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phase 2a mine > cv middle tier > Flashcards

cv middle tier Flashcards

1
Q

bradycardia

  • put a speed on it
  • symptoms
  • who is it normal for
A
  • Less than 60bpm daytime and 50bpm night
  • Usually asymptomatic
  • Normal in athletes due to increased vagal tone and so increased parasympathetic activity
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2
Q

tachycardia

  • put a speed on it
  • two types
A
  • More than 100bpm
  • Supraventricular tachycardias - arise from atrium / AV junction — Atrial fibrillation/ atrial flutter
  • Ventricular tachycardias - arise from ventricles
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3
Q

atrial fibrilation

  • irregular?
  • put a speed on it
  • what is happening
A
  • irregularly irregular - chaotic, atrial spasm
  • 300-600bpm
  • rapid activation of atria by multiple meandering re-entry wavelets. AV node responds intermittently , only a portion of impulses conducted on→ irregular ventricular rate
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4
Q

atrial fibrillation

  • persistent
  • permanent
  • paroxysmal
  • recurrent
  • acute
A
  • Persistent = continuous for 7days+, not self terminating
  • Permanent = long term
  • paroxysmal = self-terminating within 7 days
  • Recurrent: two + episodes
  • Acute = onset on last 48h
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5
Q

atrial fibrillation

  • gender
  • commonness
  • age
A
  • m>f
  • most common arrythmia
  • old
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6
Q

atrial fibrillation risk factors

A
  • 60y+
  • Diabetes
  • Hypertension
  • Coronary artery disease
  • Previous MI
  • Structural heart disease (valve/congenital defects)
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7
Q

atrial fibrillation causes/ risk factors

A

cardiac

  • Increased atrial pressure, increased atrial mass, atrial fibrosis/ inflammation/ infiltration
  • Hypertension
  • Heart failure
  • MI
  • Coronary artery disease
  • structural heart disease inc Valvular
  • Cardiac surgery
  • Cardiomyopathy
  • Rheumatic heart disease

non cardiac

  • Acute excess alcohol intoxication, exposure to caffeine tobacco etc
  • hyperthyroidism
  • chest infection
  • age
  • DM
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8
Q

atrial fibrillation symptoms

A
  • None at all /
  • Dizziness
  • Palpitations
  • Syncope
  • Chest pain
  • Heart failure
  • Fatigue
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9
Q

atrial fibrillation ecg

A
  • Rapid, irregular QRS,
  • Absent p waves - jaggedy
  • No steady isoelectric baseline
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10
Q

atrial fibrillation/ flutter treatment

A

treat precipitating cause

control ventricular rate

  • beta blockers
  • CCB
  • digoxin
  • amiodraone
  • lidocaine

restore sinus rhythm
- cardioversion (electricla DC shock)- defibrillator

catheter based therapy – ablate/ destroy cells

do CHADVASC (Stroke risk) to see if anticoagulation medication needed

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11
Q

why is verapamil (phenylalinine CCB) more effective than amlopifine (dihydropiridine CCB)?

A

dont act on calcium channels at rest

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12
Q

which beta blocker is best for post MI arrythmias and why

A

propanolol

additional quality of blocking sodium channels

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13
Q

cardioversion is associated with what risk

so what is given alongside

A

risk of thromboembolism, so need to give LMW heparin

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14
Q

lidocaine action

A

blocks the inactivation gate of Na channels so prolongs inactivation meaning higher depolarization threshold and early action potentials less likely to get through

for arrythmias (vent trach)

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15
Q

digoxin action

A

Slows HR

Increases contractility

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16
Q

atrial fibrillation complications

A 
Sudden death
Syncope (fainting)
Heart failure
Chest pain
Dizziness
Palpitations
Stroke
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17
Q

atrial flutter

  • irregularity
  • put a speed on it
  • what is happening
A
  • regularly irregular, organised but rapid
  • 250-350bpm
  • Due to re-entry circuit in RA from AV back to sinus
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18
Q

atrial flutter ecg

A

“saw tooth” ECG
Narrow tachycardia
Flutter waves

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19
Q

.

A

.

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20
Q

atrial flutter symptoms

A 
Dizziness
breathlessness
Palpitations
Syncope
Chest pain
Heart failure
Fatigue
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21
Q

heart block

  • brady/tachy
  • what is happening
  • which part of ecg is changed (what is normal)
A
  • brady
  • Conduction issue- signals not properly propogated from SAN to AVN to His-Purkinje system
  • PR interval. normal is 120-200ms. heart block= greater
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22
Q

first degree heart block symptoms

A

asymptomatic

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23
Q

second degree mobitz type 1 symptoms

A

lots asymptomatic
light headed
dizzy
syncope

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24
Q

second degree mobitz type 2 symptoms

A 
less likely to be asymptomatic
light headed
dizzy
syncope
chest pain
SOB
postural hypertension
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25
Q

third degree heart block symptoms

A 
syncope
fatigue - extreme
chest pain
breathlessness
confusion
palpitations
brady
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26
Q

first degree heart block

  • what is it
  • causes
A
  • 1:1 a:v (each is conducted but slower than normal, no dropped beats )
  • PR interval prolonged, PR intervals are constant
  • block in AV node – delay
  • Hypokalemia
  • Myocarditis
  • Inferior MI
  • AVN blocking drugs (B blockers, CCB, digoxin)
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27
Q

second degree heart block - mobitz type 1

  • aka
  • what is it
  • causes
A
  • wenckebach
  • AVnode issue
  • PR interval increases progressively, then a failure of a P wave proper conduction so a ‘dropped’/missing QRS wave (then reset)
  • AVN blocking drugs (B blockers, CCB, digoxin)
  • inferior MI
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28
Q

heart block treatment and when

A

only need treatment if symptomatic

  • transcutaneous pacing (TCP) to restore heart rate (temporary)
  • pacemaker (permenant ) may follow
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29
Q

second degree heart block- mobitz type 2

  • what is it
  • causes
A
  • Distal conduction issue
  • PR interval lengthened but no PR interval change - it is constant. then a beat is dropped (missing QRS-P wave not conducted)
Anterior MI 
mitral valve surgery
SLE,
lyme disease
rheumatic fever
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30
Q

third degree heart block

  • what is it
  • causes
A
  • 3rd degree is no relation between a and v - they contract independently- so P and QRS appear independent.
  • Constant p to p intervals. Constant q to q intervals. They are constant with themselves, but independent of the other
  • Large space between each QRS.
  • P waves may be buried in the QRS complex so can be hard to distinguish - look for intervals as said above
Structural heart disease
ischaemic heart disease
hypertension
endocarditis
lyme disease
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31
Q

bundle blocks

  • a:v ratio
  • what is the pathology
  • ecg looks like?
A
  • 1:1
  • No depolaristation down L or R branch so one side of the heart is delayed as the depolarisation has to spread across the septum from the other ventricle
  • Broad QR
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32
Q

LBBB
ecg
sound
causes

A

wiLLiam
W in v1
M in v6
L eaving each other

Reverse splitting of second heart sound

  • Ischaemic heart disease
  • aortic valve disease
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33
Q

RBBB
ecg
sound
causes

A

maRRow
M in v1
W in v6
R eaching towards each other

Splitting of second heart sound

  • Pulmonary embolism
  • ischaemic heart disease
  • atrial/ ventricular septal defect
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34
Q

supraventricular tachycardia

  • age
  • arises from where
A
  • Young patient (12-30)

- Arises from atria / atrioventricular junction

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35
Q

slow fast AVNRT means?

A

atria contract slowly then fast in different cycles

AVNRT = AV nodal reentrant tachycardia

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36
Q

wolf parkinson white pathophysiology

AVRT

A
  • Accessory pathway = bundle of Kent. bypasses the AV node (which normally slows/delays conduction) so this causes early abnormal depolarisation of part of the ventricle (=pre-excitation)
  • Pre excitation = short PR interval, wide QRS
  • Circuit loop = down normal pathway (AVN) as accessory bundle of kent is in refractory period, depolarizes ventricles and up bundle of kent accessory pathway (now out of refractory period) so impulse back to atria and down AVN again – reentry circuit

this is AVRT (AV reentrant tachycardia )- not AVNRT - no node!

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37
Q

AVNRT/AVRT treatment

A
  • Hold breath / carotid massage
  • Adenosine (temporary rapid heart block - stops loops)
  • Surgical ablation of accessory pathway(AVRT) / modification of slow pathway (AVNRT)
  • pacemaker
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38
Q

AVNRT/AVRT

  • supravent/ vent
  • tachy/brady
A

supraventricular tachy

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39
Q

AVNRT pathophysiology

A
  • AV nodal reentrant tachy AVNRT:
    • One of the conducting pathways in AV node is fast, the other is slow
  • -Fast one is used preferentially. If an impulse is early, the fast one may still be in the refractory period, so the slow one is used and propagates signal to ventricles
  • -This impulse travels back up fast pathway (now out of refractory period) and goes down slow pathway again (now out of refractory period)
  • This sets up re-entrant loop
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40
Q

prolonged QT syndrome

  • =
  • causes
  • presentation
A

Ventricular repolarization (QT interval) is greatly prolonged

Congenital

  • Jervell-lange-nielsen
  • romano-ward

Acquired

  • Hypokalemia
  • hypocalcaemia *
  • drugs (amiodarone (antiarrhythmic), antidepressants)
  • bradycardia
  • acute MI
  • diabetes

Syncope
palpitations

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41
Q

aortic aneurysm risk factors

A 
Hypertension
Age
Smoking
bicuspid/unicuspid aortic valves
Atherosclerosis
Renal failure
Previous aneurysm 
Family history 
Male
COPD
Hyperlipidemia
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42
Q

aortic dissection risk factors/ causes

A

Male
Age
Atherosclerosis
Genetics

Inherited
Degenerative
Atherosclerotic
Inflammatory
Trauma
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43
Q

what is aortic aneurysm

where

types

A
  • permanent dilation of artery to twice the normal diameter
  • can be abdominal or thoracic
  • can be true (ruptured or unruptured) or false (psuedoaneurysm)
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44
Q

true aneurysm

A

Abnormal dilation involves all layers of arterial wall
Loss of elastic lamellae
Smooth muscle cell loss

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45
Q

Is abdominal aortic aneurysm AAA true or false

A

true

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46
Q

two types of true aortic aneurysm

- symptoms

A

unruptured

  • often asymptomatic, picked up with routine xray etc
  • Pain in abdomen /back/ loin/ groin
  • Pulsatile abdominal swelling

ruptured

  • Pronounced pulsatile abdominal swelling
  • Collapse
  • Hypotension
  • Tachycardia
  • Anemia
  • Sudden death
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47
Q

what makes a person more likely for their aortic anuerysm to rupture

A

more likely if

high BP,
female,
smoker,
family history

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48
Q

psuedoaneurysm / fake aneurysm

A

collection of blood in the adventitia (/ tunica externia , outer layer) -

like a pocket of blood causing a bulge out the side of the vessel rather than the whole wall thickenness being deviated

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49
Q

aortic dissection =

A

the wall comes apart- the intima and media seperate :

  • tear in intima / media
  • blood enters wall –> haematoma
  • intima (And sometimes part of media) comes away
  • secondary blood flow, false lumen in the wall
  • true lumen is narrowed
50
Q

direction of dissection

two type systems

A

anterograde = towards bifurcation, further downstream (in direction of blood)

retrograde = towards aortic root, backwards

DeBakey
1 . ascending and descening (lots of aorta involved)
2. ascending (proximal aorta)
3. descending (distal)

stanford
A. first part of aorta involved (solo or + distal)
B. only distal aorta invo

51
Q

aortic dissection symptoms / signs

A
  • Hypertension (some present with hypo but more hyper)
  • Unequal BP in each arm maybe
  • Acute limb ischaemia
  • May have hemorrhagic shock
  • Peripheral pulses absent maybe
  • syncope, MI, stroke
  • Sudden onset of severe central chest pain (ripping /stabbing / tearing pain)
  • Radiates to back and down arms
52
Q

aortic aneurysm / dissection investigations

A
  • CT
  • MRI
  • US
  • Xray
  • echo - transoesophageal /aortagraphy (contrast xray) to locate anuerysm
53
Q

Aortic aneurysm management

A
  • Monitor small aneurysms
  • Treat underlying causes/risk factors inc smoking cessation
  • Control BP
  • Lower lipids
  • Surgical repair
54
Q

aortic dissection management

A 
Antihypertensive
-- Beta blockers
-- GTN
Analgesia
Surgery 
-- replace aortic arch
-- Stents
55
Q

PVD

  • commonness
  • age
  • most common where
A
  • common
  • old- 80+
  • most common near vessel bifurcation
  • most common in legs, esp femoro popliteal region (lower thigh/knee)
56
Q

PVD risk factors / causes

A

Risk factors for atherosclerosis (thrombus) –> stenosis
- Smoking, high glucose, lipids, cholesterol , obesity, low activity, high blood pressure

Genetics

  • vasculitis –> plaque
  • collagen disease –> weakened walls –> aneurysm
  • – Marfan, Ehlers danlos
  • arteriomegaly

embolus also (often from heart / atherosclerotic plaque)

57
Q

where is the most common aneurysm location

A

infrarenal, abdominal aorta

58
Q

PVD pathophysiolology

A
  • narrowing of arteries distal to the aorta
  • reduced blood supply so ischaemia/ infarction
  • The tissue ischaemia is often distal to the pathology

Narrowing
- Claudication (intermittent)
Blockage
- Critical limb ischaemia (chronic, narrowed over time)
- Acute limb ischaemia (acute - from thrombosis /embolism) – Limb threatening

59
Q

PVD mortality

A

high

increases with time/ severity of PAD

60
Q

acute limb ischaemia (limb threatening) symptoms

A 
6 P'S
pulseless
palor
perishingly cold
pain (claudication, angina)
paraesthesia
paralysis
61
Q

claudication

  • type of pain
  • where
  • cause
A
  • intermittent, on exercise
  • thigh/calf / buttock (not foot)
  • Due to oxygen demand outdoing supply, blood supply barely allows basal metabolism and so no reserve left for exercise. Lactic acid production - anaerobic
62
Q

calf claudication suggests?

A

femoral PVD disease

63
Q

buttock claudication suggests

A

iliac PVD disease

64
Q

iliac PVD presents as

A

buttock claudication

65
Q

femoral PVD presents as

A

calf claudication

66
Q

moderate/ severe PVD presentation

complications

A

moderate

  • claudication
  • angina

severe

  • critical limb ischaemia
  • – rest pain, gangrene, ulceration, infection
  • acute limb ischameia
  • – 6 p’s

stroke/TIA, amouris fugax

abdominal aortic anyuerysm

67
Q

what may post-prandial pain and weight loss/fear of eating be due to?

A

stenosis in gut arteries (coeliac, superior/inferior mesenteric)

68
Q

critical limb ischaemia

  • chronic/acute
  • where
  • symptoms
A
  • chronic
  • legs often
  • Rest pain (esp night – horizontal = less flow due to gravity. Relieved when hung over bed/sitting) - blood supply barely allows basal metabolism so no reserve for increased demand. May need to sleep sitting in a chair
  • Gangrene
  • Ulceration/ infection
69
Q

PVD investigations

A

Bloods

  • Looking at risk factors of atherosclerosis
  • Glucose
  • Lipids
  • Vasculitis screen
  • BP
  • ESR/CRP to exclude arteritis / vasculitis
  • FBC to exclude hematologic disorders

Buerger’s angle

  • Assess arterial supply
  • Raise leg slowly with them lying flat on bed
  • The point when their leg goes pale is buerger’s angle (the smaller the angle, the more severe the disease)
  • <20 degrees

Capillary refill time

  • Assess arterial supply
  • > 15 second

Imaging the vessel

  • Doppler ultrasonography
  • — site and extent of blockage , also looks for blood flow
  • — Harder to do deeper vessels eg renal
  • CT/MRI

ECG - many patients also have coronary artery disease

70
Q

what investigations can GP do to assess arterial supply

A

capillary refill time

  • should be less than 3 secs.
  • pvd =more than 15? - temperature affects

buerger’’s angle

  • Raise leg slowly with them lying flat on bed
  • The point when their leg goes pale is buerger’s angle (the smaller the angle, the more severe the disease)
  • <20 degrees
71
Q

PVD management

A

Reduce risk factors

  • Diet
  • Exercise prescribed (programmes, encourage them to the point of maximum pain)
  • Weight loss
  • Smoking cessation
  • Statins
    • Even if normal/low cholesterol + one other risk factor
  • Control of diabetes
  • Control of hypertension

Antiplatelets

Revascularization for critical ischaemia

  • Stent
  • Bypass
  • – Especially for long occlusions
  • – vein>prosthetic
  • Endarterectomy = surgical removal of plaque/ obstructive deposits, commonly in the carotid

Amputation
- Unreconstructable vessel plumbing or irreversible ischaemia

Heparin post op

72
Q

pericarditis causes

A
  • Idiopathic
  • Virus (adenovirus, enterovirus) / Bacteria (TB)(immunosuppressed)
  • Trauma - injury etc = early onset, after stent etc = delayed onset
  • Autoimmune (SLE, RA, sjorgens)
  • Neoplastic - secondary metastatic tumours, esp lung+breast
  • Aortic dissection
  • (fungal- rae)
73
Q

how common is pericarditis

A

not that rare

74
Q

pericarditis =

A

Inflammation of the pericardium +/- effusion

75
Q

pericarditis signs

A
  • Fever
  • Sinus tachycardia
  • Pericardial rub (sound of rubbing leather/crunching snow)= pathognomic
  • Signs of effusion
  • Becks triad: raised jugular venous pressure, low blood pressure, quiet heart sounds
76
Q

beck’s triad =

A
  • raised jugular venous pressure
  • low blood pressure
  • quiet heart sounds
77
Q

pericarditis symptoms

A 
Chest pain
-- Severe
-- Sharp
-- Pleuritic
-- Rapid onset
-- Left anterior chest /epigastrium, trapezius ridge! (superior bit between shoulder and neck)
-- Radiates to arm
-- Relieved by sitting forward, exacerbated by lying down !! -- This is very specific
Dyspnea
Cough
Viral symptoms - preceding/during
-- Fever
-- Rash 
-- Joint pain 
(hiccups)
78
Q

pericarditis diagnosis

other investigations

A

Diagnosis = 2 of

  • ECG
  • – saddled ST elevation (no ST depression in reciprocal leads)
  • – PR depression
  • Pericardial effusion
  • Friction rub
  • Chest pain
  • bloods (high wbc, SLE ANA+, troponin indicated myopericarditis)
  • CXR (assoc with pneumonia)
  • Echo
79
Q

pericarditis ecg

A
  • – saddled ST elevation (no ST depression in reciprocal leads)
  • – PR depression
80
Q

pericarditis management

A

Anti inflam

  • NSAIDs/aspirin
    • Colchicine
  • This reduces recurrence but severe diar/vom side effects mean patient rarely take for full course

restrict physical activity
for athletes
- sedentary rest for 3m until symptoms/ ECG resolves

81
Q

tamponade

  • pathophysiology
  • acute/ chronic
  • treatment
A
  • Fluid build up in pericardium
  • Thickening and reduced stretch of pericardium means limited stretch
  • Heart compressed
  • Filling of heart is reduced
  • Compliance is reduced
  • Stroke volume is reduced, low CO
  • Blood pressure is reduced!
  • high pulse
  • Left side fills less than right side to left pressure drops?

acute/chronic (either)

Treatment

  • life threatening
  • keep heart strong and fast
  • drainage, if effusion (pericardiocentesis)
  • treat underlying cause eg antibiotics
82
Q

normal amount of fluid between inner visceral and outer parietal pericadium

A

50ml

83
Q

constrictive pericarditis =

causes

A
  • pericardium becomes thick, fibrous, calcified
  • interferes with diastolic filling
  • chronic
  • bacterial infection, TB
  • rheumatic heart disease
  • can occur after any pericarditis
84
Q

A man enters A&E with severe acute pleuritic chest pain that radiates to the ridge of the trapezius. The pain is worse on inspiration and on lying flat, but is relieved by sitting forward. He also has hiccups. what is it

A

acute pericarditis

85
Q

why are hiccups involved in pericarditis

A

if phrenic nerve involved

86
Q

how do you differentiate ST elevation in STEMI vs pericarditis

A

pericarditis = in all leads

STEMI = elevation in leads depending on infarcted area eg anterior

STEMI = pain radiates to arm, jaw neck

pericarditis= pain radiates to trapezius ridge (superior bit between shoulder and neck). pain relieved by sitting forward

87
Q

valve disease gender

A

m>f

BUT mitral regurgitation is f>m

88
Q

which valve is the mitral valve

A

AV one, L side
this is the only one with two rather than 3 flaps

(R= tricuspid, aortic/ pulmonary valves )

89
Q

aortic stenosis pathophysiology

A

Obstructed LV outflow → increase LV pressure → compensatory LV hypertrophy → ischaemia, it exhausts, function decline → angina, arrhythmia, LV failure

90
Q

aortic stenosis causes

A
  • Degenerative calcification - of aortic valve
  • Rheumatic Heart disease
  • Congenital bicuspid aortic valve
91
Q

symptoms of aortic stenosis

A
  • Syncope
  • Angina
  • Dyspnoea
  • Sudden death
92
Q

signs of aortic stenosis

A
  • Ejection systolic murmur
  • Slow rising pulse (pulsus tarud)
  • Sustained apex beat
  • 4th heart sound
  • Soft 2nd heart sound
93
Q

aortic stenosis investigations

A
  • Echo - shows valve’s area, LV size and function, pressure gradient
  • ECG - LV hypertrophy, any blockages
  • CXR - LV hypertrophy, calcified aortic valve
94
Q

aortic stenosis management

A

Surgery, if symptomatic/severe

    • TAVI - transcutaneous aortic valve implantation – balloon inflated to crack calcification + stent with new valve placed over top
    • Percutaneous angioplasty (ballooning)

Infective endocarditis prophylaxis

95
Q

aortic regurgitation causes

A
  • Bicuspid aortic valve
  • Rheumatic heart disease
  • Infective endocarditis
  • Marfans
  • Aortic dissection
96
Q

aortic regurgitation pathophysiology

A

aortic valve fails to prevent backflow of blood during diastole → LV hypertrophy and LV dilatation due to combine volume and pressure overload

97
Q

aortic regurgitation symptoms

A
  • Angina
  • Dyspnoea
  • Palpitations
  • LV failure (and its signs/symptoms)
98
Q

aortic regurgitation signs

A
  • Water-hammer (collapsing) pulse - forceful. it rapidly increases then collapses
  • Displaced and hyperdynamic apex beat
  • Early diastolic murmur
  • Austin flint murmur
  • Head bobbing (deMussets sign, along with pulse)
99
Q

aortic regurgitation investigations

A
  • ECG - LV hypertrophy
  • X ray - cardiomegaly, pulmonary oedema, aortic root enlargement
  • Echo - LV hypertrophy
100
Q

aortic regurgitation management

A
  • Mild = vasodilators
  • Severe = valve replacement
  • Infective endocarditis prophylaxis
101
Q

mitral stenosis causes

A
  • Rheumatic heart disease (strep) = most common
  • Infective endocarditis
  • Mitral valve calcification
  • Congenital
102
Q

mitral stenosis pathophysiology

A

Obstruction of LV inflow → LA pressure rises, dilatation, hypertrophy → pulmonary congestion → can lead to AF and right heart failure

103
Q

mitral stenosis symptoms

A
  • Breathlessness
  • Fatigue
  • Palpitations
  • Chest pain
  • PND - paroxysmal nocturnal dyspnoea
  • Orthopnoea- SOB when lying
  • Hemoptysis
  • Recurrent chest infection
104
Q

mitral stenosis signs

A
  • AF
  • Tapping apex beat
  • Malar flush (cheeks)- due to decreased Cardiac output, increased CO2 retention
  • Low volume pulse
  • Signs of rheumatic heart failure
  • Loud first heart sound
  • Opening snap (= sound at beginning of diastole, could be called early diastolic maybe)
  • Rumbling mid-diastolic murmur
105
Q

mitral stenosis investigation

A
  • Echo - valve mobility/ area, pressure gradient
  • CXR - enlargement and pulmonary congestion/ oedema
  • ECG - AF, LA enlargement
106
Q

mitral stenosis management

A
  • Manage AF (anticoagulate, B blockers, diuretics, digoxin)

- Valvotomy (incisions in valves/ ballooned open)/ replacement

107
Q

mitral regurgitation causes

A
  • Myxomatous degeneration (MVP) → floppy mitral valve → Mitral valve prolapse
  • Rheumatic heart disease
  • Infective endocarditis
  • Ischaemic mitral valve
  • Papillary muscle dysfunction / rupture
  • Dilated cardiomyopathy
  • Marfans
  • Ehler danlos
108
Q

mitral regurgitation pathophysiology

A

Regurgitation into the LA → increased LA pressure → LA enlargement, dilatation, LV hypertrophy (less blood so needs more pump to maintain CO).

109
Q

mitral regurgitation symptoms

A
  • Palpitations
  • Dyspnoea
  • Orthopnoea
  • Fatigue
  • Right heart failure
110
Q

mitral regurgitation signs

A
  • Laterally displaced
  • Hyperdynamic
  • Systolic thrill
  • Soft 1st heart sound
  • Loud pan-systolic murmur at apex radiating to axilla
  • Third heart sound
111
Q

mitral regurgitation investigations

A
  • ECG - LV hypertrophy, palpitations
  • Echo- LV hypertrophy, valves, LA enlarged
  • Xray- LA enlarged, central pulmonary artery enlargement (feeding into L side)
112
Q

mitral regurgitation management

A
  • Echo monitoring
  • Infective endocarditis prophylaxis
  • Valve replacement
  • AF treatment (anticoagulate, B blockers, diuretics, digoxin)
113
Q

infective endocarditis pathophysiology

A
  • Infection of heart valves or other endocardial lined structure
  • infection spreads in blood
  • mainly bacteria
114
Q

why is medication not very good for valve diseases

A

mechanical issue so medication not v good

115
Q

infective endocarditis causes

A
  • prosthetic valves
  • septal defects
  • pacemaker leads
  • surgical patches
116
Q

why is the infective endocarditis types: L/R native but only L prosthetic

A

R sided surgery is rarer

117
Q

infective endocarditis epidemiology

A
  • V young/ old
  • IV drug abusers
  • Congenital heart disease (young)
  • Prosthetic valves
  • Males (more valve operations)
  • Rare
  • Poor dental hygiene/ teeth abnormality
118
Q

infective endocarditis symptoms/signs

A
  • Night sweats,
  • fever
  • Elevated INR
  • Petechial rash
  • Janeway lesions - small non tender purpley/red macular lesion on fingers and hands
  • Splinter hemorrhages - vertical short red lines under nail
  • Osler’s nodes- tender purple dots on subcutaneous digits
  • Roth spots = on eye
  • Clubbing
119
Q

infective endocarditis complications

A
  • may present as symptoms
  • Embolisation (stroke, PE, MI, bone infections, kidney dysfunction)
  • Arrhythmias , heart failure (due to valve dysfunction)
  • Abcesses
120
Q

infective endocarditis diagnosis/investigations

A
  • Vegetation seen in echo
  • – 2D TTE (transthoracic echo) not 100%.
  • – Transoesophageal echo more sensitive but need probe down throat
  • Bugs grown in blood cultures (not present in 2-5% due to previous antibiotic use)
  • Fever
  • Predisposition - history
  • Raised CRP (liver protein, marker of inflammation)
  • ECG- ischaemia, infarction, new heart block
  • Negative results dont exclude (in isolation)
121
Q

infective endocarditis treatment

A
  • Antimicrobials IV for 6w, based on culture sensitivity findings- to make sure treatment effective
  • Treat complications (eg arrythmias)
  • Surgery - if cannot cure with antimicrobials alone (CRP doesn’t fall, infection comes back) OR if severe complications OR large vegetations that may embolise
  • Remove infected devices / valves, and replace
122
Q

what lifestyle management is key for valve diseases and why

A

Fastidious dental hygiene to reduce risk of infective endocarditis

phase 2a mine (38 decks)

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