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Year 3 > Block 31 Week 3 > Flashcards

Block 31 Week 3 Flashcards

1
Q

most common cause of palpitations?

A

extrasystole

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2
Q

frequent ectopics in > 55 yrs may indicate

A

clandestine coronary artery disease

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3
Q

very frequent ectopics may cause

A

(>20% of all heart beats) may cause LV systolic dysfunction

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4
Q

what can palpation during exercise/ immediately after reflect?

A

during exertion or immediately afterwards need urgent specialist review as they can reflect cardiomyopathy, myocardial ischemia, or a channelopathy

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5
Q

cough/ SOB w palpations?

A

extrasystoles

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6
Q

persistent breathlessness w palpations?

A

sign of HF or myocardial ischaemia

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7
Q

chest pain during palpations?

A

may reflect coronary artery disease or a tachyarrhythmia

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8
Q

sudden termination of palpations?

A
  • sudden termination suggests paroxysmal supraventricular tachycardia
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9
Q

what else suggests paroxysmal supraventricular tachycardia?

A
  • end attacks by coughing
  • straining - Valsava manouvre
  • by breath holding especially under water - diving reflex
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10
Q

drugs that may be proarrhythmic?

A
  • B agonists like salbutamol
  • antimuscarinics like amitriptyline
  • theophylline
  • dihydropyridine calcium channel blockers (nifedipine),
  • class 1 anti-arrhythmics (flecainide, disopyramide
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11
Q

drugs that can prolong QT interval?

A
  • erythromycin, moxifloxacin
  • cocaine, amphetamines
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12
Q

what can provoke extra-systoles and AF?

A
  • alcohol excess, caffiene, illicit drugs provoke extrasystoles and AF
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13
Q

other social/ medical factors associated with ventricular extrasystoles and AF?

A

stress, lack of sleep and fever

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14
Q

Medical conditions that may be associated with atrial fib and flutter?

A
  • HTN
  • HF, CAD
  • valvular hD
  • thyrotoxciosis and diabetes
  • alcohol misuse
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15
Q

tachycarrythmias?

A
  • anemia
  • thyrotoxicosis
  • FHx of sudden cardiac death - which may have caused drowning, epilepsy or road traffic accident under age of 40 is suggestive of an arrhythmia and raises possibility of an inherited cardiac condition
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16
Q

examination for palpations?

A
  • look for signs of HF, thryotoxicosis and anemia
  • BCP, FBC, TFT and 12 lead ECG required
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17
Q

palpations with SVT?

A
  • often present with palpitations
  • rarely syncope, presyncope or chest pain
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18
Q

WPW syndrome

A
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19
Q

Medical management of palpitations ?

A
  • beta blockers
  • CCBs
  • class 1C agents = flecainide propafenone
  • class 3 agents - amiodranone
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20
Q

what else can be done for palpations?

A

catheter ablation

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21
Q

catheter ablation for AF?

A
  • Risk of pacemaker if in persistent flutter
  • patient needs to be AC for procedure
  • 30% go on to develop AF
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22
Q

Cathether ablation - first line management conditions?

A
  • AV nodal re-entrant arrhythmia
  • AV re-entrant arrhythmia
  • Atrial flutter
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23
Q

catheter ablation - second line management conditions?

A
  • Atrial fibrillation
  • Atrial tachycardia
  • Ventricular tachycardia
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24
Q

median age of AF patients?

A

75

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25
Q

palpitations - malignant arrythmia ?

A
  • VT and VF
  • mostly occur in failing hearts
  • often presentation is death or aborted death
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26
Q

malignant arrythmias ECG

A
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27
Q

VF ECG

A
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28
Q

AF?

A
  • 10% of over 65s will have this
  • as multiple foci and chaotic atrial rate, it’s random as to when the signal passes to the ventricles so there’s an irregular ventricular rate
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29
Q

AF ECG?

A
  • no P wave
  • irregular rhythm
  • narrow QRS complexes (less than 120ms)
  • rate (complexes in rhythm strip x6 for irreg rhythm)
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30
Q

complications of AF?

A
  • tachy-induced cardiomyopathy
  • perisistent fast AF undiagnosed can lead to reduced cardiac function anf heart failure
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31
Q

AF and filling failure?

A
  • loss of atrial contraction leads to loss of 30% of ejection of blood into left ventricle prior to ventricular systole
  • can be v significant in those with already impaired ventricular function or diastolic/ filling failure
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32
Q

stroke risk with AF?

A
  • loss of co-ordinated activity means blood remains static in the atria
  • blood clots settle out espec in left atrial appendage
  • blood clots from LA can pass into LV and occlude cranial arteries resulting in ischaemic stroke
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33
Q

Classification of AF?

A
  • Paroxysmal
  • perisistent
  • permanent
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34
Q

Paroxysmal AF?

A
  • intermittent episodes (go back into sinus rhythm in between)
  • terminate spont w/o medical intervention
  • pAF
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35
Q

Peristent AF?

A
  • ep can be terminated but requires medical intervention
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36
Q

permanent AF?

A
  • medical intervention doesn’t re-establish sinus R or does not hold it in sinus rhythm for long
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37
Q

calculating risk of stroke?

A
  • CHAS2DS2-VASc score
  • assesses patient w AF’s risk of stroke
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38
Q

CHADSVASC score?

A
  • Score of 1 (unless if the 1 is due to the patient being female) = consider AC
  • 2+ offer oral AC
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39
Q

AC protects against ? stroke but can

A

cause haemorrhagic stroke

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40
Q

risk of bleeding scoring system

A
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41
Q

first line for stroke prevention in AF?

A

DOAC

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42
Q

Warfarin?

A
  • patients already established on warfarin may choose to remain on it
  • still used as first line in patients w metal heart valve replacement
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43
Q

LMWH?

A
  • Used as bridging therapy - easy to start and stop e.g. for surgery
  • used in patients with severe renal failure who are unable to take DOAC or warfarin
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44
Q

E.g.s of DOACs?

A
  • Edoxaban
  • apixaban
  • rivaroxiban
  • dabigatran
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45
Q

excretion of DOACs?

A
  • all largely excreted renally
  • imp to check creatinine clearance - CI if creatinine clearance less than 15
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46
Q

Management of AF - rate control?

A
  • 1st line: BBs e.g. bisporolol, metoporolol (can drop BP though)
  • rate limiting CCB: Diltiazem
  • Digoxin (check renal function)
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47
Q

1st line for rate control in AF?

A

beta blockers

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48
Q

Rhythm control in AF?

A
  • consider if symptoms continue despite rate control
  • pharmacological cardioversion: amiodrane & flecanide
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49
Q

when should electrical cardioversion be done for rhythm control in AF?

A
  • electrical cardioversion in those w life-threatening haemodynamic instability acutely
  • also done electively for those w persistent AF
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50
Q

Procedures that can be done for AF?

A
  • Left atrial ablation
  • left atrial appendage occlusion
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51
Q

left atrial ablation?

A
  • if drug tx failed or unsuitable
  • pulm veins often the source of abn electrical impulses in AF - these can be isolated where scar tissue is formed near PV to stop abn electrical impulses transferring
  • uses catheter
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52
Q

left atrial appendage occlusion?

A
  • either surgically or percutaneously
  • useful for those w AF with a high bleeding risk
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53
Q

atrial flutter?

A
  • multiple foci, chaotic contraction
  • self perpertuating loop (re-enterant circuit) often around RA
  • saw-toothed pattern on ECG
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54
Q

what is the HR usually with atrial flutter?

A

usually 150bpm every time for flutter w 2:1 block

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55
Q
A
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56
Q

what to do for AF?

A
  • calc CHADS2VASC score for stroke risk
  • and HAS-BLED score for AC
  • rhythm, rate control and check LV function - echo
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57
Q

cardiac pacing?

A
  • pacemaker sends electrical impulses to the heart to keep it beating regularly and not too slowly
  • used for: tachycardia, bradycardia, heart block, cardiac arrest
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58
Q

Implantable cardioverter defibrillators (ICDs)?

A
  • Sends large electrical shock to the heart which reboots it getting it to pump again
  • ICDs are often used as a preventative treatment for people thought to be at risk of cardiac arrest at some point in the future.
  • If the ICD senses the heart is beating at a potentially dangerous abnormal rate, it’ll deliver an electrical shock to the heart.
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59
Q

what can cause fast AF in young patients?

A

alcohol and amphetamines

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60
Q

cardiac failure =

A

failure of the heart to meet the circulatory demands of the body

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61
Q

HF epidemiology?

A
  • 10% of over 75s
  • HF can mildly elevate troponin levels
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62
Q

how can HF be classified?

A
  • Systolic: heart failure with reduced EF
  • Diastolic: HF with preserved ejection fraction
  • Left vs right ventricular failure
  • acute vs chronic
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63
Q

causes of HF?

A
  • Cardiomyopathies
  • congenital HD
  • ischaemic HD
  • arrythmuias
  • hypertension
  • hyperthyroidism
  • anemia
  • chemotherapy
  • alcohol
  • drugs
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64
Q

Steps of the cardiac cycle?

A
  • passive filling
  • atrial contraction
  • start of ventricular contraction
  • closure of mitral and triscupid valves
  • as pressure increases the aortic and pulmonary valves are forced open
  • blood forced into aorta from lV and into pulmonary arteries by RV
  • ventricles relax causing bloodflow back down aorta which closes the aortic valve
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65
Q

3 mechanisms of HF?

A
  • Myocardial ischaemia - not enough oxygen and nutrients to do its function
  • hypertension - increased peripheral resistance which is too much demand on the heart
  • cardiac abnormality - valvular disease, cardiomyopathy
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66
Q

what is the most common cause of HF in the developed world?

A

ischaemic

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67
Q

ischaemic HF?

A
  • Most common cause of HF in the devloped world
  • eventually the heart muscle thins and becomes impaired -> ischaemic cardiomyopaThy
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68
Q

Things that put too much pressure on the heart leading to HF?

A
  • Hypertension
  • obesity
  • tachycardia
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69
Q

hypertension -> HF?

A
  • longstanding hypertension
  • cardiac remodelling (concentric LVH) due to longstanding pressure overload
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70
Q

Obesity -> HF?

A
  • puts the heart under extra strain which can exacerbate or cause HF
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71
Q

tachycardia induced HF?

A
  • Most commonly AF
  • atrial flutter
  • AVNRT
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72
Q

Muscle disease causing HF?

A

Cardiomyopathies

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73
Q

types of cardiomyopathy?

A
  • dilated
  • hypertrophic
  • restrictive
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74
Q

Dilated cardiomyopathy?

A
  • usually massive and global hypokinesis
  • usually very dilated on echo
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75
Q

causes of dilated cardiomyopathy?

A
  • cocaine - especially in younger patients
  • long standing multi vessel coronary disease - ischaemic HD
  • idiopathic
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76
Q

hypertrophic cardiomyopathy?

A
  • genetic disorder
  • develops obstruction of outflow tract from LV = hypertrophic obstructive cardiomyopathy
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77
Q

restrictive cardiomyopathy?

A
  • rigid, stiff thickened myocardium usually as a result of infiltration of material or fibrosis
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78
Q

causes of restrictive cardiomyopathy?

A
  • amyloid
  • sarcoid
  • scleroderma
  • hypereosinophilic syndromes
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79
Q

cardiac output =

A
  • heart rate x stroke volume
  • Usually abt 5L
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80
Q

Ejection fraction =

A

stroke volume/ total volume

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81
Q

normal ejection fraction ?

A

55-70%

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82
Q

mild LVSD?

A

45 -54%

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83
Q

severe LVSD?

A

<35%

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84
Q

diastolic HF?

A
  • problem with the ability of the left ventricle to fill with blood
  • preserved ejection fraction
  • cardiac output significantly reduced
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85
Q

What can cause diastolic HF?

A
  • processes such as LV hypertrophy can result in less left ventricular cavity space therefore less blood volume in the left ventricle
  • less blood volume to be pumped out
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86
Q

Left systolic HF?

A
  • failure to pump as much blood out as is coming in
  • blood backs up into heart
  • back up of volume into the pulmonary circulation
  • capillary hydrostatic pressure increases so fluid moves into surrounding space around alveoli
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87
Q

HF -> pulm oedema?

A
  • increased hydrostatic pressure from LV failure
  • fluid between alveoli and capillary meaning gas exchange is impaired due to this barrier - pulmonary oedema
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88
Q

left sided cardiac failure signs and symptoms ?

A
  • SOB
  • coughing
  • cardiac wheeze
  • marked orthopnea
  • pink/ white frothy sputum
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89
Q

clinical sign of pulm oedema?

A

bibasal crepitations

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90
Q

causes of left HF - diastolic?

A
  • inadequate LV filling
  • Mitral stenosis: less flow from LA to LV
  • LVH: smaller cavity for filling to occur
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91
Q

LHF - pressure overload?

A
  • aortic stenosis - tight aortic valve that the LV has to pump against
  • hypertension - pumping against high pressure system
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92
Q

LHF - volume overload?

A
  • aortic regurgitation
  • mitral regurgitation
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93
Q

LHF - LV muscle disease?

A
  • ischaemia
  • cardiomyopathy
  • -> muscle can’t contract properly
94
Q

RHF pathophys?

A
  • pulmonary diseases cause increased pressure in the pulmonary artery - pulmonary hypertension
  • RV pumps against higher resistance will impair and eventualy fail
  • volume and pressure backs up from right heart into venous circulation
95
Q

signs and symptoms of RSHF?

A
  • raised JVP - raised pressure in RA
  • pressure can go into portal veins -> ascites and liver cirrhosis (enlarged cirrhosis)
  • pitting oedema (increased cap hydrostatic pressure)
  • tiredness/ SOB
  • skeletal muscle wasting
96
Q

RSHF signs and symptoms summary?

A
  • raised JVP
  • pitting oedma
  • ascites and
    • hepatomegaly
97
Q

pitting oedema?

A
  • pitting oedema usually in legs/ feet
  • lying flat - sacral oedema
98
Q

causes of right sided HF?

A
  • Pulmonary hypertension
  • PE
  • lung disease
  • left sided failure
  • atrial septal defect
99
Q

Left sided -> Right Failure?

A
  • LV impaired contraction and ejection fraction
  • volume and pressure builds up on left side
  • increased pressure in pulmonary veins/ capillaries
  • increased hydrostatic pressure causes fluid leak around alveoli
  • impairs gas exchange and hypoxia
  • increased pressure in pulmonary veins increases pressure within PAs
  • right heart now pumping against increased pressure causing it to fail
  • volume and pressure builds up in the right heart and backs up into venous system causing increased hydrostatic pressure and peripheral oedema
100
Q

left sided to right sided failure is called?

A

congestive HF

101
Q

acute HF?

A
  • largely synonymous w left sided failure
  • sudden failure to maintain cardiac output
  • insufficient time for compensation
  • clinical picture dominated by pulmonary oedema
102
Q

Chronic HF?

A
  • Largely synoymous of comb of R and L sided failure
  • gradual decline in function allowing for compensation
103
Q

Summary of congestive HF?

A
  • chronic LV failure leads to pulmonary congestion -> pulmonary hypertension -> right ventricular failure
104
Q

HF - compensatory mechansims?

A
  • decreased CO -> reduced BF to kidneys
  • kidneys attempt to restore circulating volume by retaining sodium and water
105
Q

how can AHF present?

A
  • Acute heart failure may present suddenly with cardiogenic shock or subacutely with decompensation of chronic heart failure.
106
Q

definition of chronic HF?

A
  • due to progressive cardiac dysfunction from structural and or functional cardiac abns
  • characterised by progressive symptoms with episodes of acute deterioration
107
Q

Primary right side failure is uncommon and broadly related to 3 categories:

A
  • Pulmonary hypertension
  • Pulmonary/Tricuspid valve disease
  • Pericardial disease
108
Q

Low output cardiac failure?

A
  • cardiac output can’t meet the demands of the body
  • results in increased systemic vascular resistance in order to maintain mean arterial pressure
  • patients have a weak pulse, cool peripheries and low BP
109
Q

high output cardiac failure?

A
  • normal cardiac function but there’s an increased demand
  • problem is with reduced systemic vascular resistance often due to diffuse arteriole vasodilation or shunting - transfer of blood from arteries to veins bypassing capillary beds that increase venous flow and overloads the heart
110
Q

causes of high output cardiac failure?

A
  • generally due to states ofincreased metabolic demand(e.g. hyperthyroidism),
  • reduced vascular resistance(e.g. thiamine deficiency, sepsis)
  • orsignificant shunting(e.g. large arteriovenosu fistula).
111
Q

summary of causes of high output cardiac failure?

A
  • anaemia
  • sepsis
  • thyrotoxicosis
  • liver failure
112
Q

stroke volume =

113
Q

Compensation - increasing preload?

A
  • increases EDV compensating for the reduced EF -> maintaing cardiac output
  • In severe disease, large increases result inpulmonary oedema,ascitesandperipheral oedema.
114
Q

compensation - increasing HR?

A
  • increasing HR - sinus tachycardia
  • RAAS
  • sympathetic activation via baroreceptors
115
Q

? can lead to decompensation and development of symptoms in HF?

A

Physical activity

116
Q

Clinical features of HF?

A
  • Raised JVP
  • Displaced apex
  • Crackles
  • Ankle swelling
  • Heart sounds S3/S4
  • Pulsus alternans
  • Hepatomegaly
  • Ascites
117
Q

Diagnosis of HF?

A
  • Measuring BNP = >2000
  • ECG
  • Echo to confirm
118
Q

BNP?

A
  • Released by cardiomyocytes in response to excessive stretching
  • used to assess likelihood of HF
119
Q

Diseases raising BNP?

A

diabetes, sepsis, old age, hypoxaemia (PE and COPD),kidney disease, and liver cirrhosis.

119
Q

Echo for HF?

A
  • in patients with elevated BNP
  • looks at the ejection fraction
120
Q

Classification of HF?

A

New York Heart Association

121
Q

Investigations for HFs?

A
  • FBC- exclude anaemia, infective cause.
  • U&Es- exclude renal failure as a cause of oedema.
  • LFT- exclude liver failure as a cause of oedema.
  • Cholesterol and HbA1c- cardiovascular risk stratification.
  • TFT- exclude thyroid disease.
  • BNP
122
Q

imaging for HF?

A
  • Echo
  • CXR
  • cardiac MRI
123
Q

Echo?

A
  • Evidence of previous MI
  • Left ventricular strain / hypertrophy
  • Conduction abnormalities / AF
124
Q

CXR for HF?

A
  • Cardiomegaly (Cardiothoracic ratio > 50% on PA film)
  • Alveolar shadowing oedema
  • Kerley B lines (fluid in septae of secondary lobules)
  • Pleural effusion
  • Upper lobe diversion
125
Q

cardiac MRI?

A
  • May be used to determine the aetiology of heart failure (e.g. ischaemic versus non-ischaemic in dilated cardiomyopathy)
126
Q

Management of HF - fluid overload?

A

furosemide

127
Q

LVSD Tx?

Heart failure

A
  • ACEi like ramipril and BBs like bisoprolol - both used first line
  • ARB if intolerance to ACEi
  • third - MRA like eplerenone added if symptoms continue
  • if symptoms persist cardiac resynchronisation therapy or digoxin
128
Q

When are BBs CI?

A

severe asthma, COPD, pulmonary oedema or bradycardia

129
Q

MRA CI?

A

hyperkalaemia, hyponatraemia, acute kidney injury.

130
Q

Second lines for HF?

A
  • Ivabradine
  • Valsartan/ Sacubitiril
  • Digoxin
  • Dapagliflozin: SGLT2 blocker on PCT
131
Q

Interventions if symptoms persist despite Tx for HF?

A
  • Implantable cardiac defib
  • cardiac rescyncronisation therapy
  • PCI
  • cardiac transplant
132
Q

Implantable cardiac defibrillator (ICD):

A

important for primary and secondary prevention of sudden cardiac death (specific indications).

133
Q

cardiac resynchorisation therapy?

A

biventricular pacing, which is indicated in certain patients with HFrEF (i.e. ≤ 35%) & prolonged QRS (i.e. ≥ 130 ms). Usually receive combined device with defibrillator.

134
Q

PCI?

A

patients with ischaemic heart disease may be offered revascularisation therapy

135
Q

Preserved LVEF Tx?

A
  • limited evidence for ACEi, ARBs, BBs
  • loop diuretic like furosemide may be given for fluid overload
136
Q

Left vs right sided HF

137
Q

acute HF inital Mx?

A
  • IV diuretic
  • Closely monitor the person’s renal function, weight and urine output during diuretic therapy.
  • Start or restart beta‑blocker treatment during hospital admission in people with acute heart failure due to left ventricular systolic dysfunction, once their condition has been stabilised
138
Q

Chronic HF - HF MDT?

A
  • consultant cardiologist
  • specialist HF nurse
  • HCP with expertise in prescribing w HF
139
Q

specialist HF MDT should:

A
  • diagnose HF
  • give information on HF
  • manage HF
  • optimise Tx and start new meds that need specialist supervision
  • manage HF that is not responding to Tx
140
Q

CCBs and HF?

A

avoid verapamil, diltiazem and short-acting dihydropyridine agents in people who haveheart failure with reduced ejection fraction.

141
Q

Monitoring for chronic HF?

A
  • a clinical assessment of functional capacity, fluid status, cardiac rhythm (minimum of examining the pulse), cognitive status and nutritional status
  • a review of medication, including need for changes and possible side effects
  • an assessment of renal function.
142
Q

what causes destabilisation of HF?

A
  • drugs such as NSAIDs, verapamil, diltiazem
  • infections
  • alcohol abuse
  • PE
  • thyroid dysfunction
143
Q

Cardiac causes of destabilisation of HF?

A
  • AF
  • arrythmias
  • bradycardia
  • MI
144
Q

Impact of living w uncertain prognosis?

A
  • depression
  • distress
  • anxiety
  • stress
  • hyperaware of physical changes
  • focusing excessively on the medical details
145
Q

role of HF specialist nurses?

A
  • co-ordinate care for the patient promotoing MDT approach
  • assisting patient with self management
  • accessible to patients and ehtir families - rapid response
  • support and counselling
  • easy access to a profressional who knows the patient and can provide consistent care
146
Q

Referral to MDT/ cardiology?

A
  • severe HF (NYHA class 4)
  • HF that doesn’t respond to tx
  • HF from valvular disease
  • LVEF of <35%
  • women w HFrEF who are plannig a pregnancy
147
Q

BNP levels and referral for HF?

A
  • pro-BNP of >2000 - urgery referral and transthoracic echo within 2 weeks
  • bnp between 400-2000 for echo within 6 weeks
148
Q

Pleuritic chest pain?

A
  • caused by inflammation of the parial pleura
  • ‘sharp, knife like, catches my breath, worse when i breathe, too painful to breathe
  • pleural rub - walking in snow, creaking of a sailing ship
149
Q

causes of pleuritic chest pain ?

A
  • Pneumonia
  • Pulmonary embolus
  • Pneumothorax
  • Malignancy e.g. mesothelioma
150
Q

Other conditions can mimic pleuritic chest pain:

A
  • Musculoskeletal e.g. costochondritis, fractured ribs
  • Intercostal neuritis e.g. herpes zoster infection (shingles)
151
Q

SQQ3T3 pattern?

A
  • PE
  • Deep S wave in lead 1
  • Q wave in lead 3
  • inverted T wave in lead 3
152
Q

Tx of PE - whilst waiting investigations?

153
Q

other Txs for pE?

A
  • Oxygen to be given if the patient is hypoxic
  • Analgesia pain relief from the pleurisy
154
Q

PE - prevention?

A

if a patient is at risk of developing a PE they should be given a low dose (prophylactic) of subcutaneous heparin if they are going to be immobile for a prolonged period of time e.g post operatively

155
Q

pneumothorax - 2 Tx methods?

A
  • Aspiration of air via cannula/ 50ml syringe and 3 way tap inserted in midclavicular line in second intercostal space
  • Chest drain inserted in 5th intercostal space in the anterior axillary line if aspiration is unsuccessful
156
Q

What else can be done for pneumothorax?

A
  • Surgery sometimes if there is a persistent air leak and the lung does not reinflate then a surgical procedure may need to be performed.
157
Q

health advice for pneumothorax?

A

stop smoking - more likely to reoccur if they continue smoking

158
Q

tension pneumothorax?

A
  • life threatening
  • air enters the pleural space but can’t escape which increases pressure which causes displacement of the mediastinum
  • this causes cardiac compromise - needs immediate aspiration followed by chest drain
159
Q

tension pneumothorax CXR?

160
Q

Pneumonia Ix?

A
  • Sputum should be sent for culture and sensitivity.
  • Blood culture
  • Urine can be sent to look for antigens to pneumococcus or legionella
  • atypical serology can be sent to look for other causes of pneumonia.
161
Q

most common cause of CAP?

A

Strep pneumonia

162
Q

other causes of CAP?

A
  • mycoplasma pneumoniae
  • viruses e.g influenze
  • legionella
  • staph a
  • haemophilus influenza
163
Q

Nomosocial (HAP) causes?

A
  • gram negative organsims cause 50%
  • staph a
  • strep pneumoniae
  • anaerobes
164
Q

Scoring pneumonia severity?

A

CURB-65 score

Confusion- new mental confusion

Urea – urea > 7mmol/l

Respiratory Rate >30/min

Blood pressure SBP<90mmHg and/or DBP,60mmHg

65 – age > 65 years

165
Q

CURB score indicating severe pneumonia risk?

166
Q

CURB score indicating moderate risk of pneumonia?

A

2 (score of 2+ consider hospital care)

167
Q

CURB 0/1?

A

low risk of pneumonia

168
Q

Tx of pneumonia?

A
  • Ab - IV if severe, may be oral if disease mild
  • oxygen
  • iV fluids if dehydration/ poor oral intake
  • analgesia if pleurisy
169
Q

pneumonia - prophylactic ?

A

heparin to prevent DVTs if patient likely to be immobile

170
Q

when to consider empyema?

A
  • If patient was getting better but spikes temperarures again
  • dull percussion note
  • decreased air entry
171
Q

transudate pleural effusion?

A
  • less than 25g is a transudate Pleural effusion
172
Q

exudative pleural effusion?

A
  • more than 35g/l = exudative
  • if the pleural LDH is high its more likely to be exudate
173
Q

causes of transudate pleural effusion?

A
  • congestive HF
  • cirrhosis
  • nephrotic syndrome
  • PE
  • pericardial disease
174
Q

causes of exudative pleural effusion?

A
  • infections - pneumonia, TB
  • malignancy
  • connective tissue disease
  • abnd disorder - pancreatitis, oesophaeal rupture
175
Q

Pleural effusion - Ix?

A
  • gram stain on samples taken
  • fluid can be sent in blood culture bottles
  • pH below 7.2 indicates sig infection which should be drained
176
Q

low severity CAP Tx?

A
  • 5 day course of amoxicillin
  • consider macrolide/ tetracycline in those allergic to penicillin
177
Q

Moderate CAP?

Treatment

A
  • 7-10 day course
  • moderate severity: mcacrolide and amoxillin
178
Q

high severity CAP?

Tx

A
  • high severity: beta lactam and macrolide
179
Q

clinical presentation of PE?

A
  • Chest pain and haemoptysis
  • dyspnoea
180
Q

Which scoring system is used to categorise if PE is likely?

A

Wells score

181
Q

chest radiograph in PE

182
Q

Plasma D dimer?

A
  • D-dimer levels elevated in the presence of a clot
  • A negative D-dimer test reliably excludes PE
  • The specificity of D-dimer for VTE is poor and the positive predictive value (PPV) is low; D-dimer is not useful for confirming PE
183
Q

a normal CXR in the presence of ? is suggestive of PE?

A

Dyspnoea, tachypnoea, hypoxaemia

184
Q

CT pulmonary angiography (CTPA)?

A
  • Permits assessment of clot load
  • visualises right ventricular dilatation/ strain
  • some false negatives (v small peripheral emboli)
185
Q

Tx of PE?

A
  • LMWH usually for 5 days
  • oral anticoagulation for 6 weeks post op
186
Q

When should thrombolysis be used for PE?

A

if shocked - SBP <90mmHg

187
Q

Risk markers for PE?

A
  • shock/ hypotension
  • RV dysfunction
  • myocardial injury
188
Q

Traditional AC Tx for VTE

189
Q

Treating and preventing recurrent DVTs and PEs in adults - DOACs?

A
  • Rivaroxaban
  • Apixaban
  • Dabigatran
  • Edoxaban
190
Q

VKAs?

A
  • can be used in severe renal impairment
  • AC can be reversed
  • monitoring of INR required
191
Q

what can be seen on a CXR for a PE?

A
  • normal CXR
  • or wedge shaped and peripheral consolidation
  • can get bibasal consolidation
192
Q

history of PE?

A
  • history of RF for DVT
  • history lacking infective symptoms
  • breathlessness, pleurisy
193
Q

CTPA showing filling defects in the PAs

194
Q

presentation of PE

A
  • abrupt onset SOB
  • pleuritic chest pain
  • cough
  • deterioration in those w underlying chronic CR disease
  • leg pain and swelling
  • haemoptysis
  • syncope
  • dizziness
195
Q

saddle embolus in PE

196
Q

signs of PE

A
  • tachycardia
  • low grade fever
  • hypoxia
197
Q

PE - signs of right heart failure?

A
  • hypotension
  • elevated JVP
  • tricuspid regurgitation - pansystolic murmur
  • split second heart sound - elevated pulmonary pressure leads to delay in pulmonary valve closure.
198
Q

clinical exam for PE?

A
  • tachypnea
  • crackles
  • DVT
199
Q

Predisposition for PE

A
  • imobility
  • pregnany
  • major surgery
  • cancer
  • HF
  • FH
  • lower limb trauma/ fracture
  • active cancer
200
Q

drugs linked to DVT

201
Q

Massive PE is reduced by

A

thrombolysis in those that are unstable (shock or ventilator dependent)

202
Q

risk of thrombolysis?

A
  • major bleeding
  • intercranial haemorrhage
203
Q

VTE includes

A

PE and DVT

204
Q

Location of PE - segmental and subsegmental?

A

lower order pulmonary vessels. Unilateral or bilateral occlusion

205
Q

location of PE - lobar?

A

right or left main pulmonary arteries. Unilateral or bilateral occlusion

206
Q

location of PE - saddle?

A

embolus lodged at the bifurcation of the pulmonary arteries (3-6% of cases).

207
Q

DVT pathophys - Virchow’s triad?

A

venous stasis, hypercoaguable state, endothelial injury

208
Q

Wells score for PE

A
  • PE likely (score over 4): CTPA
  • PE unlikely (Score under 4): d-dimer within 4 hrs - if positive arrange CTPA
209
Q

ECG findings for PE?

A
  • Common: tachycardia
  • right heart strain: RBBB, ST depression and T wave inversion anteriorly (V1-V4) and/or inferiorly (II, III, aVF)
210
Q

bloods for PE?

A
  • FBC
  • D-dimer
  • ABG
  • troponin - right heart strain
211
Q

Imaging for a suspected PE?

A
  • CXR
  • CTPA
  • lower limb US to confirm presence of DVT
  • echo: assesment of RV strain in patients w suspected massive PE
212
Q

Acute management of PE?

A
  • AC for a minimum period of 3 months
  • LMWH or DOAC, uFH, warfarin
  • LMWH usually used before confirmation of PE
  • DOAC FIRST LINE
213
Q

Diagnosis of PE pathway

214
Q

VTE AC choice pathway

215
Q

complications of PE?

A
  • long term PE can lead to chronic thromboembolic pulmonary hypertension and is associated with RSHF
  • Factors associated with this complication are inadequate anticoagulation, large or residual thrombi and recurrent disease.
216
Q

Which DOACs used for confirmed PE?

A
  • apixaban or ribaroxaban for confirmed DVT or PE
  • if neither are suitable offer LMWH for at least 5 days followed by dabigatran or edoxaban
  • or LMWH with VKA
217
Q

PE w haemodynamic instability?

A
  • PE w haemodynamic instability: offer UFH infusion and consider thrombolytic therapy
  • consider DOAC for active cancer
218
Q

VTE risk assessment tool?

A
  • DoH VTE risk assessment tool
219
Q

VTE prophylaxis - mechanical prophylaxis?

A
  • anti-embolism stockings
  • NOT for:
  • suspected or proven peripheral arterial disease
  • peripheral arterial bypass grafting
  • severe leg oedema
  • peripheral neuropathy
220
Q

VTE prophylaxis - pharm?

A
  • apixaban
  • aspirin
  • dabigatran etexilate
  • fondaparinux sodium
  • low-molecular-weight heparin (LMWH)
221
Q

VTE prophylaxis for renal impairment?

A

LMWH or UFH

222
Q

Patients that should be considered for VTE prophylaxis:

A
  • all surgical and trauma patients
  • pregnant, gave birth or miscarriage or termination of pregnancy in the last 6 weeks
  • people admitted to critical care
  • acute psychiatric patients
  • lower limb immobilisation
  • fragility fractures
223
Q

X ray features of pneumothorax?

A
  • absent lung markings - Air collects in the pleural space, causing the underlying lung to collapse partially or fully.
  • visible lung edge - air collects in pleural space causing lung edge to be pushed away and become visible as a line
224
Q

pneumonia Sx

A
  • pleuritic chest pain
  • cough
  • fever
  • malaise
  • bronchial breathing
225
Q

pneumonia clinical signs?

A
  • bronchial breathing
  • increased vocal resonance, tactile vocal fremitus, and whispering pectoriloquy
226
Q

Provoked vs unprovoked PE

A
  • a provoked VTE is due to an obvious precipitating event e.g. immobilisation following major surgery. The implication is that this event was transient and the patient is no longer at increased risk
  • an unprovoked VTE occurs in the absence of an obvious precipitating event, i.e. there is a possibility that there are unknown factors (e.g. mild thrombophilia) making the patient more at risk from further clots
227
Q

Provoked PE AC for

228
Q

Unprovoked PE AC for

229
Q

PE w haemodynamic instability?

A

thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)

230
Q

PE Tx summary?

A
  • first line: DOAC - even for cancer
  • if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
231
Q

PE w renal impairment?

A
  • V/Q scan instead of CTPA
  • if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

Year 3 (45 decks)

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