Cardio Flashcards
causes of MI
CAD, aortic stenosis, hypertrophic cardiomyopathy, tachyarrhythmias, cocaine use, anaemia, thyrotoxicosis
causes of cardiovascular non-ischemic chest pain
pericarditis, aortic dissection
causes of upper GI chest pain
gastro-oesophageal reflux disease, gallstones, peptic ulcers, pancreatitis
causes of respiratory chest pain
pulmonary embolism, pneumothorax, pneumonia, pleurisy
causes of musculoskeletal chest pain
costochondritis, Herpes Zoster, shingles
diagnosing visceral and somatic pain (in history taking)
visceral: diffuse, poorly localised
somatic: localised
def angina
discomfort in chest and/or jaw, shoulder, back, arm caused by myocardial ischaemia. most common cause in CAD
symptoms/characteristics typical angina
- discomfort in chest and/or jaw, shoulder, back, arm
- symptoms bought on by exertion
- symptoms relieved within 5 minutes (rest or GTN)
def atypical angina
chest discomfort that meets 2/3 characteristics of typical angina
risk factors for CAD
age, gender, diabetes, hyperlipidaemia, smoking, hypertension
def dyspnoea
shortness of breath
what do you look for on an ECG?
- heart rate
- rhythm (sinus-rhythm starting at the P wave): PR interval 120-200 ms
- axis: QRS complex upright
- QRS complexe: les than 120 ms
- Q waves
- isoelectric ST interval
- T waves: less than 5mm in height in limb leads and less than 15 mm in chest leads
- QT interval should be less than half the preceding RR interval
ECG indictions of CAD
- Q waves: more than 40 ms wide, 2 mm deep, 25% of depth of QRS complex, seen in leads V1-3
- Left bundle branch block: broad QRS (more than 0.12 sec), dip S wave in V1, no Q wave in V5/V6
- ST depression, T wave flattening or inversion
types of angina
stable, unstable, decubitus angina (lying flat), variant (prinzemetal) angina
ECG: difference between ischemic and infarcting endocardium
ischemic: depressed ST
infarcting: elevated ST + inverted T waves
branches of left coronary artery
Lad
circumflex
obtuse marginal
diagonal
branches of right coronary artery
right marginal
poster descending artery
venous drainage of heart
oblique vein of left atrium great cardiac vein left marginal vein posterior vein of left ventricle middle cardiac vein small cardiac vein --> coronary sinus
markers of cardiac cell death
troponin (T or I) 2-12 hours after MI (peak at 24-48 hours after MI) and can be elevated for up to 2 weeks post MI creatine kinase (non specific to cardiac cells)
Increase Proportionally to cardiac death and mortality
where are troponin T and I found in cells
actin filaments
causes of ventricular fibrillation
- IRRITABLE VENTRICULAR CELLS: Cad, electrolyte abnormalities (low Ca, high K, low Mg)
- SCAR: MI, cardiomyopathy (infection, genetic disorders, CAD)
- ELECTROCUTION
different types of Ventricular tachycardia
focal
reentrant
causes of focal vtach
cell irritation due to
- hormones
- low oxygen
- stretch
(CAD, electrolyte abnormalities)
causes of reentrant vtach
scar (MI, hypertrophic and dilated cardiomyopathy)
Afib ecg: what does it look like?
irregularly irregular heart rate
-no distinct P waves
risk factors for Atrial fibrillation
diseased atrial tissue
- age
- inflammation
- enlarged atria (high BP, valve disease, lung disease, Afib)
hormonal abnormalities (thyroid)
alcohol abuse
complications post MI
-decreased contractibility
—> embolism (ventricular thrombus)
—> cardiogenic shock (decrease contractibility —> hypotension—> decrease vessel perfusion —> ischemia —> decrease contractibility)
-electrical instability (arrhythmia)
-tissue necrosis causing inflammation
—>pericarditis
—>cardiac tamponade (rupture of cardiac muscle causing blood to fill space between pericardium and serous sac)
—>mitral regurgitation (rupture of papillary muscles)
—>hypoxemia + stress on pulmonary vessels
–> congestive heart failure
Def orthostatic
Relating to or caused by an upright posture
Stages of hypertension
Grade 1 (mild): 140-159/90-99 Grade 2 (moderate): 160-179/100-110 Grade 3 (severe): >180/>110 Isolated systolic hypertension: >140/<90
Types of hypertensive crisis, BP measurement, symptom and management
Hypertensive urgency:
- BP: >180/>110 mmHg
- symptoms: no target organ damage, headaches, nosebleeds, SoB, severe anxiety
- management: oral medication, outpatient
Hypertensive emergency:
-BP: >180/>120 mmHg
-symptoms: target organ damage, chest pain, SoB, numbness/weakness, vision change, difficulty speaking, back pain
Management: IV medication, (vasodilator, Ca channel blockers, beta blockers), intensive care BUT reduce BP over 24-48 hours (25% over first few hours) to minimise ischemia
Assessment cardiovascular risk and target organ damage in hypertension
QRISK2 risk assessment
Urinalysis: protein, albumin:creatinine ratio, Haematuria
Blood test: FBC, glucose, electrolyte, creatinine, eGFR, total and HDL cholestérol
ECG
Fundoscopy for hypertensive retinopathy
Grade of hypertensive retinopathy
– Grade 1 – tortuosity of the retinal arteries with increased reflectiveness (silver wiring)
– Grade 2 – grade 1 plus the appearance of arteriovenous nipping, produced when thickened retinal arteries pass over the retinal veins
– Grade 3 – grade 2 plus flame-shaped haemorrhages and soft (‘cotton wool’) exudates due to small infarcts
– Grade 4 – grade 3 plus papilloedema (blurring of the optic disc)
Pharmacological Management of hypertension
Aged <55:
A -> A+C -> A+C+D -> (resistance hypertension): A+C+D+other diuretics, alpha or beta blockers + consider sealing expert advice
Aged >55 or black person of African or Caribbean family origin of any age:
C -> A+C -> A+C+D -> (resistance hypertension): A+C+D+ (IF K=4.5) low dose spironolactone OR (IF K> 4.5) alpha or beta blocker + consider sealing expert advice
A: ACEi or ARB
C: Ca channel blocker (CCB)
D:thiazides like diuretics
IN PREGNANCY:
-labetalol, nifedipine or methyldopa
Pathophysiology of increase BP
Usually due to increase peripheral resistance (PR)(increased arteriolar vasoconstriction)
-increased sympathetic action (constriction of muscles)
-decreased blood flow to kidneys: release of renin (RAAS citation causing increase in PR) + aldosterone (increase absorption if H2O + Na+ causing increase in CO)
—> increase in BP causes decrease blood flow to kidneys (iCloud circle)
What are the end organ damage in hypertension
Eyes hypertensive retinopathy (papilloedema, flame haemorrhage, cotton wool spot, hard exudate, arteriovenous nicking)
Brain: hypertensive cerebrovascular disease, haemorrhage/infarction, seizures, vascular dementia
Heart/blood vessels: LVH, IDH (w/ or w/out HF), pulmonary oedema, MI, atherosclerosis, aneurysms, sorti dissections
Kidneys: hypertensive nephropathy (shrunken kidneys), CKD
Examples of causes of secondary hypertension
Common:
Renal parenchyma disease
Renal artery stenosis
Primary aldosteronism
Uncommon:
Phaeochromoytoma
Cushing’s syndrome
Def orthopnoea
SoB when lying flat
Describe the waveforms of JVP and what they correspond to
- A wave: atrial contraction
- C wave: closure of tricuspid valve
- X descent: atrial relaxation
- V wave atrial filling during systole
- Y descent: passive ventricular filling
Classification of murmurs based on intensity
Grade 1: can only be heard if listen intensely for some time
Grade 2: faint murmur heard immediately on auscultation
Grade 3: loud murmur with no palpable trills
Grade 4: loud murmur with a palpable thrill
Tests and investigations in diagnosis of HF
ECG Chest X ray Blood tests: -BNP -NT-proBNP -Renal, liver, thyroid and lipid function profile -HbA1c -FBC Trans thoracic echo (exclude valve disease, assess left ventricular function, detect intracardiac shunts)
What produces the sound of heart murmurs
Turbulent blood flow:
- low viscosity of blood
- decreased radis of vessel/valve
- increased velocity of blood through morphologically normal structures
- regurgitation against incompetent valve
Causes of murmurs due to decreased blood viscosity
Anaemia
Causes of murmurs due to decreased diameter of vessel, valve, or orifice
Valvular stenosis
Coarctation of the aorta
Ventricular septal defect
Causes of murmurs due to increased velocity of blood through normal structures
Hyper dynamic states (ie sepsis, hyperthyroidism)
Causes of murmurs due to regurg acros an incompetent valve
Valvular regurg
Initial treatment of acute HF
- IV diuretic therapy
- increase dose of the diuretic the patient is already on
- monitor closely weight, renal function and urine output during diuretic therapy
- do not offer routinely opiates, nitrates inotropes or vasopressors
- do not offer sodium nitroprusside
- consider inotropes or vasopressors in people with reversible cardiogenic shock
- if person in cardiogenic pulmonary oedema with severe dyspnoea and acidaemia OR respiratory failure OR reduced consciousness OR physical exhaustion : NIV
- consider ultrafiltration for people with confirmed diuretic resistance
Treatment of acute HF after stabilisation
- Treat underlying cause
- montor renal function, electrolytes, HR; BP and overall clinical status
- offer surgical aortic valve replacement therapy if severe aortic stenosis or mitral vale regurg
HF with preserved LV function ( EF > 45%)
- diuretics
- tract co-morbidities
HF with impaired systolic function ((EF <45%)
- diuretics
- beta blockers (first line)
- ACEi (first line)
- aldosterone receptor antagonist (second line)
HF symptoms
—> SoB
- orthopnoea
- on exertion/at rest
- paroxysmal nocturnal dyspnoea
—> tiredness/fatigue
HF signs
- pulmonary oedema/pleural effusion
- raised JVP
- pitting oedema
- ascites
- tachycardia
- S3 gallop
Which beta blocker is not licenced for HF
Atenolol
AF management
In new onset:
-If life threatening haemodynamic instability: Emergency electrical cardio version
-If no life threatening haemodynamic instability: rate (beta blockers or rate limiting Calcium channel blocker) or rhythm control
—> electrical or pharmacological cardioversion (flecainide or amiodarone)
If in AF for more than 48 hours: anticoagulate, long term rhythm control and rate control
What is the Frank-Sterling curve
Relationship between the volume of blood in the heart at the end of diastole (pre-load/end diastolic volume) and the force of contraction of the ventricle
Stroke volume/EDV
(If myocardial cells stretched: increase force and velocity of contraction
BUT only until 15 mmHG pressure)
Causes of mitral valve regurg
Rheumatic heart disease
IHD (papillary muscle rupture)
Valvular vegetation (endocarditis)
Dilated left atrium
What is ejection fraction and what is a normal value?
Measurement of how much blood is being pumped out of the heart with each contraction. It is measured in percentage (stroke volume/end diastolic volume)
Normal value: 50-70%
What are the phase of the action potential
0: rapid depolarisation
1: early repolarisation
2: plateau phase
3: repolariasation
4: resting membrane potential
How long is the cardiac AP
300 ms
Ion channel activity during cardiac AP
Sodium (short but intense)
Calcium (long )
Potassium (delayed, repolarisation)
Properties of cardiac AP
- Long duration and refractory period:
- prevent premature re-excitation (which is different to skeletal muscle)
- long refractory: inactivation of Na channels and persistence of K channels - Fast conduction velocity (for uniform activation, esp in His-Purkinje system)
- Pacemaker activity
Different types of arrhythmias depending on categories
Abnormal pacemaker/triggered activity
- early afterdepolarisation
- delayed afterdepolarisation
Re-entry
What is the difference between pacemaker and triggered activity
Pacemaker: spontaneous
Triggered: set of after being excited by a stimulation
Pathophysiology of early after depolarisation and the medical issue it underlies
Decreased outward K currents: prolonges AP (+ can lead to re-activation of L-Type Ca channels)
Medical issue: long QT syndrome (genetic or acquired: anti histamines, anti cancer)
Pathophysiology of delayed afterdepolarisation
Cellular calcium overload
- spontaneous Ca release from SR
- activates depolarising membrane currents
Medical issue: HF
Pathophysiology of re-entry arrhythmia
- unidirectional block (AP can propagate in one direction but not the other)
- slow conduction (cell excitability is decreased)
- short AP (shortens refractory period, increase activation of K channels)
Medical issue: post MI
What is Ca induced Calcium release and how does it work
Ca entry on Ca current triggers SR release
L-Ca channel: infux of Ca into cell
Ca activates RyR charnels
Uptake into SR by SERCA (ATPase): influences by availability of Ca and by phosphorylation of phospholamban (during sympathetic stimulation)
NCX (exchange 1 Ca for 3 Na)
Def inotropic
Influencing the contractibility of muscular tissue
Def lusitropy
Relaxation of cardiac muscle
Effect of catecholamines on cardiac muscle
Inotropic: Increase L-Ca current (more trigger and loading)
Lusitropic: increase SERCA (increased SR Ca) via phosphorylation of phospholamban
What are peripheral signs for infective endocarditis
Splinter haemorrhages Clubbing Janeway lesions Osler’s nodes Roth spots Petechiae
Diagnostic criteria for infective endocarditis
Modified Duke criteria:
- 2 major criteria
- 1 major criteria and 3 minor criteria
- 5 minor criteria
BE FIV(E) PM
Major criteria: -+ blood culture - evidence of endocardial involvement: A. + echo (vegetation, abscess or valve dehiscence) B. New valvular regurg
Minor criteria:
- Fever
- Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor)
- Vascular phenomena (maj arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions)
- Predisposition (heart condition or IVDU)
- Microbiological evidence (+ blood culture but not meeting major criteria or serologic evidence of active inf w/ org consistent with IE)
Which beta blockers can be used in treatment of HF
Bisoprolol
Carvedilol
Nebivolol
Metoprolol (modified release)
Components of the CHADS2 score
Congestive HF Hypertension Age> 75 DMT2 Stroke or TIA symptoms
Chest pain history timing differentials
Seconds: Musculoskeletal/non cardiac
Minutes: ACS, GORD, musculoskeletal
Hours: all
Days (dull, persistent): not ACS
Chest pain history associated symptoms differentials
Nausea/vomiting: ACS, upper GI pathology
Sweating/clammy: ACSS, PE, aortic dissection
SoB: ACS, resp causes
Hypotension/syncope: PE, ACS, aortic stenosis
ECG paper:
Time of small square and big square
Small: 0.04 sec
Big: 0.2 sec
Which leads on ECG look at:
- inferior part of the heart
- lateral part
- anterior
- septal
Inferior: II, III and aVF Lateral: V5, V6, aVL, I Anterior: V1, V2 Septal: V3, V4 AVR: right atrium (always neg deflection)
How long should each part of the ECG be?
PR interval: 3-5 small squares/ 120-200 ms
QRS complex: < 3 ss/ <120ms
QT interval: female 350-470ms/ male 350-450ms (no more than 2 big squares)
Diagnostic investigations for angina chest pain
(Resting 12 lead ECG (if can’t exclude stable/unstable angina from clinical history))
(Go down first, second, third line of results are inconclusive/non-diagnostic)
First line: 64 slice CT coronary angiography: significant CAD
Second line: non invasive functional testing: reversible myocardial ischemia
—> MPS/ with SPECT
—> stress echo
—> first pass contrast enhanced magnetic perfusion
—> MRI for stress wall motion abnormalities
Third line: invasive coronary angiography
Type of systolic murmurs
Tricuspid/mitral regurgitation
Aortic/pulmonary stenosis
Mitral valve prolapse
Types of diastolic murmurs
Tricuspid/mitral stenosis
Aortic/pulmonary regurgitation
Which valves close on S1? On S2?
S1: tricuspid/mitral
S2: aortic/pulmonary
Why do we listen to the different places on the chest wall for the heart sounds
Places we expect the blood to travel towards
Describe an aortic/pulmonic stenosis murmur
Systolic ejection murmur S1 then nothing EC (ejection click) Crescendo descrenscendo murmur S2
(Radiates to the carotid: only for aortic stenosis murmur)
Describe a mitral(/tricuspid) regurgitation murmur
Holo/pan sysolic murmur
S1
Flat murmur: no change in intensity
S2
Radiates to axilla (mitral)
Treatment of unstable angina and NSTEMI
- Aspirin 300mg
- clopidogrel/ticagrelol + glycoprotein inhibitors (for people at high risk)
- Unstable angina: LMWH
NSTEMI: LMWH, PCI/thrombolyis, angiography/CABG or Fondaparinux (if not planning angiography w/in 24h)
Post MI: ACEi, dual antiplatelet therapy (aspirin + another), beta blocker, statin
Treatment for acute STEMI
- Aspirin +clopidogrel/ticagrelol
- PCI (percutaneous coronary intervention) or fibrinolysis
- give PCI if presenting w/in 12 hours of onset of unprompted if can be delivered w/in 120 minutes of the time fibrinolysis could have been given - After PCI: anti-platelets, ai thrombin drugs? Look into this
How does ACS present
Silent ischemia (in the elderly, T2DM) Stable angina Unstable angina NSTEMI STEMI Heart failure Sudden death
How can an ECG be normal in ACS
Ischemia in circumflex artery (need V7-V9 lead)
Isolated RV ischemia (V3R and V4R leads)
Transient episodes of bundle branch block
What is the drug treatment for ACS
Anti-ischemic agents (beta blockers, nitrates, Ca channel blockers, nicorandil, ivabridine, ranolazine)
Antiplatelet agents (aspirin, P2Y12 receptor inhibitors)
Anticoagulants (LMWH, factor Xa inhibitors, inhibitors of coagulation)
Long term management of ACS
Aspirin for life + another antiplatelet therapy (for 12 months) Statins Beta blockers (if LVEF<40%) ACEi (to all) Aldosterone antagonists (if LVEF<35%) Secondary prevention (lifestyle)
Which arteries are blocked in Inf Ant Lateral MI?
Inf: RCA
Ant: LAD
Lateral: circumflex
Consequences of Vfib
No pulse
Not enough oxygen circulating
Signs and symptoms of Vtach
pulse >120 BPM Palpitations SoB Chest pain Lightheaded/dizzy/syncope
ECG: regular R waves in absence of atrial rhythm, can be broad complex (>3ss) or narrow complex (<3ss)
What does GRACE score calculate?
Estimate admission-6 month mortality for patients with ACS
Takes into account
Age, HR/pulse, systolic BP, creatiine, cardiac arrest on admission?, ST segment deviation on ECG?, abnormal cardia enzymes?, Killip class (CHF,JVP, pulmonary oedema, cardiogenic shock)
What does CRUSADE score calculate?
Stratified bleeding risk post MI
Looks at:
HR, systolic BP, hématocrite, creatinine clearance, sex, signs of CHF at presentation, history of vascular disease or DM
physiological difference between a STEMI and a NSTEMI
STEMI: full thickness of the ventricular wall
NSTEMI: partial thickness of wall affected
type 1 and 2 MI
type 1: spontaneous MI due to ruptured atherosclerotic plaque
type 2: secondary to ischemia due to either increase oxygen demand or decreased supply
NYHA classification of heart disease
Class I: no limitation of physical activity
Class II: sight limitation of physical activity, comfortable at rest
Class III: marked limitation of physical activity, comfortable at rest
Class IV: inability to carry out physical activity without discomfort + discomfort at rest
ACC/AHA stage of heart failure
stage A: at high risk of dvlpt of HF (no abnormalities or signs/symptoms)
stage B: dvlpt structural Heart disease that is strongly associated w/ dvlpt go HF (w/out sign/symptoms)
stage C: symptomatic HF associated with underlying structural heart disease
Stage D: advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy
what are the 5 problems aneurysms can cause
- grow
- burst
- embolise
- compress other structures
- thombose
what is the cutoff for surgery with AAA
5.5 cm in men and 5 cm in women
what is an aortic aneurysm?
swelling of the aorta greater than 1.5 times its normal size
Fontaine description of peripheral arterial disease?
stage 1: asymptomatic
stage 2: intermittent claudication
stage 3: rest pain/nocturnal pain
stage 4: gangrene/necrosis
signs of chronic limb ischemia
lower limb cold, dry skin, lack of hair
pulses diminished/absent
ulceration may occur + dark discolouration of toes or gangrene
(must examine abode for AAA)
symptoms of acute lower limb ischemia?
5Ps: pain, pallor, parasthesia, paralysis, perishing cold
pain unbearable and requires opioids for relief
aetiology of acute limb ischemia
embolic or thrombotic disease (i.e. previously reported symptoms of claudication)
symptoms/signs of ruptured AAA
severe epigastric pain radiating to the back hypotension tachycardia profound anaemia sudden death
management of AAA
- medical: BP, smoking, hyperlipidemia and diabetes + regular ultrasounds
- surgical: graft, stent, endovascular repair (EVAR)
treatment of chronic limb ischemia
- comorbidities (BP, cholesterol, diabetes, smoking, diet etc)
- low dose aspirin or other anti platelets
- angioplasty
when do you do surgical treatment of carotid stenosis
symptomatic patients (in last 6 months) >70% stenosis of ICA
aetiology of aneurysms?
- atherosclerotic
- mycotic (infection of arterial wall)
- infammatory
- connective tissue disorder
- false
where ca you find aneurysms
aortic/iliac
popliteal
visceral (splenic most common)
intracerebral
what shapes can aneurysms be?
fusiform
saccular
causes of aortic dissection
hypertension
connective tissue disease
aneurysm
trauma of the chest
Stanford classification of aortic dissection
- type A: ascending aorta
- type B: descending aorta, distal to left subclavian origin
causes of shock
- hypovolaemia (exogenous losses)
- cardiogenic (intrinsic cardiac pump failure)
- obstructive ( obstruction to cardiac outflow OR restricted cardiac filling)
- distributive (vasodilatation and malperfusion)
examples of hypovolaemic shock
haemorrhage
burns
GI losses
dehydration
examples of distributive shock
- SIRS related (sepsis, pancreatitis, trauma, burns)
- neurogenic (spinal cord injury)
- anaphylaxis
examples of cariogenic shock
- MI/ischemia
- arrythmis
- acute valve pathology
examples of obstructive shock
- tension pneumothorax
- pericardial tamponade
- PE
physiological response to shock
- sympathetic system activated
- adrenal catecholamine release
- compensatory cardiovascular responses
- sodium and H2O retention
- coagulation system activation
- cortisol release
def shock
acute circulatory failure with inadequate or inappropriately distributed tissue perfusion, resulting in generalised cellular hypoxia and/or inability of cells to utilise oxygen
aetiology of shock
- failure of heart to act as effective pump
- mechanical impediments to forwards flow
- loss of circulatory volume
- abnormalities of peripheral circulation
