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CP1 > Cardiovascular Medicine > Flashcards

Cardiovascular Medicine Flashcards

1
Q

What are the main causes of chest paint?

A
  • Myocardial ischaemia
  • Aortic dissection
  • Pleural disease
  • Oesophageal disease
  • MSK Ddisease (e.g.costochondritis)
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2
Q

Describe the symptoms of myocardial ischaemia

A
  • Crushing, gripping or heavy pain centrally on the chest
  • Can radiate to shoulder or jaw
  • Associated with parasthesia (prickling sensation)/heaviness in one or both arms
  • Associated with dyspnoea, nausea and sweating
  • Comes on other minutes
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3
Q

What is aortic dissection?

A

Aortic dissection (AD) occurs when an injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart.

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4
Q

What are the symptoms of pleural disease?

A
  • Localised sharp pain, worse on deep breathing and coughing
  • Associated with costo-chondral tenderness
  • Pain in the shoulder tip is suggestive of diaphragmatic pleural irritation
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5
Q

What are the symptoms of oesophageal disease?

A
  • Retrosternal chest pain.

- Worse on bending over or lying down, relived by antacids

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6
Q

What are the symptoms of MSK chest pain e.g. costochondritis?

A
  • Can cause very server pain, importantly associated with local tenderness
  • Worse with certain movements, often a history of trauma of causative event
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7
Q

What is the common pathology of acute coronary syndromes?

A
  • Atheromatous plaque formation in the coronary arteries
  • Fissuring/ulceration of the plaque leading to platelet aggregation
  • Localise thrombosis,vasoconstriction and disf thromboembolism
  • Myocardial infraction
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8
Q

What are the Acute coronary syndromes?

A
  • Unstable angina
  • STEMI
  • NSTEMI
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9
Q

Define unstable angina

A

Angina occurring at rest, or sudden increased frequency/severity of existing angina

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10
Q

What causes unstable angina?

A

Pathologically caused by fissuring of plaques, thus there is a risk of subsequent total vessel
Occlusion and progression to Acura myocardial infarction (AMI)

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11
Q

What causes a regional MI?

A

Infact if one segment of the ventricular wall, nearly always due to thrombus formation on an atheromatous plaque giving prolonged ischaemia

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12
Q

What causes a regional subcutaneous infarction?

A

If there is lysis of the thrombus or a strong collateral supply the infarct is limited to the subendocardial zone (most distal point from the bloody supply)

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13
Q

What is a circumferential subendocardial infarction?

A

Caused by a general hypoperfusion of the coronary arteries, usually dyes a hypotension episode in arteries already af free ted by high grade atherosclerosis

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14
Q

How do you disagrees an MI?

A
  • Elevations in serum cardiac tropinin levels (i.e. cardiac myocyte death) with additional categorisation based on they ECG
  • ST elevation/ new LBBB (The hallmark of left bundle branch block is QRS duration ≥0,12 seconds, deep and broad S-wave in V1/V2 and broad clumsy R-wave in V5/V6) = STEMI
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15
Q

What does the right coronary artery supply?

A

Right atria, right ventricle, posteriorly septum and AVN In 80% and SAN in 60%

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16
Q

What part of the heart does a right coronary artery effect?

A

Posterior/ inferior

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17
Q

What leads depict a right coronary artery blockage?

A

Leads II, III, VF

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18
Q

Describe the symptoms of aortic dissection

A
  • Severe, central chest pain, radiating to the back and down the arms
  • Patients may be shocked and can have neurological symptoms secondary to loss of blood supply to the spinal cord
  • There may be signs of distal ischaemia or absent peripheral pulses
  • Comes on over seconds
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19
Q

What does e left coronary artery split into?

A

Circumflex and left anterior descending arteries

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20
Q

What part of the heart does an occlusion to the left coronary artery try affect?

A

Anterior lateral

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21
Q

What leads does a left coronary artery occlusion show on?

A

Leads 1, aVL, V5/6

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22
Q

What does the left anterior descending artery supply?

A

Left ventricle and anterior septum

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23
Q

What part of the heart does a left anterior descending artery affect?

A

Anterior septal

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24
Q

What leads does a left anterior descending artery occlusion show on?

A

Leads V1-V4

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25
Q

How does a collagenous scar develop after an MI with time?

A

0-12 hours: infarct not visible, loss of oxidative enzymes
12-24 hours: infarct pale and blotchy with intercellular oedema
24-72 hours: infarcted area excites acute inflammatory response with dead area soft and yellow with neutrophilic infiltration
3-10 days: organisation of infarcted area by vascular granulation tissue
10 days- several months: collagen disposition, infarct replaced by collagenous scar

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26
Q

What causes deaths in ischaemic heart disease (IHD)?

A

Ventricular fibrillation

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27
Q

What are ACS symptoms?

A
  • Severe crushing gripping or heavy chest pain lasting longer than 20 seconds- not relive by 3 x GTN sprays at 5 minute intervals
  • Radiates to the left arm, neck or jaw
  • Associated with dyspnoea, nausea, fatigue, sweatiness and palpitations
  • May present without chest pain (silent infarct) particularly in elderly or diabetics who can present later with a verity of symptoms
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28
Q

How does ACS present on examination?

A
  • Sympathetic activation: tachycardia, hypertension, pallor, sweatiness
  • Vagal stimulation: bradycardia, vomiting
  • Myocardial impairments: hypotension, narrow pulse pressure, raised JVP, basal crepetatations, 3rd heart sound
  • Tissue damage: low grade pyrexia (fever)
  • Later a pericardial rub and peripheral oedema may develop or pansystolic murmur due to papillary muscle rupture/ventriculo-septal defect
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29
Q

What is the differential diagnosis of the central chest pain from ACS?

A
  • Coronary spasm
  • Pericarditis/myocarditis
  • Aortic dissection
  • PE
  • pneumothorax
  • Oesophageal disease
  • Mediastinitis
  • Costochondritis
  • Trauma
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30
Q

What investigations would you order for ACS?

A
  • ECG
  • Bloods- FBC and U&E, glucose (lowered) and lipids (raised), cardiac enzymes (cardiac troponin)
  • CXR (cardiomegaly, pulmonary odema, widened mediastinum in aortic dissection)
  • If in doubt transthoracic echocardiography May confirm or help detect alternative diagnosis such as PE
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31
Q

Describe the ST changes in a non-reperfused STEMI

A

5 minutes- tall, pointed T-waves
30 minutes- ST elevation
2+ hours after- T wave inversion, Q waves develop
Days after- ST segment returns to normal
Weeks after- T wave may return to normal, Q wave remains

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32
Q

How is an NSTEMI different you a STEMI?

A

STEMI generally correlates with a full-thickness myocardial infarct, whereas NSTEMI is often a partial thickness elision
There may be ST depression, T wave inversion or other non-specific changes

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33
Q

How does unstable angina present in clinical tests?

A

May be ischaemic ST depression in the leads affected and there will be no tropes rise

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34
Q

What is the early management of ACS?

A
  • A-E: oxygen only required if SpO2 <94%, Baseline bloods including tropics and clotting
  • 300mg aspirin chewed
  • Morphine starting at 5mg and titrated up, plus anti-emetic
  • GTN spray/IV nitrates unless hypotensive
  • if there is ST elevation on ECG, immediate referral to cardiology for PCI is required (Primary percutaneous coronary intervention (PCI) refers to the strategy of taking a patient who presents with STEMI directly to the cardiac catheterization laboratory to undergo mechanical revascularization using balloon angioplasty, coronary stents, aspiration thrombectomy, and other measures.)
  • if there is no ST elevation, assess mortality risk using the GRACE score, continue regular ECG monitoring and add further medication (clopidogrel 300mg blood thinner, fondaparinoux anticoagulant)
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35
Q

Whats the GRACE score?

A

takes into account age, heart rate, blood pressure, class of CHF, renal function, ST segment changes, troponin elevations and whether there was an arrest at admission to give a mortality risk at various time intervals

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36
Q

How do you treat a STEMi?

A

Percutaneous coronary intervention (PCI) is the gold standard if available in a timely fashion: door to balloon in 90 minutes, patient transfer advised if intervention can occur within this window
If contraindicated then thrombolysis should be given

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37
Q

How do you treat NSTEMI/UA?

A
  • high risk if GRACE mortality >3% in 6m or raised troponins, persistent pain, ST depression or diabetes –> organise semi-elective PCI as inpatient
  • Low risk i.e. resolved unstable angina or GRACE <3% –> potentially can be discharged with long-term medication and outpatient follow up (e.g. elective angiography)
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38
Q

What is long term ACS management?

A
  • 48h bed rest with continuous ECG monitoring
  • Daily U and Es and cardiac enzyme for 2-3days
  • Thomoprophylaxis; fondaparinoux SC 2.5mg OD (if undergoing/undergone PCI within 24h, discuss need with cardiology)
  • Asprin 75mg OD continued for life
  • Clopidogrel 75mg OD continued for one year
  • Bisoprolol for life, titrated to reduceHR to around 60bpm
  • start Stanton and ACEi after 24-48 course (atorvastatin 80mg o.n. rampipril 2.5mg b.d.)
  • address modifiable risk factors
  • Start oral nitrates if there is ongoing angina (isosorbide mononitrate 50mg bd.)
  • discharge at 5-7 days
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39
Q

What are the immediate complications of AMI?

A

Arrhythmias (VT and VF are common following AMI, particularly after reperfusion, AF occurs frequently and relapse is frequent, bradycardia or AV block can occur ion the MI affects the SAN/AVN

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40
Q

What are the short term complications of AMI?

A
  • pulmonary oedema
  • cardiogenic shock
  • thromboembolism
  • venticulo-septal defect
  • ruptured chordae tendinae
  • rupture of ventricular wall
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41
Q

How does pulmonary oedema occur as a result of AMI?

A

-left heart fails to pump effectively, with poor systolic emptying leading to dilation: ‘a dilated chamber is a failing chamber’
-the back pressure in the pulmonary veins is reflected into the capillaries, leading to extravasation of low-protein fluid into the alveolar sacs
-

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42
Q

How does pulmonary oedema present?

A
  • extreme breathlessness, with sweating and anxiety
  • there may be a cough. producing frothy, blood-stained sputum
  • on examination there are signs of acute heart failure, with cracks throughout the chest
  • arterial PO2 falls, and initially PCO2 falls also due to over breathing, but later the PCO2 rises due to impaired gas exchange
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43
Q

What is cardiogenic shock?

A

hypotension causing a further reduction in coronary flow and thus further pump failure leading to a vicious cycle and a high mortality rate

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44
Q

How does thromboembolism occur due to AMI?

A

mural thrombus formation over the inflamed area of endocardium can cause emboli to the brain, kidney, gut, lower limbs etc. causing infarction

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45
Q

What is a venticulo-septal defect?

A

inter cardiac rupture through the septum causing left-right shunt and development of sever left ventricular failure if large

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46
Q

What does a ruptured chordae tendiae cause?

A

mitral valve incompetence

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47
Q

Why does AMI cause rupture of the ventricular wall?

A

2-10 days after due to re-organisation and softening of the wall

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48
Q

What does rupture of the ventricular wall cause?

A

haemopericardium, cardiac tamponade and rapid death

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49
Q

what are the long term complications of an AMI?

A
  • heart failure
  • Dressler’s syndrome
  • ventricular aneurysm formation
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50
Q

What is Dressler’s syndrome?

A

immune mediated pericarditis, associated with a high ESR and sometimes anti-myocardial antibodies

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51
Q

How long after an infarct does Dressler’s syndrome occur?

A

2-10 months

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52
Q

How does Dressler’s syndrome present?

A
  • sharp chest pain exacerbated by ,movement and lying down, relieved by sitting forwards
  • on examination, there is a classical pericardial friction rub at the lower left sternal edge with the patient leaning forwards
  • there may also be a pericardial effusion, leading to dyspnoea if it compresses adjacent bronchi
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53
Q

How is Dressler’s syndrome treated?

A

high does aspirin/NSAIDs

54
Q

How does a ventricular aneurysm form?

A

gradual distention of the infarcted part of the ventricle wall, which has been replaced by a collagen scar

55
Q

What happens if a ventricular aneurysm ruptures?

A

cardiac tamponade and death

56
Q

Define angina

A

Episodic pain that takes place when there is increase myocardial demand, usually upon exercise, in the presence of impaired perfusion by blood

57
Q

What are the causes of myocardial ischaemia?

A
  • reduced perfusion
  • reduced blood oxygenation
  • increase tissue demands
58
Q

What can cause reduced perfusion?

A

Atheroma, embolus, thrombosis, spasm or inflammation of coronary arteries, generalised hypotension

59
Q

What can cause reduced blood oxygenation?

A

Anaemia, carboxyhaemoglobinaemia

60
Q

What can cause increased tissue demands?

A

Increased Cardiac output

Cardiac hypertrophy

61
Q

What is the most common cause of stable angina?

A

Low flow in atherosclerotic coronary arteries

62
Q

What is ateriosclerosis?

A

Non-specific thickening and hardening id the walls of arteries causing a loss of contractility and elasticity and decreased blood flow. Often due to prolonged hypertension in smaller arteries

63
Q

What is atheroma?

A

Specific degenerative disease affecting large/medium sized arteries. When this leads to thinking and hardening of the arterial wall it is termed atherosclerosis.

64
Q

How does an atheroma form?

A
  • damage to the endothelium due to a variety of risk factors allows entry of LDLs into the intima
  • This lipid is taken up macrophages in the intima and accumulates excessively as it is able to bypass normal receptor mediated uptake, forming a ‘fatty streak’
  • as the macrophages take up more and more lipid, they release free lipid into the intima
  • the macrophages also stimulate cytokines, which leads to collagen deposition by inflammatory cells, and the intimal lipid plaque becomes firbrotic
  • at this stage it appears raised and yellow and leads to pressure atrophy of the media and disruption of the elastic lamina
  • increased secretion of collagen forms a dense fibrous cap to the plaque, which is now hard and white
  • advances places also show free lipid as well lipid in macrophages
  • the endothelium is fragile and often ulcerates, allowing platelet aggregation
65
Q

What are the risk factors for atheroma?

A

-age
-gender: higher in men than Pre-menopausal women
-family history: higher rates in first degree relative had IHD before 50
-smoking: stopping reduces immediate risk by 25%
-diet: high fat, low fresh fruit and vegetables implicated
-obesity: worse if primarily abdominal
Obesity
-hypertension: both systolic and diastolic hypertension
-hyperlipidaemia: High serum cholesterol, especially for high HDL/TGs
-diabetes mellitus: DM, IGT (impaired glucose tolerance) , IFG (impaired fasting glucose) all associated

66
Q

How does stable angina present?

A
  • ischameic pain of the myocardium, varying from a mild ache to a severe pain that provokes sweating and fear
  • the pain is provoked by exercise, especially after meals, in the cold, and if the patient is angry/excited
  • it fades quickly with rest/GTN, and in some the pain occurs predictably at certain. Me ems of exertion
  • there may be associate breathlessness
  • there a re no abdominal findings on examination, occasionally a 4th heart sound, and BP should always be taken
67
Q

What are the variants of stable angina?

A

Decubitus angina

Variant/prinzmetal’s angina

68
Q

What is decubitus angina?

A

Angina precipitated by lying down as there is increase venous return to the heart, is associated with LVF

69
Q

What is variant/prinzmetal’s angina?

A

Occurs without provocation at rest as a result of coronary spasm. There is ST elevation during the episode but no troponin rise

70
Q

What investigations do you run for stable angina?

A

FBC, glucose, lipids, TFTs

Resting 12-lead ECG

71
Q

How do you assess the likelihood of coronary artery disease?

A

Use ECC findings and clinical assessment using the NICE tool

72
Q

What are the different categories for the nice tool for assessment of coronary heart disease in stable angina?

A
  • if >90% treat as stable angina
  • if 61-90% coronary angiography is indicated
  • if 31-60% functional imaging is indicated (SPECT myocardial perfusion scan, exercise echo, stress MRI)
  • if 10-30% CT calcium scoring is used
  • if <10% investigate for another cause
73
Q

How do you carry out a stress 12-lead ECG?

A

If resting ECG normal, use Bruce protocol on treadmill, with ST depression >1mm indicating ischaemia. If positive within 6 minutes then angiography indicated

74
Q

How do you manage stable angina?

A
  • Inform patients that their disease holds a good prognosis
  • treat underlying problems and co-morbidities
  • manage risk factors
  • symptomatic treatment (GTN spray and beta blocker or rate limiting calcium-channel blocker) then combination therapy with a non-rate limiting CCB or add nicotandil for refractory disease
  • secondary prevention: statin/ low-dose aspirin
  • refer to cardiology if any doubt over the diagnosis, atypical features, or refractory symptoms
75
Q

What advice do you give for GTN spray?

A
  • sit down, rest and spray once beneath the tongue, wait for 5 minutes, spray again if there is still pain. If there still pain at 10 minutes, call 999 and unlock the door
  • they can be used prior to performing activities that will provoke angina
  • they can cause postural hypotension and dizziness
76
Q

How does a GTN spray work?

A

They affect large muscular arteries, reducing aortic pressure and cardiac afterlife, as well as dilating coronary vessels. Decreased pre-load and after-load decreases the oxygen requirement of the myocardium, and coronary vasodilation leads to increased oxygen delivery

77
Q

What are beta blockers used for?

A

Beta 1 sensitive blocks used as anti-hypertensive and decrease renin release from juxta-glomerular cells

78
Q

What are the side effects of beta blockers?

A

Bronchoconstriction: contraindicated in asthma, caution in COPD
Cardiac depression/bradycardia: can be critical if combined with other rate limiting agents
Hypoglycaemia: impair the sympathetic warning signs of hypos
Fatigue

79
Q

What are the types of calcium channel blockers?

A

Digydropyridines (amlodipine/nifedipine)

Rate limiting agents (verapamil/diltiazem)

80
Q

How do calcium channel blockers work?

A 
All work to prevent smooth muscle contraction, reducing afterlife and causing coronary vasodilation 
The rate-limiting agents also act on calcium channels in the AVN to control the heart rate, exhibiting class IV anti-arrhythmic effects
81
Q

What are the side effects of calcium channel blockers?

A

Flushing and headache (as with all vasodilators), ankle swelling and constipation (GI SM inhibition)

82
Q

How does nicorandil work?

A

It is a combined NO donor and also an activator of ATP-sensitive K-channels in vascular smooth muscle cells, leading to hyperpolerisation

83
Q

Describe the anatomy of the cardiac chambers, valves, coronary arteries, great arteries and cardiac conduction system

A
  • the anterior view of the heart is mainly the RV, with RA and LV also visible
  • the tricuspid valve separate the right atrium/ventricle
  • the mitral valve separates the left atrium/ventricle
  • aortic/pulmonary valves are at the base of each vessel
  • major branches of the aortic arch are the brachiocephalic trunk (giving right common carotid/right subclavian), left common carotid artery and left subclavian artery
84
Q

What is pulmonary oedema?

A

-pulmonary oedema is due to an increase in fluid in the alveolar wall (pulmonary interstitium), which then affects the interstitial spaces

85
Q

Describe the pathophysiology of pulmonary oedema

A
  • the most common cause is left ventricular failure, which causes increased pressure in the alveolar capillaries and leakage of fluid into the intersitium
  • this leads to subjective dyspnoea, but can remain stable for some time
  • severe LVF causes leakage of fluid from the interstitial into the alveolar spaces, leading to severe acute impairment of respiratory function
  • capillary rupture can lead to leakage of red cells also, which are taken up by macrophages containing iron pigment in the alveoli/intersitium and are thus termed “heart failure cells”
86
Q

What are the clinical features of pulmonary oedema?

A
  • dyspnoea
  • paroxysmal nocturnal dyspnoea
  • orthopnoea: due to increased venous return on lying down and can be measure objectively by number of pillows required to sleep
  • cough: producing frothy, blood stained sputum
87
Q

What is the acute presentation of pulmonary oedema?

A
  • severe dyspnoea
  • productive cough
  • anxiety and perspiration
  • cheyne-strokes respiration in LVF- cycling apnoea/hyperventilation due to impaired response of respiratory centre to CO2
88
Q

How does someone with pulmonary oedema present on examination?

A

-tachypnoea
-tachycardia, with gallop rhythm
-raised venous pressure
-peripheral shutdown
widespread crackles/wheezes on auscultation

89
Q

What investigations should be down for suspected pulmonary oedema?

A
  • ABG (arterial blood gas)-initial type 1 respiratory failure due to hyperventilation, with later type 2 respiratory failure due to impaired gas exchange
  • FBC, U and E, d-dimer, CRP
  • CXR-diffuse haziness (bat wing oedema) with Kerley B lines and upper zone vessel enlargement, cardiomegaly, pleural effusions
  • ECG: tachycardia, arrhythmia, signs of cardiac cause
  • Echocardiography: to demonstrate a cardiac cause e.g. MI/valvular disease
90
Q

what are the causes of pulmonary oedema?

A
  • increased capillary pressure
  • increased capillary permeability
  • reduced plasma oncotic failure
  • lymphatic obstruction
  • other
91
Q

What can cause increased capillary pressure?

A
  • cardiogenic: LVF, valve disease, arrhythmias, VSD, cardiomyopathy, negative inotropic drugs
  • pulmonary venous obstruction
  • iatrogenic fluid overload
92
Q

What can cause increased capillary permeability?

A
  • ARDS (acute respiratory distress syndrome)
  • infection: pneumonia/sepsis
  • DIC (disseminated intravascular coagulation)
  • inhaled toxins
93
Q

What can cause reduced plasma oncotic pressure?

A

renal/liver failure

hypoalbuminaemia

94
Q

What other causes of pulmonary oedema are there?

A

neurogenic: raised ICP/head injury
PE
Altitude

95
Q

What is the management of acute/decompensated heart failure causing pulmonary oedema?

A
  • sit the patient upright, administer 100% oxygen
  • IV diamorphine 1.25-5mg
  • IV furosemide 40mg-80mg IV
  • GTN spray 2 puffs sublingual (unless SBP <90)
  • if SBP >100 start an IV infusion of nitrate (consider non-invasive ventilation if not improving)
  • if SBP <100 treat as cardiogenic shock, alert ICU (may require invasive ventilation)
96
Q

Define heart failure

A

heart failure is complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as pump

97
Q

what are the common causes of heart failure?

A
  • ischaemic heart disease
  • dilated cardiomyopathy
  • hypertension
98
Q

What is cardiac output a function of?

A

pre-load, after-load and myocardial contractility

99
Q

Describe maladaptive neurohormonal response in heart failure?

A
  • reduced cardiac output leads to activation of the sympathetic nerves system and renin-angiotensin-aldosterone system
  • RAAS activation leads to vasoconstriction (increasing after load) and sodium/water retention (increasing preload), thus further increasing blood pressure and cardiac work
  • SNS activation initially maintains cardiac output by increasing contractility yet prolonged stimulation leads to myocyte apoptosis and necrosis
  • these changes are maladaptive creating a vicious cycle
100
Q

Describe the adaptive response to heart failure

A

atrial natriuretic peptide is released in response to atrial stretch, and acts to antagonise the fluid conserving effects of aldosterone

101
Q

What are the symptoms of left heart failure?

A

-fatigue
-exertional dyspnoea
-paoxysmal nocturnal dyspnoea
otheropnea

102
Q

What are the signs on examination of left heart failure?

A
  • cardiomegaly with displaced apex beat
  • 3rd heart sound, plus gallop rhythm if tachycardic
  • bibasal course crackles
103
Q

What is the most common cause of left heart failure?

A

long standing hypertention

104
Q

What are the common causes of right heart failure?

A
  • lung disease

- pulmonary valve stenosis

105
Q

What are the symptoms of right heart failure?

A
  • fatigue
  • breathlessness
  • anorexia/nausea (hepatomegaly)
  • swollen ankles
106
Q

What are the signs of right heart failure on examination?

A
  • jugular venous distension
  • hepatomegaly/ascities
  • dependent pitting oedema
  • pleural effusions
  • cardiomegaly, gallop rhythm
107
Q

What is the New York association classification of heart failure?

A
  • Stage I: disease present, no undue dyspnoea from normal activity
  • Stage II: dyspnoea present on ordinary activities
  • Stage III: less than ordinary activity causes dyspnoea, which is limiting
  • Stage IV: dyspnoea present at rest, any activity causes discomfort
108
Q

What investigations should be done for heart failure?

A
  • bloods: FBC, LFT, U and Es, TFTs, cardiac enzymes in acute failure
  • B-type natriuretic peptide: a normal level will exclude heart failure, so a good screen for breathlessness in practise
  • CXR: cardiomegaly and pulmonary oedema
  • ECG: for signs of ischaemia, hypertension or arrhythmias
  • Echo: if ECG or BNP are abnormal, gold standard for diagnosis (Ejection fraction <45% diagnostic)
109
Q

What is the management for LV dysfunction?

A
  • lifestyle advice
  • ACEi + B-blocker are first line drug therapy
  • Add diuretic if sympathetic oedema
  • aldosterone antagonists (e.g. spironolactone)/ angiotensin II receptor blocker/hydralazine plus nitrate second line
  • cardiac resyncronisation therapy/digoxin ivabradine third line therapy
110
Q

What lifestyle advice can be given?

A
  • patient education, obesity control, dietary modification (fluid and salt restriction in severe heart failure), smoking cessation
  • physical activity: bed rest is important following exacerbation of congestive heart failure, however in all patients with compensated heart failure then low level endurance activity is recommended (strenuous exercise should be avoided)
  • Vaccination: against pneumococcal disease and influenza
  • Sex: Patients should not take viagra as it may cause hypotension
111
Q

What are some. examples of ACE inhibitors?

A

ramipril, catopril, lisinopril

112
Q

What prescribing points should be given with ACE inhibitors?

A
  • risk of first dose hypotension

- dry cough

113
Q

What is contraindicated with ACE inhibitors?

A
  • NSAIDS (renal damage)

- diuretics until settled on medication

114
Q

When should ACE inhibitors not be prescribed?

A

Systolic BP <100

115
Q

How should people on ACE inhibitors be monitored?

A

renal side effects so monitor urea, creatine, K+ before and during treatment

116
Q

Give example of beta blockers?

A

bisoprolol, metoprolol, nebivolol

117
Q

Why are beta blockers used in heart failure?

A

block sympathetic activity that causes maladaptive and have anti-arrhythmic effects and thus reduce sudden death

118
Q

Why are diuretics prescribed?

A

mainly used for symptomatic relief of oedema, but also venodilate

119
Q

Which diuretics are favoured and why?

A
  • thiazides are used in mild failure or in elderly patients where massive diuresis may be intolerable
  • loop diuretics (furosemide) are used in pulmonary oedema
  • both may cause hypokalaemia so useful if taking ACE inhibitor
120
Q

Why is spironolactone used?

A

used at non-diuretic dose to reverse neurohormonal adaption

121
Q

When is digoxin used?

A

refractory heart failure and AF

122
Q

How does digoxin work?

A
  • it is a positive ionotrope and chronotrope, increasing the force of contraction yet decreasing heart rate
  • it is an inhibitor of the Na/K pump, leading to Na accumulation in he myocyte, which can be exchanged for calcium
  • it impairs AVN conduction and also increases vagal activity, yet the major clinical use is now AF
123
Q

What are the symptoms of digoxin overdose?

A
  • anorexia
  • nausea
  • visual disturbance
  • diarrhoea
124
Q

What is dosing of digoxin reliant on?

A

eGFR

125
Q

Why does renal function need to be monitored in heart failure patients?

A
  • digoxin is renally cleared
  • thiazides are ineffective in renal failure
  • diuretics and ACEi can lead to hyperkalaemia
126
Q

What are the consequences of valvular inflammation?

A
  • collagen exposure and thrombus development in the short term
  • post-inflammatroy scarring, leading to long-term functional impairment
127
Q

Which side of the heart is usually the site of endocarditis?

A

left

128
Q

Where do embolisms usually go from endocarditis?

A

systemic organs

129
Q

What is rheumatic fever?

A

an immune disorder that occurs in children, usually following tonsillitis/pharyngitis caused by group A B-haemolytic streptococci (GAS)

130
Q

Describe the pathology of rheumatic fever

A
  • there is antibody production to GAS, yet these antibodies cross-react with cardiac antigens to cause a self-limiting myocarditis/pericarditis
  • although this is self-limiting there is damage to heart valves that heals by progressive fibrosis of the valve leaflets, often with secondary calcification
131
Q

What causes congenital valvular heart disease and which valve does it affect?

A

Aortic stenosis due to calcification of a congenital bicuspid aortic valve

132
Q

What causes ischaemic valvular disease and what valve does it affect?

A

mitral regurgitation caused by papillary muscle dysfunction post-infarction

CP1 (2 decks)

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