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Year 5 Conditions > cardio > Flashcards

cardio Flashcards

1
Q

what is pericarditis

A

inflammation of the pericardium - the sac which surrounds the heart

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2
Q

aetiology of pericarditis

A
  • viral – cosackies, mumps, EBV, CMV, varicella, rubella, HIV, Parvo-19
  • MI + Dressler’s, aortic dissection, uraemia, SLE, IBD
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3
Q

clinical features of pericarditis

A
  • Classic triad of pericardial rub, chest pain, ECG changes
  • Retrosternal/ precordial pleuritic chest pain worse lying flat or inspiration, coughing,
  • Pain relieved by sitting forward, radiate to trap/ neck/ shoulder.
  • Fever.
  • Dry cough.
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4
Q

what are the pericarditis specific ECG changes

A

PR depression, widespread saddle ST elevation

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5
Q

Ix and Mx of pericarditis

A

ECG

  • Refer to cardiology  if tamponade  pericardiocentesis
  • If bacterial  pericardiocentesis + systemic Abx (vancomycin + ceftriaxone)
  • Treat cause
  • NSAID + PPI
  • Colchicine – used to prevent further pericarditis
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6
Q

what is accelerated hypertension

A

recent inc in BP to over > 180 and > 110 + papilloedema or retinal haemorrhage

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7
Q

clinical features of accelerated HTN

A

papilloedema
retinal haemorrhages

signs of end-organ damage - headache, fits, N+V, visual disturbances, chest pain, bleeding due to DIC, microangiopathic haemolytic anaemia

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8
Q

Investigation and treatment of accelerated HTN

A

medical emergency
same day referral for pt with accelaterd HTN with papilloedema/retinal haemorrhage

aim - reduce BP steadily over 24-48 hours - IV nitroprusside, labetalol or nifadipine

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9
Q

what is pericardial effusion

A

collection of fluid in the pericardial space

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10
Q

what are the different types of pericardial effusion?

A

transudate - fluid pushed through capillaries due to high pressure within them

exudate - fluid that leaks around the cells of capillaries due to inflammation

haemopericardium - blood

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11
Q

causes of pericardial effusion

A 
pericarditis 
MI 
AKI/CKD 
malignancy nearby 
autoimmune conditions
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12
Q

clinical features of pericardial effusion

A
  • Depend on speed and size of effusion
  • Chest pain: relieved by sitting up and leaning forward and intensified by lying down.
  • Light-headedness and syncope
  • Palpitations
  • Cough
  • SOB
  • Anxiety
  • Beck’s triad of pericardial tamponade: hypotension, muffled heart sounds, jugular venous distention.
  • Pulses paradoxus (significant drop in BP on inspiration)
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13
Q

ix and Mx of pericardial effusion

A

echo -diagnostic

refer to cardiology

treating underlying cause

pericariocentesis

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14
Q

what are the 2 shockable rhythms?

A

pulseless ventricular tachycardia

ventricular fibrillation

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15
Q

what are the 2 non-shockable rhythms?

A

pulseless electrical activity

asystole

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16
Q

what is the sequences of action in cardiac arrest

A

discover a patient unresponsive and not breathing normally –> call for help –> CPR 30:2 –> attach defib pads + airwya mx + IV access –> assess rhythm (pause CPR for rhythm analysis and pulse check)

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17
Q

what are the reversible causes of cardiac arrest

A

4Ts

  • tamponade
  • thrombosis
  • tension pneumothorax
  • toxins

4HS

  • hypothermia
  • hypoxia
  • hypovolaemia
  • hypo/hyperkalaemia/metabolic
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18
Q

what is acute left ventricular failure

A
  • Left ventricle is unable to adequately move blood through the left side of the heart and out of the body.
  • This causes a backlog of blood that increases the amount of blood in the left atrium, pulmonary veins and lungs.
  • As the vessels in these areas are engorged with blood due to increased volume and pressure, they leak fluid and are unable to reabsorb fluid from the surrounding tissues.
  • This causes pulmonary odema where the lung tissues and alveoli become full of interstitial fluid
  • This results in lack of gas exchange and desaturation.
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19
Q

aetiology of acute left ventricular failure

A

iatrogenic - aggressive IV fluids in frail people with impaired left ventricular function

sepsis

MI - think if flash pulmonary oedema

arrythmias

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20
Q

clinical features of acute left ventricular failure

A
  • rapid SOB
  • looking unwell
  • dry cough - due to irritation of pleura
  • inc RR
  • reduce O2 sat
  • tachycardia
  • 3rd HS
  • bilateral pulmonary basal crackles
  • hypotensions in severe cases
  • cold and clammy due to peripheral shutdown

signs of underlying causes

  • chest pain in ACS
  • fever in sepsis
  • palpitation in arrrythmias

if RHS failure as well

  • raised JVP
  • peripheral oedema
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21
Q

ix for acute left ventricular failure

A

ECG - arrythmias and ischaemias

ABG - low o2, high co2

bloods - FBC, U&Es, LFT, CRP, BNP, Trop

CXR - pulmonary oedema pictures - Kerley B line, cardiomegaly, dilated upper lobe vessels, pleural effusions

ECHO - main measure of left ventricular function is ejection fractions, <40 = LHeart failure

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22
Q

management for acute ventricular failure

A

A-E approach
PODMAN

Position pt - sit up
oxygen 
Diuretics - furosemide 40mg IV  + fluids restrction 
morphine - consider
anti-emetics - consider 
nitrites - consider

other consideration

  • nitrate (must have SBP > 90) - for MI, severe HTN, aortic regurg or mitral stenosis
  • IV opiates to act as vasodilator
  • CPAP if dyspnoea and acidaemia
  • inotropes - those with potentially reversible cardiogenic shock
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23
Q

what are some causes of secondary hypertension

A

renal disease - glomerulonephritis, pylonephritis, PCKD)

endocrine disease - Cushing’s, Conn’s, acromegaly, hyperPTH, pheochromocytoma, hyperthyroidism

other

  • pregnancy
  • steriods
  • coarctation
  • OCP
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24
Q

what is chronic cardiac failure?

A

the ability of the heart to maintain the circulation of blood is impaired as a result of a structural or functional impairment of ventricular filling or ejection

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25
Q

aetiology of chronic cardiac failure

A

coronary artery disease and heart attack - most common cause

HTN
valvular disease - aortic stensois
AF
other - hyper/hypothyroidism, haemochromatosis, protein powder?

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26
Q

clinical features of chronic cardiac failure

A

SOB - on exertion, lying flat, nocturnal cough, PND

fluid retention - ankle, abdomen, weight gina

fatigue, dec exercise tolerance

light headed/Hx syncope

tachycardia

LHF
- SOB, pulmonary oedema, displaced apex, heaves, murmurs, gallop rhythm, basal creps

RHF
- fatigeu, SOB, anorexia, inc JVP, hepatomeglay, pitting odema, ascites

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27
Q

what is Vicrchow’s triad

A

altered flow - turbulence, stasis, varicose veins

altered vessl - HTN

hypercoagulable - nephrotic syndreom, trauma or burns, cancer , pregenancy, inc age, race, smoking, obese > 30

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28
Q

what medications are used in DVT prophylaxis?

A

LMWH
UFH if renal/low platalet
graduated comprssion stockings (not if PVD, ischaemia)

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29
Q

management of DVT

A
  • Refer for same day assessment. High wells/ +ve D-dimer should try 4hr.
  • Anticoagulate: LMWH (enoxaparin 1.5mg/kg/24h SC) (unfractioned heparin in renal failure guided by APTT) or Fondaparinux.

IVC filter if not possible to have LMWH

Following.
• Stop heparin when INR 2-3 or 24 hrs after.
• Warfarin/DOAC 3 months (provoked), 6 months (unprovoked) review and aim INR 2-3.

if cancer 6 months

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30
Q

aetiology of acute ischaemic leg

A

embolism - from AF, mural thrombus after MI, prosthetic and abnor valves, aneurysm, maliganat tumour, trauma - fat embolism in long bone fracture

thrombosis

Raynaud’s
compartment syndrome
aortic dissection
diabetes

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31
Q

investigation of acute ischaemic leg

A

examine limb - last palpable pulse

Doppler US

BLoods - FBC, U&Es, LFT, ESR, glucose, lipids, thrombophilia screen (esp antiphospholipid syndrome)

source of emboli - ECG, ECHO, aortic/femoral/popliteal US

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32
Q

management of acute ischaemic leg

A

• Initial
o urgent admission + analgesia
o percutaneous catheter-directed thrombolytic therapy
o emergency embolectomy if life threatening
o endovascular revascularisation
o amputation
o fasciotomy (cut fascia – relive pressure) (compartment syndrome)

• long term management
o Heparinisation  after thrombolysis and surgery
o Aspirin
o lifestyle  diet, exercise, HTN management, hyperlipidaemia management, smoking cessation

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33
Q

management of acute ischaemic leg

A

• Initial
o urgent admission + analgesia
o percutaneous catheter-directed thrombolytic therapy
o emergency embolectomy if life threatening
o endovascular revascularisation
o amputation
o fasciotomy (cut fascia – relive pressure) (compartment syndrome)

• long term management
o Heparinisation  after thrombolysis and surgery
o Aspirin
o lifestyle  diet, exercise, HTN management, hyperlipidaemia management, smoking cessation

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34
Q

what is superficial thrombophlebitis

A

a superficial vein, usually the long saphenous vein of the leg or its tributaries becomes inflamed secondary to a blood clot inside it

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35
Q

which vein is most suspectible for superficial thrombophlebitis

A

long saphenous veins

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36
Q

aetiology of superficial thrombophlebitis

A

varicose vein - trauma to a varicose vein accounts for 65-80% of presentations

IV cannula

prev superfiical thombophlebitis or DVT or chronic venous insufficiency

> 60 yrs old 
obesity 
smoking 
IVDY 
hpercoagulability states
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37
Q

clinical features of superficial thrombophlebitis

A

hard and painful to palpation - the vein feels like a hard cord if it is not varicosed and like a hard knot if it is varicosed

inflammed, erythema, warmth and welling of the skin

associated bruising

maybe some features of cellulitis (acute onset of red, painful, hot, swollen and tender skin) or an abscess

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38
Q

investigation for superficial thrombophlebitis

A

clinical diagnosis

doppler to rule out DVT

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39
Q

differential for superficial thrombophlebitis

A

DVT - generalied pain

cellulitis - systemic features

lymphangitis - red streaks from infected area to groin/armpit

erythem nodusm

lipodermatosclerosis - chronic venous insufficiency leading to hardened, tight, red or brown skin typcially affecting htye inner part of the calf and cuasing champagne bottle appearance

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40
Q

treatment for superficial thrombophlebitis

A

Treat pain with a simple analgesic -paracetamol/NSAIDs

Manage swelling and discomfort with compression stockings.

If very big  anticoagulation  tinzaparin or enoxaparin

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41
Q

what are some complication for superficial thrombophlebitis

A

septic thrombophlebitis

DVT/PE

varicose veins

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42
Q

what is cannula-related phlebitis

A

Inflammation of a vein following the insertion of a cannula

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43
Q

aetiology of cannula-related phlebitis

A
  • Mechanical damage to the vessel wall/ foreign body irritation from the insertion of a cannula OR chemical irritation from the medicine
  • Increased length of stay of cannula in-situ
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44
Q

clinical features of cannula-related phlebitis

A
  • Redness
  • Swelling
  • Warmth
  • Visible streaking at the site of the cannula
  • Tenderness
  • Rope/cord like structure which can be felt through the skin.
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45
Q

investigations of cannula-related phlebitis

A

diagnosis of clinical features

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46
Q

Mx of cannula-related phlebitis

A
  • remove cannula
  • treat pain- analgesia
  • warm and cold compresses can be applied to areas to increase flow of blood around the area and reduce the swelling.
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47
Q

what is complete heart block?

A

3rd-degree heart block between the SA and AV node

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48
Q

what are some causes of complete heart block

A

inferior MI, IHD
cardiomyopathy
idiopathic degen of conducting system (lenegre’s or Leves disease)
inflam cardiac disease - SLE, myocarditis, RA
AV node blockign agents - B-blocker, CCB, digoxin
hyperkalaemia

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49
Q

what are the different types of complete heart block

A

nodal block - (intermittent delay at the AV node, narrow QRS) - good progress

infra-nodal block - (in or below the bundle of His, wide QRS) - bad progress

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50
Q

what is the heart rate of complete heart block like?

A

atrial > 75

ventricular rate > 45

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51
Q

clinical feature of nodal complete heart block?

A

mild fatigue, dizziness, reduced exercise tolerance, palpaitation

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52
Q

clinical features of intranodal complete heart block?

A

haemodynamically compromised, syncope, confusion, dyspnoea, severe chest pain, sudden death

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53
Q

investigation of complete heart block

A

ECG - P waves occur regularly at 75 bpm + unconnected with the rhythm of QRS complex

bloods - FBC, glucose, trop, U&Es, Ca, mg

ECHO - for structural abnor

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54
Q

management of complete heart block?

A

should follow the resus bradycardia algorithm

A-E assessment

check if any adverse features present? (shock, syncope, myocardial ischaemia, heart failure)

if yes - atropine 500mcg IV
and check if satisfactory response obtain?

long term mx
- ifAv block irresversible -

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55
Q

what defines postural hypotension?

A

a drop in systolic BP upon standing of > 20 mmHg

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56
Q

aetiology of postural hypotension

A 
Venous pooling of blood
•	Severe varicose veins
•	Prolonged standing
Reduced muscle tone
•	Prolonged bed rest
Impaired vasomotor tone
•	Diabetic autonomic neuropathy
•	Shy-Dager syndrome
Hypovolemia
•	Dehydration
•	Exsanguination e.g. gastro-intestinal bleed.
Drug
•	Hypotensive agents
•	Tranquilliser
•	Phenothiazines
•	Levodopa
Addisonian Disease
•	Addison’s disease
•	Hypopituitarism
•	Abrupt cessation of steroid therapy.
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57
Q

clinical features of postural hypotension

A

dizziness or syncope upon standing up (too fast)

relieved by sitting back down or lying down

blurring of vision

falls

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58
Q

INvestigation for postural hypotension

A
  • Lying and standing blood pressure

* HR

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59
Q

management of postual hypotension

A

conservative management

meds
1st line - fludrocortisone
2nd - midodrine

60
Q

what is aortic dissection

A

• Disruption of medial layer of aortic wall provoked by intramural bleeding  separation of aortic wall layers  formation of true lumen and false lumen +/- communication.

61
Q

aetiology of the aortic dissection

A
  • Most common cause = essential hypertension
  • Marfan syndrome and ehlers danlos syndrome
  • Bicuspid aortic valve • trauma
  • infection
  • Aortic manipulation to associated with cardiac surgery  iatrogenic causes
62
Q

what are the types of aortic dissection?

A

Standford

  • Type A - involves the aortic arch and ascending aorta
  • Type B - involve the descending aort

Debakey

  • type 1 - both aortic arch and descending aorta
  • type 2 - jsut the aortic arch
  • type 3 - just the descending aorta
63
Q

clinical features of aortic dissection

A

chest pain - sudden onset, sever on the chest or back, ripping/tearing/sharp, moving downward

o Signs related to haemopericardium – pulsus paradoxus, faint/absent heart sounds, distended neck veins and shocked.

o Signs related to aortic root dilatation – wide pulse pressure, diastolic murmur over the aortic area.

o Hypertension. (may also be hypovolemic if there is a massive haemothorax.

64
Q

what is abdominal aortic aneurysm

A

Defined as a 50% increase in dilation of the aorta.

65
Q

what are some fo the causes of AAA

A 
coactation of the aorta 
marfan syndrome, Ehlers Danlos
previous aortic surgery 
pregnancy 
trauma
tertiary syphilis 
atherosclerosis
> 65
66
Q

clinical features of AAA

A

unruptured - asymptomatic, can be an incidental finding or epigastric pain to loin, grain.back, pulsate +expanile mass. can obstruct duodenum causgin vomiting or IVC casuing oedeam, DVT

ruputre - sudden pain in lower back or central abdo , can radiate to loin, groin . collpase (if hypovolaemic shock). grey turners

67
Q

what are the investigations for AAA

A

abdo exam
USS abdo = gold standard
CT angiography if stable and consider for surgery

bloods - FBC, U&Es, LFT, G+S, crossmatch, crp

68
Q

management of AAA

A

NICE guideline

if <5.5cm - monitor, treat RF

  • if > 5.5cm/rapid growth >1cm a year/ rupture , will need surgical repair

the repair can be done through open lapratomy or endovascular aneurysm repair (EVAR via femoral artery)

69
Q

what are some risk factor for AF?

A

PIRATE

P- pulmonary causes - obstructive sleep apnoea, PE, COPD, pnemonia)

I - chaemia/infarction/CAD

Rheumatic fever and mitral regurgitation

alcohol/anaemia

thyrotoxicosis/toxins

electrolytes/endocarditis

Sepsis/sick sinus syndrome

70
Q

what is atrial flutter?

A

atria beat regularly, but faster than usual and more often than the ventricles, so you may have 4 atrial to every 1 ventricular beat

71
Q

what are the 2 types of atrial flutter

A

typical - rhythm has its origins in the right atrium at the level of the tricuspid valve - saw tooth on ECG

atypical - atypical - origin is elsewhere in the right atrium or the left atrium

72
Q

aetiology of atrial flutter

A
  • Age
  • Structural abnormalities of the heart e.g. left atrial dilatation.
  • Previous heart surgery
  • Pericarditis
  • Thyroid disease/COPD.
  • Alcohol, obesity
  • Atrial fibrillation – those who are on long term suppression
73
Q

how common is atrial flutter?

A

1/10th less common than AF

2nd most common arrhythmia

74
Q

clinical features of atrial flutter

A
  • Asymptomatic and incidental finding on ECG
  • Mild symptoms: palpitations, irregular heartbeat, fatigue, dyspnoea, chest pain, dizziness
  • Syncope
  • Heart failure
  • Irregular or regular pulse BUT tachycardia.
75
Q

investigation of atrial flutter

A

ECG - saw tooth best seen in the inferior lead II, III, aVF with atrial rte of 240-340, variable AV conduction (commonly present with 2:1, 3:1)

bloods - TFT< FBC, ESR, UE, LFT

ECHO - assess underlying cardiac function and assess for structural abnor

76
Q

management of atrial flutter?

A

same for AF

rate control if > 48 hours

rhythm control if <48 hours, DC cardioversion if unstable and < 48 hours. if > 48 hours the nanticoagulant for 3 weeks prior to cardioversion

prevention of thromboembolism

  • use CHADS2VASC/HASBLEED
  • warfarin or NOAC
77
Q

aetiology of 1st degree heart block

A

physiological - during sleep, in athletes

cardiac causes - AV block or sinus node disease

non-cardiac causes - vasovagal, hypothermia, hypothyroidism, hyperkalaemia, lyme

drugs - beta-blocker, diltiazem, digoxin, amiodarone

congential

78
Q

what is the most common cause of 1st-degree heart block?

A

amiodarone overdose

79
Q

clinical features of 1st-degree heart block

A 
•	Asymptomatic: incidental finding on ECG.
•	Bradyarrythmias < 60
•	Syncope 
•	Dyspnoea 
•	Chest pain, palpitation, N+V
HTN (or less commonly low)
80
Q

ix for 1st degree heart block

A
  • ECG
  • Trop
  • If metabolic cause suspected check UE’s.
81
Q

what are the ecg finding of 1st degree heart block

A

PR interval of greater than 0.2 (> 5 small squares)

each atrial activation leads to a ventricular activation with a 1:1 correspondence - just prolonged

82
Q

management of first-degree heart block

A

typically no management at all

if bradycardia - go with the resus bradycardia pathway

83
Q

what are the 2 types of 2nd degree heart block

A

Mobitz type 1 - Wenckebach - stepping back
- There is progressive prolongation of the P-R interval following each atrial impulse, until an atrial impulse fails to be conducted to the ventricles

Mobitz type 2 - There is intermittent failure of conduction of atrial impulses to the ventricles without progressive lengthening of the P-R interval, thus the P-R interval of conducted beats is constant. Ratio (2:1)

84
Q

aetiology of 2nd degree heart block

A
  • Physiological - during sleep, in athletes
  • Cardiac causes - AV block or sinus node disease.
  • Non-cardiac causes - vasovagal, hypothermia, hypothyroidism, hyperkalemia, Lyme
  • Drugs - beta-blocker, diltiazem, digoxin, amiodarone in therapeutic use or OD
  • Congenital
85
Q

clinical features of 2nd-degree heart block

A
  • Bradyarrythmias < 60
  • Mobitz Type 1: asymptomatic, may experience mild headedness or dizziness, fainting.
  • Mobitz Type 2: mild light-headedness or dizziness, fainting, chest, SOB, feeling very dizzy suddenly when standing up from a lying or sitting position- this is caused by having low blood pressure.
86
Q

investigation for 2nd-degree heart block

A

ecg
trop
u&Es

87
Q

management of 2nd degree heart block?

A

treat through the resus bradycardia algorithym

type 1 - no management of treat through the asystole part

type 2 - treat through the aystole part

permanent pacemaker for type 2 onward for sure, type 1 can be considered

88
Q

pathophysiology of AVRT

A

Accessory bypass tract (Wolff Parkinson White syndrome) -involves tracts of conducting tissue that partially or totally bypass normal AV connections (bypass tracts).

They run most commonly from the atria directly to the ventricles. Triggered by atrial or ventricular premature beats.

89
Q

what are the 2 different types of re-entrant supra-ventricular tachycardia

A

AVNRT - re-entry caused by nodal pathwyas

AVRT - the type of SVT where you have an abnor loop of electricity/re-enrant circuit between 2 pathways

90
Q

pathophysiology of AVNRT

A

AV node: a reentrant circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. this creates a re-entrant loop

91
Q

what is the classic ECG appearance of Woof-Parkinson White Syndrome/AVRT

A

Delta wave - upward slope of P wave

shortend PR interval - < 0.12

prolonged QRS

HR > 100

92
Q

what is the classical ECG appearance of AVNRT

A

like SVT

  • shortned QRS
  • rate > 100
93
Q

clinical features of re-entrant SVT?

A

20-40s

sudden episodes of palpitations that begin and terminate abruptly

attacks may last from few seconds to several hours

SOB, chest pain, dizziness, neck pulsation

severe tachycardia

94
Q

ix for re-enterant SVT?

A

ECG = diagnostic

blood test - U&Es, TFT, trop, calcium, magnesium

95
Q

management of re-enterant SVT?

A

vagotonic maneuvers eg holding breath and straining, dunking face in ice water pr coughing

IV adenosine

electrical cardioversion if unstable

prevention

  • beta-blocker
  • ablation - fore frequent recurrence
96
Q

what is ventricular tachycardia?

A

broad complex tachycardia

97
Q

risk factor of VT?

A

caffeine
cocaine
TCA
acidosis

98
Q

symptoms of ventricular tachycadia?

A

symptoms of IHD or haemodynamic compromise

  • chest pan
  • palpitations
  • dyspnoea
  • dizziness
  • sncope
  • tachy, palor, shock, low GCS
99
Q

investigation of ventricular tachycadia

A

ECG - HR > 120, wide QRS complex (>120m), no obvious p wave

FBC, U&Es, ca, mg, po4, troponin, glucose

level of therapeutic drugs eg Digoxin

CXR

ECHO

drug screen for cocaine

100
Q

treatment of ventricular tachycardia

A

A-E assessment

go through the resus council tachycardia algorithm -amiodarone 300mg IV over 20-60 mins then 900mg over 24 hours

if adverse features - synchronized DC shock

101
Q

aetiology of ventricular fibrillation

A

MI
AF
digoxin toxicity, TCA

102
Q

management of ventricular fibrillation

A

shockable - 1 shock, resume CPR for 2 mins - assess rhythm

IV adrenalien 1:1000 1mg

IV amiodarone

103
Q

aetiology of mitral regurgitation

A

primary - valve causes ventricular damage

  • rheumatic fever - following a throat infection, fever + joint swelling
  • infective endocarditis
  • mitral valve prolapse

secondary - ventricule casues valve damage

  • cardiomyopathy
  • CHD
  • AF
104
Q

what are some symptoms of mitral regurgitation

A

mild maybe asymptomatic

acute - pulmonary oedema, dizziness, fatigue, chest pain, palpitation

chronic - SOB, LHF (dyspnoea on exertion, orthopnoea, PND)

105
Q

signs of mitral regurgitation

A

pan systolic murmur at apex radiating to the axilla

displaced apex beat

development of LHF as enlarged left atrium and ventricular can no longer cope with inc volume

106
Q

Ix of mitral regurgitation

A

ECG - AF, left ventricular hypertrophy (tall QRS complexes)

CXR - left atrial and ventricular enlargement

ECHO - enlarged left atrium and left ventricle with abnormal mitral valve.

doppler - size/site of regurgitation

BNP - for heart failure

107
Q

management of mitral regurgitation

A

acute - medical stabilisation with diuretics and vasodilator (reduce the afterload) and so less regurgitation volume

medical

  • treat AF
  • LFT - diuretics and ACEi + aldosterone agonist
  • prophylaxis abx for infective endocarditis

surgical
- mitral valve replacement

108
Q

what is the most common cause of mitral stenosis

A

rheumatic heart disease - most common 99% of cases

109
Q

aetiology of mitral stenosis

A

rheumatic heart disease = most common 99% of cases

degenerative calcification

infective endocariditis
amyloid deposition
congenital mitral stenosis
SLE, RA

110
Q

symptoms of mitral stenosis

A 
asymptomatic for years 
progressive dyspnoea - main symptoms 
orthopnoea 
PND 
AF 
haemoptysis - rupture of a bronchial vein due to left atrial pressure 
systemic emboli - MI 
RVF - ascites
111
Q

what are some signs of mitral stenosis

A

mid-diastolic murmur (low picthc) –> best heard with bell at apex with patient rolled to the left holding breathing after expiration

Malar flash

AF common

raised JVP

laterally displaced apex beat

raised pressure in left atrium transmitted to pulmonary vessles

right ventricular heave

RV failures - hepatosplenomegaly, ascites, due to LHSHF which put strain on RHS

112
Q

investigation of mitral stenosis

A

ECG - AF, left atrail enlargement - tall QRS waves

CXR - left atrial enlargement, pulmonary oedema

ECHO - left atrial enlarement

113
Q

treatment for mitral stenosis

A

medical therapy
- diuretics and vasodilators (nitrates) - lessen pulmonary venous pressure

  • AF management - beta-blocker/calcium antagonist/digoxin, anticoagulant
  • prophylactic abx for rheumatic fever

surgical

  • percutaneous mitral commissurotomy PMC
  • balloon valvuloplasty
  • open mitral valve replacement
114
Q

what is aortic stenosis

A

obstruction of blood flow across the aortic valve due to pathological narrowing

115
Q

aetiology of aortic stenosis

A

snile calcific aortic stenosis - most common cause

bicupsid valve

childhood hx of rheumatic disease

116
Q

what is the most commonly affect valvular disease

A

aortic stenosis

117
Q

clinical features of aortic stenosis

A

usually on exertion
triad of symptoms - syncope, angina, dyspnoea

-palpitations

118
Q

examination finding of aortic stenosis

A

ejection systolic murmur - S2 is often diminished

pulse - slow rising

BP - narrow pulse pressure, but normal

Left ventricular heave - hypertrophy as more force is needed

aortic thrill

best heard over the aortic valve area with radiation to the carotid and apex

119
Q

what are the ecg finding of aortic stenosis

A

LVH, left anterior hemiblock (LAD)

LBBB - cardiomyopathy//LV strain

120
Q

investigation for aortic stenosis

A

ECG

CXR - calcific aortic ring, cardiac enlargement, post stenotic dilatation of the aorta

ECHO - diagnostic –> thickened, calcified valve, LV hypertrophy

Doppler echo - site/severity of AS

BNP

121
Q

management of aortic stenosis

A

if asymptomatic
• Monitor + advise against competitive sports.
• Lifestyle changes and symptoms control e.g. BP/HF.

if symptomatic

  • aortic valve replacement
  • TAVI (transcatheter aortic valve implantation) - less complication than AVR
  • balloon valvuloplasty - risk of failure
  • prophylactic abx against bacterial endocarditis
122
Q

aetiology of aortic regurg

A

bicuspid aortic valve - most common congenital cause

rheumatic fever

infective endocarditis

Collagen vascular diseases - marfan’s ehlers danlos

degeneartive aortic valve disease

123
Q

clinical features of aortic regurg

A

early stages - asymptomatic

end stage

  • dyspnoea
  • orhtopnoea
  • angina
  • syncope.dizzy
  • palpitations
124
Q

exam finding of aortic regurg

A

high pitched early diastolic murmur - best heard when patient lean forward on expiration

pulse - collapsing water hammer

BP - wide pulse pressure (high systolic and low diastolic)

displaced apex beat to the left

corrigan’s sign - carotid pulsation

de Musset - head bobbing

Quincke’s - nail bed bobing

125
Q

Investigation for aortic regurg

A

ECG - LVH

CXR - LVH, dilated ascending aorta, pulmonary oedema and cardiomegaly

ECHO - dilated left aortic root, reverse flow from aorta, LVH

126
Q

management of aortic regurg

A

acute
- diuretic and vasodilator

chronic
- monitoring

  • or medical
  • ACE reduced BP -when surgery contraindicated/LV dysfunction post-surgery
  • B-bloack - marfan’s prevent aortic root dilatioan
  • prophylactic ABx against infective endocarditis

surgical

  • AVR
  • aortic root surgery
127
Q

what is infective endocarditis

A

infection of the endocardium of the heart

128
Q

what is the most common causative agent in infective endocarditis

A

staphoccous infection
- S aureus via vascular line

Streptococcus = 2nd most common
- S viridian via oropharynx

Enterococci - following instrumentation of bowel or bladder

129
Q

what is the clinical feature of acute endocarditis

A

Acute - Staph A

  • rapid onset
  • infective organism damages normal valve
  • clumps of bacteria form - septic emboli in circulation
  • toxic presentation with metastatic infection
130
Q

what is the clinical feature of subacute endocarditis

A
  • Gradual onset
  • Weakly infective organism damages defected valve.
  • No septic emboli
  • Mild toxic infection with not metastatic infection
131
Q

RF for infective endocarditis

A

valvular heart disease - with stenosis or regurgitation

valvular replacement

structural congenital heart disease- septical defect or repaired defect

previous IE

hypertrophic cardiomyopathy

IVDU

invasive vascular procedure

132
Q

clinical feature of infective endocaritis

A

fever + chills, reduced appetitse, weight loss

new-onset murmur

LHS - major systolic emboli anywhere in the body
RHS - prominent pulmonary symptoms and numerous septic embolic in lungs

Roth spot - red spot on retina with characterisitic white spot centre
Osler’s node - painful on tips of hands and toes
Jane way lesions - non-painful on palms and soles of feet
splinter haemorrhages
ROJS

  • Petechiae (conjunctiva, hands, feet, chest, abdomen)
  • Splenomegaly – long standing
  • Haematuria- long standing and glomerulonephritis.
  • Clubbing-longstanding.
  • Arthritis- longstanding
  • Arterial emboli
  • Septic infarcts
133
Q

investigation for infective endocarditis

A

bloods - FBC, U&Es, LFT, CRP/ESR
ECG/CXR
blood culture - 2 sets of bloods within 1 hour
transthoracic echo - repeat in 7 days

134
Q

what is the diagnostic criteria of infective endocarditis

A

duke criterai
- requires 2 major criteria or 1 major and 3 minor to diagnose

major

1) +ve blood culture of IE
2) evidence of endocardial involvment –> ECHO evidence (intra-cardiac mass on valve or supporting structure, abscess, new partial dehiscence of prosthetic valve or new valvular regurgitation)

minor

1) predisposing heart condition or IVDU
2) fever > 38
3) vascular pheonoma - major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage and Janeway’s lesion
4) immunological phenomena - glomerulonephritis, Osler’s node, Roth’s spot and rheumatoid factor
5) PCR - +ve broad-range PCR 16
6) echo findings consistent wit hIE but do not meet a majror criteria

135
Q

management of infective endocarditis

A

IV Abx 4-6 weeks

native valve - empiriacal abx (amoxicillin and gentamicin)

prosthetic valve - empirical (vancomycin + gentamycin + rimgamicin)

surgical dariange of abscess if abx ineffective or valvular damage

136
Q

pathophysiology of varicose vein

A
  • Veins contain valves that only allow blood to flow one direction – towards the heart
  • In the legs this means that as the leg muscles contract, they squeeze blood upwards against gravity
  • When these valves become incompetent, the blood pools (drawn by gravity) in the veins and is not effectively pumped back to the heart
  • The deep vs superficial veins have a connection called the “perforators” that allow blood to flow from the superficial veins to the deep veins
  • When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them
  • This leads to dilatation and engorgement of the superficial veins
137
Q

aetiology of varicose vein

A

primary - unknow, congenital valve absence

secondary

  • obstruction (DVT, foetus, ovarian tumour, obesity)
  • valve destruction - DVT, AV malformation, constipation, overactive muscle pumps (cyclist)

RF - prolong standing, FHx, OCP

138
Q

symptoms of varicose vein

A
  • “Legs are ugly”
  • Pain
  • Cramps
  • Tingling
  • Heaviness/ dragging sensation in legs
139
Q

signs of varicose vein

A

oedema

ulcers

haemodersrin deposit - veins become leaky and blood starts to pool and being broken down (Haemodersrin - area of blackness)

thrombophlebitis and DVT

atrophie blanche - white scarring with red dot (capillaries)

varicose eczema - skin becomes dry and inflamed

lipodermatosclerosis - champagne bottle legs - skin and soft tissue become fibrotic causing tight narrowed lower legs

saphenex varix - dilation of saphenous vein at its confluence with the femoral vein

140
Q

investigation of varicose vein

A

exam –> assess with pt standing up - palpaitae for tenderness or hardness

  • feel for cough impulse at saphenofemoral junction - 4cm lateral and inferior to pubic tubercle to exclude

percussion test - tap SFJ and palpate for transmitted impulse at the varicose vein identified

auscultate for bruits

Trendelenburg test - • Ask the patient to lie down. Elevate the leg, and empty the veins by massaging distal to proximal.
• Using a tourniquet, occlude the superficial veins in the upper thigh. Ask the patient to stand.
• If the tourniquet prevents the veins from re-filling rapidly, the site of the incompetent valve must be above this level i.e. at the sapheno-femoral junction.
• If the veins re-fill, the communication must be lower down. Repeat at lower levels in the legs (knee and ankle)

dopper = diagnostic

141
Q

management of varicose vein

A

treat underlying causes

educate - avoid longstanding, elevate legs, lose weight
stockings

endovenous ablation
• Radiofrequency (catheter inserted into vein and probe generated and then closed)
• Laser ablation (catheter inserted into vein and heated and then closed.
• Injection sclerotherapy –liquid foam (below the knee), obliterates the lumen and damages the endothelium
• Stripping- veins pulled out of leg

142
Q

symptoms of chronic limb ischaemia

A

cramping pain in the calf (popliteak) or thigh (femoral) or buttock (iliac)

worse when walking on flat/hill

relieved by rest - intermitten caludication

change in leg - think, coolor, paler, ulceration, eczemam haemosiderin deposition gangree

ischaemic rest pain - nocturnal burning foot pain relieved by handing legs over the side of the bed

143
Q

signs of chronic limb ischemia

A
  • Absent femoral, popliteal, foot pulses.
  • Punched out skin ulcers.
  • Irregular borders
  • Capillary refill > 15 secs
  • Buerger’s test: raise leg to 45 degrees and look for pallor (+ve). Look for reperfusion by allowing the patient to sit with their legs over the edge
  • Postural dependent colour change :pallor on leg elevation
  • Calf wasting.
144
Q

investigation for chronic limb ischemia

A

bloods - FBC, ESR, throbophilia screen, fasting glucose, lipid level

BP

ECG - CHD

patient <50 - homocysteine taken

doppler - gold standard - ABPI, normal =1, claudication 0.6-0.9, rest pain 0.3-0.6, impending gangrene < 0.3
DM = >1

duplex USS - site and degree of stenosis

145
Q

what is fontaine classfication

A

I - ABPI > 0.9
II - ABPI 0.6-0.9
III - ABPI 0.3-0.5
IV < 0.3

146
Q

management of chronic limb ischemia

A 
ABCDES 
	Atorvastatin 80mg
•	Blood pressure control
•	Clopidogrel 75mg
•	Diabetes control
•	Exercise training – first line intervention for claudication
•	Smoking cessation

surgical

  • endovascular revascularistaion (stent)
  • surgical reconstruction - bypass for dffuse disease
  • amputation - last resort

peripheral vasodilator - naftidrofuryl oxalate - for those who can not have revascularisation and exercise fails to improve

Year 5 Conditions (19 decks)

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