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5. Cardio 2 Flashcards

1
Q

A patient has a diagnosis of HOCM, and presents with cerebellar ataxia symptoms, and you notice kyphoscoliosis. What is the most likely diagnosis?

A

Friedrich’s ataxia

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2
Q

First and second most common causes of sudden cardiac death:

A

HOCM

ARVD (arrhythmogenic right ventricular cardiomyopathy)

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3
Q

Pathophysiology of ARVD + presentation:

A

Inherited AD with variable expression
RV myocardium is replaced by fibrous fatty tissue

Palpitations
Syncope
Sudden cardiac death

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4
Q

Investigations and results in ARVD:

A

ECG - T wave inversion in T1-T3. 50% epsilon wave terminal ‘notch’ on QRS
Echo - enlarged hypokinetic RV with thin free wall
MRI = fibrofatty tissue

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5
Q

Management of ARVD:

A

Sotalol, which must be avoided in long QT

Catheter ablation to prevent VT

ICD

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6
Q

Pathophysiology of HOCM, which is usually due to a mutation in the beta-myosin heavy chain protein:

A

AD disorder of contractile protein genes
Left ventricular hypertrophy causes reduced compliance and a reduced cardiac output, diastolic dysfunction.
Disarray and fibrosis is seen on biopsy.

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7
Q

HOCM is often asx, but features can include exertional dyspnoea, angina and syncope, and sudden death. Discuss the pathophysiology of syncope in HOCM:

A

Subaortic hypertrophy of the ventricular septum causes functional aortic stenosis causing syncope.
Syncope typically follows exercise.

*HOCM asymmetrically affects the heart

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8
Q

Discuss murmurs, echo findings and ECG findings in HOCM:

A

Ejection systolic murmur due to LVOT obstruction
Increases with valsalva, decreases on squatting
Pansystolic = systolice anterior motion of mitral valve = mitral regurgitation

MR SAM ASH

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9
Q

Drugs to avoid in HOCM:

A

Nitrates, ACEi, inotropes

They worsen LVOT obstruction

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10
Q

Spectrum of outcomes in HOCM:

A

Mostly asx
Arrhythmia
Syncope
Mitral regurgitation
Heart failure and symptoms
Sudden cardiac death

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11
Q

Management of HOCM depends on the severity and symptoms. Give some lifestyle advice, and pharmacological / surgical options:

A

No strenuous exercise
Avoid heavy lifting
Avoid dehydration

BB / verapamil for symptoms
Amiodarone
If at risk of sudden cardiac death = ICD

?Surgical myectomy, alcohol ablation, ?transplant

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12
Q

What is the most common form of cardiomyopathy, including pathophysiology:

A

Dilated

Dilated heart leading to predominantly systolic dysfunction.
4 chamber dilation, LV > RV.

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13
Q

Features of DCM:

A

Heart failure symptoms
Systolic murmur - stretching of valves may result in regurgitation
S3
Balloon on CXR

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14
Q

Around 1/3 of patients with DCM are thought to have a genetic predisposition, some due to specific syndromes e.g. DMD, and some familial. What is the inheritance mechanism seen in the majority of cases?

A

AD

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15
Q

Causes of DCM;

A

Idiopathic
Viral, coxsackie
IHD
Peripartum
HTN
Doxorubicin
Cocaine
Alcohol
Infiltrative e.g. haemochromatosis, sarcoid
Wet beri beri

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16
Q

3 causes of restrictive cardiomyopathy:

A

Amyloidosis
Post radiation
Loeffler’s endocarditis

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17
Q

When would peripartum cardiomyopathy typically develop, and give 3 risk factors for its development:

A

1 month pre delivery and 5 months psot

Older
High parity
Multiple pregnancy

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18
Q

The classifications of cardiomyopathies have changed in recent years. Many causes of dilated cardiomyopathy, among others, are now classed as secondary cardiomyopathy, with types including infective, infiltrative, storage, toxicity, inflammatory, neuromuscular, nutritional deficiency and autoimmune. Group the causes into these headings:

A

Infective - coxsacki B, HIV, chagas
Infiltrative - amyloidosis
Storage - haemchromatosis
Toxicity - doxorubicin, alcohol
Inflammatory - sarcoidosis
Endocrine - DM, acromegaly, thyroid
Neuromuscular - DMD, Friedrich’s ataxia
Nutritional deficiency - beri beri
Autoimme - SLE

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19
Q

Drug therapy in chronic heart failure:

A
  1. BB and ACEi, start separately. (If preserved EF there is no effect on mortality)
  2. MRA / aldosterone antagonist e.g. spiro / eplerenone, must monitor potassium

+ SGLT2i

  1. Specialist - ivabridine, ARNI, hydralazine +? nitrate / digoxin
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20
Q

Criteria for starting ivabradine, sacubitril-valsartan, digoxin, hydralazine with nitrate and CRT:

A

Ivabridine - sinus rhythm >75bpm, LVF <35%

Sacubitril/valsartan ARNI - LVF <35%, symptomatic on acei/arb. Needs acei/arb wash out period

Digoxin - definitely give in coexistant AF. Does not improve mortality but does improve symptoms.

Hydralazine - Afro-caribbean

CRT - widened QRS LBBB on ECG

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21
Q

Causes of chronic heart failure split into cardiac, high-output state and other:

A

Cardiac; IHD, CMO, HTN, valve disease, pericardial

High output; anaemia, thyrotoxicosis, phaeochromocytoma, liver failure, sepsis, beri-beri, Paget’s,

Other
Alcohol, obesity, cocaine, NSAIDs, BB

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22
Q

3 mechanisms that may explain PND:

A

Fluid settles over large area during sleep = breathless, resolving when wakes up.

Resp centre in the brain in less reactive during sleep, so resp rate and effort do not increase in response to O2 sats until they’re worse than normal.

Reduced adrenaline during sleep, myocardium relaxed, reduced cardiac output.

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23
Q

You have taken a comprehensive history and examination which gives you high suspicion of chronic heart failure. What is the investigation you will do next, and what will the results lead to?

A

NT-proBNP

High = >2000 2 week referral
Raised = 400-2000 4 week referral

BNP is produced by myocardium in response to strain.
Very high = poor prognosis.

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24
Q

Describe CRT and when it may be indicated in HF:

A

<35% ejection fraction.

Biventricular triple chamber pacemakers, with leads to RA,RV and LV. Synchronises the contractions in these chambers to optimise heart function.

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25
Factors that may decrease BNP levels and therefore mask how severe heart failure might be:
Obesity Diuretics ACEi BB ARB Aldosterone antagonists
26
Oxygen targets in acute heart failure:
94-98%
27
Respiratory failure + acute heart failure = ?intervention
CPAP
28
Regular medication for heart failure such as BB or ACEi should be continued in acute heart failure most of the time. What situations might you consider stopping the beta-blockers?
HR <50 2nd or 3rd degree AV block Shock
29
Why are patients with acute heart failure with hypotension <85 systolic / cardiogenic shock particularly difficult to manage, and give the options:
Some of the medications usually used to treat heart failure may exacerbate hypotension e.g. loops and nitrates. Inotropes - e.g. dobutamine, used in severe LV dysfunction with reversible cardiogenic shock Vasopressors if insufficient response to inotropes Mechanical circulatory assistance e.g. intra-aortic balloon pump / LVAD devices
30
Nitrates should not be given to all patients with acute heart failure; when should they be considered?
Concomittal myocardial ischaemia, severe hypertension, regurgitant aortic / mitral valve disease
31
Acute LV failure is often the result of decompensated chronic heart failure. Give some potential triggers:
Sepsis Arrhythmia MI Iatrogenic e.g. fluid overload Hypertensive emergency
32
Causes of a raised BNP:
LVH Ischaemia Tachycardia RV overload Reduced o2 sats GFR <60 Sepsis COPD Diabetes Cirrhosis
33
Assessment of patients with acute LV failure:
Clinical A-e ECG for ischaemia and arrhythmias Bloods - anaemia, infection, renal function, BNP ?Trop if suspected MI ABG in LV failure = T1RF CXR and Echo
34
Action of BNP;
Relaxes smooth muscle in blood vessels, reduces systemic vascular resistance. Also acts on kidneys to promote water excretion, and therefore reduces circulating volume.
35
Preserved vs reduced EF heart failure:
Preserved = reduced cardiac RELAXATIon due to increased ventricular stiffness. No signs of fluid overload. Reduced = IMPAIRED cardiac contractility, reduced cardiac output and increased end diastolic volume / pressure.
36
Aortic dissection is rare, but a serious cardiac pathology. What happens?
Tear in the tunica intima, blood pools between the layers of the aortic wall, creating false lumen.
37
Stanford and DeBakey Classifications:
Stanford: Type A = ascending aorta, before brachiocephalic Type B = descending, after left subclavian DeBakey: I - ascending aortic arch II - asc only IIIa - descending but only above diaphragm IIIb - descending but can go below diaphragm
38
CV/PAD risk factors apply in aortic dissection too, with hypertension being a big factor. Give some non-peripheral arterial disease related risk factors:
Rapid rises in BP --> weight lifting, cocaine Bicuspid Coarctation Acute volume replacment CABG Ehlers danlos and marfans Trauma Turners and Noonans Syphilis Pregnancy
39
What investigation is usually done to confirm the diagnosis of aortic dissection?
If STABLE , first line in CT angiogram MRI later if planning surgery CXR will usually be done, may exclude other differentials, may showed widened mediastinum
40
What investigation is more likely to be used in aortic dissection if the patient is unstable?
TOE
41
Aortic dissection is a surgical emergency. Analgesia, BP and HR management are needed, often involving beta-blockers. Discuss the different management options for type A vs type B tears:
Type A - open surgery with midline sternotomy, synthetic graft +/- aortic valve replacement Type B = TEVAR via femoral artery + stent graft. IV labetalol to reduce BP, ?conservative in type B.
42
Common features include severe chest / back pain, changes in BP, pulse deficits, syncope etc. Other features may result from involvement of specific arteries, give 3:
Spinal - paraplegia Distal aorta - limb ischemia Coronary = angina
43
Which valve pathology is likely after an aortic dissection, and give features:
Aortic regurgitation Early diastolic murmur Collapsing pulse Quincke's sign = nail bed pulsation De Musset's sign = head bobbing
44
Acute and chronic presentations of aortic regurgitation exist. Aortic dissection and infective endocarditis exist as acute causes. Give chronic causes, split into valve disease and aortic root disease.
Valve - rheumatic fever, calcification, CTD e.g. RA and SLE, bicuspid Aortic root - bicuspid, spondyloarthropathies e.g. ankylosing spondylitis, hypertension, syphilis, Marfan's, Ehlers Danlos
45
What does coarctation of the aorta describe, what are 4 associations, and give some features:
Congenital narrowing of the descending aorta Turner syndrome, bicuspid valve, berry aneurysms, neurofibromatosis Radiofemoral delay, Midsystolic murmur heard loudest over back,
46
Which risk assessment tool should be used for patients aged 84 and under to define their 10-year risk of cardiovascular disease and what does it include?
QRISK3 Age, gender, postcode, cholesterol, hypertension, smoking, alcohol, RA/DM/CKD presence etc. Low risk = <10%
47
Which groups should the QRISK2 NOT be used in as there are more specific guidelines available?
Diabetes mellitus eGFR <60 +albuminuria FHx of familial hyperlipidaemia
48
NICE suggest that QRISK2 may underestimate CVD risk in certain population groups:
Treated for HIV Severe mental health problems Certain medications including antipsyhotics, steroids, immunosuppressants Autoimmune / systemic disorders QRISK3 is better for this
49
Who should we offer a statin to in terms of QRISK score?
>10% 20mg atorvastatin first line
50
Statin and an antibiotic interaction:
Macrolide! Stop taking statin whilst on clarithro or erythromycin
51
Statins reduce cholesterol production in the liver. When should bloods be checked after commencing statins, and what should be checked?
3 months after commencing LFTs - can cause transient / temporary rise in ALT/AST but don't need to change anything unless >3x upper limit of normal Lipids; should aim for >40% reduction in non-HDL cholesterol, if not increase statin to 80mg
52
When should statins be offered regardless of QRISK score?
T1DM if over 40, have been diagnosed for >10 years, nephropathy present or other CVD risk factors CKD ALL patients All patient with CVD have high intensity 80mg atorvastatin
53
Side effects of statins:
Myopathy muscle pain ?Rhabdo - must check CK in all patients with muscle pain + statin T2DM Haemorrhagic strokes
54
Statin has not been effective / tolerated in reducing non-HDL cholesterol by >40%. The dose was increased and this didn't help either. What is a further drug option?
Ezetimibe - inhibits absorption of cholesterol in the intestine +/- bempedoic acid
55
Familial hypercholesterolaemia is AD, with most genotypes being heterozygous. When should it be suspected?
Total cholesterol >7.5 AND / OR: Personal / family history of premature coronary artery disease <60 years OR in first degree relative
56
A child has parents affected by familial hypercholesterolaemia. When should they be tested?
By 1 years old if 1 parent By 5 years old if 2 parents
57
Clinical diagnosis of familial hypercholesterolaemia is based on the Simon Broome criteria:
Adult: Total chol >7.5 // LDL-cholesterol >4.9 Child: Total chol >6.7 // LDL-cholesterol >4 + (definitive) = tendon xanthomata in patient or 1st / 2nd degree relative + (likely) = FHx, MI <50 years old 2nd degree, <60 in first degree, FHx of raised cholesterol levels
58
Management of familial hypercholesterolaemia:
High dose statin e.g. 80mg atorvastatin Offer family screening
59
Statins in pregnancy?
Discontinue statins 3m prior to conception due to risk of congenital defects
60
Ezetimibe is a lipid-lowering drug which inhibits cholesterol receptors on enterocytes, reducing the cholesterol absorption in SI. It can be used second line in non-familial hypercholesterolaemia. When should it be offered in familial hypercholesterolaemia?
If they have started statin therapy and the serum total OR LDL is not controlled after titration, or because they cannot tolerate the higher titrated dose (same as in non-familial)
61
Postural hypotension can be defined as a fall of systolic BP >20 mmHg / >10 dbp within 3 minutes of standing. Give some causes:
Dehydration / Hypovolaemia Autonomic dysfunction e.g. Parkinson's, diabetes Drugs e.g. diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives and alcohol
62
Treatment options for postural / orthostatic hypotension:
Midodrine Fludrocortisone
63
Investigation of postural hypotension:
Lying and standing BP - after 5 mins of lying down, then 1 and 3 mins post standing. Adequate fluid and fibre intake (to reduce dehydration and constipation) Avoid caffeine, alcohol No hot baths Compression stocking
64
Constrictive pericarditis can be caused by any cause of pericarditis, particularly TB. Give some clinical features of constrictive pericarditis:
SOB Right heart failure symptoms JVP x and Y descent Kussmaul's sign = paradoxical rise in JVP during inspiration Loud S3 / pericardial knock
65
What can be seen on CXR in constrictive pericarditis?
Pericardial calcification
66
Pericarditis is inflammation of the pericardium, and acute refers to it lasting <4-6 weeks. Most commonly idiopathic, next most common is viral. What is the most common virus, and give some other causes:
Coxsackie B virus TB uraemia post MI (1-3 days = fibrinous, weeks = autoimmune Dressler's) Radiotherapy SLE/RA Hypothyroidism Malignancy
67
Clinical features of acute pericarditis, including investigations and results:
Chest pain, pleuritic Relieved on sitting forwards Pericardial rub on auscultation Raised wcc, crp, esr ?Troponin ECG changes = saddle shaped st elevation widespread + PR depression All patients should get a TTE for ?pericardial effusion
68
The majority of patients with acute pericarditis can be managed as outpatients. Who should be managed as an inpatient, and what is the first line management?
High risk e.g. fever >38, elevated troponin should be managed inpatient. NSAIDs for symptomatic management Colchicine until symptom resolution + normalisation of inflammatory markers e.g. 1-2 weeks high dose then taper Colchicine for ?3 months total
69
Other management options that may be indicated in acute pericarditis:
Steroids used 2nd line / if inflammatory condition e.g. RA or recurrent TB and renal failure treat directly ?Pericardiocentesis if evidence of pericardial effusion (?tamponade)
70
What should be avoided until symptom resolution and normalisation of inflammatory markers in acute pericarditis?
Strenuous physical activity
71
Beck's triad and then other features of cardiac tamponade:
Muffled heart sounds Hypotension Raised JVP SOB, tachycardia, absent Y descent of JVP (due to limited RV filling), pulsus paradoxus
72
Where does the value for systemic vascular resistance come from?
SVR = 80 (mean aortic pressure - mean RA pressure) / cardiac output
73
Pulmonary artery occlusion pressure monitoring is an indirect measure of what?
Left atrial pressure e.g. filling pressure of the left heart. Normal = 8-12 Low PAOP = hypovolaemia Low + pulmonary oedema = ARDS High = overload
74
Who should be offered antihypertensive treatment?
>135/85 Stage 1 hypertension and under 80 years + one of: Target organ damage, established CV disease, renal disease, DM or QRISK >10% >150 Stage 2, regardless of age
75
Diagnosing hypertension:
Both arm BP measurements done. If >20mmHg difference, repeat. If remains higher, record the higher one and examine the patient. If first reading >140, repeat and then offer ABPM/HBPM If first reading >180, treat immediately
76
Lifestyle management strategies for hypertension:
Low salt diet (<3g per day) Reduce caffeine intake Stop smoking Drink less alcohol Balanced diet Exercise more Weight loss
77
Examinations and investigations in patients with newly diagnosed hypertension:
Fundoscopy Urine dipstick ECG looking for LVH / IHD U&Es HbA1c Lipids ECG
78
Symptoms of angina:
1. Constricting discomfort of chest, neck, shoulders, jaw, arm 2. Precipitated by physical exertion 3. Relieved by GTN in ~5 mins 3/3 = typical 2/3 = atypical 1/3 = consider alt dx
79
Medication to receive in stable angina:
Aspirin Statin Sublingual GTN + 1. BB or CCB (rate limiting) 2. Titrate dose 3. Add in other rather than monotherapy 4. Still sx / cannot tolerate = long acting nitrate, ivabridine, nicorandil etc If a patient is taking both BB and CCB, only add in other drug whilst awaiting PCI / CABG assessment
80
How to prevent nitrate tolerance:
Standard-release - asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours. Not seen in OD modified-release isosorbide mononitrate

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