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Physician Associate > Cardiology - 1A and 1B > Flashcards

Cardiology - 1A and 1B Flashcards

1
Q

What is the presentation of stable angina?

A

3 key features
-Constricting/heavy discomfort/pain in chest, jaw, neck, shoulders, arm
-Symptoms bought on by exertion. Other triggers –. cold, stress emotion.
-Symptoms reduced within 5 mins by rest or GTN.
3/3 typical angina 2/3 atypical 0-1 not angina

Other symptoms –> SOB, nausea, sweaty

DD –> MI, pericarditis, GERD, aortic dissection

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2
Q

What is stable angina?

A

Recurrent transient episodes of cardiac chest pain/discomfort that occurs when there is mismatch between blood/oxygen supply and metabolic demand..

Symptomatic reversible myocardial ischemia

  • 1/10 >65s
  • Most common cause –> atherosclerosis coronary artery. Less common –> anaemia.
  • RF –> male, smoking, HTN, diabetes, high cholesterol
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3
Q

Investigations for stable angina

A
  • Bloods –> FBC to exclude anaemia
  • ECG –> r/o ACS
  • Possible CXR/ECHO

Diagnostic

  • Not previously diagnosed IHD –> 1st line –> CT coronary angiography
  • 2nd line e.g CTCA inconclusive –> Stress ECHO w exercise
  • In patient w symptoms and previously proven IHD –> treat as stable or if need further confirmation –> exercise ECG
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4
Q

What is the management for stable angina?

A

Antianginals

  • 1st line –> BB or CBB –> atenolo or amlodipine INTOLERANT THEN SWITCH, NOT CONTROLLED COMBINE.
  • 2nd line –> still not controlled or intolerant –> monotherapy or combine w long acting nitrate, ivabradine or nicorandil.
  • Optimal therapy inadequate –> consider revasc e.g PCI

Other management

  • Short acting nitrate –> GTN spray –> PRN symptom relief or sublingual tablets. Use once, wait 5 mins, use again and wait 5 mins, pain continues call ambulance.
  • Antiplatelet –> Aspirin 75mg 1st line. 2nd line clopi.
  • Statins
  • Consider ACEi when HTN.
  • Modify RF –> smoking, exercise, dietary advise
  • Refer hospital –> pain at rest or minimal exertion or GTN not working..
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5
Q

What is Unstable Angina?

A
  • Severe acute myocardial ischaemia without myocardial necrosis.
  • Prolonged severe angina at rest.
  • Major cause –> coronary artery atherosclerosis –> plaque rupture in coronary artery. Decrease in blood flow causes acute ischaemia of affected myocardium but not myocardial necrosis.
  • Other cause –> coronary vasospasm w/o rupture.

RF

  • Modifiable –> obesity, smoking, exercise, alcohol, high cholesterol, HTN
  • Non modifiable –> male, menopause, FH
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6
Q

What is the presentation of unstable angina?

A

Symptoms

  • Chest pain on rest >20 mins, possible palpitations
  • SOB, sweating, N&V
  • May be prolonged or worsening stable angina or new onset of severe angina symptoms
  • Possible Hx table w new onset pain an limitation activities

Signs

  • Haemodynamic instability –> tachypnoea/cardia, HTN, low O2
  • HR and BP can be high or low

DD –> MI, pericarditis, PE aortic dissection

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7
Q

What are the investigations for unstable angina?

A

Troponin -> no myocardial necrosis therefore no significant rise but can be rise. Serial trops to differentiate between unstable angina and NSTEMI. Trop detectable 3-6hours post MI, and peak 12-24 hours after.

  • FBC (anaemia), TFT, glucose
  • ECG –> may be normal or no specific changes. May be ST depression, T wave flattening or inversion.
  • CXR –> r/o other causes look for cardiomegaly
  • ECHO –> regional wall abnormalities
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8
Q

What is the management for unstable angina?

A

HOSPITAL

  • Dual antiplatelet –> aspirin 300mg loading dose then 75mg OD. AND either clopi 300/75, tricagrelor 180/90, prasugrel 60/10. Tricagrelor preferred in high risk groups e.g >60, previous stroke, MI.
  • Antithrombin/coag –> Fondaparinux (factor Xa inhibitor). 2.5mg OD.
  • Opiates –> morphine
  • GTN spray –> PRN relieve symptoms as opens coronary arteries
  • Background angina therapy –> BB
  • High dose statin –> atorva 80mg OD
  • Coronary angiography when refractory to medical Tx, possible PCI.
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9
Q

What is an NSTEMI?

A
  • Partial thickness necrosis of an area of myocardium
  • Cracking of unstable atherosclerotic plaque stimulates formation of platelet rich thrombus –> significant prolonged narrowing and part of territory supplied myocardium has ischaemic necrosis.
  • Often a retrospective diagnosis when trop and ECG results.
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10
Q

What is the presentation of an NSTEMI?

A
  • Acute unremitting central chest pain lasting >20 minutes. Usually severe may be mild or absent. At rest.
  • 1/3 occur in bed at night
  • SOB, sweating, pallor, palpitations, nausea, vomiting
  • Silent MIs –> syncope, epigastic pain, vomiting, stroke, increase confusion, hyperglycaemia.
  • In elderly/diabetics –> can be vague e.g epigastric

SITE –> central
ONSET –> often sudden
CHARACTER –> crushing and tight not sharp
RADIATION/RELATIONSHIP –> left arm, neck, jaw. Less common R arm, epigastric, back. Relationship to exertion, emotion, eating.
ASSOCIATED SYMPTOMS –> nausea, vomiting, SOB
TIMING –> >20 mins
EXACERBATING/RELIEVING SYMPS?
SEVERITY –> high can be atypically low

  • Haemodynamic instability
  • 4th heart sound
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11
Q

What are the investigations in NSTEMI?

A
  • Troponin –> Increase in troponin reflects degree of irreversible myocyte death as significant necrosis can occur w/o ST elevation. Values >99th centile diagnostic of MI. Diff. from unstable angina by rise troponin.
  • ECG –> may show ST depression, T wave inversion. Or non specific changes. Repeat, 20% MI normal initially.
  • FBC, TFT, glucose (powerful indicator survival needs tight control), U and E
  • CXR
  • ECHO
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12
Q

How should you manage an NSTEMI?

A

ACS protocol

  • Dual antiplatelet –> Aspirin w clopi/tricagrelor
  • Antithrombosis/coag –> fondaparinux
  • Pain relief –> opiates –> morphine
  • BB –> atenolol –> decrease HR, BP and contractility –> decrease O2 demand
  • Statin –> atorva 80mg
  • Consider glycoprotein inhibitor in high risk
  • Also think ACEi as part secondary prevention w statin.

Other

  • All patients w increased troponin –> coronary angio. Then potential revasc w PCI or CABG.
  • GRACE score –> predict those most at risk, targer intervention, risk mortality within 6 months.
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13
Q

What is a STEMI?

A
  • Full thickness necrosis of an area of myocardium
  • Complete occlusion of coronary artery leads to full thickness necrosis of myocardium supplies by that artery
  • 5 MI types —> Type 1 atherosclerotic plaque is most common
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14
Q

What is the presentation of a STEMI?

A
  • Acute and unremitting central chest pain lasting >20 mins. Severe at rest
  • Sweating, SOB,’pallor, nausea, vomiting, palpitations
S
O
C
R
A
T
E
S
  • Haemodynamic instability
  • HR or BP up or down
  • 4th heart sound
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15
Q

What are the investigations for a STEMI?

A
  • Troponin —> significant rise. Detectable from 3-6 hours. Peaks 12-24 hours. Serial trops
  • ECG —> ST elevation, hyperacute T waves or new left bundle branch block within hours. STEMI diagnosis initially from ECG alone as trops can take a while to rise.
  • New LBBB –> MI till proven otherwise
  • ECG —> T wave inversion and pathological Q waves over hours to days.
  • FBC,TFT, glucose, UandE
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16
Q

How do you manage a STEMI?

A

ACS protocol

  • Dual antiplatelet —> aspirin 300mg loafing then 75mg once daily. And clopi 300/75 or tricagrelor or prasugrel.
  • Antithrombin/coag —> fondaparinux
  • Opiate, morphine
  • GTN spray
  • BB
  • Consider glycoproteins
  • Statin —> 80mg atorva
  • ACEi

Surgical

  • Early coronary perfusion saves lives, particularly STEMI presenting within 12 hours
  • Immediate —> within 90 mins —> PCI. When not available working 120mins consider thrombolysis and transfer to PCI centre after infusion for PCI or angiography.
  • Beyond 12 hours —> specialist advice
  • Patients w STEMI who don’t receive repercussion (presenting >12 hours symptom onset) treat w fondaparinux.
  • PCI —> catheter you place aren’t to open up blood vessels, involves dilation of artery and balloon.
  • CABG —> take another artery, commonly internal mammary artery, attach to coronary artery above and below blockage and graft diverts blood. Improve blood supply. More invasive but manages complex e.g several blockages
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17
Q

What are the 5 types of MI?

A

Type 1 - atherosclerotic plaque rupture

Type 2 - mismatch and imbalance in myocardial O2 —> HR, anaemia, embolism, low BP

Type 3 - sudden cardiac death with ischaemia

Type 4 - During PCI

Type 5 - During CABG

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18
Q

What is essential HTN and the classification for HTN?

A

-RF –>65, smoking, diabetes, alcohol, obesity.

Classification

Stage 1

  • Clinic BP >140/90 w home BP >135/85.
  • Over 80s clinic BP >150/90 w home BP >145/85.

Stage 2 – Clinic BP >160/100 w home BP >150/95.

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19
Q

What is the management for HTN?

A

Offer treatment anyone w stage two.

Stage one
-Treat anyone <80 w diabetes, renal disease, target organ damage, Q risk >20%, established cardiovascular disease. Those w/o above, conservative w lifestyle e.g weight loss, stop smoking.

<55 –> ACEi/ARB –> +CCB –> +thiazide like diuretic (bendroflumethiazide) –> spironolactone/high dose thiazide/BB/a blocker

> 55 or afrocarribean –> CCB –> +ACEi/ARB –> +thiazide like diuretic (bendroflumethiazide) –> spironolactone/high dose thiazide/BB/a blocker

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20
Q

What is the presentation of essential HTN?

A

RF –> >65, smoking, diabetes, alcohol, obesity.
Often asymptomatic
Severe –> headache, blurred vision.

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21
Q

How should you investigate essential HTN?

A
  • Measure BP, confirm w home BP or ambulatory BP.
  • Bloods  FBC, glucose, electrolytes, eGFR, lipids. Calculate Q risk score. Check protein creatinine ratio to r/o underlying kidney cause.
  • Possible CXR (cardiomegaly) and ECG (end organ damage (LVH).
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22
Q

What are the causes of secondary HTN?

A
  • Causes –> kidney e.g PCKD, glomerulonephritis. Endocrine e.g conns, acromegaly.
  • Iatrogenic and drugs –> e.g NSAIDs, alcohol, amphetamines, antidepressants
  • In NSAIDs –> vasoconstriction of renal arteries and increase in glomerular pressure

-Can be signs of underlying cause e.g oedema, weakness and polyuria in conns.
Ix –> Those in essential
Tx –> Depend on cause e.g iatrogenic stop meds.

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23
Q

What is isolated systolic HTN?
Why does isolated systolic HTN occur?
What are the investigations and treatment?

A
  • Systolic >140 w diastolic <90
  • Compliance aorta and arteires < w ageing, stiffer aorta –> increase pressure in LV to work against resistance in systole therefore increasing systolic. During diastole, inward pressure to rebound therefore lower diatosle.

-Ix –> Those as essential
Tx >160/<90 same as essential HTN.

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24
Q

What are the types of hypertensive emergency?

How do they present?

How should they be treated?

A

Accelerated = BP >180/110
Malignant = >200/130 in malignant
WITH END ORGAN DAMAGE

  • Types of hypertensive emergency –> rapid increase in BP –> vascular damage and end organ damage.
  • Malignant w papilloedema, accelerated w/o.
  • Often already have HTN (often younger e.g 40), may present w blurred vision, headaches, seizures.
  • Usually associated w secondary causes HTN e.g renal problems
  • Hospital –> bloods to check kidney function, CXR check cardiomegaly.

Tx

  • Needs rapid Tx as may precipitate AKI or HF.
  • Decrease BP slowly over 24 hours (prevent hypoperfusion)
  • IV nitroprusside or CBB diltiazem and verapamil.
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25
Q

What is prinzmetal/variant angina and its triggers?

A
  • It develops when a coronary artery supplying blood and oxygen to your heart goes into spasm and suddenly narrows. Does not typically have episodes of angina during exercise.
  • Triggers –> emotional stress, exposure to extremely cold weather or a sudden drop in temperature, hyperventilation, allergic reactions (usually severe reactions that result in histamine release, sometimes referred to as Kounis Syndrome), inflammation of the coronary artery wall, smoking, some antidepressants, alcohol
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26
Q

What is the presentation of prinzmetal angina?

A
  • Pain or discomfort in their chest, arm or jaw.
  • Tends to be at rest and in the early morning or late at night.
  • Is often severe, but can be variable and can also be mild (a sense of unease).
  • Can occur in other locations in the body; the back, shoulders, neck, stomach and arms
  • The spasm can come in ‘clusters’ of two or three. If the spasm is persistent it can lead to anabnormal heart rhythm, for which you may need treatment, or in rare instances aheart attack.
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27
Q

What are the investigations in prinzmetal angina?

A
  • Troponin to rule out ACS
  • ECG
  • Coronary angiogram(with an injection of Acetylcholine, a chemical that can ‘provoke’ tightening and spasm of the blood vessel during the procedure, thus revealing providing the diagnosis in some patients).
28
Q

How is prinzmetal angina treated?

A
  • Sublingual nitratesor GTN spray

- Calcium channel blocker, such as Verapamil, Amlodipine or Diltiazem, to help prevent or reduce the number of spasms.

29
Q

Whats the difference between aortic aneurysm and dissection?

A

Aneurysm

  • Bulge in aorta
  • Abnormal dilatation of a blood vessel by more than 50% of its normal diameter.
  • Arteries made of three layers –> intima, media, adventitia.
  • Aneurysm when irreversible degradation of elastic lamallae (outermost part tunica intima) and associated smooth muscle loss

Dissection

  • Tear in aorta
  • Tear in the intima layer of the aortic wall, causing blood to flow between and splitting apart the tunica intima and media.
  • Acute (when diagnosed ≤14 days) or chronic (when symptoms diagnosed >14 days
  • More common in men and in connective tissue disorders
  • Most common in AA and AA

-RF – age (50-70), hypertension, smoking, trauma, marfans,

30
Q

What is the classification of aortic dissection?

A

Stanford
Group A – includes DeBakey Types I and II –> involves the ascending aorta and can propagate to the aortic arch and descending aorta; the tear can originate anywhere along this path
Group B – dissections do not involve the ascending aorta and include DeBakey Type III

Debakey
Type I – originates in ascending aorta and propagates at least to the aortic arch. <65, highest mortality,
Type II – confined to the ascending aorta
Elderly w atherosclerotic disease and HTN
Type III – originates distal to the subclavian artery in the descending aorta

31
Q

How does aortic dissection present?

A
  • Tearing or sharp pain, maximal at onset (unlike MI which builds), radiating to back.
  • Anterior pain suggest ascending aorta, posterior pain descending aorta.
  • BP –> hypertension and then hypotension as dissection becomes more severe –> hypovolaemia secondary to blood loss
  • New murmur or aortic regurgitation. Neurological deficits.
  • End-organ hypoperfusion (such as reduced urine output, paraplegia, lower limb ischaemia, abdominal pain secondary to ischaemia, or deteriorating conscious level).
32
Q

How is aortic dissection diagnosed?

A

1st line gold standard - CT angiogram. Classification can assist surgical planning.

Bloods –> (FBC, U&Es, LFTs, troponin, coagulation) with a crossmatch of at least 4 units, in addition to an arterial blood gas to aid initial assessment.

ECG –> r/o any cardiac pathology.

ECHO

33
Q

How should aortic dissection be managed?

A
  • Urgent vascular input and surgical repair, Urgent surgical stenting or repair (time critical – each passing hour increases mortality)
  • High flow oxygen and IV access

Type A –> ascending aorta

  • Surgical, synthetic graft
  • High mortality not treated

Type B –> descending aorta

  • Medical –> 1st line control HTN labetalol IV. Rapidly lower the systolic pressure, pulse pressure, and pulse rate to minimise stress of the dissection and limited further propagation.
  • Only require surgery when rupture or worsening pain
  • Chronic stable dissections can be managed medically w anti hypertension
  • In chronic may get aneurysm, endovascular repair

Lifelong antihypertensive therapy and surveillance imaging

34
Q

What is an AAA?

A
  • A dilatation of the abdominal aorta greater than 3cm
  • 1 in 70 men >65
  • Possible causes –> atherosclerosis, trauma, infection, connective tissue disease e.g marfans or inflammatory disease (e.g. Takayasu’s aortitis).
  • RF –> smoking, hypertension, hyperlipidaemia, family history, male gender, and increasing age
  • Screening, Abdominal US scan for all men in their 65th year.
35
Q

What is the presentation of an AAA?

A

-Often asymptomatic and detected on incidental finding or screening.

  • Non-specific abdominal pain, pain suggests high risk of rupture
  • Back or loin pain
  • Symptoms of peripheral vascular disease –> Distal embolisation producing limb ischaemia
  • On examination, a pulsatile mass can be felt in the abdomen (above the umbilical level), and rarely, signs of retroperitoneal haemorrhage may be evident.

Rupture AAA

  • Pain (abdominal, back, or loin) and a degree of shock or syncope
  • -Sudden severe pain, dizziness, sweaty clammy skin, tachycardia, shortness of breath (when rupture)

-DD –> renal colic

36
Q

What is the major investigation for AAA?

A
  • Abdminal ultrasound scan (USS)

- Once an USS has confirmed, CT scan with contrast when at threshold diameter of 5.5cm

37
Q

What is the medical and surgical management for AAA?

A

Medical
-<5.5cm can be monitor Duplex USS, as surgery prior to this diameter provides no survival benefit either for open repair or endovascular repair
3.0 – 4.4cm: yearly ultrasound
4.5 – 5.4cm: 3-monthly ultrasound
>5.5cm immediate referral for surgery and 3 monthly ultrasound

  • Treat reversible risk factors – stop smoking, statin and aspirin, BP control
  • Treating peripheral arterial disease

Surgical

  • > 5.5cm in diameter, AAA expanding at >1cm/year, or a symptomatic AAA in a patient who is otherwise fit.
  • Endovascular stenting, Laparoscopic repair, Open surgical repair

In the UK, any AAA >6.5cm requires notification to the DVLA and disqualifies from driving until repaired.

38
Q

What are the causes and presentation of thoracic aortic aneurysms?

A

Can involve ascending aorta or aortic root (60%), aortic arch (10%), descending aorta (40%), or thoracoabdominal aorta (10%) segments.

Main causes –> connective tissue diseases, bicuspid aortic valve

RF –> family history, HTN, atherosclerosis (specifically descending aneurysms), smoking, high BMI, male gender, age

-Commonly asymptomatic –> found incidentally

When symptomatic –> pain
Ascending aorta –> Anterior chest
Aortic arch –> Neck
Descending aorta –> Between the scapulae

Other symptoms

  • Back pain – secondary to spinal compression by descending or thoracoabdominal aneurysm
  • Hoarse voice – from damage to the left recurrent laryngeal nerve in arch aneurysms
  • Distended neck veins – from SVC compression
  • Symptoms of heart failure – from involvement of the aortic valve
  • Dyspnoea or cough – secondary to tracheal or bronchial compression

Ix –> CT w contrast

Tx

  • Depends on location
  • Medical –> Control BP, stop smoking, statin, antiplatelet
  • Surgical –> >5.5cm. When descending aorta >6.
39
Q

When may thiazide be a 1st line management for HTN?

A

When should be CCB but CI e.g due to oedema, HF

40
Q

What is acute pericarditis and its causes?

A
  • Inflamm of pericardium w or w/o pericardial effusion
  • Injury to pericardium e.g virus –> inflamm response
  • Pericardium –> visceral layer attached to epicardium of heart and parietal (fibrous) anchors heart to other structures in mediastinum. 50ml of serous fluid in between –> lubrication, when inflamed –> pain as layers rub
  • Often seasonal w viral trends, higher in young previously healthy
  • Flu, herpes
  • Autoimmune e.g RA and SLE.
  • Bacterial –> TB
  • Secondary metastatic –> breast and lung
41
Q

How does pericarditis present?

A
  • Rapid onset sharp and pleuritic central chest pain –> worse on inspiration and lying flat, relieved w sitting forwards
  • Can by SOB (effusion), fever, cough
  • Think PMH –> e.g post flu in young men when IHD not likely
  • Pericardial friction rub —> crunching snow
  • Severe w pericardial effusion progressing to tamponade –> Becks triad (hypotension, increase JVP, muffle heart sounds), pulsus paradoxus (Fall systolic BP >10mmHg on inspiration)
42
Q

What are the investigations for pericarditis?

A

Diagnosis
-Two of –> sharp pleuritic chest pain worse w lying down and eased w sitting forwards, diffuse ST elevation, pericardial friction rub w crunching snow, pericardial effusion.

Ix
-ECG –> saddle shaped ST elevation spread across all areas –> DIFFUSE. Can also be PR depression.
-Bloods –> FBC, CRP, ESR
-Trop –> if widespread inflamm on visceral peri and spread to epicardium then top can be raised in 1/3 patients (to lower levels than MI).
CXR –> cardiomegaly when effusion. Help Dx pneumonia, common in bacterial.
-ECHO –> suspected effusion

43
Q

What is the management for pericarditis?

A
  • Sedentary until resolution of symptoms and ECG and CRP.
  • NSAID ibuprofen 2 weeks or aspirin.
  • Colchicine 3 months –> reduce risk reoccurence
44
Q

What is constrictive pericarditis?

A

Permanent thickening or pericardium as result of recurrent pericarditis. Losing its elasticity and decrease ability of heart to work effectively.
Risk of developing highest in those w TB pericarditis

45
Q

What is a pericardial effusion and how is it treated?

A
  • Build up of fluid in pericardial sac
  • Often due to acute pericarditis. Can be caused by aortic dissection
  • Small effusions –> asymp w only symps acute peri
  • Large –> SOB, compression of locals structures –> hiccups (phrenic), nausea (diaphragm).
  • Progress tamponade –> BECKS –> hypoten, increase JVP, muffle heart sounds
  • CXR –> cardiomegaly when effusion >300ml
  • ECHO –> translucent free zone around heart
  • Treat cause

Tx
-Pericardialcentesis –> drain effusion, send fluid for culture

46
Q

What is cardiac tamponade?

A

Accumulation of fluid into pericardial sac –> increase intrapericardial pressure and decrease ventricular filling –> decrease CO –> rapidly lead to cardiac arrest

Causes
Trauma
Aortic dissection
Medical e.g cardiac catheterisation causing septal puncture
Pericardial effusion and its causes

BECKS

  • Hypotension, increase JVP, muffle heart sounds
  • Pulsus parodoxus –> fall of systolic >10mmHg on inspiration
  • Pericardiocentesis –> drain effusion. Treat cause
47
Q

What is infective endocarditis?

What are the most common causes of acute and subacute?

A
  • Infection of interior lining (endothelial) of surface of heart and its structures e.g valves as well as foreign bodies e.g prosthetic valves
  • Pathogen –> inflamm –> vegetation containing inflamm cells
  • Common consequence of two factors –> presence of organisms in blood (bacteriamia) and abnormal cardiac endothelium that enables their adherence and growth.
  • Causes bacteriemia –> IV drug use, poor dental hygiene, procedures e.g cannula, dental treatment

ACUTE

  • Occurs over days/weeks. Organisms affecting structurally normal heart, commonly effects valves
  • SASA –> Staph aureus in substance abusers via skin. Also common prosthetic valves

SUBACUTE

  • Occurs over weeks/months, weakly pathogenic organisms effect structurally abnormal heart. e.g valves
  • Strep viridans, access through oropharynx e.g dental procedure
48
Q

What is the presentation of infective endocarditis?

A

History –> recent surgical procedure, IV drug abuse

  • 85% FEVER AND NEW MURMUR –> Anyone w these symptoms IE until proven otherwise
  • Systemic –> fever, night sweats, malaise, fatigue

Immune complex disposition –> FROMJANE
Fever
Roth spots –> retinal haemorrhages. White spots on fundoscopy.
Osler nodes –> small tender purple s/c lesions on pulp fingertips
Murmur
Janeway lesions –> erythematous macular non tender lesions on fingers and palms hands/soles feet
Anaemia
Nail bed/splinter haemorrhages –> fine thread like blood clots running vertically up nail bed
Emboli –> vegetation can emboli to lungs and brain

Also –> petechaie –> red/purple/brown spots on skin –> arms and legs

49
Q

What are the key inevstigations needed to diagnose IE?

A
  • TOE –> gold standard –> better imaging and more sensitive than TTE
  • Blood cultures –> 3 sets at 3 diff times from 3 diff sites at peak of fever. Within 90 mins acute and 6 hours subacute. 90% sensitivity.

Bloods –> FBC, CRP/ESR. May be normocytic normochromic anaemia

  • CXR –> cardiomegaly
  • CT –> embolic
  • ECG any changes
50
Q

What are DUKEs criteria for diagnosis IE?

A

For diagnosis –> 2, major, 1 major and 3 minor or 5 minor

Major

  • 2 +ve blood cultures
  • ECHO showing vegetation abscess, problem w valves.

Minor

  • RF
  • Fever
  • Immune complex signs –> each a minor
51
Q

What is the management for IE?

A

Antibiotics as soon as blood cultures taken.
-Ab –> 4-6 weeks w at least 2 weeks IV

Staph aureus
-Flucloxacillin when native valve.
Prosthetic –> fluclox + gentamycin and rifampicin

Strep viridans
-Penicillin/amoxicillin (vancomycin when allergic) + gentamycin

Surgery

  • Needed in 50%
  • Debridement, repair, replace, remove. Remove infected device, replace valve, remove vegetations when risk emboli.
52
Q

What is heart failure in general?

A
  • Cardiac output is inadequate for bodies requirements –> inability of heart to deliver blood and oxygen at rate that meets metabolic demands.
  • Complex syndrome –> can result from any structural or functional disorder that impairs hearts ability to act as pump
  • Cases rise from >55 and peak >80

Ischaemic –> secondary to MI and ischaemia
Valvular
-Aortic and mitral –> L sided e.g SLE, bicuspid aortic valve, IE,
-Tricuspid and pulmonary –> Tricuspid failure in rheumatic fever and dilation R ventricle. Pulmonic stenosis –> congenital related e.g tetralogy of fallot.
-Hypertensive

Causes

  • Most common IHD
  • CHD
  • Cardiomyopathies
  • Valvular heart disease (aortic stenosis)
  • Arrhythmias (AF)
53
Q

What is the difference between acute and chronic HF?

A
  • Chronic –> Develops and progresses slowly

- Acute –> Sudden onset symptoms, most cases in those w chronic HF whose symptoms quickly worsen.

54
Q

What is the typical presentation of HF?

A

Typical (left sided, respiratory)

  • SOB
  • Orthopnea –> SOB lying down –> How many pillows?
  • Paroxysmal nocturnal dyspnoea –> Sudden waking in night w SOB, and nocturnal cough. Need to sit on side of bed and walk around.
  • Pink frothy sputum
  • Wheeze
  • Palpitations
  • Poor exercise tolerance
  • Decrease weight (cachexia), increase (fluid retention)
  • Tachy, displaced apex beat (LVH), crackles, murmurs, cold peripheries.

R sided

  • Liver congestion –> nausea, anorexia, early satiety, RUQ pain
  • Peripheral oedema
  • Epistaxis
  • Nocturia –> lying flat, fluid backs up from legs to kidneys
55
Q

What is the New York classification of HF?

A

1 - Asymptomatic, no limitations
2 - Mild symptoms, comfortable at rest, slight limitation w SOB on activities
3 - Clear limitation, symptoms w minor activity
4 - Symptomatically severe, SOB at rest

56
Q

Explain systolic and diastolic HF?

A

Systolic

  • Inability of ventricles to contract normally therefore decrease CO.
  • Ejection fraction <40%.
  • Causes –> IHD/MI, HTN, diabetes, valve, dilated cardiomyopathy, arrhythmias

Diastolic

  • Inability of ventricles to relax and fill normally. Preserved ejection fraction but impaired ventricular filling and less blood to start with.
  • Causes –> HTN, diabetes, constrictive pericarditis, caridac tamponade, restrictive cardiomyopathy
57
Q

How does LVF and RVF occur?

A

LVF
Decrease CO –> decrease BP baroreceptors –> sympathetic overdrive –> Increase BP but also increase HR –> increase peripheral resistance and increase blood volume –> heart works harder –> LVH –> decrease SV –> dilation and failure

RVF

  • Not common
  • Insufficient R ventricle output –> msot cases caused by chronic lung disease e.g COPD –> causes pulmonary HTN which means –> increase resistance therefore R ventricle needs increase pressure to maintain output –> hypertrophy –> dilate and failure
58
Q

What is high output HF?

A

Normal heart but increase needs –> anaemia, pregnancy, hyperthyroidism

59
Q

What are the investigations for HF?

A

1st line –> BNP –> brain natriuretic peptide –> secreted by ventricles in response to stress. N terminal (NT pro BNP) cleaved from pro BNP to release BNP. Both BNP and NT pro BNP increase in patients w HF. Levels correlate w stress and severity of HF. BNP distinguishes HF from other causes SOB, but other causes can increase BNP e.g COPD,

Gold standard –> ECHO –> key –> Assess structural/functional abnormalities. May indicate cause e.g valvular and can confirm presence/absence LV dysfunction

ECG –> may show cause –> look for arrhythmia, ventricular hypertrophy. Abnormal in 80%, can be non specific changes.
-BNP and ECG normal –> not likely HF

Diagnosis –> Requires symptoms of failure and objective evidence of cardiac dysfunction at rest.

60
Q

What is the management for chronic HF?

A

Management –> relieve symptoms, prevent and control disease

ABAL
A --> ACEi/ARB 
B- Beta blocker
A - Aldosterone antagonists
L - Loop diuretic e.g furosemide
  1. Disease influencing therapy –> neurohumoral blockade, inhibit renin-aldosterone-angiotensin system and inhibit sympathetic NS –> ACEi (ARB if cough) + BB. Low dose and slow increase.
  2. Symp. Tx of congestion –> loop diuretic
  3. Symps despite therapy –> Add aldosterone anta.
  4. Can’t have ACEi/ARB –> hydrazaline/nitrate combo –> vasodilators
  5. Digoxin or Ivabradine. Digoxin –> cardiac glycoside –> decrease HR. All other medication at high dose before add digoxin.
  • Tx cause –> e,g valve disease
  • Treat exac. factors e.g anaemia
  • Avoid exac factors –> NSAIDS in fluid retention

-Monitor U and E, ACEi, diuretics, and aldosterone antagonists can cause electrolyte disturbance

61
Q

What is acute LVF?

A

Left ventricle unable to adequately move blood through left side into the body –> backlog of blood left atrium, pulmonary veins and lungs –> vessels in these areas are engorged with blood as increased volume and pressure –> they leak fluid and are unable to reabsorb fluid from the surrounding tissues. This causes pulmonary oedema –> the lung tissues and alveoli become full of interstitial fluid –> interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.

Triggers

  • Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function)
  • Sepsis
  • Myocardial Infarction
  • Arrhythmias

Presentation

  • Rapid onset SOB –> exacerbated by lying flat and improves on sitting up.
  • Type 1 RF
  • Look ill
  • Frothy pink/white sputum
  • Increase RR
  • Reduce sats
  • Tachy
  • 3rd HS
  • Bilateral basal crackles

-If also have R sided HF –> increase JVP, peripheral oedema

Work up

  • History
  • Clinical Examination
  • ECG (to look for ischaemia and arrhythmias)
  • Arterial Blood Gas (ABG)
  • Chest Xray
  • Bloods (routine bloods for infection, kidney function, BNP and consider troponin if suspecting MI)
Management
Pour SOD
-Pour - stop IV fluids
-Sit up
-Oxygen
-Diuretics --> reduces circulating volume, heart less overloaded, pump better

Monitor fluid balancce

62
Q

You are asked to review a patient that has just started desaturating, what should be one the the initial questions?

A

How much fluid that patient has been given and whether they might not be able to process that much.

For example, an 85 year old lady with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturations. This is a common scenario and a dose of IV furosemide can often work like magic to clear some fluid and ease their breathing.

63
Q

What is rheumatic fever and its pathophysiology?

A

Bacteria mediated infection w streptococcus. Usually 3 weeks after step pharyngitis.

  • Group A b-haemolytic strep –> body produces Ab against strep cell wall, these Ab also react against cardiac proteins. Ab cross reaction –> affect joints, brain.
  • RF –> strep pharyngitis, poor hygiene, skin infection
  • Common developing countries
  • Ages 5-15
64
Q

What is the typical presentation of rheumatic fever? Involving major and minor criteria.

A

Presentation

  • Evidence strep infection –> +v throat culture (usually –ve by symptoms), rapid strep antigen, increase strep Ab titre, recent scarlet fever.
  • Sore throat, fever, abdo pain
  • Erythematous pharynx w lymphadenopathy

Major

  • Arthiritis in large joints (75%) (migratory)
  • Chest pain –> pancarditis, tachy, murmurs (mitr or aorc regurg), pericardial rub, conduction defects
  • Erythema marginatum –> macular erythematous rash –> red raised edges and clear centre –> trunk, thighs, arms
  • Sydenham chorea –> abnormal involuntary movement (bi or uni lat), can be preceded by emotional lability and uncharacteristic behaviour. Late in 10%.
  • Subcutaneous nodules –> small mobile, painless nodules on extensor surfaces of joints and spine

Minor

  • Fever
  • Arthralgia
  • Prolonged PR interval
  • Increase CRP/ESR

Diagnosis Jones criteria –> Evidence of recent strep infection plus 2 major criteria, or 1 major + 2 minor.

65
Q

What are the investigations for rheumatic fever?

A
  • Bloods –> FBC.
  • Bloods –> Strep Ab titres (ASO/anti-DNAse B check for increase two weeks apart)
  • Doppler echocardiography is more sensitive than clinical assessment in the detection of carditis in acute RF
  • Blood cultures
  • Thorat swab
  • ECG –> tachy, prolonged PR interval
66
Q

What is the management for rheumatic fever?

A

rest till CRP normal for 2 weeks

  • Benzylpenicillin IV stat and then Phenoxymethlypencilin 250-500mg PO 10 days (erythromycin when PA)
  • Aspirin for carditis and arthritis till normal CRP –> monitor salicylate level –> risk reye syndrome children. Alternative NSAIDS
  • Prednisolone when carditis
  • Haloperidol or diazepam when chorea

Physician Associate (10 decks)

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