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)
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
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.
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
5
Q
What are the symptoms of oesophageal disease?
A
- Retrosternal chest pain.
- Worse on bending over or lying down, relived by antacids
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
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
8
Q
What are the Acute coronary syndromes?
A
- Unstable angina
- STEMI
- NSTEMI
9
Q
Define unstable angina
A
Angina occurring at rest, or sudden increased frequency/severity of existing angina
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)
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
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)
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
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
15
Q
What does the right coronary artery supply?
A
Right atria, right ventricle, posteriorly septum and AVN In 80% and SAN in 60%
16
Q
What part of the heart does a right coronary artery effect?
A
Posterior/ inferior
17
Q
What leads depict a right coronary artery blockage?
A
Leads II, III, VF
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
19
Q
What does e left coronary artery split into?
A
Circumflex and left anterior descending arteries
20
Q
What part of the heart does an occlusion to the left coronary artery try affect?
A
Anterior lateral
21
Q
What leads does a left coronary artery occlusion show on?
A
Leads 1, aVL, V5/6
22
Q
What does the left anterior descending artery supply?
A
Left ventricle and anterior septum
23
Q
What part of the heart does a left anterior descending artery affect?
A
Anterior septal
24
Q
What leads does a left anterior descending artery occlusion show on?
A
Leads V1-V4
25
How does a collagenous scar develop after an MI with time?
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
26
What causes deaths in ischaemic heart disease (IHD)?
Ventricular fibrillation
27
What are ACS symptoms?
- 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
28
How does ACS present on examination?
- 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
29
What is the differential diagnosis of the central chest pain from ACS?
- Coronary spasm
- Pericarditis/myocarditis
- Aortic dissection
- PE
- pneumothorax
- Oesophageal disease
- Mediastinitis
- Costochondritis
- Trauma
30
What investigations would you order for ACS?
- 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
31
Describe the ST changes in a non-reperfused STEMI
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
32
How is an NSTEMI different you a STEMI?
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
33
How does unstable angina present in clinical tests?
May be ischaemic ST depression in the leads affected and there will be no tropes rise
34
What is the early management of ACS?
- 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)
35
Whats the GRACE score?
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
36
How do you treat a STEMi?
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
37
How do you treat NSTEMI/UA?
- 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)
38
What is long term ACS management?
- 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
39
What are the immediate complications of AMI?
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
40
What are the short term complications of AMI?
- pulmonary oedema
- cardiogenic shock
- thromboembolism
- venticulo-septal defect
- ruptured chordae tendinae
- rupture of ventricular wall
41
How does pulmonary oedema occur as a result of AMI?
-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
-
42
How does pulmonary oedema present?
- 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
43
What is cardiogenic shock?
hypotension causing a further reduction in coronary flow and thus further pump failure leading to a vicious cycle and a high mortality rate
44
How does thromboembolism occur due to AMI?
mural thrombus formation over the inflamed area of endocardium can cause emboli to the brain, kidney, gut, lower limbs etc. causing infarction
45
What is a venticulo-septal defect?
inter cardiac rupture through the septum causing left-right shunt and development of sever left ventricular failure if large
46
What does a ruptured chordae tendiae cause?
mitral valve incompetence
47
Why does AMI cause rupture of the ventricular wall?
2-10 days after due to re-organisation and softening of the wall
48
What does rupture of the ventricular wall cause?
haemopericardium, cardiac tamponade and rapid death
49
what are the long term complications of an AMI?
- heart failure
- Dressler's syndrome
- ventricular aneurysm formation
50
What is Dressler's syndrome?
immune mediated pericarditis, associated with a high ESR and sometimes anti-myocardial antibodies
51
How long after an infarct does Dressler's syndrome occur?
2-10 months
52
How does Dressler's syndrome present?
- 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
53
How is Dressler's syndrome treated?
high does aspirin/NSAIDs
54
How does a ventricular aneurysm form?
gradual distention of the infarcted part of the ventricle wall, which has been replaced by a collagen scar
55
What happens if a ventricular aneurysm ruptures?
cardiac tamponade and death
56
Define angina
Episodic pain that takes place when there is increase myocardial demand, usually upon exercise, in the presence of impaired perfusion by blood
57
What are the causes of myocardial ischaemia?
- reduced perfusion
- reduced blood oxygenation
- increase tissue demands
58
What can cause reduced perfusion?
Atheroma, embolus, thrombosis, spasm or inflammation of coronary arteries, generalised hypotension
59
What can cause reduced blood oxygenation?
Anaemia, carboxyhaemoglobinaemia
60
What can cause increased tissue demands?
Increased Cardiac output
| Cardiac hypertrophy
61
What is the most common cause of stable angina?
Low flow in atherosclerotic coronary arteries
62
What is ateriosclerosis?
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
What is atheroma?
Specific degenerative disease affecting large/medium sized arteries. When this leads to thinking and hardening of the arterial wall it is termed atherosclerosis.
64
How does an atheroma form?
- 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
What are the risk factors for atheroma?
-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
How does stable angina present?
- 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
What are the variants of stable angina?
Decubitus angina
| Variant/prinzmetal’s angina
68
What is decubitus angina?
Angina precipitated by lying down as there is increase venous return to the heart, is associated with LVF
69
What is variant/prinzmetal’s angina?
Occurs without provocation at rest as a result of coronary spasm. There is ST elevation during the episode but no troponin rise
70
What investigations do you run for stable angina?
FBC, glucose, lipids, TFTs
| Resting 12-lead ECG
71
How do you assess the likelihood of coronary artery disease?
Use ECC findings and clinical assessment using the NICE tool
72
What are the different categories for the nice tool for assessment of coronary heart disease in stable angina?
- 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
How do you carry out a stress 12-lead ECG?
If resting ECG normal, use Bruce protocol on treadmill, with ST depression >1mm indicating ischaemia. If positive within 6 minutes then angiography indicated
74
How do you manage stable angina?
- 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
What advice do you give for GTN spray?
- 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
How does a GTN spray work?
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
What are beta blockers used for?
Beta 1 sensitive blocks used as anti-hypertensive and decrease renin release from juxta-glomerular cells
78
What are the side effects of beta blockers?
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
What are the types of calcium channel blockers?
Digydropyridines (amlodipine/nifedipine)
| Rate limiting agents (verapamil/diltiazem)
80
How do calcium channel blockers work?
```
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
What are the side effects of calcium channel blockers?
Flushing and headache (as with all vasodilators), ankle swelling and constipation (GI SM inhibition)
82
How does nicorandil work?
It is a combined NO donor and also an activator of ATP-sensitive K-channels in vascular smooth muscle cells, leading to hyperpolerisation
83
Describe the anatomy of the cardiac chambers, valves, coronary arteries, great arteries and cardiac conduction system
- 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
What is pulmonary oedema?
-pulmonary oedema is due to an increase in fluid in the alveolar wall (pulmonary interstitium), which then affects the interstitial spaces
85
Describe the pathophysiology of pulmonary oedema
- 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
What are the clinical features of pulmonary oedema?
- 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
What is the acute presentation of pulmonary oedema?
- 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
How does someone with pulmonary oedema present on examination?
-tachypnoea
-tachycardia, with gallop rhythm
-raised venous pressure
-peripheral shutdown
widespread crackles/wheezes on auscultation
89
What investigations should be down for suspected pulmonary oedema?
- 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
what are the causes of pulmonary oedema?
- increased capillary pressure
- increased capillary permeability
- reduced plasma oncotic failure
- lymphatic obstruction
- other
91
What can cause increased capillary pressure?
- cardiogenic: LVF, valve disease, arrhythmias, VSD, cardiomyopathy, negative inotropic drugs
- pulmonary venous obstruction
- iatrogenic fluid overload
92
What can cause increased capillary permeability?
- ARDS (acute respiratory distress syndrome)
- infection: pneumonia/sepsis
- DIC (disseminated intravascular coagulation)
- inhaled toxins
93
What can cause reduced plasma oncotic pressure?
renal/liver failure
| hypoalbuminaemia
94
What other causes of pulmonary oedema are there?
neurogenic: raised ICP/head injury
PE
Altitude
95
What is the management of acute/decompensated heart failure causing pulmonary oedema?
- 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
Define heart failure
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
what are the common causes of heart failure?
- ischaemic heart disease
- dilated cardiomyopathy
- hypertension
98
What is cardiac output a function of?
pre-load, after-load and myocardial contractility
99
Describe maladaptive neurohormonal response in heart failure?
- 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
Describe the adaptive response to heart failure
atrial natriuretic peptide is released in response to atrial stretch, and acts to antagonise the fluid conserving effects of aldosterone
101
What are the symptoms of left heart failure?
-fatigue
-exertional dyspnoea
-paoxysmal nocturnal dyspnoea
otheropnea
102
What are the signs on examination of left heart failure?
- cardiomegaly with displaced apex beat
- 3rd heart sound, plus gallop rhythm if tachycardic
- bibasal course crackles
103
What is the most common cause of left heart failure?
long standing hypertention
104
What are the common causes of right heart failure?
- lung disease
| - pulmonary valve stenosis
105
What are the symptoms of right heart failure?
- fatigue
- breathlessness
- anorexia/nausea (hepatomegaly)
- swollen ankles
106
What are the signs of right heart failure on examination?
- jugular venous distension
- hepatomegaly/ascities
- dependent pitting oedema
- pleural effusions
- cardiomegaly, gallop rhythm
107
What is the New York association classification of heart failure?
- 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
What investigations should be done for heart failure?
- 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
What is the management for LV dysfunction?
- 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
What lifestyle advice can be given?
- 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
What are some. examples of ACE inhibitors?
ramipril, catopril, lisinopril
112
What prescribing points should be given with ACE inhibitors?
- risk of first dose hypotension
| - dry cough
113
What is contraindicated with ACE inhibitors?
- NSAIDS (renal damage)
| - diuretics until settled on medication
114
When should ACE inhibitors not be prescribed?
Systolic BP <100
115
How should people on ACE inhibitors be monitored?
renal side effects so monitor urea, creatine, K+ before and during treatment
116
Give example of beta blockers?
bisoprolol, metoprolol, nebivolol
117
Why are beta blockers used in heart failure?
block sympathetic activity that causes maladaptive and have anti-arrhythmic effects and thus reduce sudden death
118
Why are diuretics prescribed?
mainly used for symptomatic relief of oedema, but also venodilate
119
Which diuretics are favoured and why?
- 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
Why is spironolactone used?
used at non-diuretic dose to reverse neurohormonal adaption
121
When is digoxin used?
refractory heart failure and AF
122
How does digoxin work?
- 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
What are the symptoms of digoxin overdose?
- anorexia
- nausea
- visual disturbance
- diarrhoea
124
What is dosing of digoxin reliant on?
eGFR
125
Why does renal function need to be monitored in heart failure patients?
- digoxin is renally cleared
- thiazides are ineffective in renal failure
- diuretics and ACEi can lead to hyperkalaemia
126
What are the consequences of valvular inflammation?
- collagen exposure and thrombus development in the short term
- post-inflammatroy scarring, leading to long-term functional impairment
127
Which side of the heart is usually the site of endocarditis?
left
128
Where do embolisms usually go from endocarditis?
systemic organs
129
What is rheumatic fever?
an immune disorder that occurs in children, usually following tonsillitis/pharyngitis caused by group A B-haemolytic streptococci (GAS)
130
Describe the pathology of rheumatic fever
- 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
What causes congenital valvular heart disease and which valve does it affect?
Aortic stenosis due to calcification of a congenital bicuspid aortic valve
132
What causes ischaemic valvular disease and what valve does it affect?
mitral regurgitation caused by papillary muscle dysfunction post-infarction
