Week 5 Cardio Flashcards
Clinical trial
Evaluation of therapeutic intervention in humans, who are healthy or have a disease
Unbiased, accurate assessment of effect of treatment
Guidlines recommendations for evidence
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
AF (def, symptoms, diagnosis
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
Atrial flutter
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
Conditions that pre-dispose AF
HTN
HF
Valvular heart disease
Thyrotoxicosis
Diabetes
Obesity
Coronary artery disease
Treatment AF
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)
Risk factors for stroke for pts with AF
CHA2-DS2-VASCs score (out of 9 pts)
Cardiac failure
HTN
Age >75 (2pts)
Diabetes
Stroke (2pts)
Vascular disease
Age 65-75
Sex
HF definition, symptoms/signs, causes, types
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
Causes of HF
Common: coronary heart disease, HTN, idiopathic, toxic (alcohol)
Uncommon: valve disease, infections e.g. Chaga’s, congenital heart disease
HF pathophysiology
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
HF classification
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.
General investigations HF and for selected pts
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
Treatment for CHF
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
Suspected Acute HF: identification of aetiology
CHAMP
C acute Coronary syndroe
HTN
A rrythmia
M acute Mechanical cause
PE
Acute HF Wet vs dry
95% AHF pts “wet” - congested
Pulmonary congestion
Raised JVP
Peripheral oedema
5% AHF pts “dry” - hypoperfused
Oligouria
Confusion
Treatment AHF
O2
IV Furosemide
Nitrates
Dobutamine (ionotropic)
Ultra-filtration
Hypertension defintion
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
Hypertension pathophysiology
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
CHF Xray signs
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
Effects of HTN and cardiovascular mortality
Cardiovascular disease risk doubles for every systolic 20mmHg increase and diastolic 10mmHg increase
Types of HTN: primary and secondary
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
Diagosis HTN
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
Classification HTN
High normal: 130-139
HTN Grade 1: 140-159
HTN Grade 2: 160-179
HTN Grade 3: >180
HTN Treatments
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
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
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
Risk factors for NVE
Most pts have valve abnormalities (55-75%):
Aortic stenosis, Mitral valve prolapse (MVP)
IVDU
30% no identifiable risk
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
Clinical syndromes IE
Acute:
Toxic presentation
Progressive valve damage, metastatic infection
Staph. aureus
Subacute:
Mild toxicity
Presentation indolent
Metastatic infection rare
S. viridans, enterococcus
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
Fever, Roth spots, Osler’s nodes, Murmur, Janeway lesions, Anaemia, Nail bed (splinter haemorrhages), septic Emboli
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
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%
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
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
Why should ACEi not be given with ARB?
Angioedema
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.
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
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
Differential diagnosis MI
Aortic aneursym
Pericarditis
Anxiety
PE
Oesophageal rupture
Investigations MI
ECG
CXR
Troponin I or T (arises 6-12 hours after chest pain)
Changes in ECG in STEMI
ST elevation
T wave inversion
Q wave (if there is transmural infarction) - marker of ongoing or old MI
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.
What ECG changes occur in occlusion of LAD
Anterior STEMI
ST elevation in V1-V4
Reciprocal depression in inferior leads (II, III, avF)
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
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)
Posterior wall infarction
Left circumflex (mostly) or RCA
Reciprocal depression in anterior leads (V1-4)
Subtle elevation in inferior and lateral leads
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
Immediate management STEMI
ABCD
(MOHACT)
Morphine, Metoclopramide (anti-emetic)
O2 if <94% sats
Unfractionated heparin
Anti-platelets: aspirin,
Clopidogrel (in ambulance)
Tricegalor (hospital)
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
Secondary prevention MI
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
Complications MI
VT
Bradycardia (treat with atropine)
AF
HF
Cardiogenic shock
Pericarditis
Rehabilitation MI
Smoking cessation
Diet
Exercise
Driving - should not drive for a week
Work - aim back 1-2 months
Rehabilitation classes
Management NSTEMI
LMWH
Aspirin
Clopidogrel
Secondary prevention:
ACEi
BBlockers
Statins
Eplerenone (only for diabetics, LVSD, HF)
Risk assessment:
GRACE score: >140 - urgent inpatient angiogram
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)
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
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
Stenosis vs regurgitation
Stenosis: pressure overload
Regurgitation: volume overload
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
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
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)
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
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
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)
Arterial occlusion investigations
FBC
Fasting blood glucose
Lipid profile
ECG
Aortograms
Immediate and long term treatment of arterial occlusion
Immediate: Analgeisa, IV heparin
Long-term: Aspirin, antihypertensives (not BBlockers)
Lifestyle
Statins
Atheroma and disease
Cornoary artery - MI
Carotid artery - stroke
Renal arteries - hypertension, if bilateral - renal failure
6 signs of critical ischaemia
Six Ps:
Pale
Painful
Pulseless
Paresis (weak)
Perishingly cold
Parasthesia (tingling sensation)
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
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
Clinical symptoms of muscle necrosis
Loss of sensation
Muscle tenderness
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.
IE blood cultures
Before antibiotics
Asetptic technique
3 bottles 10ml, 1st and last at elast 1 hour apart
Taken from peripheral veins
When to think IE?
Pts with Staph. aureus bacteraemia
IVDU with positve blood cultures
Prosthetic valve with postive blood cultures
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
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
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)
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
Teratology of fallot
- Ventricular septal defect
- Overiding aorta
- RVOT (riht ventricular outflow tract) obstruction
- Right ventricular hypertrophy
Boot shaped heart on XR
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
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
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
Complications of IE
CHF
Stroke
Systemic emboli
PR interval
QRS
PR interval: less than 1 big box, <200ms
QTS < 3 small squares, <120 ms
