Week 5 Cardio Flashcards

(87 cards)

1
Q

Clinical trial

A

Evaluation of therapeutic intervention in humans, who are healthy or have a disease

Unbiased, accurate assessment of effect of treatment

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2
Q

Guidlines recommendations for evidence

A

Class I: General evidence shows treatment is useful/effective

Class II: Conflicting evidence

Class IIa: General evidence showing in favour of efficacy

IIb: Efficacy less well established

Class III: General evidence showing treatment not useful/effective

Level of evidence

A - multiple RCT

B - single RCT

C - consensus of opinion from experts/multiple small studies

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3
Q

AF (def, symptoms, diagnosis

A

Chaotic rhythm of atrium. Ventricular rhythm is irregular and rate controlled by AV node refractoriness.

Most common sustained cardiac arrythmia

Major risk factor for stroke

Symptoms:

Aysymptomatic, palpitations, SOB, chest pain

Diagnosis:

Irregular pulse

Confirmed by 12 lead ECG

Types: Paroxysmal (stops spontenously)

Persistent (stops with intervention)

Permanent

Investigations:

ECG, Echocardiogram, TFTs, LFTs

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4
Q

Atrial flutter

A

Circular movement of electrical activity in atrium. Usually 2:1 AV conduction, 300bpm

ECG:

Sawtooth appearence (as P waves don’t always cause QRS due to refractory period. Successive atrial depol (P) waves)

Regular narrow QRS

Treat with catheter ablation

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5
Q

Conditions that pre-dispose AF

A

HTN

HF

Valvular heart disease

Thyrotoxicosis

Diabetes

Obesity

Coronary artery disease

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6
Q

Treatment AF

A

Aims:

Prevent stroke, relieve symtpoms, rate control, correct rhythm

Prevent stroke

Warfarin

DOACs: Dabigratan, Apixiban/Edoxaban

  • increased risk of GI bleeding

Rate control

HR <110

If symptomatic <80

Pts without HF: (1st line) B-blocker (bisoprol) or Ca2+ antagonist (Verapamil)

2nd line: Digoxin

Rhythm control

Younger pts, pts with symptoms despite rate control

Anti-arrythmic drugs:

Class 1: Na+ channel blocker: Flecainide (contra-indicated with significant heart disease)

Class III: K+ channel anatagonists: Amiodarone

Sotalol (B-blocker with Class III activity)

Multi- channel blockers: Dronedarone

Catheter ablation:

Radiofrequency or cryo-ablation to create scar tissue to destroy areas (pulm. veins) triggering arrthymias

  • Indicated for paroxysmal AF

Direct current cardioversion (persistent AF, or pts who present first time with no heart disease, <48hrs)

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7
Q

Risk factors for stroke for pts with AF

A

CHA2-DS2-VASCs score (out of 9 pts)

Cardiac failure

HTN

Age >75 (2pts)

Diabetes

Stroke (2pts)

Vascular disease

Age 65-75

Sex

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8
Q

HF definition, symptoms/signs, causes, types

A

When heart fails to pump blood around the body at a rate to meet metabolic demands

Due to abnormality of cardiac funciton or filling pressure

Symptoms:

Dyspnoea, cough, ankle swelling, fatigue

Signs:

Raised JVP

Displaced apex beat (cardiomegaly)

Pulmomary oedema

Peripheral oedema e..g ankles

Causes:

HTN, Coronary artery disease, TB, alcohol. congenital heart disease

Types:

HF-REF (reduced ejection fraction)

Young, males, coronary arteries

H-PEF (preserved ejection fraction)

Old, femle, HTN (filling abnormal)

Chronic/acute

Chronic (congested) - presents for period of time, can be from acute or lead to acute

Acute - usually hospital admin, from chronic or de novo

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9
Q

Causes of HF

A

Common: coronary heart disease, HTN, idiopathic, toxic (alcohol)

Uncommon: valve disease, infections e.g. Chaga’s, congenital heart disease

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10
Q

HF pathophysiology

A

Myocardial injury

  • LV systolic dysfunction (reduced EF)
  • body percieves reduced circulatory vol
  • neurohumoral activation (increased sym activation, RAAS, natriuretic peptides)
  • systemic vasocontrction, Na+/H2O retention
  • LV dysfunction
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11
Q

HF classification

A

New York Heart Assocation Classifcation (NYHA)

Class I: No symptoms

Class II: Mild symptoms e.g. mild SOB

Class III: Moderate limitation in activites due to symptoms

Class IV: Severe limitations. Symptoms whilst at rest.

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12
Q

General investigations HF and for selected pts

A

Bloods: FBC, UEs, LFTs, CRP

BNP (brain natriuretic peptide) - released from ventricular myocytes

Echocardiogram (size, systolic/diastolic function)

CXR (exclude lung pathology)

ECG (rate, rhythm, QRS)

Selected pts

Coronary angiogram

Exercise testing

Ambulatory ECG

Myocardial biopsy

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13
Q

Treatment for CHF

A

B-blockers (Carvedilol) + ACEi (Ramipril)

MRA (spironolactone)

ARB (angiotensin II receptor blocker) - Valsartan, Socubritil (LCZ696) - inhibits renal vasoconstriction, and breakdown of neprilysin, increasing natriuretic peptides

ICD (implantable cardioverter defribillator), Ivrabadine (If current inhibitor, reduces HR)

Digoxin

Isosorbide dinitrate

Cardiac transplant

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14
Q

Suspected Acute HF: identification of aetiology

A

CHAMP

C acute Coronary syndroe

HTN

A rrythmia

M acute Mechanical cause

PE

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15
Q

Acute HF Wet vs dry

A

95% AHF pts “wet” - congested

Pulmonary congestion

Raised JVP

Peripheral oedema

5% AHF pts “dry” - hypoperfused

Oligouria

Confusion

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16
Q

Treatment AHF

A

O2

IV Furosemide

Nitrates

Dobutamine (ionotropic)

Ultra-filtration

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17
Q

Hypertension defintion

A

Persistent elevation in arterial blood pressure <140/90, without secondary cause

Increases vascular risk in pts such that invervention is needed

Leads to increased risk of coronary artery disease, stroke, HF, peripheral vascular disease, renal failiure

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18
Q

Hypertension pathophysiology

A

BP = CO x TPR

Genetics + Environment leads to:

Defects in renal sodium homeostasis (increased Na and H2O retention - increased plasma volume - leading to increased CO)

- Functional vasoconstriction

Defects in vascular smooth muscle - leading to thickened vascular wall

  • Increased total peripheral resistance
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19
Q

CHF Xray signs

A

Stage 1: Redistribution

- Redistribution pulmonary vessels (normally vessels in lower lobes larger than ones in upper. If uppe lobe vessels larger than lower lobe vessels - increased pulm venous pressure)

- Cardiomegaly (widest transvere cardiac diameter, divided by wideset transverse diameter lungs. Normally 0.5)

2. Interstitial oedema

- Kerly B lines (setpal lines - fluids leaks into interlobular septa due to oedema)

3. Alveolar oedema

- Consolidation

- Pleural effusions (fluid in parietal space, can obscure heart border)

Alveolar oedema

B - Kerley B lines

C ardiomegaly

Distended upper lobes (redistribution pulmonary vessels)

Pleural Effusion

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20
Q

Effects of HTN and cardiovascular mortality

A

Cardiovascular disease risk doubles for every systolic 20mmHg increase and diastolic 10mmHg increase

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21
Q

Types of HTN: primary and secondary

A

Primary: unknow cause (90%)

Risk factors: Age, sex, physical activity, obesity, genetics

Secondary: underlying cause (10%)

Cushing’s syndrome

Hyperaldosteronism

Phaeochromocytoma

NSAIDs

Obstructive sleep opnoea

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22
Q

Diagosis HTN

A

Multiple out of office BP measurement:

24 hr ambulatory BP

Home blood pressure monitoring

Other investigations:

Bloods, renin/aldosterone (for hyperaldosteronism), 24 hour urinary catecholamines (phaechromocytoma), TFTs, LFTs

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23
Q

Classification HTN

A

High normal: 130-139

HTN Grade 1: 140-159

HTN Grade 2: 160-179

HTN Grade 3: >180

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24
Q

HTN Treatments

A

Lifestyle Advice

Drugs

1st line: ACEi (<55yrs)/ARB or Ca2+ channel blocker (if African/Carribean origin, >55yrs)

2nd line: ACEi + Ca2+ channel blocker

3rd line: ACEi + Ca2+ channel blocker + thiazide diuretic (e.g. bendroflumethiazide)

Resistant HTN: ACEi + Ca2+ thiazide + furthur diuretic, a/b blocker

Aim: <140/90, <130/80 if tolerated

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25
Endocarditis
Infection of endocardial surface of valves Causes: damaged valve due to previous endocarditis, rheumtic valve disease, degeneration, prosthetic valve Pathophysiology: Platelets and fibrin attached to surface of damaged heart valves producing a sterile thrombotc endocarditis. Bacteria adhere to lesions and start an inflammtory response leading to more fibrin depsotion and **vegetations**. Leads to **valve damage** Vegetations can embolise to spleen, kidney, brain
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Types of endocarditis
Native valve endocarditis (NVE) - strep. **viridans** IVDU - staph. **aureus**, gram -ve, fungi Prosthetic valve endocarditis (PVE) - Staph **Epidermis** (**CoNS**), gram -ve, fungi Strep. viridans: **indolent** Staph. aureus, gram -ve, fungal: **acute**
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Risk factors for NVE
Most pts have valve abnormalities (55-75%): Aortic stenosis, Mitral valve prolapse (MVP) IVDU 30% no identifiable risk
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Aortic stenosis (causes, airtiology of rheumatic fever)
Calification due to age Calcification due to congenital abnormality Rheumatic fever - Strep. Pyogenes infection. - Releases streptolysin O exotoxin - Anti-Streptolysin O antibodies produces to fight streptolysin - Cardiac valves have simiar structure to toxin, so antibodies attack cardiac valves - Stenosis and regurgitation
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Clinical syndromes IE
**Acute:** Toxic presentation Progressive valve damage, metastatic infection Staph. aureus **Subacute:** Mild toxicity Presentation indolent Metastatic infection rare S. viridans, enterococcus
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Clinical features IE
Split into Early, Embolic, Late **Early:** Incubation period 2 weeks Faitgue, malaise Fever+ mumur = IE until proven otherwise **Embolic** Small: splinter haemorrhages, petichiae Large: stroke Righ sided Endocarditis (triscuspid - more common in IVDU) - septic emboli **Late** Immunological: Osler's nodes, finger clubbing, splenomegaly Valve damage, absccess FROMJANE **F**ever, **R**oth spots, **O**sler's nodes, **M**urmur, **J**aneway lesions, **A**naemia, **N**ail bed (splinter haemorrhages), septic **E**mboli
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Organisms that cause Endocarditis
Bacteria: - Coxiella Burnetti **Gram +ve** - Staphylococci: CoNS (epidermis), staph. aureus - Streptococci: strep. viridans, enterococci **Gram -ve** Coliforms e.g. E.coli Psuedomonas Aeruginosa HACEK **Fungal** Candida
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IE investigations
FBC, UEs, LFTs, urinalysis (haematuria, proteinuria), CXR, blood cultures **Transthoracic echocardiogram** Non-invasive Transducer in front of chest Sensitivity 50% **Transoesopheageal echocardiogram** Invasive Transducer in oesophagus, requires sedation Sensitivity 80-100%
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IE Duke's criteria
Major: 2 positive blood cultures, typical organisms Positive echo Minor: Fever \>38 Vascular phenomenon e.g. septic emboli Immunological phenomenon e.g. Osler's nodes Risk factor e.g. heart disease, IVDU Positive blood cultures
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IE Treatments
Native: IV Amox, Flucox, Gent Prosthetic: IV Vanc + Gent Streptococcus: IV Benzyl + Gent Enterococcus: IV Amox + Gent Staph aureus MSSA: IV Flucox + Gent MRSA: IV Vanc + Gent CoNS: IV Vanc + Gent +/- Rifampicin
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Why should ACEi not be given with ARB?
Angioedema
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Supraventricular tacycardia
Re-entry of circuit using extra electrical pathway, either in AV node or between atrium and ventricle. Electrical activity passes through normal conduction pathway, can conduct back from ventricle to atrium. Initiates circus movement.
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MI signs/symptoms/diagnosis
Decreased blood flow to heart leading to cardiac necrosis Symptoms: Central crushing chest pain, radiates to jaw/back, SOB, sweatiness, "impending sense of doom" Signs: Tachycardia, Raised JVP, arrythmia, shock Diagnosis: History of ischaemic type chest pain ECG changes Rise in troponin I or T
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Types of MI
Type 1: due to primary coronary event e.g. coronary plaque rupture Type 2: increaed O2 demand e.g. HF, sepsis Type 3: sudden cardiac death Difference between type 1 and 2: Type 1: narrowing due to athersclerotic plaque and rupture Type 2: narrowing not due to blood clot, or no narrowing
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Differential diagnosis MI
Aortic aneursym Pericarditis Anxiety PE Oesophageal rupture
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Investigations MI
ECG CXR Troponin I or T (arises 6-12 hours after chest pain)
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Changes in ECG in STEMI
ST elevation T wave inversion Q wave (if there is transmural infarction) - marker of ongoing or old MI
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Acute coronary syndrome
STEMI: Acute, total thrombotic occlusion of coronary artery leading to transmural infarction, unless artery opened. ECG shows ST elevation, troponin increased NSTEMI: Acute partial thrombotic occlusion of coronary artery. ECG may show ST depression. Troponin increased. Thrombolytic therapy not beneficial. Unstable angina: Acute coronary event (clinical presentation MI + ECG changes or narrowing on cardio angiography), but no increase in troponin. Investigated with exercise testing, coronary angiography.
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What ECG changes occur in occlusion of LAD
Anterior STEMI ST elevation in V1-V4 Reciprocal depression in inferior leads (II, III, avF)
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What ECG changes occur in occlusion of left cirumflex a.
High lateral STEMI ST elevation in I, avL Reciprocal depression in inferior leads (II, III, avF) Lateral: i, avL, V5, V6 pics of different morphology of ST elevations
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What ECG changes occur in occlusion of right coronary aftery
Inferior STEMI ST elevation in inferior leads (II, III, avF) ST depression in high lateral (I, avL)
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Posterior wall infarction
Left circumflex (mostly) or RCA Reciprocal depression in anterior leads (V1-4) Subtle elevation in inferior and lateral leads
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LBBB
New onset LBBB - infarction Old LBBB - can cover ST elevation Broad QRS (more than 3 squares (120ms)) in Lead I WiLLiaM W in V1 M in V6
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Immediate management STEMI
ABCD (MOHACT) **M**orphine, Metoclopramide (anti-emetic) **O2** if \<94% sats Unfractionated **h**eparin **A**nti-platelets: aspirin, Clopidogrel (in ambulance) Tricegalor (hospital)
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Reperfusion therapy STEMI
PCI (primary cutaneous intervention) - Improves survival, reduces strokes, speeds up recovery than thromobolytics Risks: vascular damage, stroke If takes more than 90 mins from call to balloon/journey time 40 mins: Thrombolytics Tenecteplase (tissue plasminogen activator) Risks: haemorrhagic stroke, bleeding Contra-indications: previous stroke, GI bleeding, bleeding disorders Diabetic retinopathy not a contra-indication Heparin
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Secondary prevention MI
BASAT(E) **B**-blockers (Bisoprol) **A**CEi (Ramipril) **S**tatins **A**spirin **T**icagrelor (reversibly blocks ADP receptors of P2Y12(protein involved in platelet aggregration) **E**plerenone - for diabetics, LVSD (left ventricular systolic dysfunction), HF
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Complications MI
VT Bradycardia (treat with atropine) AF HF Cardiogenic shock Pericarditis
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Rehabilitation MI
Smoking cessation Diet Exercise Driving - should not drive for a week Work - aim back 1-2 months Rehabilitation classes
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Management NSTEMI
LMW**H** **A**spirin **C**lopidogrel Secondary prevention: ACEi BBlockers Statins Eplerenone (only for diabetics, LVSD, HF) Risk assessment: GRACE score: \>140 - urgent inpatient angiogram
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Pericarditis
Flu-like symptoms, chest pain worse on inspiration ECG changes: Non specific ST elevation No reciprocal change PR depression Concave ST elevation "saddle back)
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Aortic stenosis
Aortic valve: Opens when systolic pressure in LV exceeds end-diastolic pressure in aorta, and closes when pressure falls Narrowing of aortic valve orifice Causes: Calcification (due to wear and tear), thickening, rheumatic valve diesease, congenital e.g. bicuspid Symptoms: Chest pain, SOB, syncope, LV hypertrophy (due to pressure overload) Complications: heart failure, sudden death
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Aortic regurgitation
Blood flows back to LV from aorta during diastole Symptoms: SOB, reduced capacity for exercise, LV dilatation (due to volume overload) - LV dimesion main indicator of severity Signs: collpasing pulse, displaced apex beat, pulsatile nail bed circulation, head nodding Causes: Degeneration, rheumatic valve disease, Marfan's syndrome, endocarditis
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Stenosis vs regurgitation
Stenosis: pressure overload Regurgitation: volume overload
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Mitral stenosis
Mitral valve: 2 leaflets Opens when pressure in LA exceeds LV pressure during diastole Closes when pressure in LV exceeds LA, during ventricular systole. Stenosis: Narrowing of mitral valve orifice Causes: Rheumatic valve disease (affects mitral valves more), pressure overload Can lead to pulmonary hypertension, AF (as LA dilates) Symptoms: SOB, palpitations, right sided heart failure symptoms
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Mitral regurgitation
Blood flows from LV to LA during systole Causes: Rheumatic valve disease, LV dilation (pulls leaflets apart), endocarditis Can lead to: Pulmonary hypertension (due to volume overload in LA), and AF (as LA is dilated - affects SA node conduction) Symptoms: SOB, palpitations, right sided heart failure symptoms
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Investigations valvular diseaese
History, exam BP ECG Exericise tolerance test Echo Doppler echo Cardioangiography (for surgeon to know if they need to do a coronary artery bypass as well as replacement)
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Treatment valvular disease
Surgical: Repair - Valvuloplasty Replacement - mechanical or tissue (porcine) - mechanical lasts longer but reuiqres anti-coagulation for life Procedural: TAVI (transcatheter aortic valve implantation/replacement) Mitral clip
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What can kind of murmurs can be heard in each valvular disease?
Aortic stenosis: low pitched ejection systolic (crescendo-decrescendo) murmur - Best heard in aortic area (2nd intercostal space right) radiates into neck Aortic regurgitation: high pitched (blowing) early diastolic (as when pressure in LV is below aorta) - Best heard at left sternal edge, with pt sitting forward Mitral stenosis: Low pitched (rumbling) mid diastolic - Best heard at apex, with pt lying on left side Mitral regurgitation: High pitched pan-systolic - Best heard at apex, radiates to axilla Pulm stenosis: soft ejection systolic mumur in pulmonary area Pulm regurg: soft early diastolic murmur in pulmonary area Tricuspid stenosis: diastolic murmur at left sternal edge Tricuspid regurg: soft high pitched pan-systolic at left sternal edge, increased during insp
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Causes of acute arterial occlusion
Thrombus (can occur at site of pre-exsisting atheromatous plaque, in pt with PVD) Embolism (from another source. More likely in pt with no history PVD)
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Arterial occlusion investigations
FBC Fasting blood glucose Lipid profile ECG Aortograms
67
Immediate and long term treatment of arterial occlusion
Immediate: Analgeisa, IV heparin Long-term: Aspirin, antihypertensives (not BBlockers) Lifestyle Statins
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Atheroma and disease
Cornoary artery - MI Carotid artery - stroke Renal arteries - hypertension, if bilateral - renal failure
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6 signs of critical ischaemia
Six Ps: Pale Painful Pulseless Paresis (weak) Perishingly cold Parasthesia (tingling sensation)
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Intermittent claudication
Pain in leg from brought on from walking, and stops on rest Commonly in calf Benign symptom but indicator of widspread vascular disease
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Investigations and treatment acute limb ischaemia
Imaging (although no point if not going to treat e.g. thrombolysis, angioplasty - balloon to stretch artery) - MRI, CT angiography, arteriography Medical: Treat HTN, avoid BBlockers, weight loss
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Clinical symptoms of muscle necrosis
Loss of sensation Muscle tenderness
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ECG AV block
**First degree heart block:** PR interval \>200ms **Second degree:** Mobitz type 1: PR interval progressivly longer, with dropped beats. Regularly, irregular. Mobitz type 2: dropped beats with no change in length of PR interval. Often needs pacemaker. Can lead to 3rd degree heart block. Third degree: Atria and ventricular depol indenpdent of each other, so p and QRS not assoc. with each other. Requires pacemaker. Can be caused by Lyme disease.
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IE blood cultures
Before antibiotics Asetptic technique 3 bottles 10ml, 1st and last at elast 1 hour apart Taken from peripheral veins
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When to think IE?
Pts with Staph. aureus bacteraemia IVDU with positve blood cultures Prosthetic valve with postive blood cultures
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Axis deviation
Normal: -30 to +90 Right axis deviation (+90 - +180) Causes: Right ventriuclar hypertrophy, COPD Left axis deviation (- 30 to -90) Causes: Left ventricular hypertrophy, LBBB Look at leads **I** and **aVF** **Normal**: Lead I: **positive**, avF: **positive** **RAD**: Lead I: **negative**, avF: **positive** **LAD**: Lead I: **postive**, avF: **negative** **Extreme LAD**: Lead I: **negative**, avF: **negative**
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Morphology of atria and ventrices
RA: broad LA: narrow, long RV: trabeculated endocardium, insertion of chordae tendinae to intraventricular septum LV: smooth endocardium, ellipsoid cavity
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Atrial septal defect
Types: Secundum (common), primum Secundum ASD: Septa between right and left atria, causing left to right shunt Examination: Pulmonary flow murmur, split S2 ascultation (as more volume in right side of heart, will delay pulmonary valve closure) Lead to: RV failure, pulmonary hypertension, Eisenmenger syndrome (left to right shunt causes pulmonary hypertension)
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Coarctation of aorta
Narrowing of aorta, usually where ductus arteriosus inserts Pre-ductal: lower limb cyanosis Post-ductal:upper body hypertension, berry aneurysms, rib notching in adults Different BP in arms and legs
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Teratology of fallot
1. Ventricular septal defect 2. Overiding aorta 3. RVOT (riht ventricular outflow tract) obstruction 4. Right ventricular hypertrophy Boot shaped heart on XR
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Transposition of great vessels
Aorta and pulmonary artery swaps So pulm a. comes off LV goes back to LA Aorta comes off RV goes back to RA Treatment: Arterial swtich Atrial switch
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Univentricular heart
Only one functioning ventricle Causes: tricuspid atresia Treatment: Fontan circulation - Pulmonary valve and artery disconnected with ventricle - IVC and SVC connected to pulmonary arteries, bypassing heart As pulmonary circ relies on high systemic venous pressure, low pulm vascular resistance, anything that causes an imbalance can cause haemodynamic compromise e.g. PE, bleeding
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Feotal circulation
Formen ovale: RA to LA - allows bypass of RV and pulm artery (as lungs aren't formed properly so resistance in pulm a. is high) Of blood pumped into RV and pulm a., most passes to aorta via ductus arteriosus Patent ductus arteriosus: PA to aorta
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Complications of IE
CHF Stroke Systemic emboli
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PR interval QRS
PR interval: less than 1 big box, \<200ms QTS \< 3 small squares, \<120 ms
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