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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define…

1) Preload
2) Afterload
3) Contractility
4) Elasticity

A

1) The volume of blood in the ventricles just before contraction (end diastolic volume).
2) The pressure against which the heart must work to eject blood in systole.
3) The inherent strength + vigour of the heart’s contraction during systole.
4) Myocardial ability to recover its original shape after systolic stress.

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2
Q

Define…

1) Compliance
2) Diastolic distensibility
3) Resistance
4) Starling’s law

A

1) How easily a chamber of the heart expands when it’s filled with blood.
2) The pressure required to fill the ventricle to the same diastolic volume.
3) A force that must be overcome to push blood through the circulatory system.
4) Increased EDV leads to increased stroke volume + so increased cardiac output leading to more forceful contraction as the sarcomeres are stretched more.

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3
Q

What are the equations for…

1) Stroke volume
2) Mean arterial pressure
3) Cardiac output
4) Poiseuille’s
5) Ohm’s law
6) Pulse pressure
7) Blood pressure

A

1) SV = EDV - ESV
2) MAP = DP + 1/3PP
3) CO = HR x SV
4) Flow = vessel radius^4
5) Flow = pressure gradient ÷ resistance
6) PP = SP - DP
7) BP = CO x PVR

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4
Q

How can the vascular system activate RAAS?

A

A reduction in CO means there is reduced renal perfusion + so there’s little/no arteriolar stretch which initiates RAAS.

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5
Q

Explain the RAAS process.

A
  • Juxtaglomerular cells located in the afferent arterioles are stimulated to release the enzyme renin.
  • Renin enters the blood where it cleaves angiotensinogen produced in the liver into angiotensin I.
  • Angiotensin I is a biologically inactive peptide which undergoes further cleavage by angiotensin converting enzyme (ACE) produced in the lungs to form the active agent angiotensin II.
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6
Q

What effects does angiotensin II have on the body?

A

Angiotensin II

  • Stimulates zona glomerulosa of adrenal cortex to secrete aldosterone.
  • Stimulates thirst + vasopressin release causing water retention.
  • Increases Na+ reabsorption in the proximal convoluted tubule + so water retention.
  • Vasoconstrictor + so increases GFR (esp. in efferent arterioles).
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7
Q

What effects does aldosterone have on the body?

A
  • Acts on principal cells of the collecting duct + stimulates transcription of epithelial sodium channels (ENaCs) causing Na+ reabsorption + so water reabsorption into the principal cells which causes more K+ excretion due to ENaC mechanism.
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8
Q

What is the counter mechanism to RAAS within the heart?

A
  • The atrial natriuretic + brain natriuretic peptide hormones (ANP/BNP).
  • They are released in response to stretching of the atrial + ventricular muscle cells as a result of raised atrial/ventricular pressures/volume.
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9
Q

What are the main effects of the ANP/BNP hormones?

A
  • Increased renal excretion of Na+ + water.
  • Relax vascular smooth muscle (renal vasodilator in afferent arterioles to increase GFR to increase Na+ excretion).
  • Increased vascular permeability.
  • Inhibits the release/actions of aldosterone, angiotensin II, endothelin + vasopressin.
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10
Q

What enzyme metabolises ANP/BNP?

A
  • Neutral endopeptidase (NEP) like neprilysin.2
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11
Q

What do the following represent…

1) P wave.
2) PR interval.
3) QRS complex.
4) QT interval.
5) ST segment.
6) T wave.
7) J point

A

1) Atrial depolarisation.
2) Time taken for atria to depolarise + electrical activation to get through the AVN (120-200ms).
3) Ventricular depolarisation (120ms)
4) Correlates to plateau phase of cardiac action potential + should be 350-450ms, heart rate can make it vary.
5) Interval between depolarisation + repolarisation.
6) Ventricular repolarisation.
7) Where the QRS complex becomes the ST segment, should be isoelectric.

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12
Q

ECG questions

1) In what leads should the QRS complex be dominantly upright?
2) In what lead are all waves negative?
3) What is the rule for R + S wave progression in the chest leads?

A

1) I + II.
2) aVR.
3) R grows from V1-4, S must grow V1-3 + disappear in V6.

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13
Q

ECG questions

1) Where might the ST segment not be isoelectric?
2) In what leads must P + T waves be upright + there be no/small Q waves?

A

1) Only V1-2 it may be elevated.

2) Leads I-II, V2-6.

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14
Q

How can you determine rhythm from an ECG?

A
  • Regular rhythm = 300 ÷ number of big boxes between two QRS complexes.
  • Irregular rhythm = number of beats present in 10 seconds x 6
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15
Q

What is the QRS axis of the heart?

A
  • Represents the overall direction of the heart’s electrical activity.
  • Normal axis is -30 to 90 degrees.
  • -30 to -90 degrees is left axis deviation.
  • 90 to 180 degrees is right axis deviation.
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16
Q

What ECG changes are seen in…

1) Right atrial enlargement?
2) Left atrial enlargement?
3) Abnormal T waves?

A

1) Tall pointed P waves (P pulmonale).
2) Notched/bifid (‘M’ shaped) P waves (P mitrale).
3) Symmetrical, tall + peaked, biphasic or inverted.

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17
Q

Define…

1) Atherosclerosis.
2) Atherogenesis.
3) Ischaemia.
4) Infarction.

A

1) Atherosclerosis is the pathology of the arteries characterised by the deposition of fatty material in the intima (inner wall), it’s an inflammatory process.
2) Atherogenesis is the development of an atherosclerotic plaque.
3) Ischaemia is reversible damage to tissues as a result of impaired vascular perfusion depriving tissues of vital nutrients + oxygen.
4) Infarction is irreversible necrosis of tissue due to ischaemia.

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18
Q

What is the effect of an atheromatous plaque? What causes the inflammation in atherosclerosis?

A
  • It thins the media of an artery + it’s distributed in the peripheral + coronary arteries with focal distribution along the artery length.
  • Endothelial cell injury leads to chemoattractants to be released which signal to leukocytes that accumulate + migrate into the vessel walls causing cytokine release (IL-1, 6) causing inflammation.
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19
Q

Why does atherosclerosis have such a major disruption to flow?

A

Poiseuille’s equation…

- Flow = vessel radius^4

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20
Q

What are the features in the first step in atherosclerosis progression?

A

Fatty streaks…

  • Earliest lesion of atherosclerosis, appears very early (<10y/o).
  • Consist of aggregations of lipid-laden macrophages (foam cells) + T lymphocytes within the intimal layer of the vessel wall.
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21
Q

What are the features in the second step in atherosclerosis progression?

A

Intermediate lesions…

  • Foam cells.
  • Vascular smooth muscle cells.
  • T lymphocytes.
  • Adhesion + aggregation of platelets to vessel wall.
  • Isolated pools of extracellular lipid.
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22
Q

What are the features in the third step in atherosclerosis progression?

A

Fibrous plaques/advanced lesions…

  • Fibrous cap that overlies lipid core + necrotic debris.
  • Foam cells + macrophages.
  • Smooth muscle cells.
  • T lymphocytes.
  • Can impede blood flow + prone to rupture.
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23
Q

What are the features in the fourth step in atherosclerosis progression?

A

Plaque rupture…
- Plaques are constantly growing + receding. The fibrous cap has to be resorbed + redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak + the plaque ruptures leading to thrombus formation + vessel occlusion.

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24
Q

What is plaque erosion and what can it lead to?

A
  • Lesions tend to be small ‘early lesions’ where the fibrous cap does not disrupt.
  • Can lead to an NSTEMI.
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25
Q

What are the complications with atherosclerosis?

A
  • Myocardial infarction.
  • Stroke.
  • Aortic aneurysms.
  • Peripheral vascular disease (gangrene, intermittent claudication).
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26
Q

What are the constituents in an atherosclerotic plaque?

A
  • Lipid.
  • Necrotic core with dead cells, debris.
  • Connective tissue.
  • Fibrous cap – layers of smooth muscle.
  • Lymphocytes – chronic inflammation.
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27
Q

What are the risk factors with atherosclerosis?

A
  • Smoking – due to free radicals, nicotine + CO.
  • HTN – due to shearing forces on the endothelial cells.
  • Hyperlipidaemia – due to direct damage to endothelial cells.
  • Diabetes mellitus.
  • Increasing age.
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28
Q

What is the treatment for atherosclerosis?

A
  • Percutaneous coronary intervention (PCI).
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29
Q

ANGINA PECTORIS

What is the pathophysiology of angina pectoris?

A
  • Angina is a symptom of oxygen supply/demand mismatch to the heart experienced on exertion.
  • Typically, an atheroma causes a narrowing of the coronary vessels meaning that at times of increased oxygen demand like exertion, there is symptomatic reversible myocardial ischaemia leading to anginal pain.
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30
Q

ANGINA PECTORIS

Explain the difference between physiological + pathological state in angina pectoris?

A
  • In the physiological state, blood vessels try to compensate for increased myocardial demand by reducing microvascular resistance to increase flow.
  • In the pathological state, at rest epicardial resistance is already high + so microvascular resistance has to fall at rest to supply myocardial demand so on exertion microvascular resistance can’t reduce any more so the flow can’t increase to meet metabolic demand.
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31
Q 
ANGINA PECTORIS
What is...
1) Stable angina?
2) Unstable angina?
3) Decubitus angina?
4) Prinzmetal angina?
A

1) Induced by effort, relieved by rest.
2) Crescendo angina; angina of increasing frequency or severity, occurs on minimal exertion or at rest; associated with higher risk of MI.
3) Precipitated by lying flat.
4) Vasospastic angina; caused by coronary artery spasm (may coexist with fixed stenoses, rare though), occurs at rest.

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32
Q

ANGINA PECTORIS

What is the aetiology of angina pectoris?

A
  • Atherosclerosis.
  • Increased distal resistance (LVH).
  • Reduced oxygen carrying capacity (anaemia).
  • Coronary artery spasm.
  • Thrombosis.
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33
Q

ANGINA PECTORIS

What are the modifiable/non-modifiable risk factors of angina pectoris?

A 
Modifiable...
- Smoking.
- Diabetes mellitus.
- Hypercholesterolaemia (LDL).
- Obesity/sedentary lifestyle.
- HTN.
Non-modifiable...
- Increasing age.
- Gender (male bias).
- Family history.
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34
Q

ANGINA PECTORIS

What is the clinical presentation of angina pectoris?

A
  • Constricting/heavy discomfort to the chest/jaw/neck/shoulders/arms.
  • Symptoms brought on by exertion.
  • Symptoms relieved with 5 mins rest or glyceryl trinitrate (GTN) spray.
  • All 3 = typical angina, 2 = atypical angina, 0-1 = non-anginal chest pain.
  • Accessory symptoms of breathlessness.
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35
Q

ANGINA PECTORIS

What are the differential diagnoses of angina pectoris?

A
  • Pulmonary embolism.
  • Pericarditis/myocarditis.
  • Musculoskeletal.
  • Gastro-oesophogeal reflux, ulceration.
  • Psychological.
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36
Q

ANGINA PECTORIS

What are the investigations for angina pectoris?

A
  • Stress ECG.
  • Coronary angiogram (high NPV, low PPV so good at excluding disease).
  • ECG may show signs of ischaemia (ST depression, flat/inverted T waves).
  • Can use pre-test probability of coronary artery disease, takes into account gender, age + typicality of pain.
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37
Q

ANGINA PECTORIS

What is the primary prevention for angina pectoris treatment?

A

Modify risk factors…

  • Smoking cessation.
  • Dietary + exercise advice.
  • Get conditions like HTN, hypercholesterolaemia, T2DM controlled.
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38
Q

ANGINA PECTORIS

What is the secondary prevention for angina pectoris treatment?

A

Pharmacological…
- Reduce CV events (aspirin, statins).
- Reduce symptoms (GTN spray, CCBs, ACEi, BBs).
Interventional…
Interventional…
- Revascularisation via PCI/CABG if there are large amounts of myocardial ischaemia.
- This in turn will help to reduce symptoms caused from stenotic coronary vessels.

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39
Q

ACS

What are acute coronary syndromes (ACSs)?

A
  • ACS encompasses a spectrum of acute cardiac conditions including unstable angina, non-ST elevation myocardial infarction (NSTEMI) + ST elevation myocardial infarction (STEMI).
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40
Q

ACS

What is the pathophysiology of ACS?

A
  • An atherosclerotic plaque ruptures causing platelet aggregation to occur leading to thrombus formation which completely occludes the artery.
  • This leads to irreversible ischaemia causing infarction + so necrosis of the cells that results in permanent heart muscle damage.
  • MI means there’s necrosis of cells which causes release of troponin – a marker of cardiac muscle injury which does not present in unstable angina as there’s only myocardial ischaemia without cell necrosis.
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41
Q

ACS

What’s the difference between type 1 and type 2 MI?

A
  • Type 1 is spontaneous MI with ischaemia due to plaque rupture.
  • Type 2 is MI secondary to ischaemia due to increased oxygen demand.
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42
Q

ACS

What are the common/uncommon aetiologies of ACS?

A 
Common...
- Rupture of atherosclerotic plaque leading to arterial thrombosis.
Uncommon...
- Coronary vasospasm.
- Drug abuse.
- Coronary artery dissection.
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43
Q

ACS

What complications are there with ACS?

A

May develop Dressler’s syndrome 2-10 weeks after an MI…

  • Myocardial injury stimulates the formation of autoantibodies against the heart, secondary form of pericarditis.
  • Presents with fever, chest pain + pericardial rub.
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44
Q

ACS

What are the modifiable/non-modifiable risk factors of angina pectoris?

A 
Modifiable...
- Smoking.
- Diabetes mellitus.
- Hyperlipidaemia.
- Obesity/sedentary lifestyle.
- HTN.
- Cocaine use.
Non-modifiable...
- Increasing age.
- Gender (male bias).
- Family history.
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45
Q

ACS

What’s the clinical presentation of unstable angina?

A
  • Constricting/heavy discomfort to the chest/jaw/neck/shoulders/arms at rest.
  • Pain with crescendo patterns (pain becomes more frequent + more easily provoked).
  • No significant rise in troponin.
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46
Q

ACS

What are the symptoms of MI?

A
  • Acute central crushing chest pain that may radiate to chest/jaw/neck/shoulders/arms.
  • Sweating.
  • Dyspnoea.
  • Palpitations.
  • Nausea/vomiting.
  • Third occur in bed at night.
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47
Q

ACS

What are the signs of MI?

A
  • Distress/anxiety/sweatiness.
  • Pallor.
  • Increased/decreased pulse + BP.
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48
Q

ACS

What are the differential diagnoses of ACS?

A
  • Stable angina.
  • Pulmonary embolism or pneumothorax.
  • Peri/myocarditis.
  • Musculoskeletal.
  • Gastro-oesophageal reflux.
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49
Q

ACS

What are the complications with ACS?

A
  • Heart failure.
  • Rupture of infarcted ventricle or interventricular septum.
  • Mitral regurgitation.
  • Arrhythmias.
  • Heart block.
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50
Q

ACS

What investigations are there for ACS?

A

ECG…
- ST elevated, hyperacute T waves or new LBBB w/ T-wave inversion of pathological Q waves later (STEMI).
- ST depression + T-wave inversion (NSTEMI + unstable angina).
Bloods…
- Serum troponin.
Echocardiogram.
Coronary angiogram.

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51
Q

ACS

What is the initial treatment for MI?

A

MONA…

  • Morphine for pain relief.
  • Oxygen to prevent hypoxia.
  • Nitrates for vasodilation.
  • Aspirin 300mg.
  • Get into hospital ASAP, call PCI centre if STEMI.
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52
Q

ACS

What is the hospital treatment for ACS?

A
  • PCI immediately or if not possible then thrombolysis with streptokinase.
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53
Q

ACS

What is the primary prevention for ACS?

A

Modify risk factors…

  • Smoking cessation.
  • Dietary + exercise advice.
  • Get conditions (HTN, hyperlipidaemia, T2DM) controlled.
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54
Q

ACS

What treatments optimise cardioprotective medications for ACS?

A 
Antiplatelets
- Aspirin 75mg once daily.
- P2Y12 inhibitor like clopidogrel.
Beta blocker to reduce myocardial oxygen demand.
High dose statin.
- Atorvastatin 80mg.
?ACEi.
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55
Q

CARDIAC FAILURE

What is cardiac failure and what happens when the heart fails?

A
  • Cardiac output is inadequate for the body’s requirements suggesting the efficiency of the heart as a pump is impaired, heart cannot deliver blood at a rate that meets metabolic demand.
  • Compensatory mechanisms attempt to maintain CO but as the cardiac failure progresses, mechanisms are exhausted + become pathophysiological.
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56
Q

CARDIAC FAILURE

What are the 4 compensatory methods in cardiac failure?

A
  • Sympathetic system.
  • RAAS.
  • Natriuretic peptides.
  • Ventricular dilation/hypertrophy.
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57
Q

CARDIAC FAILURE

Explain how the sympathetic system acts as a compensatory method + the consequence of this.

A
  • Improves ventricular function by increasing HR + contractility.
  • BUT causes arteriolar constriction which increases load + so myocardial work.
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58
Q

CARDIAC FAILURE

Explain how RAAS acts as a compensatory method + the consequence of this.

A
  • Reduced CO leads to reduced renal perfusion; activates RAAS leading to fluid retention + so increased preload.
  • BUT it also causes arteriolar constriction which increases load + myocardial work.
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59
Q

CARDIAC FAILURE

Explain how the natriuretic peptide system acts as a compensatory method + the consequence of this.

A
  • Atrial + brain natriuretic peptide hormones have diuretic, hypotensive + vasodilating properties.
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60
Q

CARDIAC FAILURE

What are the 2 broad categories for cardiac failure?

A

Systolic failure…
- Inability of ventricle to contract normally, results in reduced CO, ejection fraction <40%.
Diastolic failure…
- Inability of ventricle to relax + fill normally, causing increased filling pressure, typically EF >50% – heart failure with preserved ejection fraction (HFPEF).

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61
Q

CARDIAC FAILURE

What are the 2 types of cardiac failure and where does blood back up to?

A
  • Left cardiac failure = pulmonary circulation.

- Right cardiac failure = systemic circulation.

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62
Q

CARDIAC FAILURE

What is the New York Heart Association’s classification of cardiac failure?

A
  • Class I = no limitation (asymptomatic).
  • Class II = slight limitation (mild cardiac failure.
  • Class III = marked limitation (symptomatically moderate cardiac failure).
  • Class IV = inability to carry out any physical activity without discomfort (symptomatically severe cardiac failure).
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63
Q

CARDIAC FAILURE

What’s the aetiology of cardiac failure?

A 
Systolic failure...
- IHD.
- MI.
- Cardiomyopathy.
Diastolic failure...
- Cardiac tamponade.
- Ventricular hypertrophy.
- Cor pulmonale + obesity.
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64
Q

CARDIAC FAILURE

Why are men more likely to be affected by cardiac failure?

A

Oestrogen acts as a protective factor in menstruating women.

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65
Q

CARDIAC FAILURE

What are the symptoms of left cardiac failure?

A
  • Nocturnal cough ± pink frothy sputum.
  • Paroxysmal nocturnal dyspnoea, exercise intolerance.
  • Cold peripheries.
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66
Q

CARDIAC FAILURE

What are the symptoms of right cardiac failure?

A
  • Peripheral oedema.
  • Ascites.
  • Nausea.
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67
Q

CARDIAC FAILURE

What two initial investigations are crucial in determining if someone has cardiac failure?

A

Bloods – BNP raised levels indicates heart failure.
ECG – may indicate cause.
- NICE say if ECG + BNP levels are normal then cardiac failure unlikely so search for alternative diagnosis.
- If either abnormal – echocardiography required as it’s diagnostic, can confirm presence of LV dysfunction.

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68
Q

CARDIAC FAILURE

What could you see on the CXR of someone with cardiac failure?

A
  • Cardiomegaly.
  • Alveolar oedema “Bat’s wings”.
  • Dilated prominent upper lobe vessels.
  • Pleural effusion.
  • Kerley B lines (interstitial oedema).
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69
Q

CARDIAC FAILURE

What is the generic treatment for cardiac failure?

A

Generic lifestyle advice…

  • Smoking + alcohol cessation.
  • Optimise weight, nutrition + exercise.
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70
Q

CARDIAC FAILURE

What is the medical treatment for cardiac failure?

A

Symptomatic…
- Loop diuretics like furosemide for oedema.
- Switch to K+-sparing diuretic like spironolactone if hypokalaemic.
Disease-altering…
- ACEi (ARBs if C/I) in all those with LV systolic dysfunction as improves symptoms + prolongs life
- Beta blockers like bisoprolol to decrease mortality.
- Calcium glycoside like digoxin.

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71
Q

COR PULMONALE

What is the pathophysiology and prognosis of cor pulmonale?

A
  • Right cardiac failure due to right ventricular hypertrophy caused by chronic pulmonary arterial HTN.
  • Poor, 50% die in 5 years.
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72
Q

COR PULMONALE

What is the aetiology of cor pulmonale?

A
  • Chronic lung disease like COPD, pulmonary fibrosis.
  • Pulmonary emboli, sickle-cell disease.
  • Neuromuscular disease like myasthenia gravis, MND.
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73
Q

COR PULMONALE

What are the symptoms of cor pulmonale?

A
  • Dyspnoea.
  • Fatigue.
  • Syncope.
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74
Q

COR PULMONALE

What are the signs of cor pulmonale?

A
  • Cyanosis.
  • Tachycardia.
  • Raised JVP.
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75
Q

COR PULMONALE

What blood tests can you do for cor pulmonale and what do they show?

A
  • FBC – Hb + haematocrit increased (secondary polycythaemia).
  • ABG – Hypoxia ± hypercapnia.
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76
Q

COR PULMONALE

What would the ECG + CXR show for cor pulmonale?

A 
ECG...
- Right axis deviation.
- Right ventricular hypertrophy.
- P pulmonale (tall pointed P waves).
CXR...
- Enlarged RA + RV.
- Prominent pulmonary arteries.
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77
Q

COR PULMONALE

What is the treatment for cor pulmonale?

A
  • Treat underlying cause.
  • Treat respiratory failure with oxygen.
  • Treat cardiac failure with diuretics like furosemide.
  • Consider venesection or heart-lung transplantation in young patients.
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78
Q

HYPERTENSION

What are the four types of HTN?

A
  • Primary/essential.
  • Secondary.
  • Malignant.
  • White coat.
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79
Q

HYPERTENSION

Explain what primary/essential HTN is.

A
  • No known aetiology, typically older patients.
  • Usually asymptomatic, ?headache.
  • Always check for end organ damage/signs of renal disease, check for retinopathy, proteinuria.
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80
Q

HYPERTENSION

Explain what secondary HTN is.

A

HTN secondary to…

  • Renal disease.
  • Endocrine disease like Cushing’s + Conn’s syndromes, hyperparathyroidism, acromegaly, pheochromocytoma.
  • Others like pregnancy, cocaine.
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81
Q

HYPERTENSION

Explain what malignant HTN is.

A
  • Rapid rise in BP leading to vascular damage, commonly fibrinoid necrosis + bilateral retinal haemorrhages + exudates ± papilloedema.
  • Severe HTN >200/130mmHg.
  • Commonly symptoms like headache ± visual loss in younger, black patients.
  • URGENT TREATMENT.
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82
Q

HYPERTENSION

Explain what white coat HTN is.

A
  • Elevated clinical BP with a normal ambulatory blood pressure monitoring (ABPM) BP.
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83
Q

HYPERTENSION

What is suspected HTN in clinic and how do you confirm this?

A
  • Suspected is clinical BP ≥140/90mmHg.
  • Confirmed by using ambulatory blood pressure monitoring or multiple home BP measuring.
  • Helps with white coat HTN/borderline.
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84
Q

HYPERTENSION

How is HTN classified?

A 
Clinical BP...
Stage 1 = 140/90mmHg.
Stage 2 = 160/100mmHg.
Severe = 180/110mmHg.
ABPM...
Stage 1 = 135/85mmHg.
Stage 2 = 150/95mmHg.
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85
Q

HYPERTENSION

What is the first line treatment for HTN?

A

Primary prevention…

  • Smoking + alcohol cessation.
  • Low-fat + reduced salt intake.
  • Increased exercise, weight loss.
  • Treat underlying cause.
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86
Q

HYPERTENSION

What two systems are targeted in anti-hypertensive medications?

A
  • RAAS + sympathetic nervous system.
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87
Q

HYPERTENSION
What BP reading would mean you have to treat this patient immediately with anti-hypertensives, even before lifestyle advice?

A
  • BP >160/100mmHg.

- Only consider starting medication if >140/90mmHg.

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88
Q 
HYPERTENSION
What are the clinical/ABPM blood pressure targets for...
i) Under 80.
ii) Over 80.
iii) Diabetics
A

i) CBP = <140/90mmHg, ABPM = <135/85mmHg.
ii) CBP = <150/90mmHg, ABPM = <145/85mmHg.
iii) CBP = <130/80mmHg.

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89
Q 
HYPERTENSION
What is the first line medication for...
i) Under 55s.
ii) Over 55s.
iii) Afro-Caribbean any age.
A

i) ACEi or ARB if C/I like lisinopril or candesartan.
ii) CCB like amlodipine.
iii) CCB like amlodipine.

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90
Q

HYPERTENSION

What are the second + subsequent treatments for HTN?

A
  • 2nd step = Add ACEi/ARB or CCB.
  • 3rd step = add thiazide-like diuretic.
  • Consider addition of any other medications like beta blockers, K+-sparring diuretics.
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91
Q 
SINUS TACHYCARDIA
What is the...
i) Pathophysiology
ii) Aetiology
iii) Treatment

of sinus tachycardia?

A

i) HR >100bpm with a normal P wave, followed by a normal QRS complex – not an arrythmia.
ii) Physiological response to exercise + excitement.
Can be due to fever, anaemia, thyrotoxicosis, acute PE.
iii) Treat underlying cause, beta blockers used to slow sinus rate.

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92
Q

SUPRAVENTRICULAR TACHYS

What is the pathophysiology of Atrioventricular re-entrant tachycardia (AVRT)?

A
  • Due to presence of an accessory pathway where congenital myocardial fibres connecting the ventricles + atria, which can lead to pre-excitation of ventricles.
  • Wolff-Parkinson-White syndrome is best-known type of aVRT in which there is an accessory pathway (Bundle of Kent) between atria + ventricles.
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93
Q

SUPRAVENTRICULAR TACHYS
What is the pathophysiology of Atrioventricular node re-entrant tachycardia (AVNRT)? What are the risk factors that can aggravate the arrhythmia?

A
  • Commonest supraventricular tachycardia.
  • Circuits form within AVN causing narrow complex tachycardias.
  • Atrial impulse carried by slow pathway to ventricles but can also travel back up fast pathway to signal back down slow pathway.
  • Exertion, emotional stress, caffeine.
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94
Q

SUPRAVENTRICULAR TACHYS

What are the symptoms of AVRT/AVNRT?

A
  • Rapid regular palpitations with abrupt onset/offset.
  • Dyspnoea.
  • Chest pain.
  • Jugular venous pulsation.
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95
Q

SUPRAVENTRICULAR TACHYS
What does the ECG show in…
i) Wolff-Parkinson-White syndrome?
ii) AVNRT?

A

i) Short PR, broad QRS, delta waves (slurred upstroke to QRS).
ii) P waves hidden as embedded in QRS, QRS normal or wide.

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96
Q

SUPRAVENTRICULAR TACHYS

What is the acute treatment for AVRT/AVNRT?

A
  • Increase vagal stimulation of sinus node by Valsalva manoeuvre (ask patient to blow into 20mL syringe with enough force to push plunger back).
  • Adenosine (short acting AVN blocking drug that will terminate most junctional tachycardias).
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97
Q

SUPRAVENTRICULAR TACHYS

What is the long term treatment for AVRT/AVNRT?

A
  • Radiofrequency ablation of accessory pathway via a cardiac catheter.
  • Flecainide, verapamil + amiodarone commonly used.
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98
Q

SUPRAVENTRICULAR TACHYS

What is the treatment for haemodynamically unstable patients?

A
  • Emergency DC cardioversion.
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99
Q

SUPRAVENTRICULAR TACHYS

What is the pathophysiology of atrial fibrillation?

A
  • AF is a chaotic, irregular atrial rhythm at 300-600bpm where the AVN responds intermittently as it’s unable to keep up, hence an irregular ventricular rhythm.
  • CO drops by 10–20% as ventricles aren’t primed reliably by atria contributing to heart failure.
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100
Q

SUPRAVENTRICULAR TACHYS

What is the aetiology of atrial fibrillation?

A
  • HTN.
  • IHD.
  • Thyrotoxicosis.
  • Mitral valve disease.
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101
Q

SUPRAVENTRICULAR TACHYS

What are the symptoms of atrial fibrillation?

A
  • Palpitations.
  • Dyspnoea.
  • Syncope.
  • Chest pain.
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102
Q

SUPRAVENTRICULAR TACHYS

What are the signs of atrial fibrillation?

A
  • Irregularly irregular pulse.
  • 1st heart sound of variable intensity.
  • Signs of LVF.
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103
Q

SUPRAVENTRICULAR TACHYS

What is the main complication with atrial fibrillation and how is this calculated?

A
  • Embolic stroke caused by stagnation of blood in atria due to ineffective mechanical action of atria leading to thrombus formation.
  • Calculated initially by the CHADS2 score + if score >2 then CHA2DS2-VASc score.
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104
Q

SUPRAVENTRICULAR TACHYS

What are the components of the CHA2DS2-VASc score?

A 
Congestive cardiac failure (1)
HTN (1)
A2 (≥75 = 2 or 1 in first system, 64-75 = 1)
Diabetes(1)
S2troke/TIA (2)
Vascular disease (1)
Sex Category female (1)
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105
Q

SUPRAVENTRICULAR TACHYS

What CHA2DS2-VASc score warrants anti-coagulation?

A

1 = consider, 2 = anti-coagulate.

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106
Q

SUPRAVENTRICULAR TACHYS

What investigations would you do in someone with atrial fibrillation?

A

ECG.

- Absent P waves, irregular QRS complexes, F waves, irregularly irregular.

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107
Q

SUPRAVENTRICULAR TACHYS

What is the main goals in treatment of atrial fibrillation?

A
  • Rate control + anti-coagulation.
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108
Q

SUPRAVENTRICULAR TACHYS

How can rate control be achieved in atrial fibrillation?

A
  • Beta blocker or rate-limiting calcium channel blockers (verapamil, diltiazem).
  • Digoxin.
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109
Q

SUPRAVENTRICULAR TACHYS

How can anti-coagulation be achieved in atrial fibrillation?

A
  • Warfarin whilst maintaining international normalised ratio (INR) 2.0–3.0.
  • DOACs like apixaban, no INR testing.
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110
Q

SUPRAVENTRICULAR TACHYS

How can rhythm control be achieved in atrial fibrillation?

A
  • Elective DC cardioversion.
  • Elective pharmacological cardioversion with amiodarone (if underlying heart disease) or flecainide (if no underlying heart disease).
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111
Q

SUPRAVENTRICULAR TACHYS

What is the long term treatment of atrial fibrillation?

A
  • Catheter ablation.

- Pacemaker.

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112
Q 
SUPRAVENTRICULAR TACHYS
What is the...
i) Pathophysiology
ii) Investigations
iii) Treatment

for atrial flutter?

A

i) Associated with aF, follows the re-entry mechanisms where there is a blockage of normal circuit + so another pathway forms, takes different course + re-enters circuit.
- Atrial rate about 300bpm + AVN usually conducts every 2nd flutter beat so ventricular rate of 150bpm.
ii) ECG – sawtooth flutter (F) waves, narrow QRS.
iii) Radiofrequency catheter ablation of re-entry circuit, similar treatments as AF.

113
Q

VENTRICULAR TACHYARRYTHMIAS

What is the pathophysiology of ventricular extrasystoles?

A
  • Very common, generally benign arrhythmias caused by premature discharge.
  • Frequent ectopics (>60/h) particularly couplets/triplets should prompt testing for underlying cardiac conditions.
  • Bigeminy/trigeminy = ectopic every other/third beat.
  • Couplet/triplet = two/three ectopics together.
114
Q 
VENTRICULAR TACHYARRYTHMIAS
What is the...
i) Clinical presentation
ii) Investigations
iii) Treatment

of ventricular extrasystoles?

A

i) Palpitations, thumping sensation, feeling of heart missing beat, frequent ectopics might give irregular pulse.
ii) Broad QRS with bizarre configuration.
iii) Beta-blockers if symptomatic.

115
Q 
VENTRICULAR TACHYARRYTHMIAS
What is the...
i) Pathophysiology
ii) Aetiology
iii) Clinical presentation
iv) Investigations
(v) Treatment

for long QT syndrome?

A

i) Ventricular repolarisation (QT interval) greatly prolonged.
ii) Congenital (mutations in Na+/K+ channel genes), electrolyte disturbances, drugs like tricyclic antidepressants, amiodarone.
iii) Palpitations, syncope.
iv) Prolonged QT interval, polymorphic VT (Torsade de pointes) = rapid irregular sharp QRS, usually terminate randomly but can –> VF.
v) Treat underlying cause, stop drugs.

116
Q

VENTRICULAR TACHYARRYTHMIAS

What is the pathophysiology of ventricular tachycardia + ventricular fibrillation?

A
  • VT + VF associated with underlying heart disease.
  • VF is very rapid + irregular ventricular activation with no mechanical effect so no CO – patient pulseless, rapidly unconscious + goes into cardiac arrest.
117
Q

VENTRICULAR TACHYARRYTHMIAS
What are the…
i) ECG traces
ii) Treatment

for VT/VF?

A

i) VT = rapid ventricular rhythm, broad abnormal QRS, VF = completely irregular, rapid rhythm, fibrillation.
ii) VT = emergency DC cardioversion, IV beta-blockers + implanted cardioverter-defibrillator (ICD) if no haemodynamic compromise, VF = immediate defibrillation, if resuscitated ICD.

118
Q 
SINUS BRADYCARDIA
What is the...
i) Pathophysiology.
ii) Aetiology.
iii) Treatment

for sinus bradycardia?

A

i) HR <60bpm with normal P wave followed by normal QRS, not an arrhythmia.
ii) Physical fitness, drugs like beta-blockers, amiodraone, sick sinus syndrome, acute ischaemia/infarction of sinus node.
iii) If extrinsic, treat underlying cause. If intrinsic, atropine first-line and then permanent cardiac pacemaker.

119
Q

SINUS BRADYCARDIA

What is sick sinus syndrome? What does the ECG show + what is the treatment?

A
  • Bradycardia caused by intermittent failure of SAN depolarisation due to failure of sinus node to propagate to the atria (sinoatrial block).
  • ECG = severe sinus bradycardia or intermittent long pauses between consecutive P waves .
  • If symptomatic = permanent pacemaker insertion.
120
Q

ATRIOVENTRICULAR BLOCK

What is the pathophysiology of AV block?

A
  • Due to disrupted passage of electrical impulses through the AVN as a result of a blockage in the AVN or His bundle.
121
Q 
ATRIOVENTRICULAR BLOCK
Explain what...
i) First degree AV block
ii) Second degree AV block
iii) Third degree AV block

consist of.

A

i) Delayed AV conduction causing fixed prolongation of PR intervals.
ii) Some atrial impulses fail to reach ventricles causing there to be more P waves to QRS.
Mobitz I = block generally caused by AVN block.
Mobitz II = block at an intra-nodal level.
iii) Complete heart block, all of the atrial activity fails to conduct to the ventricles. Ventricular contractions are maintained by spontaneous escape rhythm from below site of block.

122
Q

ATRIOVENTRICULAR BLOCK

What are the aetiologies of AV block?

A 
First + second...
- Normal variant, athletes.
- IHD, acute myocarditis.
Third...
- Fibrosis of conducting tissue (elderly), cardiac surgery/trauma.
123
Q

ATRIOVENTRICULAR BLOCK

What is the clinical presentation of AV block?

A
  • 1st = bradycardia, often asymptomatic.
  • 2nd = bradycardia, ?dizziness/syncope
  • 3rd = bradycardia, if site of block is His-Purkinje system can be Stokes-Adams attacks (dizziness + blackouts).
124
Q

ATRIOVENTRICULAR BLOCK

What are the complications with AV block?

A
  • 2nd Mobitz II = dangerous rhythm as can progress to complete heart block.
  • 3rd = tissue distal to AVN paces slowly, patient becomes v bradycardia + may develop haemodynamic compromise.
125
Q 
ATRIOVENTRICULAR BLOCK
What does the ECG show for
i) First degree
ii) Second degree, Mobitz I
iii) Second degree, Mobitz II

AV block.

A

i) Prolonged PR interval >200ms, no missed beats.
ii) Progressively increasing P-R intervals until dropped QRS complex as AVN fails, pattern repeats (Wenckebach phenomenon)
iii) Sustained P-R intervals with occasional dropped QRS due to loss of AV conduction with ratio of AV conduction varying from 2/3:1, widened QRS.

126
Q

ATRIOVENTRICULAR BLOCK

What does the ECG show for third degree AV block?

A

No impulses passed from atria to ventricles + so P waves + QRS appear independently of each other, complete dissociation.

  • His bundle block = narrow complex (<0.12s).
  • His-Purkinje system block = broad complex (>0.12s).
127
Q

ATRIOVENTRICULAR BLOCK

What’s the treatment for AV block?

A
  • 1st = none.
  • 2nd = monitoring, ?pacemaker.
  • 3rd = His bundle block = may respond to atropine if not permanent pacemaker, Purkinje system block = permanent pacemaker.
128
Q

BUNDLE BRANCH BLOCK

What is the pathophysiology of bundle branch block, including the 2 types?

A
  • Complete block of a bundle branch.
  • LBBB = left bundle branch no longer conducts an impulse + the two ventricles do not receive an impulse simultaneously (right first).
  • RBBB = right bundle branch no longer conducts an impulse + the two ventricles do not receive an impulse simultaneously (left first).
129
Q

BUNDLE BRANCH BLOCK

What is the aetiology + clinical presentation of bundle branch block?

A
  • IHD, pulmonary embolism, right ventricular hypertrophy.

- Asymptomatic or syncope.

130
Q

BUNDLE BRANCH BLOCK

What do the ECGs show for LBBB + RBBB?

A

LBBB = WiLLiaM…
- Slurred S wave (V1/2), W pattern in V1 + second R wave in left ventricular leads (I, AVL + V4–6), M pattern in V6.
RBBB = MaRRoW…
- Second R wave (V1), M pattern + Slurred S wave (V5/6), W pattern.

131
Q

AORTIC ANEURYSM

What is the pathophysiology of an aortic aneurysm?

A
  • An artery with a dilatation >50% of its original diameter.
  • True aneurysm = abnormal dilatations that involve ALL layers of the arterial wall.
  • False/pseudo aneurysms = involve a collection of blood in the adventitia (outer layer) ONLY which communicates with the lumen (e.g. after trauma).
132
Q

AORTIC ANEURYSM

Explain what abdominal + thoracic aortic aneurysms are.

A
  • Both can spontaneously rupture.
  • Abdominal is degradation of the elastic lamellae, leukocytic infiltrate, enhanced proteolysis + smooth muscle cell loss.
  • Thoracic is inflammation, proteolysis + reduce survival of smooth muscle cells.
133
Q

AORTIC ANEURYSM

What is the aetiology of aortic aneurysms?

A
  • Abdominal = trauma, infection, atheroma.

- Thoracic = strong genetic link with connective tissue disorders.

134
Q

AORTIC ANEURYSM

What are the risk factors for aortic aneurysms?

A
  • HTN.
  • Family Hx.
  • Atherosclerotic damage.
  • Smoking.
  • COPD.
  • Male gender – screening offered to men 65–74y/o.
135
Q

AORTIC ANEURYSM

What is the clinical presentation of aortic aneurysms?

A

Abdominal…
- Unruptured = none, may be abdominal/back pain.
- Ruptured = intermittent or continuous abdominal pain radiates to back, iliac fossae or groins, collapse, expansile abdominal mass + shock.
Thoracic…
- Unruptured = none, chest/neck pain, symptoms related to compression of structures (cough, dysphagia).
- Ruptured = acute pain, collapse, shock + sudden death.

136
Q

AORTIC ANEURYSM

What investigations would you do in someone with suspected aortic aneurysm?

A
  • Abdominal = only investigate unruptured via ultrasound.
  • Thoracic = if unruptured, ECG, ultrasound, lung function tests, blood tests (FBC, clotting screen, renal function), if ruptured = ECG + CT with contrast.
137
Q

AORTIC ANEURYSM

What is the treatment for aortic aneurysms?

A
  • Unruptured = surgical repair/insertion of supportive stents.
  • Ruptured = immediate surgical repair.
138
Q

AORTIC DISEECTION

What is the pathophysiology of aortic dissection?

A
  • Starts with a tear in the tunica intima of the aortic lining allowing blood to enter between the layers of the aortic wall under pressure.
  • Forms haematoma which separates the intima from the adventitia + creates a false lumen, variable distance in either direction.
139
Q

AORTIC DISEECTION

What are the most common sites for aortic dissections?

A
  • Within 2–3cm of the aortic valve or distal to the left subclavian artery in the descending aorta.
140
Q

AORTIC DISEECTION

What are the Stanford types/DeBakey system for aortic dissection?

A

Stanford…
- Type A (70%) = dissections involving the ascending aorta, irrespective of site of tear.
Type B (30%) = dissections that do not involve the ascending aorta.
DeBakey…
Type I = originates in ascending aorta + propagates at least to aortic arch.
Type II = originates + confined to ascending aorta.
Type III = originates in descending aorta.

141
Q

AORTIC DISEECTION

What is the aetiology of aortic dissection?

A
  • Genetic link.
  • Atherosclerosis.
  • Inflammation, trauma.
142
Q

AORTIC DISEECTION

What are the risk factors for aortic dissection?

A
  • Cocaine use.
  • Aortic aneurysm.
  • Smoking.
  • Hypercholesterolaemia.
143
Q

AORTIC DISEECTION

What is the clinical presentation of aortic dissection?

A

Phase 1…
- Initial event with severe tearing chest pain (± radiation to back) + pulse loss, bleeding stops.
Diastolic murmur phase 2…
- Pressure builds + causes rupture either into pericardium (potentially causing tamponade), mediastinum or pleural space.
- Pain often migrates as dissection progresses.

144
Q

AORTIC DISEECTION

What is the investigation and treatment for aortic dissection?

A
  • CT scan/transoesophageal echocardiography (TOE) is diagnostic + confirmational.
  • Anti-hypertensives, stentgraft, surgery if dissection progression.
145
Q

PERIPHERAL VASCULAR DISEASE

What is the pathophysiology of peripheral vascular disease?

A

The atherosclerosis causes the narrowing/stenosis of the vessels distal to the aortic arch with the potential of blockage/spasm causing occlusion.

146
Q

PERIPHERAL VASCULAR DISEASE

What are the risk factors for peripheral vascular disease?

A
  • HTN.
  • Hyperlipidaemia.
  • Diabetes mellitus.
  • Smoking.
  • Obesity.
147
Q

PERIPHERAL VASCULAR DISEASE

What are the symptoms of peripheral vascular disease?

A
  • Intermittent claudication due to stress-induced ischaemia (muscle cramps due to increased anaerobic metabolism, lactic acid, on walking in calf/thigh/buttock).
  • Pain relieved with rest.
  • Ulceration, gangrene.
  • Burning pain at night relieved by hanging leads over side of bed (critical limb ischaemia).
148
Q

PERIPHERAL VASCULAR DISEASE

What is critical limb ischaemia?

A
  • Ischaemia due to structural/functional breakdown where the blood supply is barely adequate for basal metabolism so there is no reserve for an increased demand, oxygen supply is low even at rest.
149
Q

PERIPHERAL VASCULAR DISEASE

What are the 6 signs of acute limb ischaemia?

A
  • Pulseless.
  • Pale.
  • Pain.
  • Paralysis.
  • Paraesthesia.
  • Perishing cold.
150
Q

PERIPHERAL VASCULAR DISEASE

What are the signs of peripheral vascular disease?

A
  • Absent femoral, popliteal or foot pulses.
  • Cold, white legs.
  • Punched out ulcers.
  • Buerger’s angle (angle that leg goes pale when raised off couch) of <20 degrees.
151
Q

PERIPHERAL VASCULAR DISEASE

What are the investigations for peripheral vascular disease?

A
  • Exclude DM, arteritis.
  • Colour duplex ultrasound first line, shows blood vessels + blood flow.
  • Ankle-brachial pressure index (ABPI) normal = 1–1.2, PVD = 0.5–0.9
  • MR/CT angiography for extent + location of stenoses.
152
Q

PERIPHERAL VASCULAR DISEASE

What is the treatment for peripheral vascular disease?

A 
Risk factor modification...
- Exercise + weight reduction, smoking cessation.
- Control of HTN, DM, high cholesterol.
Medications...
- Anti-platelets, clopidogrel.
Surgery...
- Percutaneous transluminal angioplasty if severe.
- Amputation at worst.
153
Q

INFECTIVE ENDOCARDITIS

What is the pathophysiology of IE?

A
  • Infection of heart valve/s or other endocardial lined structures within the heart such as septal defects, pacemaker leads + surgical patches.
  • A mass of fibrin, platelets + infectious organisms form vegetations along the edges of the valve.
  • Virulent organisms destroy the valve, producing regurgitation + worsening heart failure.
154
Q

INFECTIVE ENDOCARDITIS

What is the aetiology of IE?

A
  • Streptococcus viridans, staphylococcus aureus + enterococci are common causes.
155
Q

INFECTIVE ENDOCARDITIS

What are the risk factors and complciations with IE?

A
  • Aortic/mitral valve disease, prosthetic valves or implanted devices, structural heart defects.
  • Large vegetations can embolise + cause a stroke/MI if not removed.
156
Q

INFECTIVE ENDOCARDITIS

What are is the typical clinical presentation in someone with IE?

A
  • Septic signs – fever, rigors, night sweats, malaise.

- Cardiac lesions – valve dysfunction, new murmur/change in pre-existing murmur.

157
Q

INFECTIVE ENDOCARDITIS

What specific immune complex deposition presentations are seen in IE?

A
  • Splinter haemorrhages (under nailbeds).
  • Osler’s nodes (painful pulp infarcts in fingers/toes).
  • Roth spots (boat-shaped retinal haemorrhage) + soft exudates (retinal infarcts).
  • Janeway lesions (non-tender lesions on finger, palm or sole).
158
Q

INFECTIVE ENDOCARDITIS

What investigations are used for someone suspected of IE?

A
  • A fever + new murmur = IE until proven otherwise.
  • Blood cultures before antibiotics.
  • Transthoracic echocardiography/Transoesophageal echocardiography (TTE/TOE).
  • Duke’s modified criteria.
159
Q

INFECTIVE ENDOCARDITIS

What is the Duke’s modified criteria used for?

A
  • Criteria used to diagnose IE.

- 2x major, 1x major + 3 minor or 5x minor.

160
Q

INFECTIVE ENDOCARDITIS

What is the major + minor criteria for the Duke’s modified criteria?

A 
Major...
- +ve blood cultures.
- Evidence of endocardial involvement, +ve TTE/TOE.
Minor...
- Predisposition.
- Fever.
- Vascular phenomena.
- Immune phenomena.
- +ve blood culture doesn't meet major criteria.
161
Q

INFECTIVE ENDOCARDITIS

What is the treatment for IE?

A
  • IV antimicrobial for around 6 weeks based on culture sensitivities.
  • Surgery if heart failure, persistent bacteraemia.
162
Q

ACUTE PERICARDITIS

What is the pathophysiology of acute pericarditis?

A
  • Inflammatory pericardial syndrome ± effusion.
163
Q

ACUTE PERICARDITIS

What is the aetiology of pericarditis?

A
  • Viral (common) – esp. Coxackie B, EBV.
  • Bacterial – TB, pneumonia., staph, strep.
  • Autoimmune like rheumatoid arthritis, SLE.
  • Post-MI (Dressler’s).
164
Q

ACUTE PERICARDITIS

What is the symptoms of pericarditis?

A
  • Sharp central chest pain, pleuritic, worse lying flat.
  • Chest pain relieved by sitting forward.
  • Dypnoea, cough, hiccups (phrenic nerve irritation).
165
Q

ACUTE PERICARDITIS

What are the signs of pericarditis?

A
  • Pericardial friction rub.
  • Fever.
  • Tachycardia + tachypnoea.
166
Q

ACUTE PERICARDITIS

What investigations would you do in someone with suspected pericarditis?

A 
- Rule out major DDx of MI.
Bloods...
- FBC, U+E, cardiac enzymes.
ECG...
- Concave, saddle-shaped ST segment elevation, PR depression.
CXR...
- ?Pericardial effusion
Echocardiogram...
- If suspected pericardial effusion.
167
Q

ACUTE PERICARDITIS

What is the treatment for pericarditis?

A
  • NSAIDs to manage inflammation + pain.
  • Colchicine for inflammation
  • Corticosteroids.
168
Q

CONSTRICTIVE PERICARDITIS

What is the pathophysiology + aetiology of constrictive pericarditis?

A
  • Chronic inflammation of the pericardium begins to cause damage, calcify + thicken thus reducing space for the heart + so affecting function.
  • Idiopathic/result from intrapericardial haemorrhage during surgery, TB.
169
Q

CONSTRICTIVE PERICARDITIS

What is the clinical presentation of constrictive pericarditis?

A
  • Raised JVP.
  • Kussmaul’s sign (JVP rising paradoxically with inspiration).
  • Peripheral oedema, dyspnoea.
170
Q

CONSTRICTIVE PERICARDITIS

What investigations and treatment would you do for constrictive pericarditis?

A
  • CXR = small heart ± pericardial calcification.
  • CT/MRI = diagnostic showing pericardial thickening + calcification.
  • Cardiac catheterisation can distinguish from effusive pericarditis.
  • Surgical excision of thickened pericardium.
171
Q

PERICARDIAL EFFUSION

What is the pathophysiology + aetiology of pericardial effusion?

A
  • Infection of the pericardium causing a build-up of fluid.

- Pericarditis, myocardium rupture (haemopericardium due to surgery, stab-wound or post-MI).

172
Q

PERICARDIAL EFFUSION

What is the clinical presentation of pericardial effusion?

A
  • Dyspnoea.
  • Chest pain.
  • Signs of local structures being compressed (hiccups).
  • Muffled heart sounds.
173
Q

PERICARDIAL EFFUSION

What is the major complication with pericardial effusion and how does it present?

A
  • Cardiac tamponade.
  • Clinical presentation is Beck’s triad of hypotension (pulsus paradoxus, BP drops >10mmHg), rising JVP + muffled heart sounds.
174
Q

PERICARDIAL EFFUSION

How can cardiac tamponade be diagnosed + treated?

A
  • Echocardiogram showing echo-free zone surrounding heart.

- Urgent drainage via pericardiocentesis.

175
Q

PERICARDIAL EFFUSION

What investigations + treatment would you do for someone suspected of having pericardial effusion?

A
  • CXR = enlarged, globular heart if effusion >300mL.
  • ECG = low voltage QRS.
  • Echocardiogram = echo-free zone surrounding heart.
  • Pericardiocentesis can be diagnostic, treat underlying cause.
176
Q

AORTIC STENOSIS

What is the pathophysiology of aortic stenosis?

A
  • Aortic valve is thickened/calcified which obstructs LV outflow causing increased LV pressure as the LV cannot eject blood properly in systole causing a pressure gradient between LV + aorta.
  • Leads to compensatory LV hypertrophy due to increased afterload.
177
Q

AORTIC STENOSIS

What is the aetiology of aortic stenosis?

A
  • Degeneration + calcification of normal valve (elderly).
  • Calcification of congenital bicuspid valve (middle-age).
  • Rheumatic heart disease.
178
Q

AORTIC STENOSIS

What are the symptoms of aortic stenosis?

A

SADS…

  • Syncope (exertional).
  • Angina.
  • Dsypnoea.
  • Sudden death.
179
Q

AORTIC STENOSIS

What are the signs of aortic stenosis?

A
  • Pulsus tardus (slow rising carotid pulse).
  • Pulsus parvus (decreased pulse amplitude).
  • Ejection systolic murmur < > character.
180
Q

AORTIC STENOSIS

What investigations would you do for aortic stenosis?

A
  • ECG = signs of LVH.
  • CXR shows LVH + calcified aortic valve.
  • Echocardiogram is diagnostic.
181
Q

AORTIC STENOSIS

What is the treatment for aortic stenosis?

A
  • General = good dental hygiene.
  • Surgical aortic valve replacement for anyone symptomatic, with decreasing EF or undergoing CABG.
  • If unfit for surgery, transcatheter aortic valve implantation (TAVI).
182
Q

AORTIC REGURGITATION

What is the pathophysiology of aortic regurgitation?

A
  • Regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.
  • Combined pressure + volume overload where compensatory mechanisms are LV dilation, LVH + this progressive dilation leads to heart failure.
183
Q

AORTIC REGURGITATION

What are the aetiologies of aortic regurgitation?

A
  • Bicuspid aortic valve.
  • Rheumatic heart disease.
  • Infective endocarditis.
184
Q

AORTIC REGURGITATION

What are the symptoms of aortic regurgitation?

A
  • Exertional dyspnoea.
  • Orthopnoea (SOB when lying flat).
  • Palpitations.
185
Q

AORTIC REGURGITATION

What are the signs of aortic regurgitation?

A
  • A collapsing (water-hammer) pulse.
  • Wide pulse pressure.
  • Early diastolic murmur.
186
Q

AORTIC REGURGITATION

What investigations would you do for aortic regurgitation?

A
  • CXR = cardiomegaly + aortic root enlargement.

- Echocardiogram = diagnostic.

187
Q

AORTIC REGURGITATION

What is the treatment for aortic regurgitation?

A
  • ACEi for symptoms or to reduce systolic HTN.

- Surgical aortic valve replacement if symptomatic, EF <50% or LV dilatation.

188
Q

MITRAL STENOSIS

What is the pathophysiology of mitral stenosis?

A
  • Obstruction of LV inflow that prevents proper filling during diastole.
  • Left atria dilation leads to pulmonary congestion (reduced emptying), which is worse with exercise, fever.
  • Increased transmitral pressures leads to LA enlargement + atrial fibrillation.
  • Pulmonary venous HTN causes RHF symptoms.
189
Q

MITRAL STENOSIS

What are the aetiologies for mitral stenosis?

A
  • Rheumatic heart disease.
  • Infective endocarditis.
  • Mitral annular calcification.
  • Congenital – Marfan’s + Ehlers-Danlos (connective tissue disorders).
190
Q

MITRAL STENOSIS

What are the symptoms of mitral stenosis?

A
  • Dyspnoea.
  • Haemoptysis (bronchial vessels rupture due to pulmonary pressure).
  • RHF symptoms like peripheral oedema.
191
Q

MITRAL STENOSIS

What are the signs of mitral stenosis?

A
  • Malar flush on cheeks.
  • Loud opening S1.
  • Rumbling mid-diastolic murmur.
192
Q

MITRAL STENOSIS

What investigations would you do for mitral stenosis?

A
  • ECG = atrial fibrillation + LA enlargement.
  • CXR = LA enlargement.
  • Echocardiogram = gold standard.
193
Q

MITRAL STENOSIS

What is the treatment for mitral stenosis?

A
  • Rate control if AF.
  • Anticoagulate with warfarin.
  • Diuretics to reduce preload + pulmonary venous congestion.
  • Percutaneous balloon valvotomy or valvuloplasty.
194
Q

MITRAL REGURGITATION

What is the pathophysiology of mitral regurgitation?

A
  • Backflow of blood from the LV to LA during systole.
  • LA volume overload results in compensatory increased LA enlargement + increased pulmonary pressure leading to pulmonary oedema.
195
Q

MITRAL REGURGITATION

What is the aetiology of mitral regurgitation?

A
  • Prolapsing mitral valve (commonest in developed world).
  • Rheumatic disease (commonest in developing world).
  • Infective endocarditis.
196
Q

MITRAL REGURGITATION

What are the symptoms of mitral regurgitation?

A
  • Exertional dyspnoea.
  • Fatigue.
  • Palpitations.
197
Q

MITRAL REGURGITATION

What are the signs of mitral regurgitation?

A
  • Pansystolic murmur at apex radiating to axilla.
  • Displaced hyperdynamic apex.
  • Soft S1.
  • ?Atrial fibrillation
198
Q

MITRAL REGURGITATION

What are the investigations for mitral regurgitation?

A

ECG = LA enlargement, AF + LVH.

  • CXR = LA + LV enlargement, central pulmonary artery enlargement.
  • Echocardiogram = diagnostic.
199
Q

MITRAL REGURGITATION

What are the treatments for mitral regurgitation?

A
  • Rate control + anticoagulation for AF using beta-blockers, CCBs, digoxin.
  • Vasodilator like ACEi.
  • Diuretics for fluid overload.
  • Surgical valve repair/replacement.
200
Q

SHOCK

Define shock.

A
  • Circulatory failure resulting in inadequate organ perfusion defined by hypotension (<90mmHg systolic) with evidence of tissue hypoperfusion (mottled skin, reduced urine output).
201
Q 
SHOCK
What is...
i) Anaphylactic
ii) Cardiogenic
iii) Haemorrhagic

shock?

A

i) Intense allergic reaction associated with major histamine release causing haemodynamic collapse.
ii) Cardiac dysfunction leads to inability to perfuse organs + tissue leading to acute hypoperfusion + hypoxia of tissues + organs despite adequate intravascular volume.
iii) Bleeding results in hypovolaemia + so lower SV causing decreased CO + so hypoperfusion.

202
Q

SHOCK
What is…
i) Neurogenic.
ii) Septic

shock?

A

i) Trauma causes a sudden loss of background sympathetic stimulation to blood vessels causing sudden vasodilation + so a sudden drop of BP. Sympathetic tone loss leads to pooling of blood in extremities.
ii) A systemic inflammatory response associated with bacterial infection (endotoxins) which can damage blood vessels causing them to leak fluid into surrounding tissues.

203
Q 
SHOCK
What are the aetiologies of these types of shock...
i) Anaphylactic?
ii) Cardiogenic?
iii) Haemorrhagic?
iv) Neurogenic?
v) Septic?
A

i) Type 1 IgE mediated hypersensitivity reaction caused by allergens (seafood, nuts, eggs, stings, drugs).
ii) Cardiac tamponade, acute MI, PE.
iii) Loss of blood (acute GI bleeding, trauma, splenic rupture) or loss of fluid (dehydration, burns).
iv) Spinal cord injury, epidural/spinal anaesthesia.
v) Infection with organism.

204
Q 
SHOCK
What is are the symptoms of these types of shock...
i) Anaphylactic?
ii) Cardiogenic?
iii) Haemorrhagic?
iv) Neurogenic?
v) Septic?
A

i) Wheeze + dyspnoea, rash, swollen lips/tongue.
ii) Chest pain + palpitations, nausea, syncope.
iii) Shallow breathing, sweating + anxiety.
iv) Instantaneous hypotension, warm flushed skin.
v) Dizziness/confusion, cold clammy skin w/ fever, tachypnoea.

205
Q

SHOCK

What are the signs of shock?

A
  • Reduced GCS/agitation.
  • Pallor, mottled skin + cold peripheries.
  • Tachypnoea.
  • Bradycardia in neurogenic shock.
  • Oliguria.
206
Q

SHOCK

What investigations would you do for the different types of shock?

A 
Cardiogenic –
- Bloods like FBC, U+E, troponin, echocardiogram.
Haemorrhagic –
- U+Es, ultrasound.
Neurogenic –
- FBC, U+Es, CT scan.
Septic –
- FBC, U+Es, lactate.
207
Q 
SHOCK
What is the treatment for these types of shock...
i) Anaphylactic?
ii) Cardiogenic?
iii) Haemorrhagic?
iv) Neurogenic?
v) Septic?
A

i) Adrenaline, chlorphenamine + hydrocortisone, wheeze = treat for asthma, supportive like oxygen, fluid replacement.
ii) Treat underlying cause, IV diamorphine for pain.
iii) Stop bleeding, oxygen + IV fluids.
iv) Inotropic (dopamine), vasopressin + vasopressors.
v) Oxygen therapy, vasopressors, cultures, IV fluids/antibiotics.

208
Q

ATRIAL SEPTAL DEFECT

What is the pathophysiology of ASD?

A
  • Hole connects the atria as there is failure of the septal tissue to form.
  • L>R shunt forms as LAp>RAp meaning increased flow into right heart + lungs.
209
Q

ATRIAL SEPTAL DEFECT

What are the 2 types of ASD?

A

Ostium primum…
- Associated with AV valve anomalies (downs syndrome), presents in childhood, opposing the endocardial cushions.
Ostium secundum…
- Hole is high in septum, presents middle age.
- Often asymptomatic until adulthood when L>R shunt develops as LV compliance decreases with age.

210
Q

ATRIAL SEPTAL DEFECT

What is the main complication with ASD?

A

Eisenmenger’s syndrome…

  • The inital L>R shunt leads to pulmonary HTN which increases right heart pressures until they exceed left heart pressure causing a shunt reversal.
  • There is cyanosis due to deoxygenated blood entering systemic circulation.
  • Risk of death, endocarditis + stroke.
211
Q

ATRIAL SEPTAL DEFECT

What is the clinical presentation of ASD?

A
  • Dyspnoea, palpitations, chest pain.

- Pulmonary HTN, pulmonary systolic flow murmur.

212
Q

ATRIAL SEPTAL DEFECT

What investigations would you do for ASD?

A
  • ECG = RBBB with left (primum) or right (secundum) axis deviation.
  • CXR = atrial enlargement.
213
Q

ATRIAL SEPTAL DEFECT

What is the treatment for ASD?

A
  • May close spontaneously.
  • Primum defects closed in childhood, secundum if symptomatic or signs of RV overlaod.
  • Transcatheter closure>surgical.
214
Q

VENTRICULAR SEPTAL DEFECT

What is the pathophysiology + aetiology + complication of VSD?

A
  • A hole connects the ventricles + as LVp>RVp there is a L>R shunt.
  • Congenital, can be aquired (post MI).
  • Eisenmenger’s syndrome, infective endocarditis.
215
Q

VENTRICULAR SEPTAL DEFECT

What is the clinical presentation of VSD?

A
  • Dyspnoea, poor feeding, failure to thrive.
  • Smaller holes = louder murmurs, pan-systolic murmur.
  • Tacyhpnoea.
216
Q

VENTRICULAR SEPTAL DEFECT

What investigations would you do for VSD?

A
  • ECG = left axis deviation, LVH or RVH.

- CXR = cardiomegaly, large pulmonary arteries.

217
Q

VENTRICULAR SEPTAL DEFECT

What is the treatment for VSD?

A
  • Medical initially in case of sponteanous closure.

- Symptomatic = surgical closure.

218
Q

COARCTATION OF AORTA

What is the pathophysiology of coarctation of aorta?

A
  • Congenital narrowing of the descending aorta, usually at level of ductus arteriosus.
  • Collateral circulation forms to increase flow to lower part of body so intercostal arteries become dilated + tortuous.
219
Q

COARCTATION OF AORTA

What are the aetiologies and complications of coarctation of aorta?

A
  • Associated with bicuspid aortic valve + Turner’s syndrome.

- Heart failure, intracerebral haemorrhage, infective endocarditis.

220
Q

COARCTATION OF AORTA

What is the clinical presentation of coarctation of aorta?

A
  • Radio-femoral delay (cold feet).
  • Right arm BP > left arm.
  • Scapular bruit.
221
Q

COARCTATION OF AORTA

What are the investigations and treatment for coarctation of aorta?

A
  • CXR = may show rib notching.
  • CT/MRI aortogram = diagnostic.
  • Surgery or balloon dilatation ± stenting.
222
Q

TETRALOGY OF FALLOT

What is the pathophysiology of TOF?

A

Condition defined by 4 abnormalities…

  • VSD.
  • Pulmonary stenosis.
  • RVH.
  • Overriding aorta (aorta overrides VSD accepting right heart blood).
  • Few patients have ASD = Pentad of fallot.
  • Stenosis of RV outflow leads to RVp>LVp causing R>L shunt + so cyanosis.
223
Q

TETRALOGY OF FALLOT

What are the complications with TOF?

A
  • High mortality rate (95% by age 20) without surgery.

- RV dilatation + failure + arrhythmias common problems in adulthood.

224
Q

TETRALOGY OF FALLOT

What is the clinical presentation of TOF?

A
  • Cyanosis + exertional dyspnoea.
  • Systolic murmur.
  • Toddlers may squat as it increases PVR + so degrees degree of R>L shunt.
225
Q

TETRALOGY OF FALLOT

What are the investigations and treatments for TOF?

A
  • CXR = boot-shaped heat.
  • Echocardiogram.
  • Early surgical repair with closure of VSD + correction of pulmonary stenosis.
226
Q

PATENT DUCTUS ARTERIOSUS

What is the pathophysiology of PDA?

A
  • Failure of ductus arteriosus to close causing a L>R shunt of blood from aorta (higher pressure) to pulmonary artery (lower pressure).
  • Pulmonary arterial + left heart flow increase, RA/RV unaffected.
227
Q 
PATENT DUCTUS ARTERIOSUS
What are the...
i) Complications
ii) Clinical presentation
iii) Investigations
iv) Treatment

for PDA?

A

i) Eisenmenger’s syndrome.
ii) Clubbed + blue toes but pink + not clubbed fingers, dyspnoea, failure to thrive.
iii) CXR = cardiomegaly, echocardiogram.
iv) Spontaneous closure if not surgical (can do percutaneously).

228
Q 
PATENT FORAMEN OVALE
What is the...
i) Pathophysiology
ii) Complication
iii) Investigations
iv) Treatment

for PFO?

A

i) Failure of foramen ovale to close inw eeks after birth causing a R>L shunt between atria.
ii) Rarely thromboembolic stroke.
iii) Echocardiogram bubble test where bubbes travel from R>L shunt rather than being filtered out in lungs.
iv) Often none, cardiac catheterisation if needing closure.

229
Q

HCM

What is the pathophysiology of hypertrophic cardiomyopathy (HCM)?

A
  • Genetic dysfunction of sarcomeric proteins cause LVH + so impaired diastolic filling leading to reduced SV + abnormal mitral valve.
  • A diagnosis in the absence of abnormal loading conditions like HTN or valvular disease.
  • Causes dynamic obstruction of the left ventricular outflow tract.
230
Q

HCM

What is the aetiology + complications of HCM?

A
  • Sarcomeric protein gene mutations (alpha-tropomyosin, beta-myosin + troponin) via an AD inheritance.
  • Most common cause of sudden cardiac death in young + athletes, atrial + ventricular arrhythmias.
231
Q

HCM

What are the symptoms of HCM?

A
  • Most asymptomatic.

- Can present with angina, dyspnoea, palpitations, syncope (unexplained = risk marker for sudden cardiac death).

232
Q

HCM

What are the signs of HCM?

A
  • Jerky carotid pulse.
  • Ejection systolic murmur.
  • Atrial fibrillation (commonest sustained arrhythmia).
233
Q

HCM

What investigations would you do for HCM?

A 
ECG = LVH (large QRS), large progressive T wave inversion, AF.
Echocardiogram = asymmetrical septal hypertrophy.
234
Q

HCM

What is the treatment for HCM?

A
  • Symptomatic = beta-blockers or verapamil (CCB).
  • Amiodarone for arrhythmias.
  • Anticoagulate for AF.
  • Implantable defibrillator to prevent sudden death.
  • If severe, septal myomectomy.
235
Q

DCM

What is the pathophysiology and aetiologies of dilated cardiomyopathy (DCM)?

A
  • Ventricular dilation + contractile dysfunction as the dilatation of the ventricular wall disrupts the heart’s ability to effectively pump blood.
  • Alcoholism, congenital (cytoskeletal gene mutations), thyrotoxicosis.
236
Q

DCM

What are the symptoms of DCM?

A
  • Heart failure symptoms (dyspnoea, fatigue, oedema).
237
Q

DCM

What are the signs of DCM?

A
  • Raised JVP.
  • Displaced + diffuse apex.
  • Tachycardia.
238
Q

DCM

What are the investigations + treatment for DCM?

A
  • ECG = tachycardia, poor R-wave progression.
  • CXR = cardiomegaly, pulmonary oedema.
  • Echocardiogram = marked dilatation.
  • Bed rest, diuretics for fluid overload, ACEi + beta blockers, ICD/transplantation if severe.
239
Q

ARVC

What is the pathophysiology of arrhythmogenic right/left ventricular cardiomyopathy?

A
  • Desmosome gene mutations mean myocytes pulled apart + myocardium is replaced with fatty fibrous tissue impairing the ability of ventricular muscle.
240
Q

ARVC

What is the aetiology of ARVC?

A
  • Desmosome gene mutations.

- Naxos disease (woolly hair, palmar plantar keratoderma).

241
Q

ARVC

What is the clinical presentation of ARVC?

A
  • Palpitations.
  • Syncope on exertion.
  • VT.
242
Q

ARVC

What are the investigations + treatment for ARVC?

A
  • ECG = epsilon waves (small +ve deflection buried in end of QRS), T wave inversion, broad QRS V1-3.
  • RV angiography, MRI shows enlargement + fatty infiltration + fibrosis.
243
Q

RC

What is the pathophysiology of restrictive cardiomyopathy (RC)?

A
  • Normal LV cavity size + systolic function but increased myocardial stiffness restricts diastolic filling.
  • Ventricle non-compliant + fills predominately in early diastole.
244
Q

RC

What is the aetiology of RC?

A
  • Idiopathic, amyloidosis, sarcoidosis.
245
Q

RC

What is the clinical presentation of RC?

A
  • Heart failure symptoms (dyspnoea, fatigue + oedema).

- Increased JVP, murmurs.

246
Q

RC

What are the investigations and treatment for RC?

A
  • Echocardiograph = thickened ventricular walls, valves + atrial septum, MRI = distinguishing between cardiomyopathies.
  • Treat underlying cause, standard heart failure medication, ICD in high risk.
247
Q

CHANNELOPATHIES

What is the pathophysiology, clinical presentation, investigations and treatment of common channelopathies?

A
  • Include long/short QT syndrome, Brugada (Na+ sodium channel mutation) + Wolff-Parkinson-White.
  • Most common symptom is recurrent syncope, dyspnoea.
  • Brugada ECG = classic coved ST elevated V1-3, T wave inversion, broad P waves.
  • ICD to treat VT + VF.
248
Q

ACE INHIBITORS

What is the mechanism of action of ACEi?

A
  • Inhibits ACE, reduces angiotensin II levels to prevent vasoconstriction + aldosterone secretion.
  • Reduces afterload as reduced peripheral vascular resistance.
  • Reduces preload as reduced aldosterone so promotes Na+ + H20 excretion.
    CKD it dilates efferent arterioles + so slows progression.
249
Q

ACE INHIBITORS

What are the main clinical indications + give some examples for ACEi?

A
  • HTN, IHD, CKD.

- Ramipril, enalapril, lisinopril.

250
Q

ACE INHIBITORS

What are some adverse effects of ACEi?

A
  • Hypotension due to reduced peripheral resistance.
  • Acute renal failure due to reduced perfusion pressure in glomeruli (efferent arteriole vasodilation = reduced GFR).
  • Hyperkalaemia.
  • Teratogenic effects.
251
Q

ACE INHIBITORS

Give an example of when ACEi would be contraindicated and why.

A
  • Dry cough, rash, anaphylactoid reactions.

- ACE isn’t specific, responsible for converting bradykinin into inactive peptides, ACEi can potentiate bradykinin.

252
Q

SARTANS
What is the mechanism of action for angiotensin II receptor blockers/sartans, their main clinical indication, examples and main adverse effects?

A
  • Angiotensin-I (AT-I) receptor blockers which block the action of angiotensin II (as angiotensin II acts on AT-I receptors.
  • HTN, heart failure, diabetic nephropathy.
  • Candesartan, valsartan, losartan.
  • Symptomatic hypotension (esp in volume deplete patients), hyperkalaemia, C/I in pregnancy.
253
Q

Ca2+ CHANNEL BLOCKERS

What is the mechanism + main clinical indications of CCBs?

A
  • L-type CCBs that decrease Ca2+ entry + therefore intracellular Ca2+ concentration in vascular and/or cardiac cells.
  • HTN, IHD, SVTs.
254
Q

Ca2+ CHANNEL BLOCKERS

What are the three types of CCBs?

A

Dihydropyridines (amlodipine, nifedipine)…
- Preferentially affect vascular smooth muscle, peripheral arterial vasodilators, stops vasospasm (Raynaud’s phenomenon treatment)
Phenylalkylamines (verapamil)…
- Main effects on heart, -vely chrono/inotropic.
Benzothiazepines (diltiazem)…
- Mainly heart effects.

255
Q

Ca2+ CHANNEL BLOCKERS

What are some adverse effects of CCBs?

A

Dihydropyridines…
- Flushing, oedema, headache.
Cardiac targeting…
- Bradycardia, AV block, conspitation.

256
Q

BETA BLOCKERS

What is the mechanism of beta blockers?

A
  • Binds to beta-adrenergic receptors.
  • Reduces force of contraction + speed of conduction.
  • Prolongs refractory period in aVN + so breaks ‘re-entry’ circuit in SVT.
  • Reduce renin secretion from kidney.
257
Q

BETA BLOCKERS

What are the main clinical indications + examples of beta blockers?

A
  • IHD, chronic cardiac failure, arrhythmias.

- Biosprolol, atenolol, propranolol.

258
Q

BETA BLOCKERS

Explain what selectivity of beta blockers mean.

A
  • Bisoprolol targets B-1 + so is selective whereas propranolol isn’t selective + so targets B-1+2, cardioselective implies B-1 selectivity.
259
Q

BETA BLOCKERS

What are the main adverse effects with beta blockers?

A
  • Fatigue.
  • Bradycardia.
  • Erectile dysfunction.
  • COPD/asthma exacerbations.
  • Can cause Raynaud’s phenomenon.
260
Q

DIURETICS

Give an example of a thiazide diuretic. Where does it act? What is its mechanism? What are the adverse effects?

A
  • Bendroflumethiazide.
  • Distal tubule.
  • Inhibits Na+/Cl- co-transporter + prevents Na+/H20 reabsorption.
  • Causes hypokalaemia/natraemia.
261
Q

DIURETICS

Give an example of a loop diuretic. Where does it act? What is its mechanism? What are the adverse effects?

A
  • Furosemide.
  • Loop of Henle.
  • Inhibits the Na+/K+/2Cl- co-transporter + so preventing these lions going from lumen>epithelial cells, dilates veins + so reduces preload.
  • Used in relieving dyspnoea in acute pulmonary oedema, symptomatic treatment for cardiac failure.
  • Can cause dehydration, low electrolyte state + ototoxicity.
262
Q

DIURETICS
Give an example of a potassium-sparring diuretic. Where does it act? What is its mechanism? What are the adverse effects?

A
  • Amiloride, often used with loop/thiazide diuretic to counter their K+ loss + enhance diuresis.
  • Distal convoluted tubule.
  • Inhibits ENaC leading to Na+/H20 excretion + K+ retention.
263
Q

DIURETICS

Give an example of an aldosterone antagonist. Where does it act? What is its mechanism? What are the adverse effects?

A
  • Spironolactone.
  • Distal convoluted tubule.
  • Acts on ENaC channels leading to increased Na+/H20 excretion + K+ retention.
  • Hyperkalaemia leading to arrhythmias/cardiac arrest.
264
Q

NITRATES

What are the mechanisms? What are the main clinical indications. Give some examples. What are the main adverse effects?

A
  • Converted to NO which is an arterial (reduced afterload) + venodilator (reduced preload).
  • Short acting = acute angina/ACS, long acting = angina prophylaxis, chronic heart failure, IV = pulmonary oedema.
  • Glyceryl trinitrate, isosorbide mononitrate.
  • Headache, GTN spray syncope (hypotension), flushing.
265
Q

CARDIAC GLYCOSIDE

What is the mechanism? Give an example? Main clinical indications.

A
  • Inhibits Na/K pump which is linked to calcium pump, -vely chronotropic +vely inotropic (HR down, force up) via vagal nerve stimulation (ACh release from parasympathetic nerves).
  • Digoxin.
  • Atrial fibrillation + flutter, severe heart failure.
266
Q

CARDIAC GLYCOSIDE

What are the main effects and adverse effects?

A
  • Bradycardia, slowing of AV conduction, increased force of contraction (but increased ectopic activity due to effects on calcium).
  • Narrow therapeutic range (digoxin toxicity), nausea, vomiting.
267
Q

AMIODARONE

What is the mechanism of action?

A
  • Blockage of Na+/K+/Ca2+ and antagonism of alpha + beta-adrenergic receptors.
  • Slow spontaneous depolarisation, slow conduction velocity, increases resistance to depolarisation in AVN.
  • Prolongs QT interval + can cause polymorphic VT.
268
Q

AMIODARONE

What is it used for? What are the adverse effects?

A
  • Anti-arrhythmic drug.

- Hyper/hypothyroidism, abnormal liver function, sun sensitivity + slate grey skin discolouration, optic neuropathy.

269
Q

AMIODARONE

What drug does amiodarone react with and how? How long after stopping amiodarone is it still present in circulation?

A
  • Warfarin by attaching to carrier proteins in the blood, displacing it + so potentiating its effects.
  • 3 months.
270
Q

ANTI-PLATELETS

What are the main clinical indications?

A
  • Used as prophylaxis of IHD + to reduce events.
  • Used after MI.
  • Used after PCI to prevent coronary stent occlusion.
271
Q

ANTI-PLATELETS

What are the 2 main mechanisms of anti-platelets, give examples of both?

A

Aspirin…
- Irreversible inhibitor of cyclo-oxygenase reducing production of thromboxane + so reduces platelet aggregation.
Clopidogrel…
- P2Y12 inhibitor as it irreversibly bind to ADP receptors (P2Y12) on surface of platelets + so prevent platelet aggregation.

272
Q

ANTI-PLATELETS

What are the main adverse effects of anti-platelets.

A
  • GI irritation + bleeding.

- Ulceration in aspirin.

273
Q

STATINS

What is the mechanism of action? What are the main clinical indications? Give examples.

A
  • HMG CoA reductase inhibitor reducing the amount of LDL-cholesterol present.
  • Used as prophylaxis of IHD to reduce events + hypercholesterolaemia.
  • Atorvastatin, simvastatin.
274
Q

NEP INHIBITORS
What is the function of natriuretic peptides? How are they metabolised? What is the function of NEP inhibitors? GIve examples.

A
  • Inhibit the RAAS system.
  • Metabolised by neutral endopeptidase (NEP, neprilysin).
  • NEP inhibitors increase levels of natriuretic peptides + so potentiates them.
  • Sacubitril = neprilysin inhibitor, valsartan = ARB.
275
Q

REVASCULARISATION

What is PCI? What does it involve? What treatment is required after?

A
  • Percutaneous coronary intervention.
  • Balloon inflated inside stenosed vessel, lumen opened, stent inserted to reduce risk of re-stenosis.
  • Dual anti-platelet therapy (aspirin + clopidogrel) for 12 months to reduce risk of in-stent thrombosis.
276
Q

REVASCULARISATION

What is CABG? What does it involve?

A
  • Coronary artery bypass graft.

- Stenosed vessel is opened via open heart surgery.

277
Q

REVASCULARISATION

What are the pros/cons to PCI + CABG?

A

PCI…
- Less invasive, faster recovery, patient satisfied.
- Restenosis, may need future surgery.
CABG…
- Less likely to need further surgery, those with multivessel disease get better outcomes.
- Open heart surgery so recovery slower, more invasive, larger wounds.

278
Q

VAUGHAN WILLIAMS

What is the Vaughan William’s classification for? What are the 4 classes and what do they do?

A
  • Anti-arrhythmic drugs.
  • Class I = Na+ channel blockers.
  • Class II = beta blockers.
  • Class III = prolong action potential.
  • Class IV = CCBs affecting heart.
279
Q

VAUGHAN WILLIAMS

Give an example of drugs in each Vaughan William’s classification

A 
Ia = disopyramide.
Ib = lidocaine.
Ic = flecainide.
II = propranolol (non-selective), biso/metoprolol (selective).
III = amiodarone.
IV = verapamil, diltiazem.

Phase 2a (12 decks)

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