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Phase 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define heart failure.

A

failure to pump blood at a rate sufficient to meet the metabolic requirements of the tissues
characterised by haemodynamic changes e.g. systemic vasoconstriction and neurohumeral changes

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2
Q

List some causes of heart failure.

A

coronary heart disease, hypertension, toxins, genetics, sepsis, tamponade, valve disease, infections

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3
Q

Describe the signs and symptoms of heart failure.

A
  • symptoms: dyspnoea, orthopnoea, PND, cough, ankle swelling, fatigue, tiredness
  • signs: peripheral oedema, elevated JVP, third heart sound, displaced apex beat, pulmonary oedema, pleural effusion
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4
Q

Discuss 4 main types of heart failure.

A
  1. HF-REF (systolic HF): young, male, coronary
  2. HF-PEF (diastolic HF): older, female, hypertension
  3. Chronic (congestive): present of a period of time
  4. Acute (decompensated): usually admitted to hospital, worsening of chronic, new onset
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5
Q

Briefly describe the pathophysiology of heart failure.

A
  • MI leads to left ventricular systolic dysfunction
  • perceived reduction in circulating volume and pressure
  • neurohumeral activation: SNS, RAAS, ET, AVP, natriuretic peptides
  • systemic vasoconstriction: renal Na+ and H20 retention
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6
Q

Discuss the NYHA classification of heart failure.

A
  1. no symptoms or limitations in ordinary activity
  2. mild SOB/angina, slight limitation
  3. marked limitation in activity due to symptoms even during less-than-activity, only comfortable at rest
  4. severe limitations, symptoms even at rest, mostly bedbound
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7
Q

What investigations would you carry out if you suspected heart failure?

A

ECG, CXR, echo, blood chemistry, natriuretic peptides (BNP raised)

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8
Q

What is the management plan in heart failure according to SIGN guidelines?

A
  1. Beta blocker + ACEi (or ARB if ACEi intolerant)
  2. If symptoms ongoing: + MRA
  3. Need specialised advice: + sacubitril/valsartan (ARNi) stop ACEi/ARB
  4. ICD or CRT-P/D, ivabradine (if sinus rhythm HR > 75)
  5. Digoxin (if renal dysfunction, hyperkalaemia etc)
  6. Consider referral for transplant
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9
Q

What is different about the management of HF-PEF according to ACCF/AHA guidelines?

A

give aldosterone receptor antagonists if:

  • EF > 45%
  • elevated BNP levels
  • eGFR > 30 ml/min
  • creatinine < 2.5 mg/dL
  • potassium < 5.0 mEq/L
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10
Q

Discuss classification and subsequent treatment of acute heart failure.

A
  • identify haemodynamic profile
    1. wet + warm = congestion + high systolic BP = vasodilator, diuretic and ultrafiltration if fluid accumulation rather than distribution
    2. wet + cold = congestion:
  • systolic BP < 90: inotropic agent, vasopressor, diuretic
  • systolic BP > 90: vasodilators, diuretic, inotropic agents
    3. dry + warm = adequately perfused, compensated: adjust oral therapy
    4. dry + cold = hypoperfused, hypovoloemic: consider fluid challenge, inotropic agent
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11
Q

What does PCWP stand for and what does it indirectly estimate?

A

Pulmonary capillary wedge pressure

left atrial pressure

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12
Q

Discuss the CXR features of congestive heart failure.

A 
A - alveolar oedema
B - kerley B lines
C - cardiomegaly
D - dilated upper lobe vessels
E - pleural effusion
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13
Q

What are Kerley B lines? What causes them?

A
  • horizontal lines of about 2cm commonly found in lung bases
  • fluid leakage into interlobular septa
  • interstitial pulmonary oedema
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14
Q

What is a subpulmonic effusion? How is it seen on CXR?

A
  • pleural effusion that collects at the base of the lung, in the space between the pleura and diaphragm
  • upper edge mimics diaphragm contour so often difficult to detect
  • principal sign: apparent elevation of diaphragm, lateral peak of hemidiaphragm, costophrenic angle ill-defined
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15
Q

Give a definition of endocarditis.

A

infection of endocardium, formation of a vegetation, results in damage to cusp of valves (commonly mitral)

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16
Q

What pathogens cause endocarditis?

A
  • fungi: Candida
  • gram+ve: rods, strep, staph
  • gram-ve: HACEK organisms, pseudomonas aeruginiosa, enterobacterials e.g. E. coli
  • coxiella burnetti (Q fever)
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17
Q

Give 3 classes of endocarditis.

A
  1. Native valve endocarditis
  2. Endocarditis in IVDUs
  3. Prosthetic valve endocarditis
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18
Q

What are some risk factors for NVE?

A 
aortic stenosis (age related calcification, congenital, RF arising from sleep Strep. pyogenes)
mitral prolapse
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19
Q

Why is endocarditis more common on the right side in IVDU?

A
  • particulate-induced endothelial damage to right sided valves
  • increased bacterial load in these patients
  • deficient immune response caused by IVDU
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20
Q

Differentiate between acute and subacute clinical features of endocarditis.

A
  • acute: toxic presentation, developing in days/weeks, commonly S. aureus, progressive value destruction and metastatic infection
  • subacute: mild toxicity, longer presentation, S. viridians, enterococcus
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21
Q

What are the early manifestations of endocarditis?

A
  • fever and murmur = IE until proven otherwise

- fatigue and malaise

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22
Q

Describe how embolic events present in endocarditis.

A
  • small emboli: splinter haemorrhage, conjunctival petechaie, haematuria
  • large: CVA, renal infarction
  • right sided endocarditis = septic pulmonary emboli
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23
Q

Discuss the longer term clinical manifestations of endocarditis.

A
  • Osler’s nodes: painful, palpable lesions on hands and feet
  • splenomegaly, nephritis, vasculitic lesions of skin and eyes, clubbing
  • tissue damage: valve destruction and abscess
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24
Q

How would you make a diagnosis of endocarditis?

A

DUKE CRITERIA
Major Criteria
- presence of new onset murmur
- sustained bacteriaemia with a typical organism - blood cultures
- echocardiogram consistent with endocarditis
Minor Criteria: predisposition e.g. heart condition or IV drug use, fever, vascular phenomena, immunologic phenomena, microbiological evidence

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25
Q

How do you manage endocarditis?

A
  • antibiotics

- surgical intervention: if HF, uncontrollable infection, prevention of embolism

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26
Q

How does rheumatic fever cause valvular damage? What are other clinical features?

A
  • antibody cross reactivity affecting connective tissue
  • recurrent inflammation and fibrinous repair and scarring
  • painful joints, fever, rash
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27
Q

What causes mitral valve stenosis?

A

rheumatic fever, calcification, pressure overload, dilated LA, AF, pulmonary hypertension

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28
Q

What are the symptoms of mitral valve stenosis?

A

SOB, palpitation, chest pain, haemoptysis, right HF symptoms

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29
Q

Which type of heart murmur is best heard at apex with the patient laying on their left hand side?

A

mitral stenosis

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30
Q

Describe when each of the four main heart murmurs are found in the cardiac cycle.

A
  • mitral stenosis: diastolic
  • mitral regurgitation: systolic (ventricle contracts, blood flows back into atria as valve is incompetent)
  • aortic stenosis: ejection systolic
  • aortic regurgitation: diastolic
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31
Q

What are the symptoms of mitral regurgitation?

A

those consistent with congestive HF = SOB, pulmonary oedema, orthopnoea, and PND

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32
Q

What causes mitral regurgitation?

A

valve prolapse, volume overload, LV and LA dilatation, pulmonary hypertension

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33
Q

Describe the causes of aortic valve stenosis.

A

degeneration, congenital bicuspid (rather than tricuspid) valve, calcification

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34
Q

Where is an aortic valve stenosis best heard?

A

aortic area radiating to the neck

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35
Q

Discuss the symptoms of aortic stenosis and briefly describe how they develop.

A
  • chest pain, breathlessness, sweating, clammy (consistent with ischaemia - too much pressure leads to left ventricular hypertrophy and increased vascular demand)
  • syncope on exertion: increased CO demand
  • HF - increased atrial pressure, increased pulmonary pressure, pulmonary oedema
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36
Q

List causes of aortic regurgitation.

A

degeneration, aortic root dissection, endocarditis, Marfan’s, ankylosing spondylitis, SLE

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37
Q

How would you best heard an aortic regurg murmur?

A

ask patient to sit up and breath out, left sternal edge

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38
Q

How does LV dilatation develop in aortic regurg and how does this manifest clinically?

A
  • volume overload as valve is incompetent so blood flows back from aorta
  • exertion dyspnoea, orthopnoea, PND
  • may have apex displacement
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39
Q

Describe the investigation of valvular heart disease.

A

ECG (LVH), echo (valves and LV dimensions), doppler US (flow), coronary angiography

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40
Q

Discuss the treatment of valvular heart disease.

A
  1. Medications: control of fluid, AF, hypertension, diabetes, rate
  2. Valve replacement
    - metallic/mechanical: need warfarin, longer lasting
    - tissue: no anticoag, shorter lasting
  3. Procedural interventions
    - transcatheter aortic valve intervention TAVI: non operative candidates, expensive, not common
    - valvuloplasty: in mitral valve disease, opens up tight valve in young rheumatic patients
    - mitraclip
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41
Q

Describe how peri-operative adverse cardiac effect risk is calculated.

A 
high risk surgery = 1
ischaemic HD = 1
history of HF = 1
CVD = 1
insulin therapy = 1
creatinine > 177 umol/L = 1
0 = 0.4%, 1 = 0.9%, 2 = 6.6%, >3 = 11.1%
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42
Q

What is the clinical importance of the difference between a STEMI and an NSTEMI?

A
  • STEMI: complete occlusion (thrombosis/embolism) of coronary artery
  • NSTEMI: variable, transient/near complete occlusion of coronary artery or acute factor that deprives myocardium of oxygen
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43
Q

List the symptoms and signs of MI.

A
  • chest pain radiating to jaw and down left arm, SOB, cold, clammy, sweating, indigestion
  • tachycardia, distressed patient, HF (crackles, increased JVP), shock, arrhythmia
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44
Q

What is troponin and what does its presence indicated?

A
  • part of cardiac myocyte

- release into blood marker of cardiac necrosis

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45
Q

What are some non-cardiac causes of troponin elevation?

A

CHF, tachyarrhythmias, PE, sepsis

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46
Q

List causes of chronically increased levels of troponin.

A

renal failure, chronic HF, infiltrative cardiomyopathies e.g. amyloidosis, sarcoidosis, haemochromatosis

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47
Q

What is unstable angina?

A

an acute coronary event without a rise in troponin i.e. clinical presentation of an MI and ECG changes or tight narrowings on coronary angiography

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48
Q

Discuss the five types of MI.

A
  1. Spontaneous MI due to a primary coronary event e.g. coronary plaque rupture and formation of thrombus
  2. Increased oxygen demand or decreased oxygen supply e.g. HF, sepsis, anaemia, hyper/hypotension
  3. Sudden cardiac death
  4. MI ass. with percutaneous coronary intervention
  5. MI ass. with CABG
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49
Q

What are the ECG patterns seen in a STEMI?

A
  • ST elevation reflects occlusion of coronary artery, occurs in regional patterns
  • exception: posterior infarct = STE not seen
  • LBBB: QRS > 3 little blocks, new = infarction, old = obscure ST elevation in infarct
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50
Q

Discuss the anatomical significance of ST elevation in the ECG leads.

A
  • anterior elevation (V1-4) + reciprocal depression in inferior (II, III, aVF) = LAD
  • high lateral elevation (I, aVL) + reciprocal depression in inferior = LCx
  • inferior elevation + high lateral depression = RCA or LCx
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51
Q

How would you detect a posterior wall infarct on ECG? And infarction of which arteries would cause it?

A
  • no ECG leads look directly at posterior wall
  • anterior leads opposite so posterior STE = anterior ST depression
  • LCx or RCA - often ass. with inferior or lateral STE
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52
Q

What are the characteristics of left bundle branch block?

A

broad QRS complex > 120 m/s
dominant S in V1 (QRS mostly down)
broad R wave in V6

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53
Q

Describe the immediate management of a STEMI.

A
  1. ABCD
  2. Ambulance attached to defibrillator
  3. Aspirin 300mg PO
  4. Unfractionated heparin 5000U IV
  5. Morphine 5-10 mg IV
  6. Anti-emetics
  7. Clopidogrel (in ambulance) = antiplatelet
    - 600mg if for PPCI
    - 300mg if for thrombolysis
  8. Ticogrelor 180mg = antiplatelet
  9. Activate PPCI team at GJNH
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54
Q

Discuss the pathway to optimal reperfusion therapy following STEMI.

A

shock = primary PCI

NO SHOCK

  1. Call to balloon time > 90 mins = PHT by SAS then PCI centre
    - reperfusion - cath/PCI in 24 hours
    - no reperfusion - rescue PCI
  2. Thrombolysis contraindicated or call to balloon time <90 mins = PPCI
55
Q

What is the subsequent management following PPCI in MI?

A
  • monitor for MI complications

- secondary prevention: ACEi, BB, statins, eplerenone, aspirin for life

56
Q

There are many complications associated with the aftermath of a myocardial infarction. Can you give some examples and how they are managed?

A
  1. Arrhythmias e.g. VT, VF, AF
  2. HF - diuretics, inotropes, vasodilators
  3. Cardiogenic shock - IABP, ventricular assist device
  4. Myocardial rupture
  5. Psychological e.g. anxiety, depression
  6. Pericarditis
  7. LV mural thrombus
57
Q

Discuss the 2 main methods of reperfusion therapy in STEMI.

A
  1. Primary PCI
    - balloon angioplasty and stent placement
    - carries risk of an invasive procedure e.g. vascular damage, stroke
    - superior to thrombolysis: improves survival, reduces stroke, further MI, angina, shortens time in hospital
  2. Thrombolysis
    - tenecteplase 8000U/8ml as IV bolus over 10s: tissue plasminogen activator, breaks up thrombus, haemorrhagic stroke risk
    - heparin IV: anticoagulation to prevent further thrombosis
58
Q

What are the contraindications to thrombolysis?

A

recent surgery, previous stroke, GI bleeding, bleeding disorders

59
Q

Describe a typical presentation of pericarditis.

A

fatigue, flu-like symptoms, sharp left-sided pleuritic chest pain

60
Q

What ECG changes are seen in pericarditis?

A

concave STE, often global, no reciprocal changes, PR depression

61
Q

Define systemic hypertension.

A
  • persistent elevation in arterial BP > 140/90 mmHg

- increases vascular risk sufficient enough to require intervention

62
Q

Give examples of modifiable and non-modifiable risk factors of primary hypertension.

A

modifiable: diet, physical exercise, obesity, stress, alcohol excess
non-modifiable: age, gender (males), ethnicity, genetics

63
Q

Describe the pathophysiology of primary hypertension.

A
  • genetic factors, environmental influences
  • defects in renal Na+ haemostasis leads to salt and water retention -> increased plasma volume
  • release of natriuretic hormone and functional vasoconstriction causes increased activity
  • defects in vascular smooth muscle growth and structure increase vascular wall thickness
  • increased CO and total peripheral resistance leads to hypertension
64
Q

Discuss some of the complications associated with hypertension.

A

TIA/stroke, retinopathy, peripheral vascular disease, LVH, CHD, HF, renal failure

65
Q

What are the causes of secondary hypertension?

A
  • endocrine: hyperaldosteronism, Cushing’s, thyroid, phaeochromocytoma
  • vascular: co-arctation of aorta
  • renal: renal artery stenosis
  • drugs: NSAIDs, cocaine, exogenous steroid use
  • obstructive sleep apnoea
66
Q

How would a diagnosis of hypertension be made?

A
  • often asymptomatic, uncommonly headache, dizziness, visual disturbance
  • office BP > 140/90
  • ambulatory BP: BP taken throughout day and night and mean calculated - 24hr mean = > 130/80
  • home BP: readings twice a day, taken over 4-7 days - mean = >135/85
67
Q

Discuss the management of hypertension in line with NICE guidelines.

A
  • lifestyle measures e.g. exercise, weight loss, reduction in salt, alcohol and smoking
  • if < 55 start with ACEi/ARB, if > 55/black start with CaCB
  • then ACEi/ARB + CaCB
  • ACEi/ARB + CaCB + K+ sparing diuretic
  • add a/b-B or further diuretic
68
Q

What are the symptoms of atrial fibrillation?

A
  • asymptomatic, palpitations, dyspnoea
  • rarely: chest pain, syncope
  • may present with complications e.g. stroke (5 fold increase stroke risk)
69
Q

How would you make a diagnosis of AF?

A
  • pulse = irregularly irregular

- confirmed on ECG: variable rate, irregular, narrow QRS, no P waves

70
Q

What are the three types of AF?

A
  1. Paroxysmal: intermittent
  2. Persistent: requiring intervention to terminate arrhythmia e.g. IV antiarhythmatic drug injection or DC cardioversion
  3. Permanent
71
Q

Describe the ECG changes in atrial flutter.

A

variable rate, regular QRS complex, sawtooth atrial activity, 300bpm, variable AV block

72
Q

How can atrial fibrillation cause stroke?

A

left atrial appendage blood clots can enter blood stream and cause stroke in patients with non-valvular AF - seen in transoesophageal ECHO

73
Q

List some of the predisposing factors to AF.

A

hypertension, symptomatic HF, valvular heart disease, cardiomyopathies, ASD, congenital HD, CAD, thyroid dysfunction, obesity, DM, COPD, sleep apnoea, chronic renal disease

74
Q

Describe the score system for calculating stroke risk in non-valvular AF.

A 
CHA2DS2-VASc:
congestive HF/LV dysfunction = 1
hypertension = 1
age > 75 = 2
diabetes = 1
stroke/TIA/thromboembolism = 2
vascular disease = 1
age 65-74 = 1
sex category (female) = 1

0=0% risk, 9=15% risk

75
Q

How does the CHA2DS2-VASc score determine the management of stroke risk in non-valvular AF?

A 
0 = no treatment
1 = consider OAC
>2 = NOAC, consider warfarin and LAA occluding devices
76
Q

Describe how rhythm is controlled in AF.

A
  1. Direct current cardioversion (persistent AF)
  2. Antiarrhythmic drugs e.g. Na+CB, K+CB, multichannel blockers, often used with BB
  3. Catheter ablation
    - radiofrequency current ‘burning’ or cyro-ablation ‘freezing’ pulmonary vein commonly
    - most effective in patients with normal or minimal heart disease
77
Q

What are the consequences of secundum ASD?

A
  • shunts left to right when in isolation
  • right heart volume loading
  • RV failure, tricuspid valve regurg, atrial arrhythmias, pulmonary hypertension
78
Q

What would be seen in a clinical examination of a patient with secundum ASD?

A

pulmonary flow murmur

fixed, split second heart sound

79
Q

Where does coarctation of aorta commonly occur?

A

after LSA in a juxta-ductal position

80
Q

What are some of the consequences of coarctation of aorta?

A

upper body hypertension, berry aneurysms, claudification, renal insufficiency

81
Q

Defect of which valve is commonly associated with coarctation of aorta?

A

bicupsid aortic valve

82
Q

Discuss the treatment of coarctation of aorta.

A

surgical repair by thoracotomy

  • subclavian flap - used to enlarge constricted area of aorta
  • end to end - constriction removed
  • balloon angioplasty
83
Q

What is the transposition of the great arteries?

A
  • aorta and pulmonary artery switch so aorta is now connected to RV and pulmonary artery to LV creating two separate circulation systems
  • systemic blood returning to heart is not oxygenated
  • cyanotic lesion
84
Q

How is transposition of the great arteries treated?

A
  • newborns given prostaglandins to keep ductus arteriosus open
  • atrial switch: complications = RV dilatation, tricuspid regurg, HF, atrial arrhythmias
  • arterial switch: coronary artery problems, LVH
85
Q

What are the four components of tetralogy of Fallot?

A
  1. Ventricular septal defect
  2. Overriding aorta
  3. Pulmonary stenosis
  4. Right ventricular hypertrophy
86
Q

What symptoms are seen in TOF?

A

Episodes of bluish colour to the skin, difficulty breathing, heart murmur, finger clubbing

87
Q

What is the treatment of TOF?

A
  • BT shunt

- complete repair: pulmonary a. and RV enlarged using a patch, muscular obstruction removed, VSD closed with patch

88
Q

Are there complications following TOF surgery?

A

yes

  • significant pulmonary regurg
  • arrhythmia - ventricular arrhythmia
  • pulmonary arterial/branch PA stenosis
89
Q

Give an example of an anatomical defect which causes a univentricular heart.

A

tricuspid atresia - reliant on shunts through PFO and PDA for mixing

90
Q

Discuss treatment of univentricular heart.

A
  • aim for 2 functional ventricles

- if not - Fontan circulation, where IVC and SVC directly into pulmonary arteries bypassing heart altogether

91
Q

What issues are associated with Fontan circulation in management of univentricular heart?

A

pulmonary circulation imbalances: PE, arrhythmias, dehydration, bleeding - HAEMODYNAMIC COLLAPSE

92
Q

Give two examples of recombinant tPAs and describe their mechanism of action.

A

tenecteplase + alteplase

catalyses conversion of plasminogen to plasmin, thus promotes clot lysis

93
Q

Give 2 indications of rtPA use.

A

acute MI (within 12hr of onset), massive PE

94
Q

Describe the mechanism of action of clopidogrel.

A

Irreversibly blocks ADP-R on platelet cell membranes. Consequently inhibits formation of GPIIb/IIIa complex, required for platelet aggregation. Decreased thrombus formation.

95
Q

Which drug is a direct thrombin inhibitor and prevents conversion of fibrinogen to fibrin?

A

dabigatran

96
Q

When is dabigatran used clinically?

A

post-op prophylaxis of venous thromboembolism

97
Q

What type of drug are rivaroxaban and apixaban?

A

factor Xa antagonist: inhibits prothrombin to thrombin conversion, decreased fibrin clot formation

98
Q

What are the indications of rivaroxaban and apixaban use?

A
  • prophylaxis of venous thromboembolism
  • thromboprophylaxis in non-valvular AF
  • treatment of venous thromboembolism
99
Q

Describe the mechanism of action of aspirin.

A

Irreversible inactivation of cyclooxygenase (COX) enzyme. This reduces platelet thromboxane (TXA2) production and endothelial prostaglandin (PGI2) production. Reduced platelet thromboxane production reduces platelet aggregation and thrombus formation. Reduced prostaglandin synthesis decreases nociceptive sensitisation and inflammation.

100
Q

Which drug enhances activity of antithrombin III and inhibits other factors of coagulation cascade?

A

heparin

101
Q

What are the clinical uses of heparin?

A
  • thromboembolic diseases, including inducion of vit K antagonists
  • renal dialysis
  • ACS treatment
102
Q

How doe unfractionated heparin and LMWH differ?

A

LMWH 2-4x longer plasma half-life than unfractionated

103
Q

Describe the mechanism of action of warfarin.

A

Inhibits vitamin K epoxide reductase. Prevents recycling of vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X. Prevents thrombus formation.

104
Q

In what conditions is warfarin indicated?

A
  • venous thromboembolism treatment

- thromboprophylaxis of AF, metallic heart valves, cardiomyopathy

105
Q

Name two cardioselective beta-blockers.

A

bisoprolol and atenolol

106
Q

What are uses of bisoprolol/atenolol?

A

hypertension, angina, rate-control in AF, supportive therapy in mild/moderate HF

107
Q

What is the mechanism of action of bisoprolol?

A

Cardioselective beta-1-adrenoceptor antagonist.
Preferentially blocks beta-1 receptors in cardiac and renal tissue. Inhibits sympathetic stimulation of the heart and renal vasculature. Blockade of the sino-atrial node reduces heart rate (negative chronotropic effect) and blockade of receptors in the myocardium depresses cardiac contractility (negative inotropic effect). Additionally, blockade of beta-1 adrenoceptors in renal tissue inhibits the release of renin, depressing the vasoconstrictive effects of the renin-angiotensin-aldosterone system.

108
Q

Give two examples of noncardioselective beta-blockers.

A

propranolol

carvedilol

109
Q

Propranolol should be avoided in the case of which diseases?

A

asthma and COPD

110
Q

Describe the mechanism of action of non-cardioselective beta-blockers.

A

inhibits sympathetic stimulation in the heart and vascular smooth muscle

111
Q

In what conditions is the use of propanolol/carvedilol indicated?

A

hypertension, angina, anxiety, migraine prophylaxis, post-MI prophylaxis

112
Q

Ramipril is an example of which drug? And how does it work?

A

ACE inhibitor
Inhibits conversion of Angiotensin I to Angiotensin II (a more potent systemic vasoconstrictor). This action subsequently inhibits Aldosterone release from the adrenal cortex, depressing renal sodium and fluid retention, thereby decreasing blood volume.

113
Q

What are the clinical indications of ACEi? What is the main side effect associated?

A

hypertension, HF, nephropathy, prevention of CV events in high risk patients
dry cough

114
Q

Differentiate the mechanism of action of rate-limiting and non rate-limiting calcium channel blockers.

A

BOTH
Prevent cellular entry of Ca2+ by blocking L-type calcium channels. Myocardial and Smooth muscle contractility depressed. Dilate coronary blood vessels and reduce afterload.

RATE-LIMITING
Cardiac contractility will be reduced. Antidysrhythmic actions due to prolonged atrioventricular node conduction - depresses heart rate.

115
Q

Name two rate-limiting and two non-rate-limiting CaCB.

A

RL: verapamil, diltiazem
NRL: amlodipine, nifedipine

116
Q

Give three indications for use of verapamil.

A

supraventricular arrhythmias, angina, hypertension

117
Q

Name a statin and describe their mechanism of action.

A

simvastatin
HMG CoA reductase inhibitors - the rate-determining enzyme in the mevalonate pathway synthesis of cholesterol. This causes an increase in LDL-receptor expression, on the surface of hepatocytes. Increases hepatic uptake of cholesterol, reducing plasma cholesterol levels. Reduces development of athersclerotic plaques.

118
Q

What type of drug is digoxin and how does it work?

A

cardiac glycoside
Increases vagal parasympathetic activity and inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly. In an effort to remove Na+, more Ca2+ is brought into the cell by the action of Na+/Ca2+ exchangers. The buildup of Ca2+ is responsible for the increased force of contraction and reduced rate of conduction through the AV node.

119
Q

When is digoxin used?

A

heart failure

rate control in atrial fibrillation

120
Q

Which drug works by blocking cardiac K+ channels, prolonging repolarisation of the cardiac action potential?

A

amiodarone - restores regular sinus rhythm and slow AV nodal conduction

121
Q

What is the main clinical use of amiodarone?

A

supraventricular/ventricular arrhytmias

122
Q

Photosensitivity skin reactions occur in up to 75% of patients taking which drug?

A

amiodarone

123
Q

Differentiate the symptoms of left and right sided heart failure.

A
  • left: exertional dyspnoea, orthopnoea, PND, tachycardia, fatigue, elevated PCWP, cyanosis, pulmonary congestion (cough, crackles, wheezes, haemoptysis, tachypnoea)
  • right (cor pulmonale): fatigue, increased peripheral venous pressure, ascites, hepato/splenomegaly, raised JVP, peripheral oedema, weight gain
124
Q

What changes are seen on ECG in 1st-degree heart block?

A

the PR interval is prolonged and unchanging; no missed beats

125
Q

What changes are seen on ECG in 2nd-degree HB: Mobitz 1?

A

the PR interval becomes longer and longer until a QRS is missed, the pattern then resets - Wenchkeback phenomenon

126
Q

What changes are seen on ECG in 2nd-degree HB: Mobitz 2?

A

QRSs are regularly missed, ratio may be 2:1 or 3:1

127
Q

What are some of the causes of 1st and 2nd degree heart block?

A

IHD, acute myocarditis, drugs (digoxin, BB), athletes, sick sinus syndrome

128
Q

Name three drugs associated with sinus bradycardia.

A

BB, digoxin, amiodarone

129
Q

What changes are seen on ECG in 3rd-degree HB: complete HB?

A

no impulses are passed from atria to ventricles so P waves and QRSs appear independently of each other

130
Q

List the causes of complete heart block.

A

IHD, fibrosis, congenital, aortic valve calcification, cardiac surgery, digoxin toxicity, infiltration

131
Q

What changes are seen on ECG in RBBB?

A

broad QRS, M pattern on V1, sloped S wave (and with eye of faith, a W shape) on V5 - MaRRoW = RBBB

132
Q

What are the causes of RBBB?

A

normal variant, PE, cor pulmonale

133
Q

What changes are seen on ECG in LBBB?

A

broad QRS, W pattern on V1 with dominant S, M pattern on V6 - WiLLiaM = LBBB

134
Q

What are the causes of LBBB?

A

IHD, hypertension, cardiomyopathy, idiopathic fibrosis

Phase 3 (10 decks)

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