CVS Flashcards
Cardiac chest pain
Angina Aortic Aneurysm dissection Myocardial infarction Myocarditis Pericarditis
Considerations on history
SOCRATES Character Constricting -> angina, spasm, anxiety Sharp -> pleural, pericardium, chest wall Prolonged crushing -> MI
Radiation
Shoulder, arms, neck and jack -> ischaemia
Instantaneous interscapular -> aortic dissection
May also be epigastric
Relieve - GTN, antacid, leaning forwards (pericarditic pain)
Exacerbation - Exercise
Associations
SOB
Nausea, vomiting or sweating
Underlying CAD
Cardiac History
Types of Qs
Presenting • Chest pain - SOCRATES - Comparison to previous - NB think heart burn if: associated with food worse lying flat associated with dysphagia
• Palpatation
- Awareness of heartbeat
- Onset, duration
- Association - pain, SOB, caffeine
- Regular (SVT or VT) or irregular (paroxysmal AF or flutter)
- Drop of beats
- ?Anixiety
- NB drugs - e.g. beta-blockers
• SOB
- Duration, what brought it on, worsening or acute
- Exercise tolerance
- NYHA class
- Lying flat (orthopnoea), number of pillows, wake up gasping (paroxysmal nocturnal dyspnoea)
- Ankle swelling
• Dizziness
- Clarify
- Onset, duration, frequency
- Doing at the time, pre warning
- Associated, residual symptoms
- Tongue biting, seizure, incontinence, witnessed
- Vertigo, imbalance, faintness
• Others
How were you yesterday?
How are you normally?
Past Angina Previous heart attack and stroke Rhuematic fever Hypertension, Hyperlipidaemia Previous tests
Drugs Aspirin GTN beta-blocker ACEi Digoxin Statins Anti-coagulant
Family
Heart disease - particularly 1st degree relative <60 with IHD
Social
Smoking, alcohol, exercise
IHD risk factors: HTN Smoking DM Family history
Cardiac SOB
Ischaemic heart disease
Left ventricular failure
Valvular heart disease
Considerations on history
At rest or on exertion
Number of pillows at night
Do you wake up gasping
DVT risk factors
New York Heart Association Classification
I - no limitation of physical activity or SOB
II - ordinary physical activity does cause SOB
III - less than ordinary activity causes SOB
IV - SOB may be present at rest
Full cardiac examination
WIPER
IPPA
45 degrees
Inspection:
Environment - Obs Medication - GTN, Yellow book (Warfarin) ECG Drip/Oxygen Board Mobility
Patient- SOB Palor Comfort Scars
Hands Clubbing - congenital cyanosis Capiliary refill - central prioritisation. Also feel fr Quincke's sign (pulsation of nails) - AR Splinter haemorrhage (microemboli, can be very small), Janeway lesions (palm and painless), Osler's nodes (fingers) - infective endocarditis Arachnodactyly - Marfans Xanthomata Tar staining Warmth Redness
Wrist
Pulse - rate and rhythm
Collapsing pulse - felt as a waterhammer pulsation, sign of aortic regurg (i.e. next pulse is stronger)
Radial:radial delay - aortic coarctation (radio-fem), dissection, peripheral arterial disease
Character at brachial - fast rising (regurg), slow rising (stenosis)
BP - hypo or hyper, narrow (stenosis) or wide (regurg)
Face Conjuctival palor Xantholesma and corneal arcus - hyperlipidaema Malar flush - mitral stenosis Graves' (bulging eyes or goitre)
Neck
Carotid pulse
JVP - comment on height and waveform. Can do hepato-jugular reflex. NB to get to its level and feel for it.
Expose and note scars
Subclav - pacemaker or ICD
Midline sternotomy - CABG, congenital, valve
Lateral thorocotomy - mitral valve repair
Comment on chest wall deformities
Precordium
Apex beat - location, heaving (outflow obstruction), thrusting (volume overload), tapping (mitral stenosis), diffuse (LHF, dilated cardiomyopathy), double impulse, if not palpable (habitus, COPD, dextrocardia)
Heave (left) - RV enlargement
Thrill - palpable murmur
Auscultate Chest APTM - NB bell and diaphragm for mitral Sounds 1 and 2 Added sounds - murmurs, tinkering, click Sit up for aortic and go into carotid Roll over for mitral and go into axilla Hold in expiration for aortic and mitral, inspiration for pulmonary and tricuspid Take pulse at the same time to ID whether diastole or systole
Back
Lung bases - pleural effusion (CF)
Sacral oedema
Legs
Pitting oedema
To complete Other examinations - respiratory and peripheral vasc Look at notes - obs Bedside investigations - ECG, Bloods, Urine dip, Fundoscopy (retinopathy, papilloedema, Roth spots (IE)) Further investigations: Bloods - FBC, U&Es, LFT Imaging - CXR, echo Special - Troponin/cardiac enzymes
Presenting
From the end of the bed there was no paraphernalia of…
On general inspection
No stigmata of HF or IE
Pulse - rate, rhythm, volume and character
JVP
Apex beat - displacement and character
On auscultation - type, louder where
- Heart sounds - normal, abnormal, additional
- ?Murmurs
These findings are in keep with… but differentials
Heart sounds
Comment on: Sounds 1 and 2 Added sounds Whether they were diastolic or systolic Where they are loudest
S1 - closure of mitral and tricuspid
Splitting normal in inspiration
Loud - MS, tachycardia (i.e. if there is deficient diastole)
Soft - if diastole is prolonged
S2 - closure of aortic and pulmonay
A2 loud in HTN, tachycardia and transposition
P2 loud in pulm HTN, soft in pulm stenosis
Splitting (best heard in pulm area):
Wide - BBB, pulm stenosis, deep inspiration, MR, VSD and fixed in ASD
Reversed (i.e. P then A) - LBBB, AS, PDA
Additional
S3 - just after S2, low pitch (bell)
Pathological if >30y
Indicative of poor LV function, e.g. dilation
If earlier and more high pitch - constrictive pericarditis, restrictive cardiomyopathy
S4 - just before S1
Always abnormal
Atrial contraction against stiff venticle
Triple and gallop
S3 - Ken-tucky
S4 - Tenne-ssee
Ejection systolic click - bicuspid aortic valve
Mid-systolic click - M prolapse
Prosthetic - usually tilting disc
Murmurs What do you expect to hear NB whether to use bell (low pitch) or diaphragm Comment on: Character Loudness Area loudest Radiation Accentuating manoeuvres
Pansystolic radiating to axilla - MR
Rumbling mid-diastolic - MS
Ejection systolic radiating to carotid - AS
Early diastolic when held on expiration - AR
HF
Def: Inability of heart to meet body’s demand at normal filling pressure
Clinicopathological, heterogenous (requires justification i.e. secondary to…)
Classification: Eitiology Severity R/L vs congestive Acute vs chronic Forward (can't pump at a sufficiently high rate to supply body demands) or backward (can only pump at sufficient rate when filling pressures are abnormally high) Low or high output Whether EF is preserved or not
Symptoms Fluid congestion SOB - L backwards failure, leading to pulmonary oedema Orthopnoea PND - waking up gasping Decreased supply Fatigue - L forwards failure Dizziness
Signs Leg oedema - R failure Raised JVP - increase RAP Tender hepatomegaly - R backward Generalised anasarca - R backward Fine expiratory creps, bibasal - L forwards
Investigations
ECG - look for cause. Decrease in R wave amplitude is suggestive of HF
Echo - EF (EDV vs ESV, reduced if <30%), ?cause (consider wall abnormalities), compensation
CXR - ABCDE
A -veolar shadowing (pulmonary oedema)
B - lines (kerley)
C - ardiomegaly
D - ivergence of upper lobes
E - ffusion
Bloods
U&Es - kidnet function for medication
BNP - >400, released on ventricular stretch
Management Acute (RR = 40 and low sats) 1) Sit up at 90 2) Oxygen on non-rebreathe mask 15L 3) IV furosemide 40mg
Chronic Improve mortality Beta blocker ACEi Spirolactone Improve contraction Digoxin
Others
Cardiac rehab
Resynchronisation
Transplant
JVP
Internal Jugular Vein
Observe - height and waveform
Patient at 45 degrees, look left and relax
NB good lighting
Position - just medial to the clavicular edge of SCM to the earlobe
Height from the manubriosternal angle
Differentiating from the carotid:
Usually impalpable
Exacerbated by hepatojugular reflex
Double pulse for every beat (dual waveform)
Raised (>5cm) - fluid overload, RHF
Could be secondary to various things
LQT
Congenital - Romano-Ward, Jervell and Lange-Nielsen
Cardiac - MI/ischaemia, mitral prolapse
Metabolic - decreased K, Mg or Ca
Drugs:
Anti-arrhythmics - Amiodarone
Anti-microbials - Erythomycin, levofloxacin
Anti-histamines - terfenadine
Motility - Domperidone
Psychoactive - haloperidol, tricylcics, SSRIs
Toxins - Organophosphates
Pulses
Bounding - CO2 retention, LF, sepsis
Small volume - AS, shock, pericardial effusion
Collapsing - aortic incompetence, AV malformtion, patent ductus arteriosus
Slow-rising - AS
Bisferiens - AS and AR combined
Pulsus alernans (alternating strong and weak) - LVF, cardiomyopathy, AS
Jerky - HOCM
Pulsus paradoxus (>10mmHg decrease in systole on inspiration) - children, severe asthma, pericardial constriction, tamponade
Sinus rhythms
Sinus Rhythm
• Originating from sinus node
• Modulated by autonomic nervous system
• Characterized by P waves that are upright in leads I, II and aVF but inverted in leads AVR and V1
Sinus Arrhythmia
• Fluctuations in autonomic tone -> changes of the sinus discharge rate
• Inspiration -> parasympathetic tone falls à heart rate quickens
• On expiration heart rate falls
• Normal, particularly in children and young adults
Sinus tachycardia • Sinus rate >100 Causes: • Shock • Anxiety • Exercise • Caffeine • Enhance sympathetic drive - Drugs - Phaeochromocytoma - Hyperthyroidism • Infection
Sinus Bradycardia
• Sinus rate <60bpm during day (<50bpm at night)
• Usually asymptomatic unless rate is very slow
• Normal in athletes
Causes:
• Extrinsic factors -
- Hypothermia
- Hypothyroidism
- Cholestatic jaundice
- Raised ICP (Cushing Reflex: raised BP, irregular breathing, and bradycardia)
- Drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs
- Neurally mediated syndromes (see below)
• Intrinsic sinus node disease
- Acute ischaemia and infarction of the sinus node (eg. complication of MI)
- Chronic degeneration changes such as fibrosis of the atrium and sinus node
Manage:
• Atropine or isoprenaline
• Pacemaker
[Neurally Mediated Syndromes]
• Are due to a reflex that may result in both bradycardia and reflex peripheral vasodilatation
• Examples:
- Carotid sinus syndrome
- Neurocardiogenic (vasovagal) syncope
- Postural orthostatic tachycardia syndrome (POTS)
• Sudden and significant increase in HR associated with normal or mildly reduced BP produced on standing
• Failure of peripheral vasculature to appropriately constrict in response to orthostatic stress
Heart block
Heart Block
1) AV block - Block in either AV node or His bundle
2) Bundle branch block - Block lower in conduction system
Three forms of AV block:
1st Degree AV Block -
• Prolongation of PR interval >0.22s
2nd Degree AV Block -
Mobitz I Block (Wenckebach Block Phenomenon)
• Progressive PR interval prolongation until P wave fails to conduct QRS complex
• Generally due to block in AV node
Mobitz II Block
• Dropped QRS complex is not preceded by progressive PR interval prolongation
• Usually a wide QRS complex (>0.12s)
• Signifies block at an infranodal level such as His bundle
• Risk of progression to complete heart block is greater and reliability of resultant escape rhythm is less
• Therefore pacing usually indicated
• 2:1 or 3:1 block
• When every second or third P wave conducts to the
ventricles
2nd Degree AV Block and MIs
• Inferior & Anterior MI
2nd Degree AV block associated with high risk of
progression to complete heart block
o Temporary pacing followed by permanent
pacemaker implantation is usually indicated
3rd Degree (Complete) AV Block -
• All atrial activity fails to conduct to the ventricles
• Life is sustained by a spontaneous escape rhythm
• MANY causes, some include:
o Ischaemic heart disease
o Idiopathic fibrosis (Lev’s and Lenegre’s disease)
o Cardiac surgery
o Drug induced
o Infections (eg. endocarditis, Lyme disease)
o Neuromuscular diseases (Duchenne muscular
dystrophy)
Bundle Branch Block
Bundle Branch Block
RBBB - ‘Marrow’
Late activation of right ventricle
• Deep S waves in leads I and V6
• Tall late R wave in lead V1
[Late activation moving towards right- and away from left sided leads]
• Broad QRS >120ms
• Can also get ST depression and T wave inversion in the right precordial leads (V1-V3)
LBBB - 'William' • QRS duration >120ms • R wave in lateral leads (V5-V6) may be either: - M-shaped - Notched - Monophasic - RS complex • QRS complex of V1 may be either: - rS complex (small R wave, deep S wave) - QS complex (deep Q/S wave with no preceding R wave)
RBBB can be a normal finding in 1% of young adults and 5% of elderly adults
Unusual for LBBB to exist in absence of organic disease
Supraventricular tachycardia
Supraventricular Tachycardias
- Arise from the atrium or the atrioventricular junction
- Conduction is via the His-Purkinje system (narrow QRS complex)
Atrioventricular nodal re-entry tachycardia (AVNRT)
•Presence of two functionally and anatomically different pathways predominantly within AV node
- Short effective refractory period and slow conduction
- Longer effective refractory period and conducts faster
• In sinus rhythm, fast pathway used
• If atrial impulse (eg. an atrial premature beat) occurs early when fast pathway still refractory, the slow pathway takes over
- Impulse travels back through fast pathway which has already recovered its excitability, thus initiating the most common ‘slowfast’,or typical, AVNRT
• Normal regular QRS at rate of 140-240 bpm
• P waves either not visible or are seen immediately before or after the QRS complex (due to simultaneous atrial and ventricular activation)
Atrioventricular Reciprocating Tachycardia (AVRT)
• Abnormal connection between ventricle and atrium (aka accessory pathway or bypass tract)
• Results from incomplete separation of the atria and the ventricles during fetal development
• Current can move either anterograde (towards ventricles) or retrograde (away from ventricles) or in both directions
Wolff-Parkinson-White Syndrome
• Accessory pathway (bundle of Kent) that does not have rate slowing properties of AV node
• Can conduct at a significantly higher rate than AV node
• Types A (left atrium to left ventricle) or B (right atrium to right ventricle)
- Short PR interval and presence of delta wave (slurred upstroke in QRS complex)
- WPW syndrome + AF -> rapid polymorphic wide-complex tachycardia (looks similar to polymorphic VT but does not show torsades de pointes)
• If sustained treat with immediate electrical
cardioversion
Adverse features: • Syncope • Chest pain • Hypotension • SOB, fine bibasal creps, pedal oedema (acute HF)
Rate control:
• Carotid message
• Forced valsalva
• Face in cold water
• Adenosine - to reveal underlying rhythm
- may require beta blocker or Ca blockers
Atrial tachyarrhythmias
Atrial Tachyarryhthmias - arise from the atrial myocardium
Atrial Fibrillation
• Common (1-2% of general population, 5-10% of patients >75 years of age)
Cause:
Any condition resulting in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium, may cause AF.
• There may also be genetic and systemic causes
of AF.
Classified as (this is helpful in decision-making between rhythm restoration and rate control):
- First detected (should not be regarded as necessarily the true onset as can be asymptomatic)
- Paroxysmal (stops spontaneously within 7 days)
- Persistent (requires cardioversion to stop)
- Permanent (no spontaneous or induced cardioversion
ECG shows:
- Fine oscillations of the baseline (so-called fibrillation or f waves) and no clear P waves
- QRS rhythm rapid and irregular
Management:
- Rate control (AV nodal slowing agents):
• Digoxin
• Beta-blockers
• Verapamil or diltiazem
- Rhythm control
• Antiarrhythmics (classes 1a, 1c or III)
• Left atrial ablation
• DC Cardioversion
- Anticoagulation
CHA2DS2VASc Score - estimates risk of stroke
• 2 or more = anticoagulation required
• 1 = consider anticoagulation
• 0 = no anticoagulation needed
Atrial Flutter
• Regular atrial rhythm with an atrial rate usually of 250-350 bpm
• Typically involves macro re-entrant right atrial circuit around the tricuspid annulus
• ECG shows regular sawtooth-like atrial flutter waves (F waves) between QRS complexes
• Symptoms depend on degree of AV block
- Most often 2:1 (150bpm)
Ventricular tachyarrhythmia
Ventricular Tachycardia
• Rapid ventricular rhythm with broad, abnormal QRS complexes, no P
• Supraventricular tacycardia with bundle branch block may resemble VT on ECG
Ventricular Fibrillation
• Very rapid and irregular ventricular activation with no mechanical effect
• Patient is pulse-less and becomes rapidly unconscious, and respiration ceases (cardiac arrest)
• ECG shows shapeless, rapid oscillations with no hint of organised complexes
• Burgada Syndrome
- Inheritable condition, idiopathic VF
- Classic ECG changes: RBBB with coved ST elevation in V1-3
Long QT Syndrome
• Can be congenital or acquired
• Prolongation of ventricular repolarization -> predisposes to ventricular arrhythmias
• Polymorphic VT (torsades de pointes)
- Usually terminate spontaneously but may degenerate to VF, resulting in sudden death
• Torsades de pointes
- Rapid, irregular, sharp complexes that continuously change from an upright to an inverted position
