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Year 3 > Week 5 Cardio > Flashcards

Week 5 Cardio Flashcards

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
Q

Endocarditis

A

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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26
Q

Types of endocarditis

A

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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27
Q
A
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28
Q

Risk factors for NVE

A

Most pts have valve abnormalities (55-75%):

Aortic stenosis, Mitral valve prolapse (MVP)

IVDU

30% no identifiable risk

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29
Q

Aortic stenosis (causes, airtiology of rheumatic fever)

A

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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30
Q

Clinical syndromes IE

A

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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31
Q

Clinical features IE

A

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

Fever, Roth spots, Osler’s nodes, Murmur, Janeway lesions, Anaemia, Nail bed (splinter haemorrhages), septic Emboli

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32
Q

Organisms that cause Endocarditis

A

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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33
Q

IE investigations

A

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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34
Q

IE Duke’s criteria

A

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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35
Q

IE Treatments

A

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

36
Q

Why should ACEi not be given with ARB?

A

Angioedema

37
Q

Supraventricular tacycardia

A

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.

38
Q

MI signs/symptoms/diagnosis

A

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

39
Q

Types of MI

A

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

40
Q

Differential diagnosis MI

A

Aortic aneursym

Pericarditis

Anxiety

PE

Oesophageal rupture

41
Q

Investigations MI

A

ECG

CXR

Troponin I or T (arises 6-12 hours after chest pain)

42
Q

Changes in ECG in STEMI

A

ST elevation

T wave inversion

Q wave (if there is transmural infarction) - marker of ongoing or old MI

43
Q

Acute coronary syndrome

A

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.

44
Q

What ECG changes occur in occlusion of LAD

A

Anterior STEMI

ST elevation in V1-V4

Reciprocal depression in inferior leads (II, III, avF)

45
Q

What ECG changes occur in occlusion of left cirumflex a.

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

46
Q

What ECG changes occur in occlusion of right coronary aftery

A

Inferior STEMI

ST elevation in inferior leads (II, III, avF)

ST depression in high lateral (I, avL)

47
Q

Posterior wall infarction

A

Left circumflex (mostly) or RCA

Reciprocal depression in anterior leads (V1-4)

Subtle elevation in inferior and lateral leads

48
Q

LBBB

A

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

49
Q

Immediate management STEMI

A

ABCD

(MOHACT)

Morphine, Metoclopramide (anti-emetic)

O2 if <94% sats

Unfractionated heparin

Anti-platelets: aspirin,

Clopidogrel (in ambulance)

Tricegalor (hospital)

50
Q

Reperfusion therapy STEMI

A

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

51
Q

Secondary prevention MI

A

BASAT(E)

B-blockers (Bisoprol)

ACEi (Ramipril)

Statins

Aspirin

Ticagrelor (reversibly blocks ADP receptors of P2Y12(protein involved in platelet aggregration)

Eplerenone - for diabetics, LVSD (left ventricular systolic dysfunction), HF

52
Q

Complications MI

A

VT

Bradycardia (treat with atropine)

AF

HF

Cardiogenic shock

Pericarditis

53
Q

Rehabilitation MI

A

Smoking cessation

Diet

Exercise

Driving - should not drive for a week

Work - aim back 1-2 months

Rehabilitation classes

54
Q

Management NSTEMI

A

LMWH

Aspirin

Clopidogrel

Secondary prevention:

ACEi

BBlockers

Statins

Eplerenone (only for diabetics, LVSD, HF)

Risk assessment:

GRACE score: >140 - urgent inpatient angiogram

55
Q

Pericarditis

A

Flu-like symptoms, chest pain worse on inspiration

ECG changes:

Non specific ST elevation

No reciprocal change

PR depression

Concave ST elevation “saddle back)

56
Q

Aortic stenosis

A

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

57
Q

Aortic regurgitation

A

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

58
Q

Stenosis vs regurgitation

A

Stenosis: pressure overload

Regurgitation: volume overload

59
Q

Mitral stenosis

A

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

60
Q

Mitral regurgitation

A

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

61
Q

Investigations valvular diseaese

A

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)

62
Q

Treatment valvular disease

A

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

63
Q
A
64
Q

What can kind of murmurs can be heard in each valvular disease?

A

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

65
Q

Causes of acute arterial occlusion

A

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)

66
Q

Arterial occlusion investigations

A

FBC

Fasting blood glucose

Lipid profile

ECG

Aortograms

67
Q

Immediate and long term treatment of arterial occlusion

A

Immediate: Analgeisa, IV heparin

Long-term: Aspirin, antihypertensives (not BBlockers)

Lifestyle

Statins

68
Q

Atheroma and disease

A

Cornoary artery - MI

Carotid artery - stroke

Renal arteries - hypertension, if bilateral - renal failure

69
Q

6 signs of critical ischaemia

A

Six Ps:

Pale

Painful

Pulseless

Paresis (weak)

Perishingly cold

Parasthesia (tingling sensation)

70
Q

Intermittent claudication

A

Pain in leg from brought on from walking, and stops on rest

Commonly in calf

Benign symptom but indicator of widspread vascular disease

71
Q

Investigations and treatment acute limb ischaemia

A

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

72
Q

Clinical symptoms of muscle necrosis

A

Loss of sensation

Muscle tenderness

73
Q

ECG AV block

A

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.

74
Q

IE blood cultures

A

Before antibiotics

Asetptic technique

3 bottles 10ml, 1st and last at elast 1 hour apart

Taken from peripheral veins

75
Q

When to think IE?

A

Pts with Staph. aureus bacteraemia

IVDU with positve blood cultures

Prosthetic valve with postive blood cultures

76
Q

Axis deviation

A

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

77
Q

Morphology of atria and ventrices

A

RA: broad

LA: narrow, long

RV: trabeculated endocardium, insertion of chordae tendinae to intraventricular septum

LV: smooth endocardium, ellipsoid cavity

78
Q

Atrial septal defect

A

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)

79
Q

Coarctation of aorta

A

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

80
Q

Teratology of fallot

A
  1. Ventricular septal defect
  2. Overiding aorta
  3. RVOT (riht ventricular outflow tract) obstruction
  4. Right ventricular hypertrophy

Boot shaped heart on XR

81
Q

Transposition of great vessels

A

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

82
Q

Univentricular heart

A

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

83
Q

Feotal circulation

A

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

84
Q

Complications of IE

A

CHF

Stroke

Systemic emboli

85
Q

PR interval

QRS

A

PR interval: less than 1 big box, <200ms

QTS < 3 small squares, <120 ms

86
Q
A
87
Q
A

Year 3 (15 decks)

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