Cardio Flashcards

(238 cards)

1
Q

How to do ECG rate?

A

300/number of squares in R-R interval
OR
Number of QRS X6 (10 sec strip)

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2
Q

Normal ECG axis and how to calculate

A

-30 - +90
Look at leads I and aVF If these are both positive then axis is between -30 and +90

Also Leads I and II leaving returning rule for L and R deviation

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3
Q

What is P-wave & what increases & makes absent

A

This is atrial depolarisation

Inc = Cor pulmonale, PE
Absent = AF
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4
Q

What is PR interval
Prolonged = ?
Shortened = ?

A

Time from atrial to ventricular depolarisation (120-200ms)

Prolonged = AV block, digoxin, hypokalaemia, rheumatic fever, sarcoidosis (RF and Sarc give AV node fibrosis)

Shortened = Accessory pathway e.g. WPW (assoc with Delta wave - upstroke on QRS due to retrograde impulse activity).

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5
Q

QRS breadth

Narrow =
Broad =

A

Normally 80-120ms

Narrow = normal HIS/Purkinje

Broad = ventricular ectopic, accessory pathway (non His-Purkinj)

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6
Q

What is R-wave progression?

A

This is normal phenomenon where QRS become more positive

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7
Q

What can cause tall T-waves

A

Hyperacute STEMI

Hyperkalaemia

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8
Q

What can cause inverted T-waves

A
Ischaemia
Digoxin toxicity
SAH
PE
Brugada syndrome
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9
Q

What can cause prolonged QT (interval over 500ms)?

Why is this important?

A

Citalopram
Antipsychotics
Macrolides (erythromycin)
Genetic

Risk of arrhythmias (longer relative refractory period means ectopics can cause arrhythmias)

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10
Q

First 4 steps in ECG interp

A

Patient name
Rate
Rhythm
Axis

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11
Q

Leads for Circumflex occlusion?

A

Leads I, V5, V6

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12
Q

Leads for Right coronary occlusion?

A

Leads II, III, aVF

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13
Q

Leads for LAD occlusion?

A

V1-V4

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14
Q

What are some causes of an irregular tachycardia

A

VF
Torsades (give Mg Sulphate)
AF+WPW (can be seen in association)

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15
Q

What can cause Left axis deviation

A

LBBB
WPW with right sided accessory pathway
hyperkalaemia
ASD

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16
Q

Causes of right axis deviation

A

RV hypertrophy

lung disease: cor pulmonale, PE

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17
Q

ST elevation causes

What causes prolonged ST elevation

A

MI
Pericarditis
LV aneurysm (cause of persistent STEMI)
Prinzmetals angina

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18
Q

ST depression causes

A

Can be seen secondary to abnormal QRS (LVH, RBBB/LBBB)
Ischaemia (e.g. inferior infarct)
digoxin
hypokalaemia

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19
Q

LBBB (WiLLiaM) causes

A

ALWAYS pathological
Ishcaemia: Ischaemic heart disease, MI (Sgarbossa criteria helps diagnose)
Aortic stenosis
Cardiomyopathy

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20
Q

RBBB (MaRRoW) causes

A

Can be normal variant seen with age

RVH e.g due to corpulmonale/PE

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21
Q

Hypokalaemia ECG

A
U waves
small/absent T-waves
Prolonged PR
Long QT
ST depression
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22
Q

Hyperkalaemia ECG

A

Widened QRS
ST depression
Tall Tented T-waves
p-wave depression

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23
Q

Hypothermia ECG

A

Brady - 1st degree heart block
Long QT
Arrhythmia

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24
Q

Degrees of Heart Block

A

1st - PR over 0.2 (benign)

2nd type 1 Wenkebeck

  • Inc PR until dropped beat
  • AV nodal failure

2nd type 2
- PR constant until dropped beat (bundle branch conduction failure - can progress to complete block)

3rd

  • Complete.
  • P not assoc with QRS
  • Broad complex QRS
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25
Which 2nd degree heart block is higher risk?
Type II - due to bundle branch failure More commonly progress to complete failure Pacing might be required
26
What is Bradycardia? Physiological and pathological causes.
Under 60bpm Phys = young (increased Nodal tone), fit Pathological = acute MI, drugs (BB, digoxin, amiodarone), hypothyroid, hypothermia, inc ICP
27
Bradycardia symptoms & Tx
``` Syncope Fatigue Dizzyness Ischeamic chest pain Palpitations ``` Tx: only if less than 40 bpm - IV atropine: anti-cholinergic. reduces vagal tone - Temp pacing wire
28
Sick sinus pathophys, ECG changes and Tx.
Cause = fibrosis of AV node (idopathic, ischemis, digoxin, toxicity, sarcoid/amyloid) ECG = sinus block/arrest with escape rhythms. Bursts of atrial tacky interspersed with Brady Brady: dual chamber pacing Tachy: Digoxin or Verapamil (CCB)
29
Investigating Bradycardia
ECG, U&E, Glucose, Ca, Mg, TFT, drugs, FBC
30
Tx in Bradycardia
``` Treat any underlying (remove negative chronotrope, tx electrolyte disturbances) IV atropine (if poor response e.g. heart block do transcutaneous pacing ```
31
Tachycardia Presentation
``` Palpitations Fatigue Dizzyness Chest discomfort Syncope ```
32
Tx of tachycardia (Acute pres) Tx if unstable (high HR, low BO) Tx if irregular tachy Tx if regular tachy
``` O2 and IV access If HR over 200, BP under 90, MI or HF then GA + IV amiodorone (class III - K+ channel block) ``` If irregular tachycardia (usually AF) control with IV BB or Diltiazem. If onset less than 48 hours amiodarone cardioversion If regular IV adenosine
33
Tachy Precipitating factors
MI/Ischamia Thyrotoxicosis Electrolyte disturbances Drug/Caffeine/Alcohol
34
SVT - What is it, possible site or origin and what is the main concern
HR over 100bpm Narrow complexes Can be from Atria (AF and flutter) Can be from AV node (nodal re-entry tachycardia) Increased HR means decreased coronary filling time (angina type symptoms, chest pain, faintness, SOB)
35
Causes and Tx of sinus tachycardia (100-200bpm, regular with P-waves)
Physiological - pain, anxiety, exertion Pathological - fever, anaemia, hypovolaemia, thyrotoxicosis, phaeo Pharmacological - sympathomimetics, adrenaline, alcohol, caffeine, salbutamol Tx: treat underlying (e.g. hypovolaemia), vagal manoeuvres (carotid massage, valsalva). If ongoing sinus SVT give BB or non-dihydropyridine CCB (diltiazem, verapamil-
36
AV node re-entry pathophysiology.
- Two pathways in AV node one fast with slow refractory and one slow with fast refractory - usually slow pathway is blocked as common pathway is in refractory when impulse arrives - if an impulse goes down the slow pathway when not in refractory then impulse can travel up fast pathway giving a re-entry circuit
37
AV node re-entry ECG
Narrow QRS Rate 130-250 retrograde conduction = inverted P=waves in II, III and aVF
38
AV node re-entry Tx
Vagal manoeuvres 1st line Adenosine 2nd line (transient AV block fees like death) Long term: Beta block or digoxin, diltiazem, verapamil, flecanide (class 1c Na channel blocker – increases QRS time) Cure: Radiofrequency ablation
39
AVRT ?
WPW
40
WPW pathophys
Bundle of Kent usually light sided. formed due to developmental failure. Accessory pathway allows re-entry circuit formation (critical timing needed when pathways not in refractory) Broad complex (anterograde) Narrow (Orthodromic 90% - retrograde up accessory path used to get impulse back to atria)
41
WPW Tx - Acute - Prophylaxis - Cure
Vagal manoeuvres ± adenosine Prophylaxis Flecainide (1c- inc refractory period) or sotalol (3) Cure: RFA
42
What is AF
Chaotic firing of ectopics in atria. | Leads to irregularly irregular ventricular rhythm on ECG
43
AF complications
Stagnation of blood in atria can cause thrombus and inc risk stroke. Reduced cardiac output may lead to HF
44
Types of AF
Paroxysmal: spontaneous termination in less than 7 days (usually 48hr) Recurrent: 2+ episodes Persistent: lasts over 7 days (may become permanent) Permanent: long-standing (over 1 year) not terminated by cardioversion
45
AF Symptoms & Signs ECG Other Presentations
Symptoms: Palpitations, Dyspnoea, Chest pain Signs: Irregularly irregular heart beat ECG: No P-waves, Oscillating baseline Other: Syncope, TIA, stroke
46
AF Investigations
24 hour ECG TFT, FBC (anaemia can cause), U&E (Potassium), LFT/Coag Imaging - trans thoracic echo
47
AF management: Three areas to address
Rate Rhythm Anticoagulation
48
Rate control in AF
Beta blocker or CCB (Diltiazem) 1st line Combination therapy 2nd line (NOT Verapamil - risk heart block) adding the above two OR adding in Digoxin
49
Rhythm control in AF - What should be considered - Who should get this - What is used
- Thromboembolism - Only those with short term symptoms (less than 48 hours) or anticoagulant for over 3W - DC cardioversion or Amiodarone
50
Risk Control score in AF
``` Chronic heart failure (1) HTN over 140/90 (1) Age of 75 (2) DM (1) Prior Stroke/TIA (2) Vasc disease (PVD, MI)(1) Age over 65 (1) Sex: Female (1) ```
51
When to offer anticoagulant in AF
CHA2DS2VASc Consider Warfarin or NOAC in males with 1 and anyone over 2 points INR 2-3 (n.b prostetic heart valves/post MI = 2.5-3.5) If poor warfarin control switch to NOAC
52
Bleeding Risk score
``` Hypertension Abnormal Liver/Renal Stroke Bleeding Labile INRs Elderly (over 65 years) Drugs or alcohol (1 point each) ``` in those with score one 3 use Warfarin with care
53
What is atrial flutter, causes and ECG
This is due to re-entry circuits in the atria Causes: HTN, CAD, hyperthyroid, Obesity, alcohol ECG: sawtooth appearance Tx: anticoagulation then DC cardioversion / Amiodarone / sotalol / flecainide Recurrent = RFA
54
What causes broad complex tachycardia?
Ventricular origin. Either ventricular conduction (BBB) problem OR not using AV node. Note any SVT with poor conduction can present as broad complex too
55
Causes of: Regular VT Irregular VT
Reg - monomorphic VT (all QRS look the same) most commonly due to MI Irregular - Torsades de Points (Plyomorphic VT), VF
56
Pathophysiology of Monomorphic VT
Re-entry circuits in zones of fibrosis/ischaemia e.g. iscahmia/damaged myocardium post MI
57
Pathophysiology of Torsades
Commonly due to electrolyte disturbance. Treated by giving Magnesium sulphate
58
ECG in VT - P waves and capture beats
Broad complex (ventricular) - VT: regular - VF: irregular P wave dissociation: AV node continues independently of ventricle Capture beats are when some P-waves translate into normal QRS complexes intermittently
59
Broad complex Tachy symptoms
Dizziness, palpitations, syncope, chest pain, HF
60
Broad complex Tachy Tx
ABC, O2 and venous access in unstable DC cardioversion (3 shocks) may be needed Amiodarona IV In Plyomorphic VT give magnesium 2g for non-Torsades, IV Mg sulphate for TdP VT is usually due to damage so BB/CCB and consider Implantable cardioversion defibrillator
61
Torsades de Points Causes Morphology Tx
Hypokalaemia, hypomagnesia, Class III antiarrhythmics (amiodarone/sotalol) Antibacterials (erythromycin, trimethoprim) Varied axis and amplitude of QRS Tx: Magnesium sulphate IV
62
VF - Causes - Morphology - Acute/Long term Tx
Cause of cardiac arrest and sudden death. Random contracting of ventricular fibres giving failed ventricular function. - Antiarrhythmic drugs, AF, hypoxia, ischaemia, heart disease - Chaotic (varying amplitudes, no identifiable P, QRS, T -Acute: Defibrillation Long term: BB, implantable cardioverter defibrillates
63
What are shockable rhythms?
VF and Pulseless VT
64
Non-shockable rhythms?
Asystole and PEA (Pulseless electrical activity)
65
Brugada What is? ECG? Tx?
- Geneticalli inherited condition affecting sodium channels. Family history of sudden death less than 45 yrs - Risk of sudden death - Coved ST segment elevation followed by negative T - ICD (implantable defibrillator)
66
PE ECG
S1Q3T3 Deep S in I, Deep Q in III Deep T in III
67
Class 1 Class 2 Class 3 Class 4
``` 1 = Na channel blocker 2 = CCB 3 = Potassium channel blocker 4 = Beta blocker ```
68
Amiodarone - Use - Mech - Adverse
For irregular tachycardia (AF, SVT) Block/Na/K/Ca, antagonist alpha and beta adrenergic Reduces automaticity/conduction in atria Hypotension, Pneumonitis (upper lobe fibrosis), AV block, grey skin, hypothyroidism
69
Adenosine - Use - Mech - Adverse
- Used in certain SVT that don't respond to Vagal maneouvers - Causes trainsient block in the AV node by causing hyperpolarization through inc potassium flux - Short term: Feeling of impending doom - Long term: Chest pain, Bronchospasm (caution in asthmatics), can cause increased conduction down accessory pathways - caution here
70
Digoxin (cardiac glycoside) - Use - Mech - SE
Reduces ventricular rate after CCB and BB 3rd line in HF Negative chronotropic(reduced AV node conduction), positive inotropic (Ca accumulation intracellular) Toxicity - arrhythmias, low therapeutic index - GI upset - nausea - Hypokalaemia (competes with K+ and Na/K pump - visual disturbance (yellow)
71
Types of CCB
Dihydropyridine (More smooth muscle relax) - Amlodipine Non-dihydropyridine (more cardiac depression - SA and AV node block) - Verapamil, Diltizem
72
Mechanism of CCB
Decrease Calcium entry to vascular and cardiac cells - induce relaxation and vasodilation in arterial smooth muscle - suppress cardiac conduction esp at the AV node
73
CCB effect in HF/IHD
Reduced rate and after load, decreases oxygen demand preventing angina
74
Amlodipine SE
ankle swelling, flushing
75
Verapamil facts
ONLY CCB which can be given IV in SVT DONT give with BB (both negatively chronotropic and inotropic so = Heart block
76
Beta blockers use
IHD - reduces angina Congestive HF - improves prognosis AF - reduces rate and maintain rhythm SVT - restore sinus rhythm
77
Receptors and action of BB
B1 (heart) - reduces force and rate of conduction in heart (prolonged AV refractory period). = reduced cardiac work and oxygen demand. increased myocardial perfusion B2 (vasc smooth muscle) - lower peripheral vasc resistance and also lowers BP through reducing renin secretion.
78
SE of BB
Fatigue, cold extremities, headache, impotence Asthma - causes bronchospasm so contraindicated (choose B1 specific e.g. atenolol not non-specific e.g. Bisoprolol)
79
Where to listen for mitral area?
Mid clavicular | 5th intercostal space
80
Where to listen for Tricuspid?
inferior right sternal | 4th intercostal space
81
Where to listen for Pulmonary valve?
Left 2nd intercostal | Next to sternum
82
Where to listen for Aortic valve?
Right 2nd intercostal next to sternum
83
S1 and S2?
S1 = closure of mitral and tricuspid S2 = closure of aortic and pulmonary there may be delayed P2 (pulm part of S2) in inspiration. Third heart sound in diastole (aka after s2 is pathological)
84
Mitral regurgitation
Pansystolic blowing murmur at apex radiating to axilla
85
Mitral stenosis
Loud opening snap in S1 and mid-diastolic murmur
86
Aortic stenosis
Radiates to carotids Soft S2 crescendo decrescendo murmur between S1 and S2
87
Aortic Regurg
Diastolic murmur Collapsing pulse not well transmitted to carotids
88
PDA murmur
Late systolic best heard across back Continusous machinery murmur
89
VSD murmur
Harsh systolic murmur best a left sternal edge
90
Starlings Law
Preload or degree fo stretch is critical factor for stroke volume. Thus increased end-diastolic volume increases stretch and also contractility giving a lower end systolic volume (after load)
91
Aortic stenosis - Triad - other features - Cause - Investigations
- Chest pain, HF (LV hypertrophy due to obstruction), syncope (insufficient blood) - slow rising pulse, narrow pulse pressure (higher pressure needed to eject), transmitted to carotids - calcification of aortic ring - ECG (LV strain), Transthoracic echo, CXR (Calcifications)
92
Aortic valve anatomy
Tricuspid valve | Coronary sinus sits behind
93
Aortic stenosis Tx and complications of Tx
1st line is valve replacement 2nd line saloon valvuloplasty SE of infection (need Abx prophylaxis) and risk emboli (esp metal valves) needing anticoagulant aiming for 2.5-3.5 INR
94
Aortic regurgitation - Causes - Associated diseases - Presentation
- Bicuspid aorta, thematic fever (autoimmune), infective endocarditis, collagen disease, age (degenerative) - SLE, Marfans, Ehlers-Danlos, Turner's, Ank spond - Shortness of breath, orthostatic/nocturnal dyspnoea - Wide pulse pressure and collapsing water hammer pulse
95
Aortic regurgitation - Investigations - Tx - screening
- ECG (may have LVH), CXR (HF due to fluid overload), Transthoracic echo - acute surgery (valve replace) is symptomatic, give ace inhibitor if chronic screen those with assoc diseases e.g. marfans
96
Mitral stenosis | - complications
- Inc LA and pulmonary artery pressure. - May progress to cause RV failure and subsequent raised JVP, liver congestion, ascites and peripheral oedema - Thromboembolic risk due to blood stasis in atria
97
Mitral stenosis - Causes - Pres - Signs
- congenital, rheumatic fever, degenerative calcification in elderly - progressive breathlessness, palpitations due to AF, systemic emboli effects, hoarseness (LA hypertrophy) - Malar flush (CO2 retention), raised JVP, Laterally displaced apex, RV heave, signs of RHF (hepatomegaly, ascites etc)
98
Mitral Stenosis - Investigation - Tx - Prevention
- ECG (P- mitrale = bifid), CXR - LA enlargement & interstitial oedema (Kerly B lines) & prominent pulmonary vessels - diuretics and nitrates fo SOB, BB or CCB for exercise tolerance, valve balloon if symptomatic - Prophylaxis for rheumatic fever and infective endocarditis is penicillin
99
Mitral regurgitation - Causes - Presentation - Complications - Investigations - Tx
- advancing age, rheumatic fever (less commonly), MI, IHD, post surgical, ehlers-Danlos, SLE - Acute forms lead to rapid pulmonary oedema (e.g. papillary muscle rupture). - Chronic forms give HF, Breathlessness, can cause pulmonary HTN - ECG P-mitrale, CXR left heart hypertrophy, Echo - Surgery (valve repair), ACEi, nitrates, diuretics
100
Rheumatic fever
- Antigen mimicry to strep pyoges (Group A beta haemolytic) - affects joint skin heart and nervous system 2-4 weeks post infection (sore throat) - IV Benzylpenicillin for strep, NSAIDs suppress inflammation - long term MR due to papillary muscle fibrosis and shortening
101
Why is Rhematic fever less common
Group A - Strep Pyogenes infection is less common
102
infective endocarditis - Pathogenesis - presentation - complications - RF
- strep viridian's (dental procedures), Staph aureus (invasive procedures IVDUs). Poor blood supply to valves (hard for WBC and drugs to reach), fibrin-platelet/organisms vegetation formed --> destroys valve leaflets - Fever + New Murmur = endocarditis until proven otherwise - valvular insufficiency, systemic emboli (can have embolic or infective effect (block or make abscess), immune complexes (cutaneous, kidney, arthritis) - structural heart defect, IVDU, previous IE
103
Infective endocarditis features
Fever + new murmur (usually MR, tricusp with Staph aureus) Roth’s spots - eyes, retinal haemorrhage with pale centre Osler’s nodes - painful red blisters @ terminal phalanges and toes Janeway lesions - painless red maculae on thenar eminence Nail haemorrhage - splinter - red and linear Embolic phenomena e.g. stroke Subacute: clubbing
104
Infective endocarditis Tx
Amoxicillin + Gentomycin IV Surgery may be needed if damaged heart valves
105
What is cardiomyopathy
Functional/Structural abnormality of heart muscle WITHOUT Coronary/valvular/congenital disease HTN
106
Classification of cardiomyopathy
Dilated - most common. imparted contraction, most common need for transplant Hypertrophic - (HOCM) L/R ventricular hypertrophy. usually familial due to data-myosin dysfunction Restrictive - rare. reduced diastolic filling
107
Causes of cardiomyopathy
Dilated - Ischaemic, Alcohol, Thiamine deficiency (Beri Beri), SLE Hypertrophic = familial Restrictive - amyloidosis, sarcoidosis, radiation, haemochromatosis
108
Presentation, Investigation and Tx of dilated cardiomyopathy
- congestive HF, Right sided HF, cardiomegaly, AF or VT, thromboembolism by stasis - CXR ABCDE (Alveolar oedema, Batwing, kersey B, interstitial Cardiomegaly, Dilated upper lobe vessels, pleural Effusion Bloods - BNP (b-type natriuretic peptide) - Loop diuretics / thiazide, ACEi (Digoxin if doesn't respond) Nitrates, Warfarin, pacing Most common cause for heart transplant
109
Most common cause of sudden cardiac death in young people
Hypertrophic cardiomyopathy. Genetic inheritance gene coding for Beta myosin Mitral regurgitation may be present giving atrial enlargement
110
Management of Restrictive cardiomyopathy
Amiodarone if ventricular arrhythmia, anticoagulant, BB and CCB if AF Transplant sometimes indicated
111
What is Myocarditis and how does it occur?
acute/chronic inflammation of myocardium (fatigue, chest pain, fever) might be due to viral (Coxsakie), immune mediated (SLE, Sarcoid, scleroderma), Alcohol, Heavy metals, Electric shock
112
Heart failure features
``` Dyspnoea Cough - worse at night (pink frothy sputum) Orthopnoea/nocturnal dyspnoea Wheeze Weight loss Bibasal crackles Peripheral oedema/ascites ```
113
HF acute management
``` O2 diuretics (furosemide) Opiates (for SOB) Vasodilators Inotropes CPAP ```
114
HF - Drug management
1st - ACei and BB 2nd - Aldosterone agonist or hydralazine in combo with nitrates Diuretics for fluid overload Annual influenza vaccine and pneumococcal vaccine 3rd line is digoxin
115
HF classification
NYHA I = no sympt II = mild symptoms, slight limitation III = moderate symptoms, unable to carry our physical activity without discomfort IV = severe, symptoms of HF at rest
116
HF investigations
BNP (released my myocardium stretched) ECG for aetiology at Tx Gallop murmur due to S3
117
Causes of HF
Mostly IHD and HTN, 10% valvular (AS causing LVH) Myocardial disease - ischaemia, cardiomyopathy, HTN, drugs (bb, cbb, doxorubicin), alcohol and cocaine, infiltrative (haemochromatosis, sarcoidosis) high output: anaemia, pregame's, hyperthyroidism, pagers disease of bone
118
Atherosclerosis | 4 stages
1) Fatty streak formation - this is due to endothelial dysfunction causing lipid and monocyte infiltration.monocytes engulf fat to become foam cells = fatty streak 2) Intimal hyperplasia - platelet derived growth factor, TGF-B from macrophages and SMC causes hyperplasia 3) Fibrous cap formation - SMC produce collagen 4) Plaque formation or Rupture - may have a fatty necrotic core. Plaque might continue growing to narrow lumen or become unstable and rupture
119
What can be found within intimal plaques in Atherosclerosis?
Lipid Macrophages Smooth Muscle cells
120
Two type of Cholesterol
HLD - Carries fat away from arteries to Liver for synthesis of bile salts and steroids LDL - Carry fat towards arteries causing plaque formation
121
What carries fat from intestine to muscle
Chylomicrons
122
Statins: - Mechanism - When NICE recommend - SE - Which statin - Monitoring
- HMG-CoA reductase inhibitor - QRISK2 over 10%, Hx of CVD, familial hypercholesterolaemia, over 65 - Myalgia, stiffness, weakness, cramping - Atorvastatin 20mg (primary prev), 80mg for secondary prev - LFTs
123
HTN complications
Stroke, IHD, MI, CKD
124
HTN modifiable RF
Smoking, weight, alcohol, stress, exercise, salt
125
HTN non-modifiable RF
AGe, Fam Hx, Ethnicity, Gender
126
HTN stages and when to Tx
Stage 1: over 140/90 (135/85 ABPM/HBPM) Stage 2: over 160/100 (150/95ABPM/HBPM) Stage 3: over 180/110 Intervene at stage 2
127
Symptoms of HTN and screening
Often no symptoms (unless 200 systolic then headaches etc) Screen adults every 5 years up to 80
128
Causes
Primary - Essential HTN (95%) env, gene etc Secondary - Renal disease (inc renin due to dec perfusion), Endocrine (Cushing, Conns, Thyroid, Phaeo), Pre-eclampsia and preg, Drugs (steroids, COCP, decongestant)
129
What is malignant HTN
High BP or fast inc in BP Causes end-organ damage
130
End organ damage in HTN
``` Brain - Seizure, Vomit, Stroke Dissection Pulmonary oedema (HF) Nephropathy Retinopathy (grade 1 = tortuous retinal arteries, grade 4 = papilloedema) ```
131
Investigations for secondary HTN
Lipids and FBC VMA - breakdown prod of adrenaline Urinary free cortisol Renin/aldosterone levels Plasma Ca MRI renal arteries
132
Treatment of HTN
LIFESTYLE! diet, weight, salt, all, exercise, smoking Target of under 140/90 A or C (amlodipine - ankle swelling) - A for under 55 - C for afrocarib or over 55 A + C A + C + D (indapamide ) if still then if K+ low add Spironolactone if high then inc 'D'
133
IHD Causes
Mechanical obstruction of CA (atherosclerosis, thrombosis, spasm-prinzmetals, arteritis) Decrease blood O2 (anaemia, decreased CO - HF, poor oxygenation in lung) inc heart demand = more O2 and reduced coronary filling time (HTN, valvular disease, hyperthyroid, fever, exercise)
134
IHD symptom
Angina (stable is when exercise induced, unstable is at rest)
135
IHD RF
modifiable: - smoking, poor diet, weight, low exercise, alcohol, stress, HTN, depression, diabetes, hyperlipidaemia non-modifiable: - age, male, genetics, FH
136
What is stable angina?
Narrow lumen from atherosclerosis decrease blood flow = chest pain on exertion constricting discomfort front of neck/shoulder/jaw/arms Brought on by exercise, received by rest/GTN
137
What is Prinzmetals angina?
Angina due to coronary spasm
138
Referral of new angina
All cases to acute chest pain clinic for confirmation of Dx and severity assess within 2 week
139
How does unstable angina occur
Either progressive luminal narrowing or Plaque rupture.
140
Angina Dx
``` MI - if pain over 5 mins Pericarditis - worse on inspiration or lying flat MSK - worse on moving PE - pleuritic GORD ```
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Investigation of angina
``` ECG - S/T or T flattening or inversion FBC (anaemia), Blood glucose diabetes) LFT (baseline befor statin) U&E (renal function) TFT ``` Coronary angiography will confirm (this is invasive)
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Stable angina management:
Modify CV RF + educate patient GTN (if doesn't relieve then 2nd dose after 5 min and third dose after 5 min then wait 5 min then call 999) 1s line: BB (atenolol - dec HR and BP, brady, cold hands, fatigue) or CCB (diltiazem (ankle swelling flushing) 2nd line dihydroperidine CCB + BB To reduce RF: Aspirin or Clopidogrel, Statin if indicated
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Angina not controlled by medications
PCI CABG
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ACS ECG ST elevation = No ST elevation =
STEMI NSTEMI (if cardiac markers raised) Unstable angina if they are not raised
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ACS investigation
ECG - ST elevation (acute infarct) ST depression/T-inverstion (unstable angina or NSTEMI) Cardiac enzymes: (best 3-6 hours post infarct, max at 12-24hours troponin T, troponin I, Creatine kinase --> minimal inc may suggest future risk Bloods (FBC - anaemia, glucose - if high poor prognosis, renal/tyroid function) Imaging: CXR - complications like pulmonary oedema, PE, pneumothorax, TAA
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ACS presentation
New onset angina, prolonged anginas pain at rest (over 20 min) Other: sweating, vomit, fatigue, SOB, palpitations
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Initial management of ACS
MONA morphine, O2, Nitrates, Aspirin Monitor with ECG
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Risk assessments in ACS
TIMI - bleeding risk in MI thrombolysis GRACE - assess Tx of NSTEMI
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GRACE
used in ACS to predict 6 month mortality Low risk = Clopidogrel 12 months Medium risk = angiography within 4 days High risk = PCI or CABG for revascularisation
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Dressler's syndrome
late pericarditis. Inflammatory reaction to necrotic tissue occurring 2-8 weeks after ACS
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Discharge management for ACS
Cant drive for 4 weeks (1 week if angioplasty) ACEi, dual platelet (aspirin+clopidogrel), BB, Statin, monitor BP and renal function regularly. IF HF offer Spironolactone LIFESTYLE - smoking, weight
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ACS complications
Acute MI Pericarditis Dresslers syndrome
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MI complications
``` Death Dresslers PEricarditis Rupture of free wall Aneurysm (persistent ST elevation) Tamponade (Becks) HF Shock (cariogenic) VT ```
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Cardiac arrest management
call 999 A+B C once airway secured (30:2 uninterrupted) D - automatic defibrillates 2 mins CPR between defibrillates attempts after 3rd shock adrenaline + Amiodarone 2min CPR.. Adrenaline etcetcetc
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Pericarditis - Anatomy - Pathogen - Causes
Pericardium is outer fibrous layer and inner serous membrane with 5ml fluid. Fixes heart to pericardium and prevent dilation. inflammation results in exudate/adhesions/effusions (haemorrhage or serous) viral (Coxsackie, EBV, staph) Rheum (RA, SLE, Sarcoid) MI (dresslers) Other (drugs e.g. hydralazine, fungal)
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Acute pericarditis | - Presentation, Signs/sympt
Chest pain (dull, sharp, burning), Substernal/precordial radiates to neck or leg trapezius Aggravated - Cough, lying flat Relieved - siting up tachypnoea, tachycardia, fever If tamponade may have becks 60-85% have pericardial friction rub
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Acute Pericarditis Investigations
ECG - Concave ST elevation (saddle shape) Bloods - FBC (WCC), ESR/CRP (raised), U+E (uraemia can cause), Cardiac enzymes (point to MI as cause of pericarditis) Echo - if suspecting fluid or tamponade (over 20mm free fluid)
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Pericarditis Tx
If RA or Ventricular collapse on echo - Pericardiocentesis Stable Patients: - Rest, Treat cause, NSAIDs (naproxen) - If uraemia consider dialysis
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When to admit for Pericarditis
``` Fever evidence of tamponade Large effusion (echo free space over 20mm) On Warfarin Trauma Fail to respond to NSAIDs ```
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Complications of Pericarditis
Falling BP and shock - suspect tamponade
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What is Cardiac Tamponade. | Why Important?
Blood/Fluid/Pus/Gas in pericardial space. | Large volume = reduced ventricular filling leading to haemodynamic compromise medical emergency
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Causes of Tamponade
Pericarditis, malignancy, Dressler's (post MI), infective (HIV, TB), connective tissue disease (SLE, RA, dermatomyositis, systemic sclerosis), Trauma.
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Presentation of Tamponade
Anxiety, Fatigue, Oedema (peripheral, pulmonary), SOB, tachycardia, tachypnoea
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Becks Triad: when and what
Seen in ACUTE Tamponade 1) Muffled Heart sounds 2) Raised JVP 3) Hypotension
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Tamponade ECG
Low voltage QRS
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Tamponade CXR
Water bottle shaped heart
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Gold standard Investigation in Tamponade
Transthoracic Echo
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Tamponade Tx
``` O2 Volume Expansion Increase venous return (legs up) Inotrope (dobutamine) Pericardiocentesis ```
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What is peripheral artery disease?
Narrowing of peripheral vasculature Most often due to atherosclerosis
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Peripheral artery disease classification
1) Asymptomatic 2) Intermittent Claudication 3) Ischaemic rest pain 4) Critical limb ischaemia (P's - Pulseless, perishing cold, Painful, Pale, Parasthesia, Paralysed)
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Intermittent Claudication:
Cramping pain in calf/thigh/buttock on walking. symptoms worse uphill/stairs relieved by rest
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Intermittent Claudication - determinants of severity
Claudication distance Rest time
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Ischaemic rest pain
Unremitting pain in limb. Wakes from sleep, relieved on dangling foot/cold floor
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Peripheral artery disease other signs
Skin changes (atrophic) Hairless
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Peripheral artery disease DDx
Sciatica Spinal stenosis DVT Nerve entrapment
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Peripheral artery disease investigations
``` FBC (anaemia aggravates) ESR (giant cell arteritis) Thrombophilia screen (DVT) ECG (look for coronary disease) Doppler US to calc ABPI - Normal = 1 - 0.9 mild, 0.8 mod, below 0.5 ischaemic rest pain. ```
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Acute limb ischaemia - 6 P's - Cause - Investigation - Tx - Complications
- Pulseless, Paralysed, Parasthesia, Pale, Perishing cold, Pain - Thrombus or Embolism giving sudden occlusion - Urgent doppler and urgent angiography - Revascularisation in 4-6 hours with immediate heparinisation (embolectomy for embolus, thrombolysis/angioplasty/bypass if thrombotic - Infection, poor healing, gangrene
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General management of Peripheral Limb Ischaemia.
RF: smoking, weight, statins, ACEi (beware renal artery stenosis), Manage DM/HTN Antiplatelet - Clopidogrel
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Management of intermittent claudication
Vasodilator therapy - Naftidrofuryl oxalate Supervised exercise ABPI (doppler USS) ± CT angio Revascularisation if tried lifestyle improve (angioplasty + stenting
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Management of Critical ischaemia
Pain: para+opioid doppler USS ± contrast angio Revascularisation with angioplasty and stenting Some cases may need amputation
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Aortic Dissection what is it?
Intimal tearing gives disruption of media Intramural bleeding separates layers leading to a false lumen creation
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Aortic Dissection Types
``` Type A (70%) aortic arch + ascending aorta Type B (30%) descending aorta ```
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Aortic Dissection RF
Cardiovascular disease Aortic disease Cocaine/amphetamines Bicuspid aortic valve
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Aortic Dissection Presentation - Acute - possible systemic effect
- Sudden tearing/sharp pain. Radiates to back, Pulse loss | - Spinal arteries (paraplegia), Distal aorta (limb ischaemia), Carotids (Neurological deficit), Coronary (angina)
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Aortic Dissection expansion phase
- Cardiac tamponade | - Pleural Haemothorax
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Important Dx in Aortic Dissection
Differentiate from MI as thrombolysis will be fatal in Aortic Dissection
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Aortic Dissection investigations
CXR - widened mediastinum (if -ve can't exclude dissection) TTUS - site and extent of dissection MRI - good for diagnosis and looking for other vessel involvement ECG - needed to differentiate if MI suspected
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Aortic Dissection Tx
IV access, analgesia (morphine) and O2 initially ICU Aggressive HTN management aim for BP 100-120 systolic - IV BB (labetalol) to reduce contraction - IV nitropruside (emergency Vasodilation) Surgical repair - Type A gets graft - Type B TEVAR
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TAA - True aneurysm - Location - Pathogenesis - RF
- Involves all three layers - Ascending aorta (51%), arch, descending - Inflammation, proteolysis and reduced SMC survival - CTD (marfans etc), genetic, Infective (HIV, syphilis), Aortitis (GCA, RA, Takyasu's arteritis, Trauma (weight lifting), Cocaine/amphetamines, bicuspid aortic valve, HTN, smoking, age
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What level is Aortic Hiatus in diaphragm?
T12
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TAA presentation
Pain - chest, neck, upper back, epigastrium. dissection sudden tearing Compression symptoms - hoarseness, SVC obstruction, stridor if rupture: acute pain, collapse/shock, haematemesis/haemoptysis, haemothorax/tamponade
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TAA investigations
Acute: FBC, clotting, U&E, LFT, CT contrast, ECG, MR angio Non-acute: above plus USS, TTE
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TAA Tx
Surgery: TEVAR smoking cessation, Tx CV RF 6 monthly MRI/CT Inform DVLA if above certain size
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TAA surgery complications
paraplegia (spinal ischaemia) Stroke AKI
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AAA - Location - Causes
- Mainly below level of renal arteries - Atherosclerotic disease, FH, smoking, male, inc age, cardiovasc disease/RF, Arteritis (Takyasu, Behcets), CTD ( marinas etc), infective (TB, HIV)
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AAA - Presentation - Examination findings
- Often incident finding, pain in back/loin (DDX for loin to groin), pulsatile abode swelling, rupture = shock - Bimanual palpation, Abdominal bruit, retroperitoneal haemorrhage - Grey Turner sign (flank bruising)
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AAA investigations
``` FBC, clotting, U&E (renal), LFTs, Crossmatch, USS --> initial assess ECG CXR CT --> more anatomical detail ``` MRI angio
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AAA Management
USS monitoring - 3-4.5cm = yearly - 4.5-5.5cm = 3mnthly Over 5.5 consider surgery Inform DVLA over 6cm surgery - over 5.5cm or rapid expansion over 1cm/year or if symptomatic - Open repair - EVAR
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AAA rupture - Pres - Investigation - Management - Prognosis
- Thoracic chest pain, Haemoptysis ± tamponade, pale, sweaty, weak pulse, hypotension. Triad 1) flank/back pain 2) hypotension 3) pulsatile abdo mass - FBC, crosshatch, baseline U&E, CXR, ECG - Large bore IV access, Immediate theatre - Prosthetic graft repair and stem bleeding - 1 in 3 reach hospital alive
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Types of shock
Cardiogenic - heart can't supply enough blood (dec CO) Septic - dec systemic vasc resistance Anaphylactic - Type I hypersensitivity, mast cell histamine and vasoactive mediators dec systemic vasc resistance Neurogenic - spinal cord injury, epidural/spinal anaesthesia causes dec vasc resist
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Triad seen in shock?
Triad 1) Coagulopathy 2) hypothermia 3) Metabolic acidosis
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Shock and Organ systems
Kidney - acute tubular necrosis Lung - ARDS Heart - MI Brain - Confusion, Coma
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Sepsis def | Septic shock def
- Life threatening organ dysfunction from dysreg response to host infection (dec SOFA 2 points or more) - Circulatory and metabolic dysfunction as a result of sepsis
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Hypovolaemic shock - Aim of resus - Presentation - Investigations
- correct hypo perfusion of vital organs e.g. kidneys - Pale, sweaty, tachycardia/pnoea, cold periphery, inc cap refill time, hypotension - FBC (Hb), U&E (kidney), Group and Crossmatch, ABG+Lactate, urine output
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Hypovolaemic shock | staging
``` Like Tennis: Class I 15% loss Class II 30% Class III 40% Class IV over 40% ```
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Compensation mechanisms to hypovolaemia
Baroreceptor feedback (via CN IX sensation) causes vagal inc in contractility, tachycardia, vasoconstriction Release of Vasopressin, Aldosterone, Renin (Kidney compensation)
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what is occurring in hypovolaemia which is: - Uncompensated - Irreversible
- Myocardial depression and failure of vasomotor reflex, inc capillary permeability, lactic acidosis - End organ failure
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``` Features of: Class I Class II Class III Class IV ``` When to transfuse
Class I: Physiological compensation Class II: postural hypotension, dec urine Class III: Tachycardia over 120 bpm, urine under 20ml/hr, confused Class IV: marked hypotension, tachycardia
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Tx Hypovolaemic shock
- Raise legs (venous return) - ABCDE - Fluid resus: Saline or - Hartmann's 500ml over 15 min - If haemorhhagic give O -ve blood - Pain relief (pain inc metabolic rate and inc ischaemia) IV opiates - Surgery may need fro stem blood loss
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Cariogenic shock - Cause - Presentation - Management
- MI mostly, can also be Tamponade/constrictive pericarditis/PE/tension pneumothorax - Dyspnoea, sweat, confusion, palpitations, pale, mottled, slow cap refill, hypotension - A+B = intubation and ventilation, C = venous access (may need central due to peripheral shut down, IV morphine, cardiac inotropes
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Anaphylactic shock - Definition - Presentation
- Type 1 hypersensitivity due to mast cell histamine/other vasomediator release. sudden onset, life threatening airway + circulatory problems - breathless/wheeze, profound vasodilation (warm periphery, low BP, tachycardia), angio-oedema/hives, oedema of face/pharynx/larynx
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Anaphylactic shock Tx
A (call help if signs of obstruction), B (treat rest distress - O2), C (assess with colour, pulse, BP), D (responsive?) Give: - high flow O2 - raise legs (venous return) - IM adrenaline (most important) 0.5mg adult - Expert intubation - IV fluid challenge: 500ml CRYSTALLOID in 5-10 min - IV chlorphenamine + hydrocortisone - Bronchodilators: IV salbutamol (or nets), ipratropium inhaled, Aminophylline (IV)
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Sepsis Presentation
``` Bounding pulse temperature Rigors Rapid cap refill Vasodilation warm peripheries ```
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Sepsis BUFALO
- Blood cultures - Urine output - monitor hourly - Fluid resus - Abx - Tazocin, Gent (according to local guidelines) - Lactate (ABG/VBG) - Oxygen to correct hypoxia
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Sepsis complications
DIC Renal failure Cardiorespiratory failure
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ECG Hyperkalaemia
Peaking of T waves (occurs first) Loss of P waves Broad QRS complexes Ventricullar fibrillation
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Hypercalcaemia features
Bones, Stones, Groans and Psychic moans. ShortenedQT interval on ECG
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DVLA and driving with cardio disease
``` Angioplasty - 1 week CABG - 4 week ACS - 4 week Pacemaker - 1 week AA over 6cm - tell DVLA ```
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When is BNP released? Effects on BNP What can cause a rise in BNP?
Hormone prod. mainly in LV in response to strain Vasodilator, diuretic and natriuretic (suppresses both RAAS and sympathetic tone) ischaemia, valvular disease, an LV dysfunction
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What is Buerger's Disease
Small and medium vessel vasculitis assoc with smoking Causes IgA nephropathy but also Intermittent Claudication, Ischaemic ulcers, Raynauds
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TOF
- Over-riding aorta - VSD - LVH - Pulmonary stenosis
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Types of ASD
``` Ostium Secundum (most common) Ostium primum ```
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Ostium Secundum Aetiology
70% due to failed closure of Foramen Ovale
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Clopidogrel - Action - When used - Names of similar drugs
- Blocks ADP receptor (P2Y12) inhibiting platelet activation - 1st line in ischaemic stroke and peripheral artery disease - Ticagrelor, Prasugrel
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Antiplatelet use - NSTEMI - STEMI - TIA - Ischaemic stroke - Periphreal artery disease
- Aspirin (lifelong), clopidogrel/ticagrelor (12mnth) - Aspirin (lifelong), clop 1 month - Clopi (lifelong) - Clopi (lifelong) - Clopi (lifelong)
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ACEi SE
Cough in 15% due to inc bradykinin levels Small risk angio-oedema Hyperkalaemia
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Cautions and contraindications ACEi
Pregnancy and BF Renovascular disease risk renal impairment if bilateral renal artery stenosis
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``` Action of antiarrhythmics Class 1 - Class 2 - Class 3 - Class 4 - ```
Class 1 - sodium channel blockers Class 2 - B-block (Propanolol) Class 3 - K+channel block (Amiodarone, Sotalol) Class 4 - Ca channel block (verapamil, diltiazem)
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Class 1 antiarrhythmics examples
1a (moderate): Quinidine 1b (weak): Lidocaine, phenytoin 1c (strong): Flecainide
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Action potential changes of Antiarrhythmics
Class 1: Change slope of phase 0 Class 2: decrease HR and conduction velocity Class 3: inc AP duration and absolute refractory period, prolong repolarization Class 4: slow rise of action potential. prolonged depolarisation at AV node
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When does ductus arterioles close - What drug keeps open & what one closes early
2-3 days PG NSAID
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Reduced femoral pulse / Radio femoral delay.. what is diagnosis
Coarctation (constriction) of the aorta
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What is 1st management of Pulseless electrical activity
Chest compression then | Give 1mg IV adrenaline
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In VF/VT when is adrenaline given
After chest compression started
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In Asystole what should be done
2 mins chest compressions and see if changes
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CCB used in HTN
Dihydroperidones: Amlodipine
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When is electrical rather than pharmacological cardioversion used in AF? What should be done prior?
Any AF lasting for over 48 hour s= DC cardioversion Must receive oral anticoagulant for 3 weeks prior if AF symptoms last over 48hr
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Definition of Pulseless electrical activity
Sinus tachy on eCG | No pulse felt