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All conditions - Year 3 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is Atrial fibrillation

A

Rapid, chaotic and ineffective atrial electrical conduction.

Permanent
Persistent
Paroxysmal

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2
Q

What are the causes of Atrial fibrillation

A

May be no cause

Systemic:

  • Thyrotoxicosis
  • HTN
  • Alcohol

Cardiac:

  • Mitral valve disease
  • IHD
  • Rheumatic heart disease
  • Cardiomyopathy
  • Pericarditis
  • Sick sinus syndrome
  • Atrial myxoma

Lung:

  • Cancer
  • PE
  • Pneumonia
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3
Q

What are signs and symptoms of Atrial fibrillation

A

Mainly asymptomatic

Palpitations
Syncope

Irregularly irregular pulse

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4
Q

What are the appropriate investigations for Atrial fibrillation

A

ECG - Absent P waves + Irregularly irregular QRS complex
Atrial Flutter = Saw tooth

Check Thyroid - Low TSH in Thyrotoxicosis

Check Valves - Echo

Check U&Es

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5
Q

How is Atrial fibrillation treated

A

Acute
Haemodynamically unstable Under 48hrs - DC Cardioversion or chemical cardioversion (Flecainide)

Over 48hrs - Anticoagulant for 3/4 weeks and then cardioversion

Chronic
Otherwise
- Anticoagulant or antiplatelet: - NOAX (Rivaroxaban, Apixaban, Dabigitran), Warfarin, Aspirin

Rate control (Aimed rate is 90bpm and below):

  • Beta-blocker - Propranolol
  • Digoxin (Glycoside - Positive inotropic affect but negative chronotropic - Good in CHF with AF but not CHF with sinus rhythm)
  • CCBs - Verapamil (Negative Inotropic and chronotropic affect)

Prophylaxis:
Amiodarone - Antiarrhythmic used in tachyarrhythmias as it prolongs ventricular and atrial muscle contraction

Anticoagulant depends on stroke risk stratification (CHADS-VASc):
Low risk (<2) = Antiplatelet
High risk (>2) = Anticoagulant
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6
Q

What are the complications of Atrial fibrillation

A
  • Thromboembolism - Risk of stroke 4% per year

Increased risk with left atrial enlargement or left ventricular dysfunction

  • Worsening of existing HF
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7
Q

What are the reversible cause of Cardiac arrest

A

4 Hs:

  • Hypothermia
  • Hypoxia
  • Hypovolaemia
  • Hypokalaemia/Hyperkalaemia

4 Ts:

  • Toxins
  • Thromboembolic
  • Tamponade
  • Tension pneumothorax
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8
Q

What are the signs and symptoms of Cardiac arrest

A

Potentially preceding:

  • Fatigue
  • Pre-syncope

Unconsciousness
Not breathing
Absent carotid pulse

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9
Q

What are appropriate investigation for Cardiac arrest

A

Cardiac monitor: Allows classification of rhythm

Bloods:

  • ABG
  • U&Es
  • FBC
  • X-Match
  • Clotting
  • Toxicology
  • Blood glucose
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10
Q

What is the treatment for Cardiac arrest

A

BLS - CPR & Rescue Breaths

ALS - If pulseless VT or VF then defibrillate once + Administer Adrenaline (1mg IV) every 3-5 minutes - Repeat

If pulseless electrical activity or systole then administer adrenaline and atropine (3mg IV once only) if <60bpm

Treatment of reversible causes:
- Hypothermia - Warm slowly
- K - Correct imbalance
- Hypovolaemia - IV colloids, crystalloids and blood products
- Tamponade - Pericardiocentesis
- Tension pneumothorax - Aspiration/Chest drain
- Thromboembolism - Treat as PE or MI
Toxins - Use antidote
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11
Q

What is HF?

A

This is the inability of the cardiac output to meet the body’s demands despite normal venous pressure

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12
Q

What are the causes of low output HF (Reduced CO)

A

LHF:

  • IHD
  • HTN
  • Cardiomyopathy
  • Aortic valve disease
  • Mitral regurgitation

RHF:

  • Secondary to LHF (Called CHF)
  • Infarction
  • Cardiomyopathy
  • Pulmonary hypertension/Embolus/Valve disease
  • Chronic lung disease
  • Tricuspid regurgitation
  • Constrictive pericarditis/pericardial tamponade

Biventricular failure

  • Arrhythmia
  • Cardiomyopathy
  • Myocarditis
  • Drug toxicity
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13
Q

What are the causes of high output HF (Increased demand)

A
  • Anaemia
  • Beri-Beri
  • Pregnancy
  • Paget’s disease
  • Hyperthyroidism
  • Arteriovenous malformations
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14
Q

What are symptoms of HF

A

LHF:

  • Dyspnoea/Orthopnoea/PND
  • Fatigue

Acute LHF:

  • Dyspnoea
  • Wheeze/Cough
  • Pink frothy sputum

RHF:

  • Swollen Ankles
  • Fatigue
  • Increased weight
  • Reduced exercise tolerance
  • Anorexia
  • Nausea
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15
Q

What are the signs of HF

A

LHF:

  • Tachycardia
  • Tachypnoea
  • Displaced apex beat
  • Bilateral basal crackles
  • S3 Gallop (Rapid ventricular filling)
  • Pansystolic murmur

Acute LHF:

  • Tachycardia
  • Tachypnoea
  • Cyanosis
  • Pulsus alternans
  • Wheeze
  • Bilateral basal crackles
  • S3 Gallop

RHF:

  • Raised JVP
  • Hepatomegaly
  • Ascites
  • Peripheral oedema
  • Tricuspid regurgitation

Class 1: Exertional
Class 2: With daily tasks
Class 3: Less than daily tasks
Class 4: Rest

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16
Q

What are the investigative findings in HF

A

Troponin
BNP >500

CXR

  • Alveolar shadowing (Bat-winging)
  • Kerley B lines
  • Cardiomegaly
  • Upper lobe Diversion
  • Pleural Effusion

ECG
- Potential ischaemic changes

Echocardiogram

  • Assess ventricular contraction
  • Systolic Vs Diastolic (Systolic LVEF <40%)

Catheterisation

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17
Q

How is acute HF treated

A

Sit up
Oxygen

Stable:

  • Furosemide
  • GTN

If hypotensive:
- Dobutamine

If malignant hypertension (>180/110):

  • IV BB - Metoprolol
  • GTN
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18
Q

How is chronic HF treated

A
  • BB + ACEi/ARB(Valsartan)
  • Reduced Salt + Reduced Fluid

Class 2 + AA (Spironolactone)
Class 3 + Vasodilators (Isosorbide Dinitrate + Hydralazine)/Diuretic (Furosemide
Class 4 + Inotrope (Digoxin)/Ivabrandine

LVEF <35% = ICD –> Transplant
LVEF <3O% = CRT biventricular pacemaker

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19
Q

What are complications and prognosis for HF patients

A

Respiratory failure
Cardiogenic shock
Death

50% die within 2 years

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20
Q

What are causes of DVT

A

Vessel wall damage

  • Surgery
  • Trauma
  • Previous DVT
  • Central venous catheterisation
  • Cancer

Stasis

  • Varicose veins
  • Paralysis
  • COPD
  • GA
  • Long-haul flights

Hyper-coagulability

  • HRT + Increased Oestrogen
  • Pregnancy
  • Inherited thrombophilia
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21
Q

What are signs and symptoms of DVT

A

Calf swelling
Localised pain
Oedema

  • Unilateral calf swelling (Difference between legs >3cm = bad)
  • Oedema
  • Tenderness along deep vein
  • Homan’s sign: Forced passive dorsiflexion of the ankle causes deep calf pain
  • Pratt’s Test: It involves having the patient lie supine with the leg bent at the knee, grasping the calf with both hands and pressing on the popliteal vein in the proximal calf. If the patient feels pain, it is a sign that a deep vein thrombosis exists.
  • Phlegmasia cerulea dolens (Painful blue swelling)
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22
Q

What are the investigative findings in DVT

A

Wells score 2 + = Duplex
D-Dimer - High sensitivity
Proximal duplex US

Monitor:

  • FBC
  • U&Es
  • LFTs
  • Coag
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23
Q

What are the criteria in Well’s criteria

A 
Active caner
Bedridden/surgery
Calf swelling >3cm
Collateral veins present
Entire leg swollen
Localised tenderness
Pitting oedema
Paralysis
Previous DVT
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24
Q

What is the treatment of DVT

A

No bleeding/PE

  • Anticoagulant: Heparin and Warfarin
  • Gradient stockings

Pregnant

  • Dalteparin instead
  • Gradient stockings

Bleeding
- IVC filter

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25
Q

What are complications of DVT

A

PE
Bleeding
HIT - Heparin induced thrombocytopenia
Osteoporosis

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26
Q

What are the 3 classifications for Heart block

A

1st Degree AV Block: Prolonged conduction through the AV node

2nd Degree AV Block:
Mobitz Type 1: Progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle then repeats

Mobitz Type 2: Intermittent or regular failure of conduction through the AV node. Defined by the number of normal conductions per failed or abnormal one (2:1, 3:1, etc.)

3rd Degree (Complete) AV Block: No relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle

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27
Q

What are the causes of Heart block

A
  • MI or IHD (Most common)
  • Infection (Rheumatic heart or IE)
  • Drugs - Digoxin
  • Metabolic (Hyperkalaemia)
  • Infiltration of conducting system (Sarcoidosis)
  • Degeneration of the conducting system
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28
Q

What are signs and symptoms of Heart block

A

1st and 2nd degree are usually asymptomatic

Mobitz 2 and 3rd degree may cause Stokes-Adams attacks (Syncope caused by ventricular asystole)
+ Chest pain, HF, Palpitations, Pre-syncope, Hypotension

In 3rd degree there is:

  • A slow large volume pulse
  • JVP may show cannon a waves - Atria and ventricle contract at the same time
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29
Q

What are the investigative findings in heart block

A

ECG - Gold standard

  • 1st Degree: Fixed PR interval (0.2s)
  • Mobitz Type 1: Progressively prolonged PR interval - Dropping QRS
  • Mobitz Type 2: intermittently a P wave is NOT followed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
  • Complete: No relationship between P waves and QRS complexes. If QRS is initiated in the bundle of His then there will be a narrow complex. If it is more distally then there will be a wide complex and slow rate

CXR - Cardiomegaly/Pulmonary Oedema

Bloods - TFTs/Digoxin/Cardiac enzyms/ Troponin

Echo - Wall motion abnormalities/Aortic valve disease/Vegetations

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30
Q

What is the treatment for Heart block

A

Chronic Block
- Permanent pacemaker is recommended for: Complete/Mobitz 2/Symptomatic Mobitz 1

Acute Block

  • IV atropine
  • Temporary (External) pacemaker
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31
Q

What are the complications of Heart block

A
  • Asystole
  • Cardiac arrest
  • Heart failure
  • Complications of any pacemaker instead
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32
Q

What is an AAA

A

This is the permanent dilation of the aorta (>3cm or 1.5x expected on AP film for sex and body size)

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33
Q

What are risk factors for AAA

A

Smoking

FHx
Increasing age
Male
Female (Rupture)
Connective tissue disorder
Hyper lipidaemia
COPD
Atherosclerosis
HTN
Tall
Central obesity
Non-diabetic
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34
Q

What are the signs and symptoms of AAA

A

Normally incidental findings

Rupture:

  • Abdominal, back and groin pain
  • Palpable expansile abdominal mass
  • Hypotension
  • Fever if infectious
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35
Q

What are the investigative findings in AAA

A

Abdominal US - Diagnostic
CTA - Diagnostic for rupture

ESR/CRP
FBC
Blood culture

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36
Q

What is Aortic dissection and what are the different classifications

A

Separation of the tunica intimacy leads to blood flow between the inner and outer layers of the tunica media creating a false channel

Stanford A: Ascending or Arch
Stanford B: Descending
DeBakey I: Ascending + Arch
DeBakey II: Ascending
DeBakey III: Descending

Most affect the ascending aorta

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37
Q

What are the causes of Aortic dissection

A
  • Atherosclerotic aneurysmal disease
  • HTN
  • Connective tissue disorders
  • Bicuspid aortic valve
  • Annulo-Aortic ectasia
  • Coarctation
  • Smoking
  • FHx
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38
Q

What are the signs and symptoms of Aortic dissection

A
  • Tearing chest pain radiating to the back

Potentially:

  • Syncope
  • Weakness/Paraplegia/Paraesthesia

Signs:

  • BP difference between limbs
  • Diastolic Decrescendo murmur
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39
Q

What are the appropriate investigations for Aortic dissection

A

ECG - ST Depression rarely elevation
CXR - Widened mediastinum
D-Dimer - May be raised helps with differentials

Diagnosis:
- CT Angiography

Operating theatre/ICU:
- Trans-Thoracic Echo or Trans-Oesophageal Echo

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40
Q

What are the most common causes of Aortic regurgitation

A

Worldwide: Rheumatic heart disease

Developed countries: Bicuspid valve

Connective tissue disease
Aortic dissection
Infective endocarditis
AS, TA, RA

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41
Q

What are the signs and symptoms of Aortic regurgitation

A

Acute:

  • Signs of Pulmonary Oedema and Cardiogenic Shock
  • MI

Chronic:

  • Palpitations
  • Exercise intolerance
  • CHF
  • Wide PP
  • Early Diastolic murmur
  • Severe: Austin-Flint Mid-Late diastolic rumbling
  • Collapsing pulse
  • S3 +/- S4 (LVH)
Eponymous signs of haemodynamic instability: 
Quincke's - Nail bed pulsation
Corrigan's - Visible carotid pulse
de Musset's - Head nodding
Muller's - Uvula pulsations
Traube's - Pistol shot over femoral
Becker's - Retinal artery pulsations
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42
Q

What are the appropriate investigations for Aortic regurgitation

A

Echo - Diagnostic
2D Echo - Valvular Anatomy
Doppler Echo - Severity
ECG - Left axis deviation

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43
Q

What are the most common causes of Aortic stenosis

A

Most common: Age related calcification
Bicuspid valve calcification

Rheumatic fever

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44
Q

What are the signs and symptoms of Aortic stenosis

A

Reduced exercise tolerance

On exertion:

  • Dyspnoea
  • Angina
  • Syncope

Signs of:

  • LVH
  • CHF
  • Ejection systolic murmur (Crescendo Decrescendo)
  • S2 diminished
  • Slow rising pulse
  • Narrow PP
  • S4 (LVH)
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45
Q

What are the appropriate investigations for Aortic stenosis

A

Echo

ECG - LVH, Absent Q, Block

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46
Q

What are the characteristics of Arterial ulcers

A 
Temperature: Cold
Pain: Painful
Site: Bony (Dorsum, Ankle, Toes)
Depth: Deep 
Border: Well defined (Punched out)
Base: Dry +/- infection

Delayed capillary refill
Hairlessness
Absent pulse
Pain relieved dangling leg off bed

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47
Q

What are the causes of Arterial ulcers

A

PVD

Vasculitis
DM
Renal failure
HTN
Sclerosis
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48
Q

What are the investigations of Arterial ulcers

A

Ankle Branchial Pressure Index <0.9

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49
Q

What are the characteristics of Venous ulcers

A 
Temperature: Warm
Pain: Mildly?
Site: Gaiter - Medial Malleolus
Depth: Shallow
Border: Bigger poorly defined
Base: Granulation tissue (Wet)
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50
Q

What are the causes of Venous ulcers

A

Venous valvular defect

DM
CHF
PVD
DVT
VV
Pregnancy 
Obesity
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51
Q

What are the investigations of Venous ulcers

A

Duplex US - Retrograde or reversed flow, valve closure time >0.5 seconds

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52
Q

How are Venous ulcers treated

A

Graded compression stockings
Debridement to make the wound heal acutely
Extreme cases: Surgical graft

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53
Q

What is Cardiomyopathy

A

It is primary disease of the myocardium

  • Dilated
  • Hypertrophic
  • Restrictive
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54
Q

What are the causes of Cardiomyopathy

A

Majority idiopathic

Dilated

  • Post viral
  • Alcohol
  • Drugs
  • Familial
  • Thyrotoxicosis
  • Haemochromatosis
  • Peripartum

Hypertrophic
- 50% genetic

Restrictive

  • Amyloidosis
  • Sarcoidosis
  • Haemochromatosis
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55
Q

What are symptoms of Cardiomyopathy

A

Dilated

  • Symptoms of heart failure – fatigue, dyspnoea
  • Arrhythmias
  • Thromboembolism
  • Family history of sudden death

Hypertrophic

  • Usually NO SYMPTOMS
  • Syncope
  • Angina
  • Arrhythmias
  • Dyspnoea
  • Palpitations
  • Family history of sudden death

Restrictive – similar to constrictive pericarditis

  • Dyspnoea
  • Fatigue
  • Arrhythmias
  • Ankle or abdominal swelling
  • Family history of sudden death
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56
Q

What are signs of Cardiomyopathy

A 
Dilated
RHF
- Functional mitral and tricuspid regurgitations 
- Hypotension 
- AF

Hypertrophic

  • Jerky carotid pulse
  • Double apex beat
  • Ejection systolic murmur
  • Systolic thrill at lower left sternal edge

Restrictive

  • RHF
  • Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles
  • Palpable apex beat
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57
Q

How is Cardiomyopathy investigated

A

CXR:

  • May show cardiomegaly
  • May show signs of heart failure – pulmonary oedema
ECG:
All Types
- Non-specific ST changes 
- Conduction defects 
- Arrhythmias

Hypertrophic

  • Left-axis deviation
  • Signs of left ventricular hypertrophy
  • Q waves in inferior and lateral leads

Restrictive
- Low voltage complexes

Echocardiography:
Dilated
- Dilated ventricles with global hypokinesia and low ejection fraction
- MR, TR, LV thrombus

Hypertrophic
- Ventricular hypertrophy (asymmetrical septal hypertrophy)

Restrictive:

  • Non-dilated non-hypertrophied ventricles
  • Atrial enlargement
  • Preserved systolic function
  • Diastolic dysfunction
  • Granular or sparkling appearance of myocardium in amyloidosis

Cardiac Catheterisation

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58
Q

What are the causes of Pericarditis

A

Usually Idiopathic

  • Viral - Coxsackie B virus
  • Dressler syndrome - Post MI
  • Uraemic
  • Autoimmune - RA, SLE, SS
  • Cancer + Radiation therapy
  • Medication
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59
Q

What are the signs and symptoms of Pericarditis

A
  • Pleuritic chest pain - Sharp central, radiates to neck or shoulders (Relieved by sitting forward)
  • Dyspnoea
  • Nausea
  • Fever
  • Pericardial friction rub
  • Faint HS due to effusion

Tamponade

  • Beck triad (Raised JVP, Hypotension, Muffled HS)
  • Tachycardia
  • Pulsus paradoxus

Constrictive = RHF signs

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60
Q

What are the investigations in Pericarditis

A

ECG - Widespread saddle-shaped ST elevation

Echo

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61
Q

How is Pericarditis treated

A

Pain = NSAIDS
Treat cause

Recurrent = Low dose steroids/Immunosuppressants

62
Q

What is Constrictive pericarditis

A

This chronic pericarditis leading to thickening and scaring of the pericardium

63
Q

What are signs of Constrictive pericarditis

A

RHF signs

64
Q

What are investigations for Constrictive pericarditis

A

Echo - Diagnostic
CXR - Calcification of pericardium
Pericardial biopsy

65
Q

How is Hypertension diagnosed

A

Stage 1 >140/90 in clinic and ambulatory/home readings over 135/85

  • Treat <80 + LVH, CKD, Hypertensive retinopathy, CVD, Renal disease, DM
  • <40 seek specialist advice for secondary cause

Stage 2 >160/100 in clinic and ambulatory/home readings over 150/95
- Treat all

Generally for under 80 target is

66
Q

What are the symptoms of accelerated Hypertension

A 
Visual field loss
Blurered vision
Headache
Seizures
N&amp;V
Acute HF
67
Q

What are the signs of Hypertension

A 
Retinopathy - Keith-Wagner Classification
1 - Silver wirings
2 - AV nipping
3 - Flame haemorrhages + soft exudates
4 - Papilloedema
68
Q

What are the investigations for Hypertension

A 
FBC - Polycythaemia
U+E - Hypokalaemia/Renal function
ECG - LVH
Urinalysis
Fasting glucose
Lipids

Ambulatory BP monitoring or Home readings

69
Q

How is Hypertension treated

A

Stop smoking/Lose weight/Reduced salt/Reduce alcohol

1st line
Under 55 - ACEi/ARBs
Over 55 or Black - CCBs/Thiazide diuretic

2nd line
ACEi/ARBs + CCBs/Thiazide diuretic

3rd line
+ Thiazide diuretic/CCB (whichever wasn’t previously given)

4th line
+ Alpha/beta blockers

70
Q

What are important secondary causes of Hypertension

A 
Phaeochromocytoma
Cushing's
Conns
Acromeglay
Renal artery stenosis
Co-arctation of the aorta
71
Q

What are the causes of Infective endocarditis (IE)

A

Most common cause is Streptococcus Viridans then:

  • Staph. Aureus
  • Strep. Bovis
  • Enterococci and Coxiella Brunetii
Rarely
HACEK (Gram -ve):
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
72
Q

What are risk factors for IE

A
  • Abnormal valves (Congenital, calcification, rheumatic heart disease)
  • Prosthetic heart valves
  • Turbulent blood flow - Patent ductus arteriosus
  • Recent dental work/poor dental hygiene - Source of S. Viridans
  • IVDU - Source of S. Aureus
73
Q

What are the signs and symptoms of IE

A 
Fever
Headache
Weakness
Arthralgia
Dyspnoea on exertion

Cutaneous infarcts
Chest pain
Back pain

Subacute (Weeks to months):

  • Janeway lesions
  • Osler nodes
  • Roth spots
  • Splinter haemorrhages
  • Clubbing
  • Petechiae on pharyngeal and conjunctival mucosa

New regurgitant murmur:
Mitral > Aortic > Tricuspid > Pulmonary

74
Q

How is IE diagnosed

A

FBC - Anaemia of chronic disease, Leukocytosis
U&Es - Normal or elevated urea
Urinalysis - RBC casts; WBC casts; Proteinuria; Pyuria
Blood cultures - Bacteraemia; fungaemia

ECG - Prolonged PR; Non-specific ST/T wave abnormalities; AV block

Echo - Diagnostic- Valvular, mobile vegetations

Duke classification - A method of diagnosis IE based on findings of the investigation and the symptoms/signs
- RF

75
Q

How IE treated

A

Antibiotics for 4­‐6 weeks

Empirical treatment
- Benzylpenicillin, Gentamicin

Streptococci - Benzylpenicillin, Gentamicin

Staphylococci - Flucloxacillin, vancomycin, Gentamicin

Enterococci - Ampicillin, Gentamicin

Culture Negative - Vancomycin, Gentamicin

Surgery - Urgent valve replacement may be needed if there is a poor response to antibiotics

76
Q

What are the complications of IE

A
  • Valve incompetence
  • Intracardiac fistulae or abscesses
  • Aneurysm
  • Heart failure
  • Renal failure
  • Glomerulonephritis
  • Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
77
Q

What are the 4 diseases that come under Ischaemic heart disease

A

Stable angina
Unstable angina
NSTEMI
STEMI

78
Q

What are the 3 diseases that come under Acute coronary syndrome

A

Unstable angina
NSTEMI
STEMI

79
Q

What is Stable angina and what are the causes

A

Chest pain resulting from Myocardial ischaemia that is precipitated by exertion and relieved by rest

The main cause is atherosclerotic disease
Rare causes:
- Decubitus - When lying down
- Prinzmetal - Coronary spasm
- Coronary syndrome X - Normal exercise tolerance and normal coronary angiograms

80
Q

What are the symptoms of Stable angina

A
  • Constricting discomfort in the chest or neck, shoulders, jaw and arms
  • Precipitated by exercise
  • Relived by rest or GTN after 5 minutes

Typical = All 3
Atypical = 2 features
Likely to be non-anginal pain = 1

81
Q

How may Stable angina be investigated

A

Resting ECG is often normal so an exercise ECG may help show differences.

Hb
Lipids
Blood glucose

82
Q

How is Stable angina treated

A

Conservative:

  • Smoking cessation
  • Lose weight
  • Exercise

Medical:

  • Anti-anginals (BB/CCB)
  • Symptomatic (GTN)
  • Risk factor reduction (Aspirin, statins, ACEi)

if medical treatment is ineffective then consider PCI or CABG

83
Q

What are the symptoms of Acute coronary syndrome

A
  • Acute-onset central, crushing chest pain
  • Radiates to arms/neck/jaw
  • Pallor
  • Sweating

Silent infarcts in elderly and diabetics

84
Q

How is Acute coronary syndrome diagnosed

A

ECG:

  • STEMI - ST elevation, Hyperacute T waves, New-onset LBBB
  • Unstable angina/NSTEMI - ST depression, T wave inversion

Troponins:

  • Elevated troponin suggest myocardial injury (NSTEMI/STEMI)
  • High sensitivity - 0-3hrs
  • Previous generation - 3-6hrs
  • CK-MB - 8-12hrs
  • If there has been a previous infarction in the last 10-14 days then CK-MB or Serum myoglobin should be used as cardiac markers instead
  • The gold standard diagnostic investigation is Coronary angiogram
85
Q

Which ECG leads would be affected in different sites of infarction

A
  • Inferior (Right coronary artery) - II, III, aVF
  • Anterior (LAD) - V1-5
  • Lateral (Left circumflex) - I, aVL, V5/6
  • Posterior (Posterior descending): Tall R wave + ST depression in V1-3
86
Q

How is Acute coronary syndrome treated

A

MONA BASH

Morphine
Oxygen - Saturating below 90
Nitrates (GTN)
Antiplatelets (Aspirin + Clopidogrel)

Beta-blockers (Bisoprolol) - Indefinitely with Reduced LVEF, HF
ACEi - LVEF <40, DM, HTN, CKD
Statins - All patients
Heparin (LMWH) - If coronary angiography is planned

Fondaparinux - If low bleeding risk and no coronary angiography is planned within 24hrs of admission

For a STEMI you want to give them a PCI

  • Access to PCI in 90 minutes - Perform PCI - 120 minutes latest!
  • No access to PCI in 90 minutes but under 12 hours since onset - Thrombolysis (Alteplase) followed by PCI in high risk patients (Ongoing chest pain, haemodynamically, mechanically or electrically unstable) - If thrombolysis is contra indicated then do a PCI
  • No access to PCI in 90 minutes and over 12 hours since onset - If symptoms persisted then PCI is still indicated especially is a coronary angio is done first to determine patient condition. If the patient is stable then there is no evidence that PCI is beneficial.
87
Q

What is the GRACE score

A

This is the risk stratification score used to estimate mortality of patients up to 6 months after admission

High risk patients should be given - GlpIIb/IIIa Inhibitor - Tirofiban and coronary angiography within 72 hours

88
Q

What are the complications to Acute coronary syndrome

A 
Death
Arrhythmia
Rupture
Tamponade
HF
Valve disease
Aneurysm
Dressler's syndrome
Embolism
Reinfarction
89
Q

What is Supraventricular tachycardia

A

A regular, narrow-complex tachycardia with no p waves and a supraventicular origin

90
Q

What are symptoms of Supraventricular tachycardias

A

Palpitations
Syncope
Dyspnoea
Chest discomfort

91
Q

What are the different types of Supraventricular tachycardia

A

Atrioventricular nodular re-entry tachycardia (AVNRT)
- Local circuit form around AV node

Atrioventricular re-entry tachycardia (AVRT)
- A re-entry circuit forms between the atria and ventricles due to the presence of an accessory pathway (Bundle of Kent)

92
Q

How is an Supraventricular tachycardia diagnosed

A

ECG

  • During the tachycardia - Regular, narrow complex tachycardia with absent P waves
  • After termination of SVT - AVNRT - Normal but AVRT - Delta wave (Slurred upstroke on QRS complex)

Presence of an accessory pathway resulting in a delta wave on ECG - Wolff-Parkinson-White syndrome

93
Q

How is Supraventricular tachycardia treated

A

Step 1: Is the patient haemodynamically stable
No - DC Cardioversion
Yes - Step 2

Step 2: Vagal manoeuvres - did it work?
Yes - Great
No - Step 3a

Step 3a: IV adenosine 6mg - Did it work?
Yes - Great
No - 3b then 3c - IV adenosine 12mg (Try twice) - Then step 4

Step 4:
1 - BB/CCB (Diltiazem/Esmolol/Verapamil/Metoprolol)
2 - Amidarone/Ibutilide
3 - Flecainide/Propafenone/DC Cardioversion

94
Q

What is Wolff–Parkinson–White syndrome (WPW)

A

The presence of an accessory pathway connecting the atrium to the ipsilateral ventricle

95
Q

What are causes of WPW

A

Accessory pathway (AP) is a development cardiac defect

An increased rate of stimulation causes increase AP conduction but decreased AV conduction leading to an AVRT

  • Ebstein’s anomaly (most common) - Displacement of septal and posterior tricuspid leaflets
  • Mitral valve prolapse
  • Cardiomyopathies (HOCM)
96
Q

What is the different between a WPW Pattern and WPW

A

A WPW pattern is asymptomatic but with the same ECG abnormalities as normal WPW

97
Q

Who is usually affected by WPW

A

2x in Men

Younger patients - Prevalence decreases with age

98
Q

What are the signs and symptoms of WPW

A

Often asymptomatic

Potential:

  • Palpitations
  • Syncope
  • Light-headedness
  • SOB
  • Chest pain
  • Sudden cardiac death

Paroxysmal SVT may be followed by a period of polyuria due to Atrial dilation and release of ANP

99
Q

How is WPW diagnosed

A

ECG - Delta waves if the AP conducts anterogradely (If it conducts retrograde-only then there will be no delta wave), Short PR interval, Broad QRS complex, Intermittent pre-excitation

Echo - Cardiomypoathy/Valve defects

100
Q

What is Vasovagal syncope

A

This is LOC due to a transient drop in blood flow to the brain caused by excessive vagal discharge

101
Q

What are causes of Vasovagal syncope

A
  • Emotions (Fear, severe pain, blood phobia)

- Orthostatic stress (Prolonged standing, hot weather)

102
Q

How does Vasovagal syncope present

A
  • LOC lasting short time
  • Patients may experience sweating, dizziness, light-headedness before hand
  • There may be some twitching of limbs during the blackout
  • Recovery is normally very quick
103
Q

Ventricular fibrillation

A

This is an irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death

It is the most common arrhythmia identified in cardiac arrest patients

104
Q

What are risk factors of Ventricular fibrillation

A
  • Coronary artery disease
  • AF
  • Hypoxia
  • Ischaemia
  • Pre-excitation syndrome
  • Cardiomyopathy
  • Valvular heart disease
  • Long QT syndrome
  • Brugada syndrome
105
Q

What are the signs and symptoms of Ventricular fibrillation

A

Chest pain
Fatigue
Palpitations

106
Q

How is Ventricular fibrillation diagnosed

A

ECG - Random lines

  • Cardiac enzymes to check for infarction
  • Electrolytes check for derangement
  • Drug levels and toxicology screen
  • TFTs
  • Coronary angio if survived
107
Q

How is Ventricular fibrillation treated

A
  • VF requires urgent defibrillation and cardioversion
  • Full assessment of LV function and perfusion
  • Most survivors need and implantable cardioverter defibrillator (ICD)
  • Empirical BBs
  • Radiofrequency ablation treatment in some cases
108
Q

What is Ventricular tachycardia

A

A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually >120bpm

109
Q

What are risk factors of Ventricular tachycardia

A
  • Coronary heart disease
  • Structural heart disease
  • Electrolyte deficiencies (K,Ca,Mg)
  • Use of stimulant drugs - Caffeine, cocaine
110
Q

What are the symptoms of Ventricular tachycardia

A
  • Chest pain
  • Dyspnoea
  • Syncope
  • Palpitations
111
Q

What are signs of Ventricular tachycardia

A 
Respiratory distress
Bibasal crackles
Raised JVP
Hypotension
Anxiety 
Agitation
Lethargy
Coma
112
Q

How is Ventricular tachycardia diagnosed

A

ECG - Rate >100, Broad QRS complex, AV dissociation

  • Cardiac enzymes to check for infarction
  • Electrolytes check for derangement
  • Drug levels and toxicology screen
  • TFTs
  • Coronary angio if survived
113
Q

How is Ventricular tachycardia treated

A

ABC approach
Pulseless VT - ALS
Unstable VT - Reduced cardiac output

Pulseless VT and VF require defibrillation, but other VTs can be treated with synchronised cardioversion

Correct electrolytes abnormalities
Amiodarone - Anti-ar

Stable VT - Same as above + DC cardioversion if amiodarone is unsuccessful

ICD - Implanted cardioverter defibrillator - Consider if:

  • Sustained VT causing syncope
  • Sustained VT with LVEF <35%
  • Previous cardiac arrest due to VT/VF
  • MI complicated by non-sustained VT
114
Q

What is Gangrene

A

Tissue necrosis either, wet with superimposed infection, dry or gas gangrene

115
Q

What are causes of Gangrene

A
  • Tissue ischaemia and infarction
  • Physical trauma
  • Thermal injury
  • Gas gangrene is caused by Clostridia perfringens
116
Q

What are risk factors for Gangrene

A 
Diabetes
Peripheral vascular disease
Leg ulcers
Malignancy
Immunosuppression
Steroid use
Puncture/surgical wounds
117
Q

What are the symptoms of Gangrene

A

Painful area = Erythematous region around gangrenous tissue

Gangrenous tissue = Black because of haemoglobin break down products

Wet - Tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes

Gas - Spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus

118
Q

How is Gangrene diagnosed

A

Diagnosis is clinical

May include:
Wounds swab, pus, fluid aspiration - MC&amp;S
X-Ray for Gas gangrene
CRP
Na - Low in 100% patients
119
Q

What are causes of Mitral regurgitation

A

Leading cause is mitral valve prolapse which is when the heartstrings rupture - Due to myxomatous degeneration

Rheumatic heart disease
IE
Connective tissue disease

120
Q

What are signs and symptoms of Mitral regurgitation

A 
Acute MR - LVF
Chronic - Asymptomatic or
- Exertional dyspnoea
- Palpitations if in AF
- Fatigue
  • Pulse - AF
  • Laterally displaced apex beat - LVD
  • Pan/Holosystolic murmur - Loudest at apex beat - radiates to the axilla
  • Soft S1
  • S3 Galloping - Rapid ventricular filling
  • Mitral valve prolapse - Mid-systolic click - Closer to S1 when standing and further when lying down
121
Q

How is Mitral regurgitation diagnosed

A

ECG - Normal - May show AF or P mitrale

CXR

  • Acute = LVF
  • Chronic = Cardiomegaly + LVF

Echo - Performed every 6-12 months in moderate-severe MR
- Diagnostic

122
Q

What are causes of Mitral stenosis

A

Main cause: Rheumatic heart disease (90%)

  • Congenital mitral stenosis
  • SLE
  • Rheumatoid arthritis
  • Endocarditis
  • Atrial myxoma
123
Q

What are signs and symptoms of Mitral stenosis

A

May be asymptomatic

  • Fatigue
  • SOB
  • Orthopnoea
  • Palpitations - AF
  • Peripheral cyanosis
  • Malar flush
  • Pulse - AF
  • Apex beat undisplaced
  • Parasternal heave due to RVH secondary to pulmonary hypertension (cor pulmonale)
  • Loud S1
  • Mid-diastolic murmur
  • Evidence of pulmonary oedema
124
Q

How is Mitral stenosis diagnosed

A

ECG - Normal - May show AF or P mitrale

CXR

  • Cardiac enlargement
  • Pulmonary congestion
  • Mitral valve calcification

Echo - Diagnostic

125
Q

What is Myocarditis

A

Acute inflammation and necrosis of cardiac muscle

126
Q

What are causes of Myocarditis

A

Most common in Europe and USA: Coxsackie B virus

Most common in South America: Chagas disease - Trypanosoma Cruzi

Viruses: EBV, CMV, Adenovirus, Influenza
Bacteria: Post-Strep, TB, Diphtheria
Fungal: Candidiasis
Helminths: Trichinosis
Non-infective: SLE, Sarcoidosis, Polymyositis, Hypersensitivity, sulphonamides
Other: cocaine, heavy metals, radiation
127
Q

What are the signs and symptoms of Myocarditis

A

Fever
Malaise
Fatigue
Lethargy

SOB
Palpitations
Sharp chest pain

Signs of pericarditis
Signs of complications

128
Q

How is Myocarditis diagnosed

A

ECG - Non-specific T wave and ST changes
Pericarditis - widespread saddle shaped ST elevation

CXR - CHF

Cardiac enzymes - CK, CK-MB, Trop - Elevated
BNP - Elevated in CHF

2D Echo - Diagnostic

Gold standard but rarely required - Endomyocardial biopsy

129
Q

What is Pulmonary hypertension

A

This is an increase in mean pulmonary arterial pressure which can be caused by or associated with a wide variety of other conditions

130
Q

What are causes of Pulmonary hypertension

A

Idiopathic - Rare

Problems with smaller branches of the pulmonary arteries
LVF
Lung disease (COPD, Interstitial lung disease)
Thromboses/Emboli in the lungs

131
Q

What are the signs and symptoms of Pulmonary hypertension

A

Progressive SOB
Weakness/tiredness
Exertional dizziness and syncope
Angina and tachycardia

Parasternal heave
Loud pulmonary S2
Murmur - pulmonary regurgitation
Tricuspid regurgitation
Raised JVP
Peripheral oedema
Ascites
132
Q

How is Pulmonary hypertension diagnosed

A 
CXR - Exclude lung disease
ECG - RVH and strain
PFTs - Spiro
LFTs - Liver disease - Portal hypertension
Echo - Asses right ventricular function

Right heart catheterisation - directly measure pulmonary pressure and confirm the diagnosis

133
Q

What are causes of Tricuspid regurgitation

A

Congenital

  • Ebstein’s anomaly
  • Cleft valve in osmium primum

Functional

  • Consequence of right ventricular dilation
  • Valve prolapse

Rheumatic heart disease
IE - Most common
Carcinoid, Trauma, Cirrhosis, Iatrogenic

134
Q

What are the signs and symptoms of Tricuspid regurgitation

A 
Fatigue
SOB
Palpitations
Headaches
Nausea
Anorexia
Epigastric pain made worse by exercise
Jaundice
Peripheral oedema
Pulse - AF
Raised JVP - Giant V waves
Parasternal heave
Pansystolic murmur - Louder on inspiration
Loud P2 component of S2
Pleural effusion
Hepatomegaly
Ascites
Pitting oedema
135
Q

How is Tricuspid regurgitation diagnosed

A

ECG - Normal - May show AF or P pulmonale due to right atrial hypertrophy

CXR
- Cardiac enlargement

Echo - Diagnostic
Valve prolapse and right ventricular dilation

Right heart catheterisation - Rarely necessary but may be useful for assessing pulmonary artery pressure

136
Q

What are causes of Varicose veins

A

1o - Due to genetic developmental weakness in the vein wall results in increased elasticity, dilation and valvular incompetence

2o

  • Venous outflow obstruction - Pregnancy, Pelvic malignancy, Ovarian cysts, Ascites, Lymphadenopathy, Retroperitoneal fibrosis
  • Valve damage (After DVT)
  • High flow (Arteriovenous fistula)

RFs:
Age, Female, FHx, Caucasian, Obesity

137
Q

What are the symptoms of Varicose veins

A

Patient may complain about the cosmetic appearance

  • Aching in the legs
  • Aching is worse towards the end of the day or after standing for long periods of times
  • Swelling
  • Itching
  • Bleeding
  • Ulceration
  • Infection
138
Q

What are the signs of Varicose veins

A

Inspect with patient standing

  • Tap test - Tapping over saphenofemoral junction will lead to an impulse felt distally (Valve incompetence)
  • Palpation of a thrill or auscultation of a bruit would suggest an AV fistula
  • Trendelenburg test - Allows localisation of the sites of valvular incompetence - Hand over saphanofemoral junction - Lift leg, place hand, lower leg, observe filling, remove hand, observe filling
139
Q

What are the signs of venous insufficiency

A 
Varicose eczema
Haemosiderin staining
Atrophie blanche
Lipodermatosclerosis
Oedema
Ulceration
140
Q

How is Varicose veins investigated

A

Duplex US of legs - Allows exclusion of DVT

141
Q

How are Varicose veins treated

A

Conservative:

  • Exercise - Improves skeletal muscle pump
  • Elevation of legs at rest
  • Support stockings

Plus

  • Stab avulsion
  • mechanical avulsion
  • Laser scleropathy
  • Microinjectino scleropathy
142
Q

What are complications of Varicose veins

A 
Venous pigmentation
Eczema
Lipodermatosclerosis
Superficial thrombophlebitis
Venous ulceration

Complications of treatment:
Scleropathy - Skin staining, local scarring
Surgery - Haemorrhage, infection, recurrence, Paraesthesia, Perineal nerve injury

143
Q

What is Peripheral Vascular Disease (PVD)

A

Narrowing of arteries other than those supplying the brain/heart. Most commonly seen in the legs

144
Q

What are the different types of PVD

A
  • Intermittent claudication - Calf pain on exercise
  • Critical limb ischaemia - Pain at rest (Most severe manifestation)
  • Acute limb ischaemia - A sudden decrease in arterial perfusion in a limb due to thrombotic or embolic causes
  • Arterial ulcers
  • Gangrene
145
Q

What are risk factors for PVD

A 
Smoking
Dibetes
HTN
Hyperlipidaemia
Physical inactivity
Obesity

Male
Age

146
Q

What are the signs and symptoms of PVD

A

Intermittent claudication - Cramping pain in calf, thigh or buttock after walking for a given distance (claudication distance) and relieved by rest - Calf claudication indicates femoral disease. Buttock claudication indicates iliac disease

Critical limb ischaemia:

  • Ulcers
  • Gangrene
  • Rest pain
  • Night pain - Relieved by dangling leg over edge of bed

Leriche syndrome (aortoiliac occlusive disease):
Buttock claudication
Impotence
Absent/weak distal pulses

147
Q

What is the Fontaine classification of PVD

A

Asymptomatic
Intermittent claudication
Rest pain
Ulceration/Gangrene

148
Q

What are the signs of acute limb ischaemia

A 
6 Ps
Painful
Pale
Pulseless
Perishingly cold
Paralysis
Paraesthesia

Often hairless, atrophic skin, punched-out ulcers, colour change when raising leg (to Buerger’s angle)

149
Q

How is PVD investigated

A 
ABPI - When BP in ankles is lower than brachial pressure indicates PVD (Vessel calcification - False negatives - DM, dialysis)
>0.90 - Normal
0.5-0.90 - Claudication
0.3-0.5 - Rest pain
<0.3 - Critical ischaemia

TBI - <0.6

Doppler US - Non-invasive and cheap - Poor visualisation below the knee

MR Angio - Gold standard for demonstrating anatomy

150
Q

What are prognostic signs in Acute limb ischaemia

A

Viable – No neurological signs + audible doppler at ankle

Threatened – Sensory loss, tense calf, no audible doppler

Dead – Complete neurological deficit, fixed mottling

Of the 6 Ps - Profound deficits showing Paraesthesia and Paralysis indicate a non-viable limb

All conditions - Year 3 (16 decks)

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