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Electrolyte Disorders > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Name 5 causes of HF

A 
Ischaemic Heart Disease
Hypertension
Dilated Cardiomyopathy 
Valvular Heart Disease
RHF (Cor Pulmonale, RV infarct, PHTN, PE, COPD)
Congenital Heart Disease
Alcohol
Pericarditis
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2
Q

What 4 things occur pathophysiologically in HF?

A

Activation of SNS - Raised HR and Contractility, Vasoconstriction resulting in increased preload to try and improve contractility, but this also increased afterload

Renin-Angiotensin System - reduced CO results in reduced renal perfusion, resulting in renin release. This raises water and Na retention, increasing venous return, to help maintain SV. As retention increases, can get P oedema and causes dyspnoea.

ANP and BNP released

Ventricular Dilatation and remodelling - when compensatory mechanisms become limited.

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3
Q

What x-ray findings are there in HF?

A 
Cardiomegaly
Kerley 'B' lines - interstitial oedema
Peri-hilar shadowing (Bat's wing) - alveolar oedema
Pleural Effusion
Dilated vessels in upper lobe
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4
Q

What is the normal level of BNP?

A

< 100pg/ml

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5
Q

What investigations would you order for initial suspicion of HF? If any are abnormal what would you do next?

A

CXR, Bloods (BNP), ECG (if normal, unlikely HF)

Echo -TTE (if normal, unlikely HF)

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6
Q

How do you treat HF?

A

Vasodilator Therapy : Ace-Inhibitors* (ARAs if intolerable), Isosorbide Mononitrate (reduces preload) with Hydralazine (reduces afterload)
Ivabradine (alternative to ISMN)

Beta-Blockers* - helps block chronically activated SNS

Diuretics - used in pts with fluid overload
Loop (Furosemide, Bumetanide 20-40mg daily)
Thiazide (Bendroflumethiazide 2.5mg daily)
Aldosterone antagonists (Spironolactone)

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7
Q

How do ACE-i work?

A

Inhibit Angiontensin II (which usually causes vasoconstriction)

Increase levels of bradykinin, which causes vasodilation

Enhance salt and water excretion

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8
Q

Summarise the management of HF. (General, Pharmacological, Non-Pharmacological)

A

General: Educate, light exercise, diet, vaccine against influenza and pneumococcal, social changes

Pharmacological: ACE-i, BB, Diuretics, Digoxin, Inotropes

Non-pharmacological: CABG/PCI, cardiac resynchronisation therapy, implantable defibrillator, repair underlying cardiac problems (valve, congenital), cardiac transplant

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9
Q

What is the emergency management of Acute HF (caused by hypertensive HF/acute pulmonary oedema/cardiogenic shock/RHF)?

A

Same investigations as chronic HF

High flow oxygen, sometimes CPAP
Diuretic - Furosemide iv 50mg

Measure SBP

Give vasodilator if <100
Give vasodilator and/or inotrope if 85-100
Give inotrope and/or dopamine and/or noradrenaline if <85

If no response, try mechanical assist devices

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10
Q

Give some examples of Vasodilators

A

GTN
Isosorbide Mononitrate
Nitroprusside
ACE-i

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11
Q

What does an artheroma consist of?

A

Fatty streak, macrophages, lipids, smooth muscle cells (usually in the intima of the artery)

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12
Q

Name 6 RFs for IHD

A

Reversible: High cholesterol, high fat diet, Sedentary lifestyle, smoking, HTN,

Irreversible: Age, Gender, FH

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13
Q

What assessment tool do NICE recommend for estimated CVD risk?

A

QRISK2 - gives the 10-year risk of CVD
Use in high-risk people
Takes into account DM, BP, lipid profile, age, gender, fH

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14
Q

What is prinzmetal’s / variant angina?

A

Coronary artery spasm

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15
Q

What is decubitus angina?

A

Angina on lying down

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16
Q

What is cardiac syndrome X?

A

Pt has symptoms of angina, a positive exercise test, but on investigation has normal coronary arteries

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17
Q

What investigations would you perform in suspected angina?

A

Usually diagnosis is clinical

Resting ECG - normal between attacks, ST depression or T-wave flattening during attack

Exercise ECG - Positive in most people with CAD, ST depression at a low workload or a paradoxical fall in BP with exercise indicate CAD

Angiography - Only really used if intervention is planned, so exact coronary pathology can be found out

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18
Q

What is the long term management of angina?

A

Modify lifestyle factors
Aspirin - 75mg daily - inhibits COX2 and thus thromboxane A2

Clopidogrel - 75mg daily - if aspirin intolerable

Statin - aim for cholesterol <5.0 mmol/L

If persistent despite oral treatment, consider revascularisation therapy:

PCI - Try if 2 anti-anginals and still not improving, preferred in pts with isolated disease, complications are death, acute MI, need for restenosis, give aspirin and clopidogrel for 6-12 months after

CABG - use mammary artery to bypass stenosis, recommended in pts with triple artery disease, impaired LVF

19
Q

What is the symptomatic treatment of angina?

A

GTN - tablet or spray
Encourage to use before exertion rather than waiting for pain to develop
S/E is severe headache

20
Q

What prophylaxis is given to angina patients?

A

Nitrates - reduce the pressures in the heart by dilating coronary arteries (ISM,ISD)

BBs - reduce HR and contractility thus reducing myocardial oxygen demand

Ca+ Antagonists - Relax the coronary arteries and reduce contractility thereby reducing oxygen demand

21
Q

What is most common cause of an ACS?

A

Rupture of a fibrous cap of a coronary plaque

22
Q

How is Unstable Angina different to NSTEMI?

A

In an NSTEMI, the occluding thrombus is large enough to cause myocardial damage, and thus a rise in troponin and creatine kinase.

23
Q

What are the similarities of NSTEMI and UA?

A

ECG may be normal / show ischemia with T-Wave inversion and ST depression

Troponin may be 0 on arrival to hospital (measure 12h later, if still normal it suggests UA)

Both can be complicated by a STEMI if not treated

24
Q

Name some risk stratification scoring systems for MI

A

TIMI, GRACE
Looks at age, cardiac markers, ECG results to see if there is a risk of a STEMI/death in patients with either NSTEMI or UA

25
Q

What is the immediate management of an ACS?

A

IV access

Investigations - Bloods (Troponin, CKMB), ECG

Treatment (mona)- Morphine 5mg IV, Metaclopromide, Oxygen, GTN, Aspirin 300mg/Clopidogrel/Ticagrelor

26
Q

What is the management of STEMI?

A

MONA

Pts presenting within 90minutes of onset = primary angioplasty with dual anti-platelet therapy

Between 90mins and 12h = thrombolysis (tenecteplase)

Metaprolol if HR > 100, Insulin if BM > 11 mmol/L

27
Q

What ECG changes are there in a STEMI?

A

Minutes - Tall T waves and ST elevation
Hours - Inverted T waves, pathological Q waves (broad + deep)
Days - Normal ST segment
Weeks - T wave returns upright, Q wave persists

28
Q

Which leads ‘face’ which aspect of the heart?

A

Leads II, III, aVF = Inferior
I, aVL and V5-6 = Lateral
V2 - 4 = Anterior

29
Q

What is the post-acute management of a STEMI?

A

Re-measure cardiac markers, electrolytes and repeat ECG at 24 and 48h

Initiate secondary prevention

Exercise tolerance ECG test before discharge

Refer to cardiac rehab programme

No driving for 1 month, no work for 2 months

30
Q

What is secondary prevention of STEMI?

A

ACE-i - start day 1 after attack
Continue DAPT (Aspirin + Clopidogrel/Ticagrelor)
Continue Statin, BB

31
Q

What are the complications of an MI?

A

HF, Arrhythmias, Pericarditis, Mitral Regurgitation, Heart block

Dressler’s Syndrome - weeks or months after, give NSAIDs/steroids (fever/pericardial effusion and pericarditis)

32
Q

Which bacteria causes Rheumatic Fever?

A

Group A Streptococcus (Strep Pyogenes)

33
Q

What is the modified Duckett Jones criteria for RF?

A

Requires 2 major or 1 major + 2 minor present with streptococcal infection (antistreptolysin O)

Major Criteria:

Polyarthritis - large joints
Carditis - which can cause murmurs
Subcutaneous nodules - non-tender and over the joint ususally
Erythema Marginatum - pink rings on the trunk
Sydenham’s Chorea - fidgety movements

Minor Criteria:

Fever, Arthralgia, raised ESR/CRP, Leukocytosis, previous episode of RF, ECG showing heart block

34
Q

How do you treat RF?

A

Bed rest and high-dose aspirin

Penicillin to treat the infection, given long-term for those who get cardiac damage

35
Q

What type of pt gets RF?

A

Kids, 5 - 15 year olds
But, over 50% of those who have carditis, will present again 10-20 years later with chronic rheumatic valvular disease (mainly aortic and mitral)

36
Q

What is the pathophysiology of Mitral Stenosis?

A

Thickening and immobility of the leaflets leads to stenosis between the LA and LV.
Therefore the pressure increases in the LA, leading to PHTN and right-heart dysfunction.
AF is common (increased likely hood of embolism too) due to the increased pressure in LA.
Chronically elevated pressure in LA leads to Pulmonary Oedema.
Eventually leads to RVH and RHF.

37
Q

What are the signs/symptoms of Mitral Stenosis?

A

Malar flush (cyanotic/pink discolouration of cheeks),
Low-volume pulse (irregular if AF)
Tapping apex beat
Mid-Diastolic murmur

Signs of PHTN (Raised JVP, parasternal heave, ascites, peripheral oedema)

Progressive exertional dyspnoea, coughing of blood, AF, Fatigue, Oedema

38
Q

Give 5 causes of Mitral Regurgitation.

A 
Prolapse (most common cause)
RF
Infective endocarditis
Rupture of the chordea tendinae or papillary muscle
Ehlers-Danlos syndrome
39
Q

What is the pathophysiology of Mitral Regurgitation?

A

Long-standing regurgitation does not produce a significant increase in pressure in the LA as it is accomodated by an enlarged LA.
LV dilation and hypertrophy follow, late on in the disease process.

40
Q

What are the symptoms and signs of Mitral Regurgitation?

A

Exertional dyspnoea, fatigue, lethargy, symptoms of RHF eventually

Displaced apex beat
Pan-systolic murmur

41
Q

What investigations are used in diagnosing valvular disease?

A

Echo + Doppler Echo to see severity is key

CXR and ECG can also be helpful

42
Q

How do you treat Mitral Stenosis?

A

Mild = no treatment, just treat complications (BB for AF, anti-coagulate)

Severe = Percutaenous Balloon Valvotomy (cardiac catheterisation) or Valvotomy

43
Q

How do you treat Mitral Regurgitation?

A

Serial Echo’s every 1-5 years if mild
Medical = diuretics and ACE-i
Surgical if severe (depends on symptoms and EF)

Electrolyte Disorders (6 decks)

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