cardiology Flashcards
(192 cards)
1
Q
What happens to the ductus arteriosus days after birth?
A
usually closes within a few days, becoming a fibrous cord called the ligamentum arteriosum
2
Q
what is depression in the right atrium of the heart that’s a remnant of a fetal opening?
A
fossa ovalis
3
Q
what connects the papillary muscles to the atrioventricular valves?
A
chordae tendineae
4
Q
what are the layers of the heart?
A
endocardium > myocardium > epicardium (visceral layer of serious pericardium) > pericardial cavity > parietal layer of serous pericardium > fibrous pericardium
5
Q
where does the coronary sinus drain blood into?
A
right atrium
6
Q
where is the coronary sinus?
A
sits in the atrioventricular groove posteriorly
7
Q
describe the layers of blood vessels
A
tunica intima (endothelial cells) > internal elastic membrane > tunica media (muscle) > external elastic membrane > tunica adventitia (supportive connective tissue)
8
Q
where do you auscultate for each heart valve?
A
aortic valve = 2nd right ICS sternal edge
pulmonary = 2nd left ICS sternal edge
tricuspid = 4th left ICS sternal edge
mitral = 5th left ICS midclavicular line
9
Q
what is stroke volume?
A
volume blood pumped out of the left ventricle during each systolic cardiac contraction
10
Q
how to calculate CO
A
CO = HR x SV
11
Q
what is SVR?
A
- systematic vascular resistance
- main site = ARTERIOLES
12
Q
What controls SVR?
A
extrinsic factors (sympathetic nerves fibres - noradrenaline acting on alpha receptors, vasomotor tone)
intrinsic factors (chemicals, vasodilation - increased CO2 , decreased 02, histamine, bradykinin, NO) (vasoconstriction caused by serotonin, leukotrienes, endothelin)
13
Q
how to calculate MAP?
A
MAP = CO x SVR
MAP = DBP + 1/3 pulse pressure
pulse pressure = SBP - DBP
14
Q
what is MAP?
A
the average arterial pressure throughout one cardiac cycle, systole, and diastole. MAP is influenced by cardiac output and systemic vascular resistance
15
Q
what is the definition of the frank-starling curve?
A
stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction.
16
Q
explain the physiology of cardiac muscle?
A
Striated, has no neuromuscular junctions just gap junctions (cell-to-cell excitations)
Desmosomes provide mechanical adhesion between cells and tension is transmitted
Made of muscle fibres that each contain many myofibrils
Myofibrils contain ACTIN (thin) and MYOCIN (thick)
These are arranged into SACROMERES
Muscle Fibre > Myofibril > ACTIN (thin) + MYOCIN (thick) [arranged into sarcomeres]
16
Q
explain. the path of the electrical activity from the SA node
A
SA node > Atrials > AV node > bundle of his > punkinje fibres > ventricles
17
Q
explain the phases of the pacemaker action potential
A
Phase 0 = depolarisation
Activation of L-type Ca channels opening resulting in calcium influx
Phase 3 – repolarisation
Calcium channels close
Activation of K+ channels resulting in potassium efflux
Phase 4 – slow depolarisation
Funny current – mixed Na/K inward current resulting in slow depolarisation
This stage is important to determine HR
Lots of drugs affect this stage of the pacemaker potential
Adenosine – decreases HR
Catecholamines – increase HR
18
Q
explain the phases of the cardiac action potential
A
Phase 0
Depolarisation due to Na influx
Phase 1
Closure of Na channels and transient K efflux
Phase 2 - Plateau phase
Ca++ influx through L-type Ca++ channels
Phase 3
Closure of Ca channels and K efflux
Phase 4
Resting potential due to K efflux
19
Q
where do you places the limb leads for an ECG?
A
Right arm – red
Left arm- yellow
Left leg- green
Right leg- black
(RIDE YOUR GREEN BIKE)
20
Q
how long does the QRS complex last in an ECG?
A
0.12s
21
Q
describe the limb leads of an ECG
A
LEAD 1 = RA (-) to LA (+)
LEAD 2 = RA (-) to LL (+)
LEAD 3 = LA (-) to LL (+)
22
Q
How do you read an ECG?
A
- Is there electricity activity present
- Is the rhythm regular or irregular
- What is the HR (next slide)
- Are P waves present
- What is the PR interval (0.12 - 0.2s)
- Is each P wave followed by a QRS complex?
- Is the QRS duration normal (<0.12s)
23
Q
How do you work out the heart rate using in an ECG?
A
300/ number of large squares between 2 consecutive R waves (if rhythm is regular)
count number of R waves in a ten second period (normal rhythm strip) and then times by 6
24
explain axis deviation
'left axis 1'
left axis - lead 1 positive, avF lead negative
right axis - lead 1 negative, avF positive
extreme right axis - lead 1 negative, avF negative
25
explain sympathetic innervation of the heart
- supplied via cardiac sympathetic nerves
- cardiac nerves sympathetic supply: SA node, AV node & Myocardium
- sympathetic stimulation increases HR and force of contraction - increases b rate of firing from the SA node and decreases AV node delay
Sympathetic > positive chronotropic and inotropic
26
what is the neurotransmitter for sympathetic innervation
noradrenaline via b1 receptors
27
explain parasympathetic innervation of the heart
supplied via the VAGUS NERVE
- reduces HR via lowering firing from SA node
- increasing AV nodal delay
- negative chronotropic effect (rate)
28
what is the neurotransmitter used in parasympathetic innervation?
acetylcholine via muscarinic M2 receptors
29
should you avoid using ACEi with pregnancy?
yes
30
what is a side effect os an ACEi?
dry cough
31
what does ACEs block?
blocks angiotensin converting enzyme.
- prevents angiotensin II production from angiotensin I
32
what do ARBs block?
Block angiotensin II at the level of the receptor
33
do ARBS cause a dry cough?
no
34
how does each heartbeat begin?
flow of ions across the plasma membrane of the specialised cardiac pacemaker cells within the SA node
35
how do pacemaker cells generate action potentials spontaneously?
due to their membrane potential being unstable (the membrane potential never rests)
36
what are the side effects of calcium channel blockers?
swollen ankles = peripheral oedema
37
what are the 2 classes of calcium channels blockers (+ an example)
dihydropyridines - nifedipine and amlodipine
non-dihydropyridines - verapamil and diltiazem
38
what are dihydropyridines used for?
relax and widen arteries
- used in angina and hypertension
39
what are non-dihydropyridines used for?
- help to control certain fast heart rhythms such as AF & SVT
- because they block calcium going into the conducting cells in the heart, which slows the heart down.
- used in hypertension and angina
40
what are non selective beta blockers? (+ an example)
block B1 & B2 receptors
slow down heart rate, contractility and conduction velocity
- propanolol, carvedilol
41
what are cardio-selective beta blockers? (+ an example)
only block B1 receptors (receptors in the heart)
used in angina, MI, ACS, hypertension and heart failure
- bisoprolol & atenolol
42
how do loop diuretics work and what are they used for?
inhibit Na-K-Cl cotransporter in the thick ascending loop of henle in the kidney
- used in HEART FAILURE
43
example of a loop diuretic
furosemide
44
what are the side effects of loop diuretics?
low Na/K
Gout
ototoxicity (ear poisoning)
45
how do thiazide diuretics work and what are they used for?
inhibit sodium reabsorption in the distal convoluted tubule
mainly used for hypertension
46
what are the side effects of a thiazide diuretic?
low Na/K
Gout
Hyperglycaemia (high blood sugar)
47
example of a thiazide diuretic?
bendoflumethiazide
48
what is the drug mechanism of statins?
inhibits HMG-CoA reductase
reduces hepatic cholesterol synthesis
49
what are the side effects off statins?
myalgia and rhabdomyolysis
50
when do you discontinue statins?
- pregnancy
- if patient is on macrolide antibiotics (erythromycin & clarithromycin)
51
what must you do before going on statins?
must take baseline liver function test before commencing treatment with 3 and 12 month follow up
- stop if 3x increase in ALT (alanine aminotransferase, an enzyme that helps assess liver health)
52
how is Digoxin a positive ionotropic?
Digoxin binds to the sodium-potassium pump in the heart muscle cell membrane
This blocks the pump, causing sodium to build up inside the cell
The sodium-calcium exchanger moves sodium out of the cell in exchange for calcium
The increased calcium in the cell makes the heart muscle contract more forcefull
53
how is Digoxin a negative chronotropic?
Digoxin also increases vagal activity through its action on the central nervous system, thus decreasing the conduction of electrical impulses through the atrioventricular (AV) node.
This negative chronotropic effect (slowing of heart rate) is important for its clinical use in different arrhythmias.
54
what is the drug action of Atropine?
anticholinergic - blocks acetylcholine
increases the rate of discharge by the sinus node, enhances conduction through AV junction and accelerates the HR, and improves CO
55
when is Atropine used?
sinus bradycardia
56
what are class 1 anti-arrhythmic drugs?
- reduce Na channel current
- used for rhythm control
- action potential stage 0
- lignocaine, quinidine, propaferone
57
what are class 2 anti-arrhythmic drugs?
B-Adrenergic antagonists
- used for rate control
- action potential stage 4
- propranolol, bisoprolol
58
what are class 3 anti-arrhythmic drug?
action potential prolongation
- used for rhythm control
- action potential stage 3
- amiodarone, sotalol
59
what are class 4 anti-arrhythmic drugs?
Ca channel antagonists
- used for rate control
- action potential stage 2
- verapamil
60
what are the 4 types of shock?
- cardiogenic
- obstructive
- hypovolemic
- distributive
61
what is cardiogenic shock?
heart doesn't work properly = decreased CO and MAP
- MI, drug toxicity, arrhythmia, myocarditis, valve disease
62
what is hypovolmeic shock?
losing flood = decreased MAP
- bleeding, vomiting, diarrhoea, burns
63
what is obstructive shock?
Action of pump is physically limited by pressure = decreased CO & MAP
- inside of circulation (PE)
- outside of circulation (tamponade, pneumothorax)
64
what is distributive shock?
excess vasodilation and leaking of fluid at capillaries = decreased MAP
65
what are the 2 types of distributive shock?
- Neurogenic, nerve damage cuts out sympathetics
- Vasoactive, (anaphylaxis and sepsis) systemic overactive immune response
66
what is the gold standard for testing for hypertension?
ABPM
- ambulatory blood pressure monitoring
>140/90 in clinic
> 135/85 ambulatory
- if systolic >180 consider same day referral
67
what are the target blood pressure values for hypertension?
140/90 if <80 years old
150/90 if >80 years old
68
what is the blood pressure target for a diabetic with hypertension?
aim for 135/85
69
what are the blood pressure values for stages of hypertension?
stage 1 - 140/90
stage 2 - 160/100
stage 3 (severe) - 180/110
malignant - diastolic >130
70
what are the symptoms of a very high BP?
headache
visual disturbances
seizures
71
how do we check for end organ damage in hypertension?
- Fundoscopy: to check for hypertensive retinopathy
- urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
- ECG: to check for left ventricular hypertrophy or ischaemic heart disease
72
Describe syncope
- a common cause of transient loss of consciousness (TLOC)
- Resolves quickly (not cardiac) - danger comes from the FALL
- due to sudden trigger causing cerebral hypo perfusion
73
what are the 3 types of syncope?
reflex
orthostatic
cardiac
74
what are the 3 types of reflex syncope?
vasovagal - most common 'the faint'
- prodrome of pale, sweaty and nausea
- caused by dehydration, standing too long & emotional stress
situational (uncommon) - specific trigger (e.g cough, urinating, swallowing)
carotid sinus reflex - bifurcation of the common carotid
- it contains baroreceptors
- direct stimulation (tight collar, shaving) causes sympathetic tone to decrease
- assumes more pressure is due to increasing HR so compensates through decreasing HR
75
what is orthostatic syncope?
'postural hypotension'
- standing causes BP drop
- baroreceptor reflex corrects this normally
- this reflex can work insufficiently due to age, mediation & prolonged bed rest
76
what is cardiac syncope?
MOST DANGEROUS
- as can result in death
- caused by arrhythmias, MI, structural diseases
Red flags = EXERTION, SUPINE AND PALPITATIONS
77
what is virchows triad?
thrombosis is caused by hyper coagulability, endothelial injury, stasis of blood
78
what are the risk factors for venous thromboembolism?
Immobility
Surgery
Pregnancy
Long haul flights
Malignancy
Oestrogen therapy (COP, HRT)
79
describe the symptoms of a DVT
- Leg swelling
- Leg pain, cramping or soreness that often starts in the calf
- Change in skin colour on the leg — such as red or purple, depending on the colour of your skin
- A feeling of warmth on the affected leg
80
describe the symptoms of a PE
- chest pain
typically, pleuritic
- dyspnoea
- haemoptysis
- sinus tachycardia
- tachypnoea
- in a respiratory examination
classically the chest will be clear
81
what is the scoring system used for PEs and DVTs?
Wells scoring system
82
explain the steps of atherosclerosis
Initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
This results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
Monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large foam cells'. As these macrophages die the result can further propagate the inflammatory process.
Smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
83
what are the 3 types of peripheral vascular disease?
- intermittent claudication
- severe PVD, chronic limb threatening ischaemia
- acute limb ischemia
83
what the investigations for Peripheral vascular disease?
LOOK
skin pallor
cyanosis
hair loss
ulcers
poor wound healing
dependent rubor
gangrene
FEEL
Temperature
sensation
Cap refill
Pulses
Buerger’s test
OTHER
ABPI
Duplex ultrasound
angiography (CT/MRI)
84
describe intermittent claudication
occurs when insufficient blood reaches exercising muscles due to artherosclerosis in the arteries
classical presentation is external discomfort, most commonly cramping in the calves and buttocks, relieved by REST
85
what is the treatment for intermittent claudication?
lifestyle
- manage modifiable risk factors
- optimise medical management (diabetes etc0
- exercise training
medical
Atorvastatin 80mg
Clopidogrel 75mg
Naftidofuryl oxalate
surgical
endovascular angioplasty and stenting
endarterectomy
bypass surgery
86
chronic limb threatening ischemia / critical limb ischemia
obstruction to blood flow in the artery is compromised to the point where the blood is unable to maintain oxygenation of the tissue at rest
- needs urgent referral to vascular team
87
what is the treatment for chronic limb threatening ischemia?
surgery
88
describe acute limb ischemia?
a rapid decrease in lower limb blood flow due to acute occlusion of peripheral artery or bypass graft
six Ps
- pain
- pulseless
- pale
- paresthesia
- paralysis
- perishingly cold
89
what is the treatment for acute limb ischemia?
surgical
endovascular thrombolysis
amputation
90
what is the treatment for stable angina?
acute treatment
- GTN spray (vasodilator) increases collateral spumy to the heart
maintenance
- all to receive aspirin and statin providing no contraindications
- B blocker/ CCB first line
- then combination of both
- PCI/CABG if MI develops
91
why do you not prescribe verapamil + a beta blocker?
risk of complete heart block
92
how is unstable angina diagnosed?
- when there are symptoms which suggest ACS
- the troponin is normal
and either
- a normal ECG
- other ECG changes (ST depression or T wave inversion)
93
how is an NSTEMI diagnosed?
NSTEMI is diagnosed when - - there is a raised troponin, with either:
- A normal ECG
- Other ECG changes (ST depression or T wave inversion)
94
describe the management for unstable angina and NSTEMI
initial management
- Aspirin asap (single 300mg loading dose)
- Offer fondaparinux if low bleeding risk and not immediately undergoing coronary angiography – unfractioned heparin in people with severe renal impairment.
- immediate PCI if unstable
- Oxygen if sats < 94%
- Morphine for pain
Risk assessment
GRACE score to assess risk – predicts 6-month mortality to catagorise risk.
Predicted 6-month mortality >3% = PCI within 72 hours
Predicted 6-month mortality <3% = Dual antiplatelet therapy
Ticagrelor + aspirin = low bleeding risk
Clopidogrel + aspirin = high bleeding risk
Prasugrel + aspirin = if undergoing angiography
94
how to diagnose a LBBB on an ECG
wiLLiam maRRow
in v1 lead = W shape
in v6 lead = M shape
95
how to diagnose a RBBB on an ECG
wiLLiam maRRow
in v1 lead = M shape
in v6 lead = W shape
96
what is the management for a patient with a STEMI?
INITIAL TREAMENT
Single 300mg loading dose of Aspirin ASAP
Oxygen if sats <94%
Morphine for pain
Nitrate (GTN)
Dual antiplatelet therapy
Prasugrel + Aspirin – if taking no other anticoagulants - PCI
Clopidogrel + Aspirin = if they are already taking oral anticoagulation - PCI
Ticagrelor + Aspirin = low bleeding risk - NO PCI
Clopidogrel + Aspirin = high bleeding risk - NO PCI
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with the local cardiac centre for either:
Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
Thrombolysis (if PCI is not available within 2 hours)
Offer an electrocardiogram (ECG) to people with acute STEMI treated with fibrinolysis, 60 to 90 minutes after administration. For those who have residual ST‑segment elevation suggesting failed coronary reperfusion:
offer immediate coronary angiography, with follow‑on PCI if indicated
do not repeat fibrinolytic therapy.
Assess LV function in all people following STEMI before discharge
97
Describe HF-pEF
- diastolic dysfunction
- concentric hypertrophy
impaired ventricular filling during diastole
cause
- ischaemic heart disease
- dilated cardiomyopathy
- myocarditis
- arrhythmias
98
describe HF-rEF
-systolic dysfunction
- eccentric hypertrophy
impair myocardial contraction during systole
causes
- restrictive cardiomyopathy
- cardiac tamponade
- constrictive pericarditis
99
what are the symptoms of right sided HF?
- peripheral oedema
- distended JVP
- hepatosplenomegaly
- ascites
100
what are the symptoms of left sided HF?
- exertional dyspnea
- PND
- orthopnea
- fatigue
- cyanosis
- pulmonary congestion (cough - pink frothy sputum)
(crackles / wheezes)
- pulmonary oedema
101
how do we investigate heart failure?
1st line = NT-pro-BNP
- released when the heart is under strain/stretch
then ECHO to access cardiac function and structure
CXR
A - alveolar oedema (bat wing opacities)
B - Kerley B lines
C - cardiomegaly
D - dilated upper lobe vessels
E - pleural effusion
102
what is the acute management for heart failure?
- sit them up
- oxygen at 100%
(keep oxygen saturations at 94-98%)
- Iv loop diuretic (furosemide)
- IV morphine (reduces anxiety and preload)
103
what is the management for chronic heart failure?
- 1st line = ACEI + BB dual
- if not controlled with that consider adding aldosterone antagonist
- SGLT-2i?
- if fluid overload add FUROSEMIDE (loop diuretic)
104
what are murmurs?
abnormal sound caused by turbulent blood flow
105
what are the known locations for valve auscultation?
Aortic: 2nd ICS R of sternum
Pulmonary: 2nd ICS L of sternum
Tricuspid: 4th ICS L of sternum
Mitral: Apex (5th ICS mid clavicular line)
106
what is the S3 heart sound?
S3 is heard just after S2
Indicative of heart failure
NB can be normal in younger adults and adolescents
KENTUCKY
106
what is the S4 heart sound?
S4 is heard directly before S1
Hypertrophic ventricle
Always abnormal
TENNESSEE
107
what are the systolic murmurs
Mitral Regurgitation Systolic
Aortic Stenosis Systolic
MRS ASS
Systolic murmurs coincide with pulses
108
what is aortic stenosis?
Signs and symptoms
- Breathless, chest pain, dizziness, collapse
- Displaced apex, narrow pulse pressure
Causes
Rheumatic heart disease
Bicuspid valve
Calcification
Murmur
- Ejection systolic murmur that radiates to the Carotids
Creshendo-decreshendo character
109
what is mitral regurgitation?
Signs and symptoms:
- Breathless, peripheral oedema and fatigue
- Displaced apex
Murmur
- Pansystolic murmur that radiates to the Axilla
110
what is mitral stenosis?
Signs and symptoms
- Breathless, fatigue and palpitations (AF)
- Malar flush, tapping apex beat
Causes
Rheumatic disease (prodromal illess + rash)
Murmur
- Mid diastolic murmur localised to apex. Emphasised by putting patient on their left side
111
what is aortic stenosis?
Signs and symptoms
- Breathless
- Collapsing pulse, displaced apex
Causes
CTDs (marfan’s, ehler danlos)
Murmur
- Early systolic on right sternal edge, rumbling
112
what is endocarditis?
an infection of the endothelial lining in the heart valves
damages the valve leading to the turbulent flow of blood
bacteria colonise the platelet deposits ion the valve, producing vegetation over the valve
113
What valve is most commonly infected with endocarditis?
mitral valve
114
what valve is infected by endocarditis by IVDU?
Tricuspid valve
115
what are the causes of endocarditis?
Poor dental hygiene
Previous rheumatic disease
Immunocompromised
Recent invasive therapy (dental work, cardiac lines)
IVDU
Mechanical valve
Congenital heart disease
116
describe the presentations of endocarditis?
FROM JANE
Fever + finger clubbing
Roth’s spots (eyes)
Osler’s nodes
Murmur (new)
Jane-way lesions
Anaemia
Nail (splinter) haemorrhages
Emboli
116
what criteria do you use to diagnose endocarditis?
duke criteria
and at least 2/3 blood cultures its be positive to meet major criteria
117
if you develop a fever and new murmur, what does this suggest?
endocarditis - until proven otherwise
118
what bacteria is linked with native valve?
staph aureus (most common)
119
what bacteria is most common with mechanical valve?
staph epidermidis
120
what bacteria is linked with dental work/poor hygiene?
strep viridans
121
what bacteria is linked with IVDU?
staph aureus
122
what is pericarditis?
infection of the pericarditis
caused by
- bacteria/viral infection
- post MI (dresslers syndrome)
123
what is the presentation of pericarditis?
Pleuritic (sharp, sudden, intense) chest pain – retrosternal -> radiates to neck and shoulders
Relieved by sitting forward
Aggravated by lying down + deep inspiration
Pleural rub – High pitched scratching sound
Fever
124
what does pericarditis look like on an ECG?
- Widespread saddle shaped ST elevation
- PR interval depression
125
how do you treat pericarditis?
treat underlying cause
NSAIDs + colchicine
(NSAIDs block the enzyme cyclooxygenase (COX), which the body uses to produce prostaglandins.
Prostaglandins are hormone-like chemicals that cause inflammation, pain, and fever.
By reducing prostaglandin production, NSAIDs help relieve pain and inflammation.)
126
what is cardiac tamponade?
accumulation of pericardial fluid under pressure
- can be blood in the pericardial cavity
127
what are the classical features of tamponade?
- hypotension
- raised jVP
- muffled heart sounds
128
what are other features of cardiac tamponade?
- dyspnoea
- tachycardia
- pulsus paradoxus - an abnormally large drop in BP during inspiration
- ECG: electrical alternans
- an absent Y descent on the JVP - this is due to the limited right ventricular filling
129
What are the causes of bradycardia?
- heart block
- sick sinus syndrome
- medications
129
what is the management for tamponade?
urgent pericardiocentesis
- needle is placed under the xiphoid process
130
what is sick sinus syndrome?
encompasses many conditions that cause dysfunction in the sinoatrial node. It is often caused by idiopathic degenerative fibrosis of the sinoatrial node. It can result in sinus bradycardia, sinus arrhythmias and prolonged pauses
131
what is the management of unstable patients of those at risk of asytole?
- Intravenous atropine (first line)
- Inotropes (e.g., isoprenaline or adrenaline)
- Temporary cardiac pacing (e.g. external pacing)
-
Permanent implantable pacemaker, when available
132
what heart rate indicates bradycardia?
a heart rate of less than 60 beats per minute
133
what are the 3 types of SVT?
Atrioventricular nodal re-entrant tachycardia (AVNRT)
- where the re-entry point is back through the AV node
Atrioventricular re-entrant tachycardia
- where the re-entry point is an accessory pathway. (somewhere between the atria and the ventricles)
Atrial tachycardia
- where the electrical signal originates in the atria somewhere other than the sinoatrial node (not caused by signal re-entering from the ventricles)
134
what is the treatment for SVT?
Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion
IMMEDIATE CARDIOVERSION IF
- LOC, haemodynamically unstable, signs of myocardial ischaemia, signs of severe HF
- + IV Amiodarone if DC cardioversion doesn’t work
135
what are the vagal manoeuvres?
- valsalva (a medical procedure that involves forcefully exhaling against a closed airway)
- carotid sinus massage
- diving reflex (a survival mechanism that occurs when a mammal's face is submerged in cold water)
136
what does adenosine do? and how it is taken?
slows conduction through the AV node
- has a half life of 10s therefore needs to be given as IV bolus to ensure enough drug to have an effect
- might cause bradycardia or asystole momentarily
137
what doses of adenosine and given in patients with SVT until normal sinus rhythm occurs?
6mg -> 12mg -> 18mg
138
what do people with SVT/AF with BBB present as on an ECG?
wide complex tachycardia
139
what heart rate is associated with tachycardia?
heart rate over 100 beats per minute
140
what do patients with AF and BBB present on an ECG with?
irregularly irregular rhythm
141
what do patients with SVT and BBB present on an ECG with?
a rhythm that looks very alike VT
142
what does the left bundle branch divide into?
- anterior hemi-bundle
- posterior hemi-bundle
143
what is bifascicular block?
the combination of RBBB with left anterior/posterior hemisphere-block (RBBB with left axis deviation)
144
what is trifascicular block?
features of a bifascicular block + 1st degree heart block
145
describe the different types of heart block
1st degree heart block - PR interval increases (slower conduction between aerials and ventricles)
2nd degree, mobitz type I - PR interval increases in each beat, until a whole QRS complex is missed. (ventricles do not contract I that missed beat)
2nd degree, mobitz type II, irregular rhythm where beats are dropped.
3rd degree - atrium and ventricles do not connect with eachother - irregularly irregular rhythm
- missed beats randomly
146
describe Wolff-parkinson- white syndrome
re-entrant SVT due to accessory pathway called the BUNDLE OF KENT
147
What changes are seen on an ECG for a patient with Wolff-parkinson-white syndrome?
- wide QRS >0.12s
- shortened PR interval <0.12s
- delta wave (slurred upstroke on QRS complex)
148
what is a delta wave on an ECG?
slurred upstroke on QRS complex
149
what is the definitive treatment for Wolff-Parkinson-White syndrome?
radiofrequency ablation of the accessory pathway
150
what are the 2 aims of AF treatment
1. rate & rhythm control
2. reduce stroke risk (CHAD-VASc)
151
how is rate & rhythm controlled for AF?
RATE CONTROL
1st line= bisoprolol (BB) & diltiazem (CCB)
2nd line= combination of 2 of Bisoprolol, Diltiazem & digoxin
RHYTHM CONTROL
Advised over rate control if:
- co-existent heart failure
- first onset HF
- obvious reversible causes (e.g alcohol)
Amiodarone (class 3) or flecainide (class 1c)
if haemodynamically unstable = DC cardioversion
152
what is the CHADS-VASc?
is a scoring system for atrial fibrillation stroke risk
score 0 = mo treatment
score 1 = consider AC in males
score 2 = offer AC (DOAC)
153
What is atrial flutter?
due to re-entry circuit in the right atrium
SAW TOOTH PATTERN ON ECG
atrial rate is around 300bpm, ventricular rate is around 150 bpm, resulting in 2:1 atrial to ventricle contractions
154
how is atrial flutter resolved?
radiofrequency ablation
155
what does hyperkalemia look like on an ECG?
peaked T waves
small P waves
PR prolongation
=== BROAD QRS
156
what is the normal range for Potassium levels?
3.5-5.3
157
what are severe levels of potassium?
over 6.5
158
what are the treatment options for hyperkalaemia if ECG changes are present or potassium levels >6.5?
IV calcium gluconate – stabilizes myocardium
Insulin – drives potassium from extracellular space to intracellular space
Dextrose – to prevent hypoglycemia on insulin
159
how long should the QT interval be in men & women?
men > 440ms
women > 460ms
160
what can prolonged QTs lead to in an ECG?
- prolonged re-polarisation
- this can lead to spontaneous depolarisations before complete re-polarisation.
- these are called afterpolarisations = can lead to polymorphic VT
161
what are ventricular ectopics?
- also know as premature ventricular complexes
types
bigeminy - 1 sinus beat coupled with a VPC
trigmeiny - 1 VPC every 1 sinus beats
162
what is polymorphic VT?
Torsades de Pointes
163
what medication is administered for monomorphic & polymorphic VT?
monomorphic - IV amiodarone
polymorphic - IV Mg sulphate
164
what is ventricular Fibrillation?
- form of cardiac arrest
- irregular random baseline
- no clear waveforms
not compatible with life and will be pulseless
MANAGEMENT = DEFIB
165
what are the 2 shockable cardiac arrest rhythms?
- ventricular fibrillation
- pulseless ventricular tachycardia
166
what are the 2 non-shockable cardiac arrest rhythms?
- pulse electrical activity
- asystole
167
what is HOCM?
hypertrophic cardiomyopathy
- commonest cause of sudden cardiac death in young people
168
what happens in HOCM?
left ventricle becomes hypertrophic, particularly affecting the septal wall, this can block flow of blood out of the ventricle
- autosomal dominant condition affecting myosin chain protein
169
what is the presentation of HOCM?
- SOB
- palpitations
- fatigue
- chest pain
- dizziness/syncope
- ejection systolic murmur
- 4th heart sound
- thrill at lower left sternal border
170
what is the treatment for HOCM?
- Beta blockers / CCB
- disopyramide (amtiarrhythmic)
- surgical myectomy (surgery removes part of the septum)
- ICD
- transplant
171
what is dilated cardiomyopathy?
condition where the heart muscle becomes thin and dilated.
may be genetic or secondary to the other conditions (e.g myocarditis)
172
what is restrictive cardiomyopathy?
when the heart becomes rigid and stiff, causing impaired ventricular filling during diastole
173
what is arrhythmogenic cardiomyopathy?
genetic condition
- heart muscle us progressively replaced with fibrofatty tissue.
- becomes prone to ventricular arrhythmias.
- noticeable cause of sudden cardiac death in young people
174
what is takotsubo cardiomyopathy?
rapid onset of left ventricular dysfunction and weakness.
- this often follows severe emotional stress (e.g following death of a long term partner)
- tends to resolve spontaneously with time
(broken heart syndrome)
175
what is the classifications for AAA?
normal = less than 3cm
small = 3-4.4cm
medium = 4.5-5.4cm
large = >5.5cm
176
what is the presentation of AAA?
non-specific abdominal pain
pulsatile mass
177
what investigations would be used to diagnose a AAA?
USS (ultrasound)
CT angiogram
178
what is the management for AAA?
change lifestyle
- stop smoking, optimise manangement of risk factors
elective repair
- symptomatic
- growing over 1cm a year
- width is >5.5cm
179
what is the presentation for a ruptured AAA?
- Severe abdominal pain that may radiate to the back or groin
- Haemodynamic instability (hypotension and tachycardia)
-Pulsatile and expansile mass in the abdomen
- Collapse
- Loss of consciousness
180
what are the classifications for aortic dissection?
type A - ascending aorta before brachiocephalic artery
type B - descending aorta after left subclavian artery
181
what are the presentations of aortic dissection?
- ripping or tearing chest pain that radiates to the back
- difference in BP in arms
- abdominal pain
- Hypotension
- collapse
182
what investigations are used to diagnose an aortic dissection?
- ECG
- CXR (X-ray)
- CT-angiogram/ MRI-angiogram
183
what is the management for an aortic dissection?
- analgesia
- HR/BP control (beta blockers)
SURGICAL
- type A - cardiothoracics
- type B - thoracic end-vascular repair (TEVAR) OR OPEN
184
what is buergers disease?
- Inflammatory condition
- causes thrombus formation in small/medium blood vessels
- typically affects hands and feet
- affects younger people who smoke
185
what is the presentation of buergers disease?
painful/blue fingertips or toes
pain worst at night
corkscrew collataterals seen on angiograms
186
what is the management for buerger disease?
stop smoking
IV iloprost (prostaglandin analogue tat dilates blood vessels)
