipids in artery walls -> formation of fibrous atheromatous plaques
26
What are the consequences of artheromatous plaques?
Stiffening - HTN and strain or heart as its pumping against extra resistance Stenosis - reduced blood flow (e.g. angina) Plaque rupture - creates thrombus, can block vessels and cause ischaemia
27
What are some non-modifiable risk factors of CVD?
Older age FHx Male
28
What are some modifiable risk factors of CVD?
Raised cholesterol Smoking Alcohol consumption Poor diet Lack of exercise Obesity Poor sleep Stress
29
What are some medical co-morbidities that increase the risk of atherosclerosis?
Diabetes Hypertension CKD Inflammatory conditions e.g. RA Atypical antipsychotic medications
30
What is the end results of atherosclerosis?
Angina MI TIA Stroke PAD Chronic mesenteric ischaemia
31
What is primary prevention for CVD?
Optimise risk factors Diet and exercise advice If QRISK >10% or CKD, T1DM - atorvostatin 20mg OD
32
What monitoring should be done when starting patient on statins?
Lipids - 3 months after starting LFTs within 3mths and 12mths
33
What are some significant side effects of statins?
Myopathy (causing muscle weakness and pain) Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain) Type 2 diabetes Haemorrhagic strokes (very rarely)
34
What is MOA of statin?
Statins reduce cholesterol production in the liver by inhibiting HMG CoA reductase
35
What secondary prevention of CVD is available?
4 A’s: Antiplatelet (aspirin, clopidogrel, ticagrelor) Atorvastatin 80mg Atenolol (or bisoprolol) ACEi After MI - duel antiplatelet Aspirin 75mg daily (continued indefinitely) Clopidogrel or ticagrelor (generally for 12 months before stopping) Clopidogrel is the antiplatelet of choice in peripheral arterial disease and following an ischaemic stroke
36
What investigations should be done in patients with angina for baseline?
Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI) ECG (a normal ECG does not exclude stable angina) FBC (anaemia) U&Es (required before starting an ACE inhibitor and other medications) LFTs (required before starting statins) Lipid profile Thyroid function tests (hypothyroidism or hyperthyroidism) HbA1C and fasting glucose (diabetes)
37
What imagining/investigations can be done in angina?
Cardiac stress testing - ECG, echocardiogram, MRI or a myocardial perfusion scan CT coronary angiography Invasive coronary angiography
38
How can angina be managed medically?
Sublingual GTN - immediate symptom relief Long-term symptom relief - beta blocker and CCB A specialist may consider other options for long-term symptomatic relief: -Long-acting nitrates (e.g., isosorbide mononitrate) -Ivabradine -Nicorandil -Ranolazine Secondary CVD management
39
What surgical interventions are available for angina?
PCI Coronary artery bypass graft
40
What is typical presentation of ACS?
Central, constricting chest pain Pain radiates to jaw or arms Nausea and vomiting Sweating and clamminess Feeling of impending doom SOB Palpitations **diabetes pts may not experience chest pain
41
What ECG changes may be seen in ACS?
STEMI: ST-segment elevation New left bundle branch block NSTEMI: ST segment depression T wave inversion Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms
42
If changes are seen in leads I, aVL, V3-6, what heart area and artery has been affected?
Anterolateral heart Left coronary artery
43
If changes are seen in ecg leads V1-4, what area of heart and what artery is affected?
Anterior heart Left anterior descending
44
If changes are seen in ecg leads I, aVL, V5-6, what heart area and artery has been affected?
Lateral heart Circumflex artery
45
If changes are seen in ecg leads II, III, aVF, what heart area and artery has been affected?
Inferior heart Right coronary artery
46
What investigations should be done for suspected ACS?
Troponin FBC, U&E, LFT, lipids and glucose CXR Echocardiogram ECG
47
What is the management of a STEMI?
Aspirin 300mg IV morphine anti-emetic Nitrate - GTN O2 if required PCI if within 2hrs of presenting + prasugrel Thrombolysis if PCI not available within 2hrs - alteplase
48
What scoring system can be used to determine NSTEMI management?
GRACE score gives a 6-month probability of death after having an NSTEMI. 3% or less is considered low risk Above 3% is considered medium to high risk medium or high risk are considered for early angiography with PCI (within 72 hours).
49
What are some complications post MI?
D – Death R – Rupture of the heart septum or papillary muscles E – “oEdema” (heart failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome
50
What is the medical management of NSTEMI?
B – Base the decision about angiography and PCI on the GRACE score A – Aspirin 300mg stat dose T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography) M – Morphine titrated to control pain A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography) N – Nitrate (GTN) O2 if req
51
What is dresslers syndrome?
Pericarditis post MI occurs around 2 – 3 weeks after an acute myocardial infarction. It is caused by a localised immune response that results in inflammation of the pericardium
52
What are some potential causes of pericarditis?
Idiopathic (no underlying cause) Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses) Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis) Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma) Uraemia (raised urea) secondary to renal impairment Cancer Medications (e.g., methotrexate)
53
What are some presenting features of pericarditis?
Chest pain: -Sharp -Central/anterior -Worse with inspiration (pleuritic) -Worse on lying down -Better on sitting forward Low grade fever Pericardial friction rub on auscultation
54
What ECG changes may be present in pericarditis?
Saddle-shaped ST-elevation PR depression
55
What is the management of pericarditis?
NSAIDs Colchicine to reduce risk Steroids may be used second-line, in recurrent cases or associated with inflammatory conditions Treat underlying causes Pericardiocentesis may be required to remove fluid from around the heart if there is a significant pericardial effusion or tamponade
56
What are some causes of HTN?
R – Renal disease O – Obesity P – Pregnancy-induced hypertension or pre-eclampsia E – Endocrine D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
57
What are some complications of HTN?
Ischaemic heart disease (angina and acute coronary syndrome) Cerebrovascular accident (stroke or intracranial haemorrhage) Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms) Hypertensive retinopathy Hypertensive nephropathy Vascular dementia Left ventricular hypertrophy Heart failure
58
What should new HTN patients have to investigate end organ damage?
Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage Bloods for HbA1c, renal function and lipids Fundus examination for hypertensive retinopathy ECG for cardiac abnormalities, including left ventricular hypertrophy
59
What is a hypertensive emergency?
Accelerated hypertension, also called malignant hypertension, refers to extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema
60
How should a hypertensive emergency be managed?
IV: Sodium nitroprusside Labetalol Glyceryl trinitrate Nicardipine
61
What are some complications of mechanical valves?
Thrombus formation (blood stagnates and clots) Infective endocarditis (infection in the prosthesis) Haemolysis causing anaemia (blood gets churned up in the valve)
62
What anti-coagulation is required in pts with mechanical heart valve?
Warfarin INR target 2.5-3.5

Cardio Yr 3 (2 decks)

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