cv middle tier Flashcards
bradycardia
- put a speed on it
- symptoms
- who is it normal for
- Less than 60bpm daytime and 50bpm night
- Usually asymptomatic
- Normal in athletes due to increased vagal tone and so increased parasympathetic activity
tachycardia
- put a speed on it
- two types
- More than 100bpm
- Supraventricular tachycardias - arise from atrium / AV junction — Atrial fibrillation/ atrial flutter
- Ventricular tachycardias - arise from ventricles
atrial fibrilation
- irregular?
- put a speed on it
- what is happening
- irregularly irregular - chaotic, atrial spasm
- 300-600bpm
- rapid activation of atria by multiple meandering re-entry wavelets. AV node responds intermittently , only a portion of impulses conducted on→ irregular ventricular rate
atrial fibrillation
- persistent
- permanent
- paroxysmal
- recurrent
- acute
- Persistent = continuous for 7days+, not self terminating
- Permanent = long term
- paroxysmal = self-terminating within 7 days
- Recurrent: two + episodes
- Acute = onset on last 48h
atrial fibrillation
- gender
- commonness
- age
- m>f
- most common arrythmia
- old
atrial fibrillation risk factors
- 60y+
- Diabetes
- Hypertension
- Coronary artery disease
- Previous MI
- Structural heart disease (valve/congenital defects)
atrial fibrillation causes/ risk factors
cardiac
- Increased atrial pressure, increased atrial mass, atrial fibrosis/ inflammation/ infiltration
- Hypertension
- Heart failure
- MI
- Coronary artery disease
- structural heart disease inc Valvular
- Cardiac surgery
- Cardiomyopathy
- Rheumatic heart disease
non cardiac
- Acute excess alcohol intoxication, exposure to caffeine tobacco etc
- hyperthyroidism
- chest infection
- age
- DM
atrial fibrillation symptoms
- None at all /
- Dizziness
- Palpitations
- Syncope
- Chest pain
- Heart failure
- Fatigue
atrial fibrillation ecg
- Rapid, irregular QRS,
- Absent p waves - jaggedy
- No steady isoelectric baseline
atrial fibrillation/ flutter treatment
treat precipitating cause
control ventricular rate
- beta blockers
- CCB
- digoxin
- amiodraone
- lidocaine
restore sinus rhythm
- cardioversion (electricla DC shock)- defibrillator
catheter based therapy – ablate/ destroy cells
do CHADVASC (Stroke risk) to see if anticoagulation medication needed
why is verapamil (phenylalinine CCB) more effective than amlopifine (dihydropiridine CCB)?
dont act on calcium channels at rest
which beta blocker is best for post MI arrythmias and why
propanolol
additional quality of blocking sodium channels
cardioversion is associated with what risk
so what is given alongside
risk of thromboembolism, so need to give LMW heparin
lidocaine action
blocks the inactivation gate of Na channels so prolongs inactivation meaning higher depolarization threshold and early action potentials less likely to get through
for arrythmias (vent trach)
digoxin action
Slows HR
Increases contractility
atrial fibrillation complications
Sudden death Syncope (fainting) Heart failure Chest pain Dizziness Palpitations Stroke
atrial flutter
- irregularity
- put a speed on it
- what is happening
- regularly irregular, organised but rapid
- 250-350bpm
- Due to re-entry circuit in RA from AV back to sinus
atrial flutter ecg
“saw tooth” ECG
Narrow tachycardia
Flutter waves
.
.
atrial flutter symptoms
Dizziness breathlessness Palpitations Syncope Chest pain Heart failure Fatigue
heart block
- brady/tachy
- what is happening
- which part of ecg is changed (what is normal)
- brady
- Conduction issue- signals not properly propogated from SAN to AVN to His-Purkinje system
- PR interval. normal is 120-200ms. heart block= greater
first degree heart block symptoms
asymptomatic
second degree mobitz type 1 symptoms
lots asymptomatic
light headed
dizzy
syncope
second degree mobitz type 2 symptoms
less likely to be asymptomatic light headed dizzy syncope chest pain SOB postural hypertension
third degree heart block symptoms
syncope fatigue - extreme chest pain breathlessness confusion palpitations brady
first degree heart block
- what is it
- causes
- 1:1 a:v (each is conducted but slower than normal, no dropped beats )
- PR interval prolonged, PR intervals are constant
- block in AV node – delay
- Hypokalemia
- Myocarditis
- Inferior MI
- AVN blocking drugs (B blockers, CCB, digoxin)
second degree heart block - mobitz type 1
- aka
- what is it
- causes
- wenckebach
- AVnode issue
- PR interval increases progressively, then a failure of a P wave proper conduction so a ‘dropped’/missing QRS wave (then reset)
- AVN blocking drugs (B blockers, CCB, digoxin)
- inferior MI
heart block treatment and when
only need treatment if symptomatic
- transcutaneous pacing (TCP) to restore heart rate (temporary)
- pacemaker (permenant ) may follow
second degree heart block- mobitz type 2
- what is it
- causes
- Distal conduction issue
- PR interval lengthened but no PR interval change - it is constant. then a beat is dropped (missing QRS-P wave not conducted)
Anterior MI mitral valve surgery SLE, lyme disease rheumatic fever
third degree heart block
- what is it
- causes
- 3rd degree is no relation between a and v - they contract independently- so P and QRS appear independent.
- Constant p to p intervals. Constant q to q intervals. They are constant with themselves, but independent of the other
- Large space between each QRS.
- P waves may be buried in the QRS complex so can be hard to distinguish - look for intervals as said above
Structural heart disease ischaemic heart disease hypertension endocarditis lyme disease
bundle blocks
- a:v ratio
- what is the pathology
- ecg looks like?
- 1:1
- No depolaristation down L or R branch so one side of the heart is delayed as the depolarisation has to spread across the septum from the other ventricle
- Broad QR
LBBB
ecg
sound
causes
wiLLiam
W in v1
M in v6
L eaving each other
Reverse splitting of second heart sound
- Ischaemic heart disease
- aortic valve disease
RBBB
ecg
sound
causes
maRRow
M in v1
W in v6
R eaching towards each other
Splitting of second heart sound
- Pulmonary embolism
- ischaemic heart disease
- atrial/ ventricular septal defect
supraventricular tachycardia
- age
- arises from where
- Young patient (12-30)
- Arises from atria / atrioventricular junction
slow fast AVNRT means?
atria contract slowly then fast in different cycles
AVNRT = AV nodal reentrant tachycardia
wolf parkinson white pathophysiology
AVRT
- Accessory pathway = bundle of Kent. bypasses the AV node (which normally slows/delays conduction) so this causes early abnormal depolarisation of part of the ventricle (=pre-excitation)
- Pre excitation = short PR interval, wide QRS
- Circuit loop = down normal pathway (AVN) as accessory bundle of kent is in refractory period, depolarizes ventricles and up bundle of kent accessory pathway (now out of refractory period) so impulse back to atria and down AVN again – reentry circuit
this is AVRT (AV reentrant tachycardia )- not AVNRT - no node!
AVNRT/AVRT treatment
- Hold breath / carotid massage
- Adenosine (temporary rapid heart block - stops loops)
- Surgical ablation of accessory pathway(AVRT) / modification of slow pathway (AVNRT)
- pacemaker
AVNRT/AVRT
- supravent/ vent
- tachy/brady
supraventricular tachy
AVNRT pathophysiology
- AV nodal reentrant tachy AVNRT:
- One of the conducting pathways in AV node is fast, the other is slow
- -Fast one is used preferentially. If an impulse is early, the fast one may still be in the refractory period, so the slow one is used and propagates signal to ventricles
- -This impulse travels back up fast pathway (now out of refractory period) and goes down slow pathway again (now out of refractory period)
- This sets up re-entrant loop
prolonged QT syndrome
- =
- causes
- presentation
Ventricular repolarization (QT interval) is greatly prolonged
Congenital
- Jervell-lange-nielsen
- romano-ward
Acquired
- Hypokalemia
- hypocalcaemia *
- drugs (amiodarone (antiarrhythmic), antidepressants)
- bradycardia
- acute MI
- diabetes
Syncope
palpitations
aortic aneurysm risk factors
Hypertension Age Smoking bicuspid/unicuspid aortic valves Atherosclerosis Renal failure Previous aneurysm Family history Male COPD Hyperlipidemia
aortic dissection risk factors/ causes
Male
Age
Atherosclerosis
Genetics
Inherited Degenerative Atherosclerotic Inflammatory Trauma
what is aortic aneurysm
where
types
- permanent dilation of artery to twice the normal diameter
- can be abdominal or thoracic
- can be true (ruptured or unruptured) or false (psuedoaneurysm)
true aneurysm
Abnormal dilation involves all layers of arterial wall
Loss of elastic lamellae
Smooth muscle cell loss
Is abdominal aortic aneurysm AAA true or false
true
two types of true aortic aneurysm
- symptoms
unruptured
- often asymptomatic, picked up with routine xray etc
- Pain in abdomen /back/ loin/ groin
- Pulsatile abdominal swelling
ruptured
- Pronounced pulsatile abdominal swelling
- Collapse
- Hypotension
- Tachycardia
- Anemia
- Sudden death
what makes a person more likely for their aortic anuerysm to rupture
more likely if
high BP,
female,
smoker,
family history
psuedoaneurysm / fake aneurysm
collection of blood in the adventitia (/ tunica externia , outer layer) -
like a pocket of blood causing a bulge out the side of the vessel rather than the whole wall thickenness being deviated
aortic dissection =
the wall comes apart- the intima and media seperate :
- tear in intima / media
- blood enters wall –> haematoma
- intima (And sometimes part of media) comes away
- secondary blood flow, false lumen in the wall
- true lumen is narrowed
direction of dissection
two type systems
anterograde = towards bifurcation, further downstream (in direction of blood)
retrograde = towards aortic root, backwards
DeBakey
1 . ascending and descening (lots of aorta involved)
2. ascending (proximal aorta)
3. descending (distal)
stanford
A. first part of aorta involved (solo or + distal)
B. only distal aorta invo
aortic dissection symptoms / signs
- Hypertension (some present with hypo but more hyper)
- Unequal BP in each arm maybe
- Acute limb ischaemia
- May have hemorrhagic shock
- Peripheral pulses absent maybe
- syncope, MI, stroke
- Sudden onset of severe central chest pain (ripping /stabbing / tearing pain)
- Radiates to back and down arms
aortic aneurysm / dissection investigations
- CT
- MRI
- US
- Xray
- echo - transoesophageal /aortagraphy (contrast xray) to locate anuerysm
Aortic aneurysm management
- Monitor small aneurysms
- Treat underlying causes/risk factors inc smoking cessation
- Control BP
- Lower lipids
- Surgical repair
aortic dissection management
Antihypertensive -- Beta blockers -- GTN Analgesia Surgery -- replace aortic arch -- Stents
PVD
- commonness
- age
- most common where
- common
- old- 80+
- most common near vessel bifurcation
- most common in legs, esp femoro popliteal region (lower thigh/knee)
PVD risk factors / causes
Risk factors for atherosclerosis (thrombus) –> stenosis
- Smoking, high glucose, lipids, cholesterol , obesity, low activity, high blood pressure
Genetics
- vasculitis –> plaque
- collagen disease –> weakened walls –> aneurysm
- – Marfan, Ehlers danlos
- arteriomegaly
embolus also (often from heart / atherosclerotic plaque)
where is the most common aneurysm location
infrarenal, abdominal aorta
PVD pathophysiolology
- narrowing of arteries distal to the aorta
- reduced blood supply so ischaemia/ infarction
- The tissue ischaemia is often distal to the pathology
Narrowing
- Claudication (intermittent)
Blockage
- Critical limb ischaemia (chronic, narrowed over time)
- Acute limb ischaemia (acute - from thrombosis /embolism) – Limb threatening
PVD mortality
high
increases with time/ severity of PAD
acute limb ischaemia (limb threatening) symptoms
6 P'S pulseless palor perishingly cold pain (claudication, angina) paraesthesia paralysis
claudication
- type of pain
- where
- cause
- intermittent, on exercise
- thigh/calf / buttock (not foot)
- Due to oxygen demand outdoing supply, blood supply barely allows basal metabolism and so no reserve left for exercise. Lactic acid production - anaerobic
calf claudication suggests?
femoral PVD disease
buttock claudication suggests
iliac PVD disease
iliac PVD presents as
buttock claudication
femoral PVD presents as
calf claudication
moderate/ severe PVD presentation
complications
moderate
- claudication
- angina
severe
- critical limb ischaemia
- – rest pain, gangrene, ulceration, infection
- acute limb ischameia
- – 6 p’s
stroke/TIA, amouris fugax
abdominal aortic anyuerysm
what may post-prandial pain and weight loss/fear of eating be due to?
stenosis in gut arteries (coeliac, superior/inferior mesenteric)
critical limb ischaemia
- chronic/acute
- where
- symptoms
- chronic
- legs often
- Rest pain (esp night – horizontal = less flow due to gravity. Relieved when hung over bed/sitting) - blood supply barely allows basal metabolism so no reserve for increased demand. May need to sleep sitting in a chair
- Gangrene
- Ulceration/ infection
PVD investigations
Bloods
- Looking at risk factors of atherosclerosis
- Glucose
- Lipids
- Vasculitis screen
- BP
- ESR/CRP to exclude arteritis / vasculitis
- FBC to exclude hematologic disorders
Buerger’s angle
- Assess arterial supply
- Raise leg slowly with them lying flat on bed
- The point when their leg goes pale is buerger’s angle (the smaller the angle, the more severe the disease)
- <20 degrees
Capillary refill time
- Assess arterial supply
- > 15 second
Imaging the vessel
- Doppler ultrasonography
- — site and extent of blockage , also looks for blood flow
- — Harder to do deeper vessels eg renal
- CT/MRI
ECG - many patients also have coronary artery disease
what investigations can GP do to assess arterial supply
capillary refill time
- should be less than 3 secs.
- pvd =more than 15? - temperature affects
buerger’’s angle
- Raise leg slowly with them lying flat on bed
- The point when their leg goes pale is buerger’s angle (the smaller the angle, the more severe the disease)
- <20 degrees
PVD management
Reduce risk factors
- Diet
- Exercise prescribed (programmes, encourage them to the point of maximum pain)
- Weight loss
- Smoking cessation
- Statins
- Even if normal/low cholesterol + one other risk factor
- Control of diabetes
- Control of hypertension
Antiplatelets
Revascularization for critical ischaemia
- Stent
- Bypass
- – Especially for long occlusions
- – vein>prosthetic
- Endarterectomy = surgical removal of plaque/ obstructive deposits, commonly in the carotid
Amputation
- Unreconstructable vessel plumbing or irreversible ischaemia
Heparin post op
pericarditis causes
- Idiopathic
- Virus (adenovirus, enterovirus) / Bacteria (TB)(immunosuppressed)
- Trauma - injury etc = early onset, after stent etc = delayed onset
- Autoimmune (SLE, RA, sjorgens)
- Neoplastic - secondary metastatic tumours, esp lung+breast
- Aortic dissection
- (fungal- rae)
how common is pericarditis
not that rare
pericarditis =
Inflammation of the pericardium +/- effusion
pericarditis signs
- Fever
- Sinus tachycardia
- Pericardial rub (sound of rubbing leather/crunching snow)= pathognomic
- Signs of effusion
- Becks triad: raised jugular venous pressure, low blood pressure, quiet heart sounds
beck’s triad =
- raised jugular venous pressure
- low blood pressure
- quiet heart sounds
pericarditis symptoms
Chest pain -- Severe -- Sharp -- Pleuritic -- Rapid onset -- Left anterior chest /epigastrium, trapezius ridge! (superior bit between shoulder and neck) -- Radiates to arm -- Relieved by sitting forward, exacerbated by lying down !! -- This is very specific Dyspnea Cough Viral symptoms - preceding/during -- Fever -- Rash -- Joint pain (hiccups)
pericarditis diagnosis
other investigations
Diagnosis = 2 of
- ECG
- – saddled ST elevation (no ST depression in reciprocal leads)
- – PR depression
- Pericardial effusion
- Friction rub
- Chest pain
- bloods (high wbc, SLE ANA+, troponin indicated myopericarditis)
- CXR (assoc with pneumonia)
- Echo
pericarditis ecg
- – saddled ST elevation (no ST depression in reciprocal leads)
- – PR depression
pericarditis management
Anti inflam
- NSAIDs/aspirin
- Colchicine
- This reduces recurrence but severe diar/vom side effects mean patient rarely take for full course
restrict physical activity
for athletes
- sedentary rest for 3m until symptoms/ ECG resolves
tamponade
- pathophysiology
- acute/ chronic
- treatment
- Fluid build up in pericardium
- Thickening and reduced stretch of pericardium means limited stretch
- Heart compressed
- Filling of heart is reduced
- Compliance is reduced
- Stroke volume is reduced, low CO
- Blood pressure is reduced!
- high pulse
- Left side fills less than right side to left pressure drops?
acute/chronic (either)
Treatment
- life threatening
- keep heart strong and fast
- drainage, if effusion (pericardiocentesis)
- treat underlying cause eg antibiotics
normal amount of fluid between inner visceral and outer parietal pericadium
50ml
constrictive pericarditis =
causes
- pericardium becomes thick, fibrous, calcified
- interferes with diastolic filling
- chronic
- bacterial infection, TB
- rheumatic heart disease
- can occur after any pericarditis
A man enters A&E with severe acute pleuritic chest pain that radiates to the ridge of the trapezius. The pain is worse on inspiration and on lying flat, but is relieved by sitting forward. He also has hiccups. what is it
acute pericarditis
why are hiccups involved in pericarditis
if phrenic nerve involved
how do you differentiate ST elevation in STEMI vs pericarditis
pericarditis = in all leads
STEMI = elevation in leads depending on infarcted area eg anterior
STEMI = pain radiates to arm, jaw neck
pericarditis= pain radiates to trapezius ridge (superior bit between shoulder and neck). pain relieved by sitting forward
valve disease gender
m>f
BUT mitral regurgitation is f>m
which valve is the mitral valve
AV one, L side
this is the only one with two rather than 3 flaps
(R= tricuspid, aortic/ pulmonary valves )
aortic stenosis pathophysiology
Obstructed LV outflow → increase LV pressure → compensatory LV hypertrophy → ischaemia, it exhausts, function decline → angina, arrhythmia, LV failure
aortic stenosis causes
- Degenerative calcification - of aortic valve
- Rheumatic Heart disease
- Congenital bicuspid aortic valve
symptoms of aortic stenosis
- Syncope
- Angina
- Dyspnoea
- Sudden death
signs of aortic stenosis
- Ejection systolic murmur
- Slow rising pulse (pulsus tarud)
- Sustained apex beat
- 4th heart sound
- Soft 2nd heart sound
aortic stenosis investigations
- Echo - shows valve’s area, LV size and function, pressure gradient
- ECG - LV hypertrophy, any blockages
- CXR - LV hypertrophy, calcified aortic valve
aortic stenosis management
Surgery, if symptomatic/severe
- TAVI - transcutaneous aortic valve implantation – balloon inflated to crack calcification + stent with new valve placed over top
- Percutaneous angioplasty (ballooning)
Infective endocarditis prophylaxis
aortic regurgitation causes
- Bicuspid aortic valve
- Rheumatic heart disease
- Infective endocarditis
- Marfans
- Aortic dissection
aortic regurgitation pathophysiology
aortic valve fails to prevent backflow of blood during diastole → LV hypertrophy and LV dilatation due to combine volume and pressure overload
aortic regurgitation symptoms
- Angina
- Dyspnoea
- Palpitations
- LV failure (and its signs/symptoms)
aortic regurgitation signs
- Water-hammer (collapsing) pulse - forceful. it rapidly increases then collapses
- Displaced and hyperdynamic apex beat
- Early diastolic murmur
- Austin flint murmur
- Head bobbing (deMussets sign, along with pulse)
aortic regurgitation investigations
- ECG - LV hypertrophy
- X ray - cardiomegaly, pulmonary oedema, aortic root enlargement
- Echo - LV hypertrophy
aortic regurgitation management
- Mild = vasodilators
- Severe = valve replacement
- Infective endocarditis prophylaxis
mitral stenosis causes
- Rheumatic heart disease (strep) = most common
- Infective endocarditis
- Mitral valve calcification
- Congenital
mitral stenosis pathophysiology
Obstruction of LV inflow → LA pressure rises, dilatation, hypertrophy → pulmonary congestion → can lead to AF and right heart failure
mitral stenosis symptoms
- Breathlessness
- Fatigue
- Palpitations
- Chest pain
- PND - paroxysmal nocturnal dyspnoea
- Orthopnoea- SOB when lying
- Hemoptysis
- Recurrent chest infection
mitral stenosis signs
- AF
- Tapping apex beat
- Malar flush (cheeks)- due to decreased Cardiac output, increased CO2 retention
- Low volume pulse
- Signs of rheumatic heart failure
- Loud first heart sound
- Opening snap (= sound at beginning of diastole, could be called early diastolic maybe)
- Rumbling mid-diastolic murmur
mitral stenosis investigation
- Echo - valve mobility/ area, pressure gradient
- CXR - enlargement and pulmonary congestion/ oedema
- ECG - AF, LA enlargement
mitral stenosis management
- Manage AF (anticoagulate, B blockers, diuretics, digoxin)
- Valvotomy (incisions in valves/ ballooned open)/ replacement
mitral regurgitation causes
- Myxomatous degeneration (MVP) → floppy mitral valve → Mitral valve prolapse
- Rheumatic heart disease
- Infective endocarditis
- Ischaemic mitral valve
- Papillary muscle dysfunction / rupture
- Dilated cardiomyopathy
- Marfans
- Ehler danlos
mitral regurgitation pathophysiology
Regurgitation into the LA → increased LA pressure → LA enlargement, dilatation, LV hypertrophy (less blood so needs more pump to maintain CO).
mitral regurgitation symptoms
- Palpitations
- Dyspnoea
- Orthopnoea
- Fatigue
- Right heart failure
mitral regurgitation signs
- Laterally displaced
- Hyperdynamic
- Systolic thrill
- Soft 1st heart sound
- Loud pan-systolic murmur at apex radiating to axilla
- Third heart sound
mitral regurgitation investigations
- ECG - LV hypertrophy, palpitations
- Echo- LV hypertrophy, valves, LA enlarged
- Xray- LA enlarged, central pulmonary artery enlargement (feeding into L side)
mitral regurgitation management
- Echo monitoring
- Infective endocarditis prophylaxis
- Valve replacement
- AF treatment (anticoagulate, B blockers, diuretics, digoxin)
infective endocarditis pathophysiology
- Infection of heart valves or other endocardial lined structure
- infection spreads in blood
- mainly bacteria
why is medication not very good for valve diseases
mechanical issue so medication not v good
infective endocarditis causes
- prosthetic valves
- septal defects
- pacemaker leads
- surgical patches
why is the infective endocarditis types: L/R native but only L prosthetic
R sided surgery is rarer
infective endocarditis epidemiology
- V young/ old
- IV drug abusers
- Congenital heart disease (young)
- Prosthetic valves
- Males (more valve operations)
- Rare
- Poor dental hygiene/ teeth abnormality
infective endocarditis symptoms/signs
- Night sweats,
- fever
- Elevated INR
- Petechial rash
- Janeway lesions - small non tender purpley/red macular lesion on fingers and hands
- Splinter hemorrhages - vertical short red lines under nail
- Osler’s nodes- tender purple dots on subcutaneous digits
- Roth spots = on eye
- Clubbing
infective endocarditis complications
- may present as symptoms
- Embolisation (stroke, PE, MI, bone infections, kidney dysfunction)
- Arrhythmias , heart failure (due to valve dysfunction)
- Abcesses
infective endocarditis diagnosis/investigations
- Vegetation seen in echo
- – 2D TTE (transthoracic echo) not 100%.
- – Transoesophageal echo more sensitive but need probe down throat
- Bugs grown in blood cultures (not present in 2-5% due to previous antibiotic use)
- Fever
- Predisposition - history
- Raised CRP (liver protein, marker of inflammation)
- ECG- ischaemia, infarction, new heart block
- Negative results dont exclude (in isolation)
infective endocarditis treatment
- Antimicrobials IV for 6w, based on culture sensitivity findings- to make sure treatment effective
- Treat complications (eg arrythmias)
- Surgery - if cannot cure with antimicrobials alone (CRP doesn’t fall, infection comes back) OR if severe complications OR large vegetations that may embolise
- Remove infected devices / valves, and replace
what lifestyle management is key for valve diseases and why
Fastidious dental hygiene to reduce risk of infective endocarditis
