Block 31 Week 3 Flashcards
1
Q
most common cause of palpitations?
A
extrasystole
2
Q
frequent ectopics in > 55 yrs may indicate
A
clandestine coronary artery disease
3
Q
very frequent ectopics may cause
A
(>20% of all heart beats) may cause LV systolic dysfunction
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
5
Q
cough/ SOB w palpations?
A
extrasystoles
6
Q
persistent breathlessness w palpations?
A
sign of HF or myocardial ischaemia
7
Q
chest pain during palpations?
A
may reflect coronary artery disease or a tachyarrhythmia
8
Q
sudden termination of palpations?
A
- sudden termination suggests paroxysmal supraventricular tachycardia
9
Q
what else suggests paroxysmal supraventricular tachycardia?
A
- end attacks by coughing
- straining - Valsava manouvre
- by breath holding especially under water - diving reflex
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
11
Q
drugs that can prolong QT interval?
A
- erythromycin, moxifloxacin
- cocaine, amphetamines
12
Q
what can provoke extra-systoles and AF?
A
- alcohol excess, caffiene, illicit drugs provoke extrasystoles and AF
13
Q
other social/ medical factors associated with ventricular extrasystoles and AF?
A
stress, lack of sleep and fever
14
Q
Medical conditions that may be associated with atrial fib and flutter?
A
- HTN
- HF, CAD
- valvular hD
- thyrotoxciosis and diabetes
- alcohol misuse
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
16
Q
examination for palpations?
A
- look for signs of HF, thryotoxicosis and anemia
- BCP, FBC, TFT and 12 lead ECG required
17
Q
palpations with SVT?
A
- often present with palpitations
- rarely syncope, presyncope or chest pain
18
Q
WPW syndrome
A
19
Q
Medical management of palpitations ?
A
- beta blockers
- CCBs
- class 1C agents = flecainide propafenone
- class 3 agents - amiodranone
20
Q
what else can be done for palpations?
A
catheter ablation
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
22
Q
Cathether ablation - first line management conditions?
A
- AV nodal re-entrant arrhythmia
- AV re-entrant arrhythmia
- Atrial flutter
23
Q
catheter ablation - second line management conditions?
A
- Atrial fibrillation
- Atrial tachycardia
- Ventricular tachycardia
24
Q
median age of AF patients?
A
75
25
palpitations - malignant arrythmia ?
* VT and VF
* mostly occur in failing hearts
* often presentation is death or aborted death
26
malignant arrythmias ECG
27
VF ECG
28
AF?
* 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
29
AF ECG?
* no P wave
* irregular rhythm
* narrow QRS complexes (less than 120ms)
* rate (complexes in rhythm strip x6 for irreg rhythm)
30
complications of AF?
* tachy-induced cardiomyopathy
* perisistent fast AF undiagnosed can lead to reduced cardiac function anf heart failure
31
AF and filling failure?
* 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
32
stroke risk with AF?
* 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
33
Classification of AF?
* Paroxysmal
* perisistent
* permanent
34
Paroxysmal AF?
* intermittent episodes (go back into sinus rhythm in between)
* terminate spont w/o medical intervention
* pAF
35
Peristent AF?
* ep can be terminated but requires medical intervention
36
permanent AF?
* medical intervention doesn't re-establish sinus R or does not hold it in sinus rhythm for long
37
calculating risk of stroke?
- CHAS2DS2-VASc score
* assesses patient w AF's risk of stroke
38
CHADSVASC score?
* Score of 1 (unless if the 1 is due to the patient being female) = consider AC
* 2+ offer oral AC
39
AC protects against ? stroke but can
cause haemorrhagic stroke
40
risk of bleeding scoring system
41
first line for stroke prevention in AF?
DOAC
42
Warfarin?
* patients already established on warfarin may choose to remain on it
* still used as first line in patients w metal heart valve replacement
43
LMWH?
* 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
44
E.g.s of DOACs?
* Edoxaban
* apixaban
* rivaroxiban
* dabigatran
45
excretion of DOACs?
* all largely excreted renally
* imp to check creatinine clearance - CI if creatinine clearance less than 15
46
Management of AF - rate control?
* 1st line: BBs e.g. bisporolol, metoporolol (can drop BP though)
* rate limiting CCB: Diltiazem
* Digoxin (check renal function)
47
1st line for rate control in AF?
beta blockers
48
Rhythm control in AF?
* consider if symptoms continue despite rate control
* pharmacological cardioversion: amiodrane & flecanide
49
when should electrical cardioversion be done for rhythm control in AF?
* electrical cardioversion in those w life-threatening haemodynamic instability acutely
* also done electively for those w persistent AF
50
Procedures that can be done for AF?
- Left atrial ablation
- left atrial appendage occlusion
51
left atrial ablation?
* 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
52
left atrial appendage occlusion?
* either surgically or percutaneously
* useful for those w AF with a high bleeding risk
53
atrial flutter?
* multiple foci, chaotic contraction
* self perpertuating loop (re-enterant circuit) often around RA
* saw-toothed pattern on ECG
54
what is the HR usually with atrial flutter?
usually 150bpm every time for flutter w 2:1 block
55
56
what to do for AF?
* calc CHADS2VASC score for stroke risk
* and HAS-BLED score for AC
* rhythm, rate control and check LV function - echo
57
cardiac pacing?
* pacemaker sends electrical impulses to the heart to keep it beating regularly and not too slowly
* used for: tachycardia, bradycardia, heart block, cardiac arrest
58
Implantable cardioverter defibrillators (ICDs)?
* 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.
59
what can cause fast AF in young patients?
alcohol and amphetamines
60
cardiac failure =
failure of the heart to meet the circulatory demands of the body
61
HF epidemiology?
* 10% of over 75s
* HF can mildly elevate troponin levels
62
how can HF be classified?
* Systolic: heart failure with reduced EF
* Diastolic: HF with preserved ejection fraction
* Left vs right ventricular failure
* acute vs chronic
63
causes of HF?
* Cardiomyopathies
* congenital HD
* ischaemic HD
* arrythmuias
* hypertension
* hyperthyroidism
* anemia
* chemotherapy
* alcohol
* drugs
64
Steps of the cardiac cycle?
* 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
65
3 mechanisms of HF?
* 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
66
what is the most common cause of HF in the developed world?
ischaemic
67
ischaemic HF?
* Most common cause of HF in the devloped world
* eventually the heart muscle thins and becomes impaired -> ischaemic cardiomyopaThy
68
Things that put too much pressure on the heart leading to HF?
- Hypertension
- obesity
- tachycardia
69
hypertension -> HF?
* longstanding hypertension
* cardiac remodelling (concentric LVH) due to longstanding pressure overload
70
Obesity -> HF?
* puts the heart under extra strain which can exacerbate or cause HF
71
tachycardia induced HF?
* Most commonly AF
* atrial flutter
* AVNRT
72
Muscle disease causing HF?
Cardiomyopathies
73
types of cardiomyopathy?
- dilated
- hypertrophic
- restrictive
74
Dilated cardiomyopathy?
* usually massive and global hypokinesis
* usually very dilated on echo
75
causes of dilated cardiomyopathy?
* cocaine - especially in younger patients
* long standing multi vessel coronary disease - ischaemic HD
* idiopathic
76
hypertrophic cardiomyopathy?
* genetic disorder
* develops obstruction of outflow tract from LV = hypertrophic obstructive cardiomyopathy
77
restrictive cardiomyopathy?
* rigid, stiff thickened myocardium usually as a result of infiltration of material or fibrosis
78
causes of restrictive cardiomyopathy?
* amyloid
* sarcoid
* scleroderma
* hypereosinophilic syndromes
79
cardiac output =
- heart rate x stroke volume
- Usually abt 5L
80
Ejection fraction =
stroke volume/ total volume
81
normal ejection fraction ?
55-70%
82
mild LVSD?
45 -54%
83
severe LVSD?
<35%
84
diastolic HF?
* problem with the ability of the left ventricle to fill with blood
* preserved ejection fraction
* cardiac output significantly reduced
85
What can cause diastolic HF?
* 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
86
Left systolic HF?
* 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
87
HF -> pulm oedema?
* increased hydrostatic pressure from LV failure
* fluid between alveoli and capillary meaning gas exchange is impaired due to this barrier - pulmonary oedema
88
left sided cardiac failure signs and symptoms ?
* SOB
* coughing
* cardiac wheeze
* marked orthopnea
* pink/ white frothy sputum
89
clinical sign of pulm oedema?
bibasal crepitations
90
causes of left HF - diastolic?
- inadequate LV filling
* Mitral stenosis: less flow from LA to LV
* LVH: smaller cavity for filling to occur
91
LHF - pressure overload?
* aortic stenosis - tight aortic valve that the LV has to pump against
* hypertension - pumping against high pressure system
92
LHF - volume overload?
* aortic regurgitation
* mitral regurgitation
93
LHF - LV muscle disease?
* ischaemia
* cardiomyopathy
* -> muscle can't contract properly
94
RHF pathophys?
* 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
signs and symptoms of RSHF?
* 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
RSHF signs and symptoms summary?
* raised JVP
* pitting oedma
* ascites and
* * hepatomegaly
97
pitting oedema?
* pitting oedema usually in legs/ feet
* lying flat - sacral oedema
98
causes of right sided HF?
* Pulmonary hypertension
* PE
* lung disease
* left sided failure
* atrial septal defect
99
Left sided -> Right Failure?
* 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
left sided to right sided failure is called?
congestive HF
101
acute HF?
* largely synonymous w left sided failure
* sudden failure to maintain cardiac output
* insufficient time for compensation
* clinical picture dominated by pulmonary oedema
102
Chronic HF?
* Largely synoymous of comb of R and L sided failure
* gradual decline in function allowing for compensation
103
Summary of congestive HF?
* chronic LV failure leads to pulmonary congestion -> pulmonary hypertension -> right ventricular failure
104
HF - compensatory mechansims?
* decreased CO -> reduced BF to kidneys
* kidneys attempt to restore circulating volume by retaining sodium and water
105
how can AHF present?
* Acute heart failure may present suddenly with cardiogenic shock or subacutely with decompensation of chronic heart failure.
106
definition of chronic HF?
* due to progressive cardiac dysfunction from structural and or functional cardiac abns
* characterised by progressive symptoms with episodes of acute deterioration
107
Primary right side failure is uncommon and broadly related to 3 categories:
* Pulmonary hypertension
* Pulmonary/Tricuspid valve disease
* Pericardial disease
108
Low output cardiac failure?
* 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
high output cardiac failure?
* 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
causes of high output cardiac failure?
* generally due to states of increased metabolic demand (e.g. hyperthyroidism),
* reduced vascular resistance (e.g. thiamine deficiency, sepsis)
* or significant shunting (e.g. large arteriovenosu fistula).
111
summary of causes of high output cardiac failure?
- anaemia
- sepsis
- thyrotoxicosis
- liver failure
112
stroke volume =
EDV - ESV
113
Compensation - increasing preload?
* increases EDV compensating for the reduced EF -> maintaing cardiac output
* In severe disease, large increases result in pulmonary oedema, ascites and peripheral oedema.
114
compensation - increasing HR?
* increasing HR - sinus tachycardia
* RAAS
* sympathetic activation via baroreceptors
115
? can lead to decompensation and development of symptoms in HF?
Physical activity
116
Clinical features of HF?
* Raised JVP
* Displaced apex
* Crackles
* Ankle swelling
* Heart sounds S3/S4
* Pulsus alternans
* Hepatomegaly
* Ascites
117
Diagnosis of HF?
* Measuring BNP = >2000
* ECG
* Echo to confirm
118
BNP?
* Released by cardiomyocytes in response to excessive stretching
* used to assess likelihood of HF
119
Diseases raising BNP?
diabetes, sepsis, old age, hypoxaemia (PE and COPD), kidney disease, and liver cirrhosis.
119
Echo for HF?
* in patients with elevated BNP
* looks at the ejection fraction
120
Classification of HF?
New York Heart Association
121
Investigations for HFs?
* 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
imaging for HF?
- Echo
- CXR
- cardiac MRI
123
Echo?
* Evidence of previous MI
* Left ventricular strain / hypertrophy
* Conduction abnormalities / AF
124
CXR for HF?
* 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
cardiac MRI?
* May be used to determine the aetiology of heart failure (e.g. ischaemic versus non-ischaemic in dilated cardiomyopathy)
126
Management of HF - fluid overload?
furosemide
127
LVSD Tx?
| Heart failure
- 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
When are BBs CI?
severe asthma, COPD, pulmonary oedema or bradycardia
129
MRA CI?
hyperkalaemia, hyponatraemia, acute kidney injury.
130
Second lines for HF?
* Ivabradine
* Valsartan/ Sacubitiril
* Digoxin
* Dapagliflozin: SGLT2 blocker on PCT
131
Interventions if symptoms persist despite Tx for HF?
- Implantable cardiac defib
- cardiac rescyncronisation therapy
- PCI
- cardiac transplant
132
Implantable cardiac defibrillator (ICD):
important for primary and secondary prevention of sudden cardiac death (specific indications).
133
cardiac resynchorisation therapy?
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
PCI?
patients with ischaemic heart disease may be offered revascularisation therapy
135
Preserved LVEF Tx?
* limited evidence for ACEi, ARBs, BBs
* loop diuretic like furosemide may be given for fluid overload
136
Left vs right sided HF
137
acute HF inital Mx?
* 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
Chronic HF - HF MDT?
* consultant cardiologist
* specialist HF nurse
* HCP with expertise in prescribing w HF
139
specialist HF MDT should:
* 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
CCBs and HF?
avoid verapamil, diltiazem and short-acting dihydropyridine agents in people who have heart failure with reduced ejection fraction.
141
Monitoring for chronic HF?
* 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
what causes destabilisation of HF?
* drugs such as NSAIDs, verapamil, diltiazem
* infections
* alcohol abuse
* PE
* thyroid dysfunction
143
Cardiac causes of destabilisation of HF?
* AF
* arrythmias
* bradycardia
* MI
144
Impact of living w uncertain prognosis?
* depression
* distress
* anxiety
* stress
* hyperaware of physical changes
* focusing excessively on the medical details
145
role of HF specialist nurses?
* 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
Referral to MDT/ cardiology?
* 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
BNP levels and referral for HF?
* pro-BNP of >2000 - urgery referral and transthoracic echo within 2 weeks
* bnp between 400-2000 for echo within 6 weeks
148
Pleuritic chest pain?
* 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
causes of pleuritic chest pain ?
* Pneumonia
* Pulmonary embolus
* Pneumothorax
* Malignancy e.g. mesothelioma
150
Other conditions can mimic pleuritic chest pain:
* Musculoskeletal e.g. costochondritis, fractured ribs
* Intercostal neuritis e.g. herpes zoster infection (shingles)
151
SQQ3T3 pattern?
- PE
* Deep S wave in lead 1
* Q wave in lead 3
* inverted T wave in lead 3
152
Tx of PE - whilst waiting investigations?
- DOAC
153
other Txs for pE?
* Oxygen to be given if the patient is hypoxic
* Analgesia pain relief from the pleurisy
154
PE - prevention?
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
pneumothorax - 2 Tx methods?
* 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
What else can be done for pneumothorax?
* 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
health advice for pneumothorax?
stop smoking - more likely to reoccur if they continue smoking
158
tension pneumothorax?
* 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
tension pneumothorax CXR?
160
Pneumonia Ix?
* 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
most common cause of CAP?
Strep pneumonia
162
other causes of CAP?
* mycoplasma pneumoniae
* viruses e.g influenze
* legionella
* staph a
* haemophilus influenza
163
Nomosocial (HAP) causes?
* gram negative organsims cause 50%
* staph a
* strep pneumoniae
* anaerobes
164
Scoring pneumonia severity?
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
CURB score indicating severe pneumonia risk?
3
166
CURB score indicating moderate risk of pneumonia?
2 (score of 2+ consider hospital care)
167
CURB 0/1?
low risk of pneumonia
168
Tx of pneumonia?
* Ab - IV if severe, may be oral if disease mild
* oxygen
* iV fluids if dehydration/ poor oral intake
* analgesia if pleurisy
169
pneumonia - prophylactic ?
heparin to prevent DVTs if patient likely to be immobile
170
when to consider empyema?
- If patient was getting better but spikes temperarures again
- dull percussion note
- decreased air entry
171
transudate pleural effusion?
* less than 25g is a transudate Pleural effusion
172
exudative pleural effusion?
* more than 35g/l = exudative
* if the pleural LDH is high its more likely to be exudate
173
causes of transudate pleural effusion?
- congestive HF
- cirrhosis
- nephrotic syndrome
- PE
- pericardial disease
174
causes of exudative pleural effusion?
- infections - pneumonia, TB
- malignancy
- connective tissue disease
- abnd disorder - pancreatitis, oesophaeal rupture
175
Pleural effusion - Ix?
* 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
low severity CAP Tx?
* 5 day course of amoxicillin
* consider macrolide/ tetracycline in those allergic to penicillin
177
Moderate CAP?
| Treatment
* 7-10 day course
* moderate severity: mcacrolide and amoxillin
178
high severity CAP?
| Tx
* high severity: beta lactam and macrolide
179
clinical presentation of PE?
* Chest pain and haemoptysis
* dyspnoea
180
Which scoring system is used to categorise if PE is likely?
Wells score
181
chest radiograph in PE
182
Plasma D dimer?
* 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
a normal CXR in the presence of ? is suggestive of PE?
Dyspnoea, tachypnoea, hypoxaemia
184
CT pulmonary angiography (CTPA)?
* Permits assessment of clot load
* visualises right ventricular dilatation/ strain
* some false negatives (v small peripheral emboli)
185
Tx of PE?
* LMWH usually for 5 days
* oral anticoagulation for 6 weeks post op
186
When should thrombolysis be used for PE?
if shocked - SBP <90mmHg
187
Risk markers for PE?
* shock/ hypotension
* RV dysfunction
* myocardial injury
188
Traditional AC Tx for VTE
189
Treating and preventing recurrent DVTs and PEs in adults - DOACs?
* Rivaroxaban
* Apixaban
* Dabigatran
* Edoxaban
190
VKAs?
* can be used in severe renal impairment
* AC can be reversed
* monitoring of INR required
191
what can be seen on a CXR for a PE?
- normal CXR
- or wedge shaped and peripheral consolidation
- can get bibasal consolidation
192
history of PE?
* history of RF for DVT
* history lacking infective symptoms
* breathlessness, pleurisy
193
CTPA showing filling defects in the PAs
194
presentation of PE
* abrupt onset SOB
* pleuritic chest pain
* cough
* deterioration in those w underlying chronic CR disease
* leg pain and swelling
* haemoptysis
* syncope
* dizziness
195
saddle embolus in PE
196
signs of PE
* tachycardia
* low grade fever
* hypoxia
197
PE - signs of right heart failure?
* hypotension
* elevated JVP
* tricuspid regurgitation - pansystolic murmur
* split second heart sound - elevated pulmonary pressure leads to delay in pulmonary valve closure.
198
clinical exam for PE?
* tachypnea
* crackles
* DVT
199
Predisposition for PE
* imobility
* pregnany
* major surgery
* cancer
* HF
* FH
* lower limb trauma/ fracture
* active cancer
200
drugs linked to DVT
* COCP
* HRT
201
Massive PE is reduced by
thrombolysis in those that are unstable (shock or ventilator dependent)
202
risk of thrombolysis?
* major bleeding
* intercranial haemorrhage
203
VTE includes
PE and DVT
204
Location of PE - segmental and subsegmental?
lower order pulmonary vessels. Unilateral or bilateral occlusion
205
location of PE - lobar?
right or left main pulmonary arteries. Unilateral or bilateral occlusion
206
location of PE - saddle?
embolus lodged at the bifurcation of the pulmonary arteries (3-6% of cases).
207
DVT pathophys - Virchow's triad?
venous stasis, hypercoaguable state, endothelial injury
208
Wells score for PE
* PE likely (score over 4): CTPA
* PE unlikely (Score under 4): d-dimer within 4 hrs - if positive arrange CTPA
209
ECG findings for PE?
* Common: tachycardia
* right heart strain: RBBB, ST depression and T wave inversion anteriorly (V1-V4) and/or inferiorly (II, III, aVF)
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bloods for PE?
* FBC
* D-dimer
* ABG
* troponin - right heart strain
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Imaging for a suspected PE?
* CXR
* CTPA
* lower limb US to confirm presence of DVT
* echo: assesment of RV strain in patients w suspected massive PE
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Acute management of PE?
* AC for a minimum period of 3 months
* LMWH or DOAC, uFH, warfarin
* LMWH usually used before confirmation of PE
* **DOAC FIRST LINE**
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Diagnosis of PE pathway
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VTE AC choice pathway
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complications of PE?
* 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.
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Which DOACs used for confirmed PE?
* 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
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PE w haemodynamic instability?
* PE w haemodynamic instability: offer UFH infusion and consider thrombolytic therapy
* consider DOAC for active cancer
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VTE risk assessment tool?
* DoH VTE risk assessment tool
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VTE prophylaxis - mechanical prophylaxis?
- anti-embolism stockings
* NOT for:
* suspected or proven peripheral arterial disease
* peripheral arterial bypass grafting
* severe leg oedema
* peripheral neuropathy
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VTE prophylaxis - pharm?
* apixaban
* aspirin
* dabigatran etexilate
* fondaparinux sodium
* low-molecular-weight heparin (LMWH)
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VTE prophylaxis for renal impairment?
LMWH or UFH
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Patients that should be considered for VTE prophylaxis:
* 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
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X ray features of pneumothorax?
* 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
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pneumonia Sx
* pleuritic chest pain
* cough
* fever
* malaise
* bronchial breathing
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pneumonia clinical signs?
* bronchial breathing
* increased vocal resonance, tactile vocal fremitus, and whispering pectoriloquy
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Provoked vs unprovoked PE
- 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
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Provoked PE AC for
3 months
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Unprovoked PE AC for
6 months
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PE w haemodynamic instability?
thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)
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PE Tx summary?
- 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)
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PE w renal impairment?
- 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
