Case 13 Flashcards
1
Q
What is the BP range for hypertension and when is it considered an emergency ?
A
Hypertension >140/90
Emergency >180/110
2
Q
What sx may be present when px moves into emergency hypertension ?
A
Painful headaches and visual disturbances
3
Q
What is primary hypertension and what are the risk factors?
A
Idiopathic (95% of all cases). Heterogenous risk fx, strong familial link. Epigentics
4
Q
What is secondary hypertension and how would you treat it ?
A
Secondary to an identifiable underlying cause, target the cause and BP should decrease eg. renin artery stenosis.
5
Q
Name the 3 common non invasive measurements of hypertension ?
A
Fundoscopy
Urinanalysis
NIBP - non invasive intermittent blood pressure monitor
6
Q
What would urinalysis show if hypertensive and why?
A
Proteinuria. pressure on kidneys decreases filtering capacity.
7
Q
What test would you do if you suspected a px with white coat hypertension ?
A
NIBP, records BP every hour for a 24 hour period to show trajectory of BP.
8
Q
What is vascular rarefaction ?
A
Decreased density of capillary in tissue
9
Q
What is the function of the vascular endothelium?
A
Generates NO (potent vasodilator) that blocks Ca entry into SM. This decreases vasoconstriction.
10
Q
How is vasomotor tone controlled in SM cells ?
A
Post ganglion sympathetic innervation. NA from synapse binds to a1 + a2 adrenoreceptors to ^ Ca in VSMC.
11
Q
Describe how the RAAS would incur a BP ^ ?
A
BP drop detected by juxtaglomerular cells, release Renin converts AT -> AT1. AT1 goes to lungs -> AT2 via ACE. AT2 binds to receptor ^ aldosterone + vasoconstriction BP ^
12
Q
What should be altered in a hypertensive px before drug options are considered?
A
Px modifiable fx eg. salt, sat fat, obesity, smoking, alcohol consumption all decrease. Less sedentary lifestyle.
13
Q
What is the MOA of an ACE inhibitor (kidney, cardiac, vascular) and name one ….
A
Ramipirl - inhibits ACE so no AT2, BP down.
Kidney - indirect block Na uptake
Cardiac - limits LV remodelling
Vascular - decreases vasomotor tone (block AT2 creation)
14
Q
What is Lasartan?
A
Angiotensin receptor blocker
Antagonistically blocks AT2 receptor so no effects BP down.
15
Q
Name a Ca channel blocker and describe MOA (cardiac, vascular)
A
Nifedipine. Inhibits VSMC contraction.
Cardiac - -ve ino/chronotrope stops Ca into contracting/conducting cells
Vascular - prevent SM contraction through Ca down.
16
Q
What is the general MOA of diuretics, name 3 ?
A
Prevent H2O reabsorption by blocking ion transfer from fluid to blood
Furosemide , Bendoflumethiazide, Spironolactone
17
Q
What is the specific MOA of Sprionolactone ?
A
Prevents H2O reabsorption by trapping electrolytes in the urine so fluid loss decreases. Acts in collecting duct as a weak K sparing diuretic. Blocks aldosterone receptors prevents Na reabsorption
18
Q
What is the effect of blocking b1 receptors in cardiac tissue ?
A
cAMP down -> Ca down -> -ve chronolo/inotropy -> Co Down -> BP down.
19
Q
What is the effect of Atenolol on the RAAS ?
A
Inhibits renin release
20
Q
What drug (and type) stimulates sGC that leads to relaxation through what MOA ?
A
GTN - glyceryl trinitrate
GTN -> NO -> sGC -> cGMP -> (in VSMC) K efflux -> Ca down -> MLCP up -> vasodilation.
21
Q
What is the order of the layers of the adrenal cortex from out to in ?
A
Zona ; Glomerulus
Fascicularis
Reticularis
22
Q
What is the function of androgens produced in the zona reticular ?
A
Taken up by the ovaries/testis to produce Oestrogen/testosterone
23
Q
What substances regulates androgen secretion ?
A
ACTH
24
Q
What are the qualities of funny currents (3)
A
Mixed Na/K permeability
Activation on hyperpolarisation
Very slow continual kinetics
25
Why does warfarin target clotting fx 2,7,9,10 specifically?
they contains glutamic acid. Warfarin inhibits VKOR which is required for these clotting fx to be activated enough to form clots.
26
What is the ERP?
Effective refractory period
| experimental period in which another AP won't cause depolarisation
27
How are slow and fast waves compensated ?
The fast wave will extinguish the slow wave so they continue to ventricles as one
28
How is tachycardia induced through slow wave conduction ?
Fast in ERP so can't be stimulated. Slow reaches apex and fast no longer in ERP so it loops back around in fast -> circular movement tachycardia
29
During circular movement tachycardia, how is HR calculated ?
Number of times the circuit goes round the loop, each loop stimulates atria/ventricles
30
What is the accessory pathway ?
Muscle strand between atria and ventricles, allows conduction bypassing the AVN and causing reentry (AVRT)
31
In terms of AVN dependant tachycardia, what are 10% of the population born with ?
Accessory pathway so they have dual input. Leads to AVRT due to macro reentry.
32
How does the orientation of fibres affect conduction speed ?
Conduct rapidly in the parallel direction but slowly when perpendicular
33
What are the 3 zones related to a scar related VT ?
Dense scar, peri infarct zone, unaffected area
34
How is VT initiated ?
ectopic across peri infarct zone; some signal blocked some gets through -> partial signal return -> ready to activate. Circuit overrides sinus rhythm and drives heart.
35
What is the consequence of VT ?
Too fast for ventricles to fill. Pulse decreases leads to cardiac death
36
What can occur if the QT interval prolongs too much during ^ ERP?
afterdepolarisations -> tachycardia
37
What condition shows palpitations, syncope, transient loss of consciousness, loss postural tone, pale, motionless but then leads to a quick recovery ?
Torsade de pointes (TdP)
38
What are the implications for TdP?
Torsade de pointes
V high risk for cardiac arrest. if episode doesn't terminate -> V fibrillation.
Admit px for constant monitoring and tx.
39
What drugs can prolong the QT interval ?
```
Antiarryhthmic VM class 3 lengthen refractory period and can be overdone -> long QT.
Antidepressatns/antipsychotics can prolong.
```
40
What electrolyte imbalance can result in a depolarisation abnormality and what is it common in ?
Hypokalaemia
| Chronic renal failure, K losing diuretics (esp in elderly) , vomiting/diarrhoea.
41
What are the two types of tachycardia and how are they defined ?
Broad complex >120 ms
Narrow complex <120 ms
Based on broadest QRS on whole ECG
42
What are some common NCTs that show a distinctive pattern ?
Narrow complex tachycardias
| AF, atrial flutter, multifocal atrial tachycardia (definite P waves but 3 different paths)
43
List some BCTs ?
```
Broad complex tachycardias
Ventricular tachycardia (most common) , SVT and bundle branch block, accessory pathway related tachycardias
```
44
What are the pros/cons of 24 hour tape monitoring using portable ECG ?
non invasive, useful for particular day episodes. Doc can apply so readings will be accurate.
Unlikely to pick up problems if they have weekly episodes for example.
45
How long will an injectable loop recorder last ?
Up to 3 years. Uses a base unit to upload information to Docs using wifi.
46
What is and how long is the PR interval ?
duration of atrial depolarisation and the delay during conduction through AVN. Normal is 120-200 ms
47
Where is there a difference in height in the P and R waves ?
Atria have thin walls so have reduced conduction compared to the thicker ventricular walls
48
When can sinus arrhythmia be considered normal ?
Youths
49
How can conduction velocities be varied ?
Drugs, para/sympa stimulation, ischemia
50
What do the P, QRS and T wave correspond to ?
```
P = atrial depolarisation
QRS = Ventricular depolarisation (atrial repolarisation masked)
T = Ventricular repolarisation
```
51
What are the possible sx of arrhythmias ?
nothing at all, palpitations, breathlessness (dyspnoea) , chest pain, dizziness, lightheadedness (pre-syncope) , T-LOC, syncope, sudden death
52
Palpatations; what exacerbates them?
| More common in what? (3 each)
caffeine , stress, alcohol
| Puberty, pregnancy, menapause
53
What is the cause of breathlessness ? (in tachycardia and Brady)
due to decreased CO
Tachy = decreased SV as insufficient time to fill and empty
Brady = decreased HR
54
What is the consequence if PQRST is disturbed during breathlessness ?
Loss of active atrial filling
55
Why does dizziness/lightheadness occur during chest pain ?
less blood to the brain, Co Down leads to BP down which leads to less cerebral diffusion -> T-LOC (in extreme)
56
What happens If PMVT is not tolerated ?
polymorphic ventricular tachycardia , cardiac arrest.
57
What is cardiomyopathy ?
Group term for conditions in which heart muscle problem is acquired or inherited
58
When are ILRs used ?
Injectable loop recorders , only used after T-LOC due to price
59
How would you tell the origin of an ectopic beat ?
```
Broader = ventricles
Atria = narrower
```
60
What normally follows an ectopic beat ?
Compensatory phase, inverted P wave not from sinus node
61
How does Starling's law effect emptying ?
If heart takes longer to fill then the emptying will be more vigorous
62
What lifestyle management can be put in place to limit ectopic beats ?
Smoking, alcohol, caffeine, Chinese food (monosodium phosphate)
63
What is atrial fibrillation ?
Irregular uncoordinated rhythm arising from atria. Irregularly irregular without P waves.
64
What are the 3 classes of AF ?
paroxysmal, episode lasts <48 hrs
Persistent, episode >48 hrs - 1 week
Permanent
65
What is the ventricular response to AF if px is born with an accessory pathway ?
Conduction bypasses AVN (not slowed) so ventricular rate = atrial rate
66
What cerebral thromboembolic events may be the first presentation of AF ?
Stroke, TIAs
67
Why does Athletes heart syndrome ^ risk of AF?
Enlarged LV
| Anything that enlarges the atria ^ risk of AF
68
How would you assess wether to control rate or rhythm during AF tx ? (3 tests)
Rhythm - AFFIRM study
Assessment of stroke - CHADS2VASC score
Anti coagulation - HASBLED score
69
How do beta blockers affect AF ?
target AVN to decrease conduction, still in AF but slower. Help decrease the rate
70
What is the advantage of the 'ablate and pace' method of tx ?
destroy AVN insert pacemaker. The heart beats and controlled and slower so more comfy for px.
71
What drugs can be used in rhythm control tx of AF ?
```
VW class 1c (flecainide, propapenone)
VW class 3 (amiodorone, dronedarone, sotalol)
```
72
What is the disadvantage of DC cardioversion ?
Shock to return to sinus rhythm. Px may slip back into AF over next few weeks
73
What is TOE and why is it used ?
Transosophageal echo, US
| goes just behind the heart shows area of heart contractions.
74
How would you imagine orientation on an US ?
imagine toes coming out toward you with the px lying down.
75
What would an ECG show during accessory pathways ?
short PR interval plus 'delta waves'.
76
What is the name for a slurred QRS upstroke ?
Delta wave.
77
What is 1st degree heart block?
Long PR (>200ms) no sx or tx. Often caused by AVN blocking drugs
78
Which heart block presents with; intermittent P waves, breathless, T-LOC ?
2nd degree
79
How can the heart still beat during 3rd degree heart block ?
Escape rhythms, from BoH (30-40 bpm) and ventricular myocytes (20-30)
80
How would you differentiate 2nd and 3rd degree heart block on an ECG ?
3rd has superimposed P waves. They can appear either side of QRS with no relation
81
Why can dementia tx lead to heart block and how would you rectify it ?
Uses drug Donepezil which commonly causes heart block. Better to stay on tx and put in a pacemaker rather than switch medication.
82
What are some common causes of heart block ?
age related degeneration , acute ischemia, drugs, hypokalaemia, hypothyroid, ^ intracranial pressure (Cushing's reflex)
83
Where would the scar be if px has a PPM inserted ?
Permanent pacemaker
| 5cm just below clavicle, inserted under x ray
84
How often do px with PPMs need to be seen and when are they replaced ?
at least yearly checks.
| Generator every 5 years and leads every 10
85
What would you do during ventricular tachycardia ?
1. return px to safe rhythm
| Then do an echocardiogram and a coronary angiogram.
86
What is the purpose of EPS ?
Electrophysical studies
| Put px in VT, then locate pathology area. Scarring causes non conduction
87
How do you differentiate between ICDs and pacemakers ?
ICDs appear bright white on X-ray , if not white then its a pacemaker. The shock coils are the bit that deliver the impulse.
88
What groups of inherited heart disease can pre dispose to arrhythmias ?
Cardiomyopathies
| Primary arrhythmias
89
How does parasympathetic stimulation affect heart rate ?
Increased ACh decreases HR
90
What does lusitrophy mean ?
^ rate of relaxation, heart recovers faster in diastole
91
What is the term used to refer to the rate of delay at the AVN ?
Dromotropy
92
In ionic channels, what governs the rate of flow ? (4)
Selectivity to the specific ion, which part of the heart (expression) , activation (of cAMP etc) and inactivation (relative period to how long active for)
93
What is significant about the IK1 channel ?
underlies resting potential not voltage potential. Not voltage dependant, can be phosphorylated
94
Which channels help maintain the plateau during phase 2 ?
balance between ICaL (long) in and K out (IKr+IKs)
95
What are ionic channels ?
Large complexes, contain repeats of 6 transmembrane segments each with a P loop (domain).
96
What is significant about the P loop ?
Forms the core of the segments for the ions to flow through
97
What domains are thought to influence Na inactivity ?
Na channels rapidly inactivate, thought to be linked between domains 3 and 4
98
Which Na channels can cause long QT syndrome ?
Type 3, activate for longer -> longer AP -> long QT
99
What is the difference between cardiac and neuronal channels in terms of sensitivity ?
Neuronal sensitive to TTX (tetrodotoxin) which blocks Na channels hindering conduction. Cardiac insensitive
100
What are the general properties of L type Ca channels ?
In the ventricles, powerhouse of inotropy.
| L activate rapidly and deactivate slowly allowing more time for Ca to enter.
101
How is inotropy stimulated ?
Sympathetic activation -> b1 stimulation -> protein kinase C -> Ca ^ into myocytes -> ^ inotropy
102
What is verampil ?
Phenylalkamine drug that blocks Ca entry in cardiac cells
103
What is different about the dihydropyridine class of drugs and give an example ?
More selective for SM
| Methanamine
104
What feature do the Ito channels contribute to in the ventricular action potential diagram ?
Cardiac notch in phase 1. 'current transient outward'. Flow out of myocyte channels inactive rapidly causing transient repolarisation.
105
Which channels in cardiac ventricules are voltage dependant ?
Ito , Ikr, Iks
106
Which channel is associated with long QT type 2 syndrome ?
Ikr, this is the rapid of the slow channels. No K channel function so longer depolarisation if abnormal in long QT.
107
Which channel has a slow switch on time during plateau that can lead to long QT type 1
Iks, slow channel
108
How does b stimulation favour different channels ?
stimulates the out currents (Iks, Ik1) more than the in currents (IcaL) so that repolarisation happens earlier in AP.
109
During CICR, Ca triggers the opening of which channel in what region ?
Opening of the RyR channel in the dyadic cleft (proximal to the T-tubule connection to cytoplasm)
Calcium induced Calcium release
110
What two substances inhibit RyR ?
Calsequestrin and FKBP (calstabin)
111
When does Calsequestrin stop inhibiting RyR ?
In diastole Ca ^ in SR -> Ca binds to Calsequestrin (relieves inhibition) -> Ca then released into cytoplasm
112
What are the two methods of Ca movement during diastole ?
Taken back into SR (Ca ATPase)
| Or taken across sarcolemma (Na/Ca exchange)
113
Why does Ca usage in systole have to equal Ca in diastole ?
If it doesn't equal then arrhythmias arise leading to sudden cardiac death
114
What is the function of the Na/Ca exchange at rest ?
Maintains low Ca in sarcoplasm. 3Na in for 1Ca out so net +ve charge movement causing depolarisation of myocytes.
115
Name the two Ca ATPases and their brief function ?
PMCA, transports 2Ca/atp out of sarcolemma
| SERCA, transports 1Ca/atp into SR
116
What regulates the ATP pump ?
Calmodulin, Ca dependant
117
How are PMCA2 and SERCA2a regulated ?
PMCA, calmodulin regulation ^ Ca removal from sarcolemma
| SERCA2a, phospholamban regulation inhibits Ca uptake into SR
118
What is the function of TnC relative to Ca ?
Binds to Ca removing inhibition of tropomyosin on actin and myosin
119
What happens when TnI becomes phosphorylated and when does it happen?
moves tropomyosin away allows actin to bind to myosin -> contraction. Occurs during b stimulation.
120
What causes a decrease in TnC sensitivity for Ca?
Phosphorylation of TnI , Ca released faster -> contraction shorter, lucitropy ^
121
Which membrane currents does b-adrenergic stimulation stimulate ?
IcaL , Iks, Ik1
122
What effect does b-adrenergic stimulation have on TnI ?
Decrease sensitivity for Ca.
123
How are funny currents generated ?
Flow through If channels, HCN (hyper polarisation activated cyclic nucleotide gated). phase 4 dominant.
124
When is IcaT active ?
Later end of phase 4, brings in Ca for Na/Ca exchange
125
What effects does the IkACh channel have ?
-ve inotropic effect. paired to muscarinic receptors. ACh activates it -> hyperpolarise -> -ve inotropy.
126
What process is induced through ^ cAMP binding to HCN4 allowing ^ Na into pacemaker cells -> depolarisation ?
Tachycardia
127
How is bradycardia stimulated ?
Decreased cAMP bind to HCN4 -> ^ IkACH -> depolarisation decreases
128
What is the action of Ivabradine?
selectively blocks HCN channels. Pacemaker works but slower (failsafe)
129
What is the function of connexins ?
Form connexons, facilitate current spread to adjoining myocytes.
130
Which connexons are associated with the AVN ?
30 and 45 , have ^ R so less conductivity (delay feature)
131
Where are connexons cx 40 + 43 found ?
In the purkinje fibres, ^ conduction force.
132
What are the 3 main reasons for treating somebody with an arrhythmia ?
Relieve sx/improve QoL
Prevent complications (stroke, worsening heart failure)
Prevent sudden cardiac death
133
What is the valsalva manoeuvre ?
Deep breath in hold nose and pop eardrums to ^ intrathoracic pressure. Can ^ vagal drive to transiently block AVN (terminates AVN tachys)
134
What is the approach to alcohol and caffeine during arrhythmia treatment ?
Only limit if drinking excessive amounts. No point if normal
135
What is an SVT ablation ?
burn myocardium to modify AVN input using radio frequency ablation. 1st line for AVNRT.
136
What is PVI ?
Segmental pulmonary isolation, used when v. symptomatic and has failed 1+ drug tx. Ablation strategy, day procedure LA for 2-3 hrs.
137
What is the 'ablate and pace' strategy ? Why is it limited ?
Destroy AVN, ventricles then paced whilst atria remains fibrillating. Still needDOACs but still need rate limiter (b blocker)
138
What is the scoring system used for stroke risk ?
```
Congestive heart failure
Hypertension
Age >75 (2)
Diabetes mellitus
Stroke/TIA/TE (2)
```
```
Vascular disease (prior MI, aortic plaque)
Age >65
Sex (female = 1)
```
139
What tx should be offered to a male with recurrent AF and a CHADSVAS score >1 ?
Lifeling anticoagulants.
140
Why might someone not be put on DOACs even when their CHADSVAS score is 1 ?
Risk of major bleeding on DOACs is similar to risk of stroke so px may not feel it's necessary.
141
How should AV synchrony change with rhythm tx?
Should improve. During AF you loose atrial contribution to ventricular filling so ventricles can't relax properly. Tx should allow more unified contraction.
142
What method of tx puts the px back into sinus rhythm and then uses drugs to maintain it ?
DCCV (DC cardioversion). Px may relapse in which case PVI can be used.
143
How does out of hospital cardiac arrest survival rates differ with time ?
For every 1 minute your chance of survival decreases by 10%
144
What method of tx can be used for px who may suffer cardiac arrests ?
ICD (implantable cardiac defibrillator) delivers 700v shock within 15 seconds of arrest. Success rate 99.9%
145
How does the SAN rate change during ^ sympathetic innervation ?
^ HR due to activation of b1-adrenergic receptors by NA/A.
146
Which type of Ca channel are key for stimulus of an action potential ?
L type channels
| T type only involved during later end of phase 4 but have lesser effect.
147
Which channels react to hyper polarisation?
If 'funny currents'. They cause gradual depolarisation during phase 4 as part of the 'pacemaker potential'.
148
What structures do rate and rhythm control drugs target respectively ?
```
Rate = b-1 and phase 4.
Rhythm = Ca channel blockers
```
149
When is a gate said to be in refractive state and what significance does this have ?
When it's inactive/v. depolarised. They can't be stimulated at all so no contribution to impulse propagation
150
What are the general causes of arrhythmias ? (5)
damage to cardiac tissue/nodes (eg. CAD) , automaticity/spontaneous generation , congenital abnormalities (having extra conducting pathway) , drug effects, electrolyte imbalance (hypokalaemia)
151
What are the key characteristics of AF ?
Irregularly irregular rhythm with absent P waves.
152
What are the 3 types of AF ?
Paroxysmal, self terminate within 24 hours
Persistent, sx >24 hours
Permanent, sx resistant to tx
153
What 3 major things might predispose somebody to AF ?
Hypertension (fluid overload distends pulmonary veins)
CAD (leads to ischemia)
Valvular disease eg. mitral stenosis
154
What Ca channel blocker can be used as a rate and rhythm control drug in tx of AF ?
Verapamil (IV) decreases CICR to slow nodal output. Limited ADRs
155
What is the action of Flecainide in rhythm control ?
Type 1 blocker, decreases electrical activity to extinguish tachycardia. No effect on the nodes
156
Which R+R drug has a side effect that can lead to Torsade de Pointes ?
Amiodarone. acts as b blocker (rate) and type 3 (rhythm) to ^ refractory period and QT interval. ^ QT interval too much -> TdP
157
Warfarin; what are it's actions , antidote, how would you monitor, how is it administered ?
Vit K epoxide reductase inhibitor blocks synthesis of fx 2,7,9,10.
Vit K
monitor INR for prothrombin time
Px can take orally at home, unpredictable pharmacodynamics.
158
What is the dual action of heparin ?
```
Activates prothrombin 2.
Inhibits thrombin (generates fibrin clot) and Fx Xa.
```
159
Px ODs on heparin, what would your tx plan be ?
Give them protamine sulphate. Monitor via APTT (activated partial thromboplastin time)
160
What are the pros/cons of DOACs ? give two examples ...
More predictable pharmacodynamics
Fewer antidotes so bleeding has ^ risk.
Dabigatran (thrombin) and Rivaroxaban (Fx Xa)
161
What are the key features of SVT and what is is caused by ?
Supraventricular tachycardia
Regular rate 140-280 ppm, narrow QRS with 'buried' P waves.
Normal variants in fast/slow conducting fibres around AVN.
162
What are the 3 main predisposing fx for SVT ?
Caffeine (stimulants) , psychological stress, hyperthyroidism
163
How is adenosine used as a rhythm drug?
Binds to adenosine receptors to hyperpolarise AVN to decrease nodal excitability to decrease SVT. V short half life.
164
What is the characteristic appearance of atrial flutter on ECG ?
Sawtooth flutter waves with atrial rate 300bpm. Narrow QRS.
165
What are the 3 predisposing fx for AFl?
Hypertension, cardiomyopathy, valvular dysfunction/disease
166
What rate control drugs can be used for treating AFl ?
beta blockers eg. metoprolol , decreases ventricular rate that blocks b1. decreases automaticity in nodes to slow HR
167
What is the MOA of digoxin ?
blocks Na/K ATPase in brainstem cardiac centre to ^ vagal stimulation of AVN -> refractory + limits AVN output. Stops impulses reaching ventricles
168
What are the key features of BCT on X-ray ?
regular monomorphic rhythm, QRS >120ms , HR >100 bpm.
169
What is Alteplase ?
Fibrinolytic drug used during MI , analogue of tissue plasminogen activating fx.
Plasmin release -> dissolves clot that was causing infarct.
170
What tx would you give for post MI anti platelet ?
Aspirin, blocks thromboaxane A2 mediated platelet aggregation
Clopidogrel, inhibits ADP receptor mediated platelet aggregation (clot formation).
Overall platelets can't trigger intravascular clot
171
What are the types of Na channel blocker?
```
All class 1;
a = moderate eg. procainamide
b = weak eg. lidocaine
c = strong eg. flecainade
```
172
What is voltage conduction defined as ?
How rapid the voltage channels cycle through their states and refractory periods
173
How does conduction speed and time spent in ERP vary between fast and slow channels?
Slow; slow conduction speed but short ERP
| Fast; fast conduction speed but long ERP
174
How does giving Flecainade as tx alter reentry arrhythmias ?
semi selective for the fast pathway. stays bound longer than other class 1 to remove reentrant potential because fast pathway isn't available.
175
Apart from accessory pathway defects, why does is the AVN the only pathway to the ventricles ?
atria and ventricles divided by cartilage. Creates area of CT separates A and V.
176
What other areas of the heart can control rhythm if an SAN pathology is present ?
AVN 'junctional rhythm' 50 bpm
| Purkinje fibres 'escape rhythm' 30 bpm
177
What differences would be seen on ECG for a LBBB and why ?
Wide QRS with normal HR. Slow depolarisation of the ventricles due to APs moving from R -L as only conduction.
178
What is the 'R on T' phenomenon ?
Prolonged QT , refractory period over but cells remain hyper polarised so easily repolarised. leads to tachycardia -> VF.
179
What is WPWS?
Wolff Parkinson White syndrome. deformity in ring of valve of AVN so alternate pathway between atria and ventricles. Wave forms return and depolarise atria too quickly.
180
What condition is indicated by a sloped Q wave and a shorter PR interval ?
WPWS, shows premature atrial contraction. PR (0.04-0.08) starts slow because ventricles only partially depolarised.
181
Where do the left and right bundle branches arise from ?
Originate in the bundle of his, branch off like a tuning fork
182
In what tissue does phase 4 occur and through which channels ?
Only in nodal tissue. Uses If (funny current) pacemaker channels. Gradual depolarisation until threshold for phase 0 reached.
183
How does the type of cardiac tissue affect which channels are involved in phase 0?
Nodal tissue = Slow Ca (CaL)
Other tissue = fast Na
The CaL produce a longer/slurred depolarisation that causes rate limitation in the AVN.
184
What counteracts phase 1 in non nodal tissue ?
Activation of Ca channels. Repolarisation causes the plateau that extends AP.
185
Why is there no phase 2 in non nodal tissue?
Slow Ca channels are active during phase 0 not phase 2. Ca must inactivate before repolarisation can commence.
186
What is the significance of the ARP and when does it occur ?
Absolute refractory period, between phase 1 and end of 2.
187
What is the period called when the majority of channels are inactive. Some may be activated in presence of depolarising impulse 'afterdepolarisations'.
ERP , occurs during phase 1 and the start of repolarisation in phase 3.
188
What is the RRP ?
Relative refractory period. Small no channels inactive, enough to propagate impulse. If impulse of sufficient strength then full depolarisation can occur. Between end of phase 3 and start of 4.
189
What is the supernormal period ?
all channels available. Hyperexcitable period even small impulse can trigger new/mistimed cAP.
190
What happens during an early AD in phase 2?
Afterdepolarisation. small bump but not enough Na to trigger new AP so QT interval ^.
191
How would a full new cAP be caused during AD?
early phase 3 afterdepolarisation with enough Na -> QT ^.
192
What are delayed ADs ?
^ Ca in phase 4, enough to reach Na threshold causing extrasystole. Fuels arrhythmia trains until Ca runs out.
193
What effect can Digoxin and adrenaline have on ectopic activity ?
^ slope and decrease phase 4 time through ^ Ca causing a new mistimed AP.
194
What does the valsalva manoeuvre cause ?
^ Vagal stimulation to the heart. HR decreases makes baroreceptors in aortic/carotid think there's sharp ^ BP so HR and BP down. Hyperpolarisation in AVN so decrease impulse to ventricles.
195
What does an upward trace show on an ECG?
Depolarisation toward the lead or
| Repolarisation away from the lead.
196
What is the antidote to the DOAC Dabigatran ?
Idarucizumab
197
A px overdoses on an anti arrhythmic drug and are given Magnesium sulphate. Which drug was the original cause?
Amiodarone
198
How does a lack of oxygen affect an ECG ?
causes ischemia, lack of ATP pump so more Na in cells and a higher +ve charge (stays depolarised).
199
How is the ST segment flat on an ECG even though some ventricular cells are depolarising?
ECG measures overall so an equal (or similar) amount are repolarising causing flatline.
200
What is the significance of the sub epicardial tissue ?
Last part of ventricle to depolarise so shorter AP and depolarises before the rest giving T waves +ve nature.
201
What are the two types of ischemia ?
Transient (demand driven) eg. stable angina
| Blockage (supply driven) eg. major coronary vessel blocked during an infarct.
202
How would transient ischemia been shown on ECG ?
+ve baseline shows ST depression on exertion eg. stress test.
203
Why does the ST depression occur during ischemia?
Ventricles repolarise faster than non ischemic tissue, ST more -ve. Sub endo stays ischemic so segment depressed compared to base.
204
How does blockage ischemia respond to stress ?
Not triggered so no change
205
The baseline on an ECG is more negative during blockage ischemia. What is this caused by?
Depolarisation waves are too large/too many so travel all directions including away from ECG -> more -ve.
206
What is the result of ventricular repolarisation during blockage ischemia ?
Ischemic part still depolarised so impulses travel away from electrode. Lowered base so ST elevation compared to baseline.
207
What is phase 4 and where does it occur ?
Gradual depolarisation (If) until threshold for phase 0 reached. 'Pacemaker' activity accounts for nodal automaticity + cAPs
208
How does phase 0 vary between tissue types ?
Nodal tissue - slow Ca , longer slurred depolarisation with AVN rate limiting.
non nodal tissue - Fast Na open once threshold reached
209
What is phase 2 and where does it occur ?
activation of Ca channels counteracting phase 1, repolarisation 'plateau' extends AP. Non nodal tissue (Ca are active during phase 0)
210
What phase is caused by K efflux ?
3, depolarisation. Resets in advance of next cycle
211
What happens if Na channels are stuck in refractory period ?
No AP will be generated so ventricles won't be able to empty and refill effectively
212
What is the supranormal period ?
All channels available, 'hyper excitable' period where even small impulse can trigger new/mistimed cAP.
213
Which phases involve the RRP ?
Relative refractory period
| End of phase 3
214
What will happen if an after depolarisation is stimulated in phase 2 but with not enough force ?
Small bump but not enough Na to trigger new AP so QT interval ^
215
What is an arrhythmia train and when does it stop ?
Delayed AD shows ^ Ca in phase 4 that is sufficient enough to trigger extrasystole. The train will run out when Ca runs out.
216
What are 3 main causes for ectopic activity ?
Damage to heart
Some drugs eg. Digoxin, ^ slope and decrease phase 4 time by ^ Ca so new AP
Valsalva manœuvre
217
How does damage to the heart cause ectopic activity ?
Causes sustained partial depolarisations which decrease the threshold for new APs (tissue like mini pacemaker)
218
Which electrolyte is responsible for depolarisation of cardiac myocytes ?
Sodium, causes a rapid influx.
| Slow influx Ca causes the plateau
219
Px with SVT has a carotid sinus massage but they tachycardia persists. What is the next step?
IV adenosine, rapid onset and offset.
220
Which part of the ECG corresponds to closure of the mitral valve ?
QRS = ventricular depolarisation (contraction). This means P is higher in ventricles to mitral valve is closed to prevent back flow
221
What is the normal resting potential of hearts ventricular and atrial contractile fibres resting potential ?
```
Ventricular = -90mV
Atrial = - 80mV
```
222
Px has persistent dry cough that isn't improving on abx. What type of antihypertensive meds are responsible and give an example ?
ACE inhibitors eg. Lisinopril
223
Px has 30 mins of central crushing chest pain, what feature will show MI at this stage ?
ST elevation or non ST elevation used at this stage.
| Q waves haven't had time to develop. Troponin tests used after 12 hours to indicate myocardial damage.
224
What is the sign of ischemia on an ECG ?
Inverted T waves and ST depression
225
What are the indications of first degree heart block ?
PR interval >200ms. (normal range 120-200). P wave may be 'buried' in end of T.
226
81 yo female with palpitations in AF. She's hypertensive and hypercholesterolaemic, what is the appropriate tx to reduce cardiac risk ?
CHADSVAS of 5 so high risk. Needs to be on antihypertensives (B blocker +statin). High risk = warfarin unless contraindicated.
227
What is the normal range of cholesterol for a healthy and at risk adult ?
Healthy <5 mmol/L
| Target <4 mmol/L
228
What are the indications of hypokalaemia and hyperkalaemia on an ECG ?
Hypo; U waves , ST depression, absent T waves, prolonged PR, long QT
Hyper; tall sometimes prolonged pointy P waves
229
What conditions are indicated for J and delta waves ?
Delta - WPWS
| J - hypothermia
230
What is the indication on an ECG for left atrial hypertrophy?
P wave shows twin peaks, with the second being higher.
231
What condition is indicated on ECG by a tall P wave with a singular point ?
P pulmonalae
232
Which inhibitory protein in cardiac muscle regulates the Ca ATPase pumps of the SR ?
Phospholambin
233
What are the positions of the 6 chest leads ?
```
V1; R of sternum 4th intercostal
V2; L of sternum 4th intercostal
V3; Midway between V2/V4
V4; L midclavicular line 5th intercostal
V5; L anterior axillary
V6; L mid axillary
```
234
What territories do the 6 chest leads cover ?
```
V1+2 = septal
V3+4 = anterior
V5+6 = lateral
```
235
What territories do leads 1,2 and 3 cover and where are they positioned on the body?
1; L hand to R hand gives lateral view
2; L leg to R hand gives inf view.
3; L leg to L arm gives inf view.
236
Which lead is used as the rhythm strip and why ?
Lead 2; P waves most visible
237
How are the augmented leads calculated and what view do they give ?
aVL; LA-(LL+RA) shows L shoulder to R hip giving Lat view
avR; RA-(LL+LA) shows R shoulder to left hip gives Lat view
aVF; LL-(LA+RA) shows umbilicus to neck gives inf view.
238
On an ECG, which leads give the views; septal, ant, lateral, inferior ?
Septal; V1, V2
Anterior; V3, V4
Iateral; V5, V6, aVL, aVR, 1
Inferior; aVF, 2, 3
239
What are the orientation steps during an ECG for exam purposes ?
```
Name+DOB of px
Time and reason for ECG taken
Checks stats top right, often give info/calculations
Identify rhythm strip at the bottom
Look at paper speed at bottom
```
240
What should the paper speed by on a normal ECG ?
25m/s and mV =10
241
How would you calculate HR for an irregular rhythm ?
Count no of QRS across 30 squares then x10
242
What is the normal duration of the QRS complex ?
<120ms (3 small squares)
243
What are the pathologies associated with abnormal QRS complexes ?
```
Broad QRS (>120ms) , seen in BBB forcing longer, slower conduction route. Ventricular origin common
Narrow QRS (much smaller than <120ms) , extra impulse in atria. Atrial or supraventricular tachycardia.
```
244
What are the two possible causes of ST elevation ?
Infarct; 2+ chest leads shows acute MI (specific leads indicate location)
Inflammation e.g. pericarditis
245
Which leads show T wave inversion? What is the indication if T waves are tall ?
aVR and V1
| Tall T waves = hyperkalaemia
246
What is the normal range for QT interval?
360-440 ms (9-11 small squares)
247
What are the indications on an ECG and the px sx for AF ?
Atrial fibrillation. ECG; irregularly irregular rhythm with absent P waves.
Sx; irregular pulse (BP around 180/100), breathless, paroxysmal palpitations
248
What course of tx would you advise for px in AF ?
Drugs; anticaogulants (warfarin in emergency) R+R (verapamil, amiodarone)
Procedures; DCCV, catheter ablation
249
What condition shows regularly irregular rhythm with abscent/hidden P waves?
Supraventricular tachycardia
| HR v ^ (140-280bpm) narrow QRS
250
What are the causes of SVT, what px sx will be experienced ?
Causes; caffeine/stimulants , hyperthyroidism, stress
| Px sx; sudden onset 'racing heart' , syncope, chest pain (if assoc CAD), light headed
251
What tx can be used for SVT ?
acute use of adenosine , Ca blocker, vagal manoeuvres (first) eg. valsalva
252
What are the features of WPWS on an ECG?
Long QRS, long QT, short PR, Slurred Q (delta waves).
253
Why is AF in WPWS dangerous ?
WPWS is congenital and often asymptomatic. AF can be life threatening as impulse propagates to ventricles directly through accessory pathway causing ventricular fibrillation.
254
How would a STEMI show on an ECG ?
ST elevation in 3 adjacent leads . Irregularly irregular R+R. May show reciprocal depression in leads 3+aVF.
255
What course of tx would you advise for a px with a STEMI?
PCI is gold standard. Maybe thrombosis if required. Can give pain relief eg. morphine
256
If a px's ECG shows; notched R waves, long QRS and large Q downstroke, what condition are they likely to have ?
Left bundle branch block.
| V1 shows W and V6 shows M pattern
257
What investigations would you do for a LBBB?
Cardiography and coronary angiography (catheter insertion)
258
What is the normal PR interval ? What condition makes it longer ?
120-200ms
1st degree heart block is >200ms.
P wave may be 'buried' in T wave.
259
What are the causes of 1st degree heart block?
AVN blocking drugs, hyperkalaemia, may be normal in athletes
260
What are the px sx associated with 1st degree heart block and what tx plan would you advise for them ?
sx; may be asymptomatic, dyspnoea/fatigue on exertion
| Tx; none if asymptomatic, if serious issue a dual pacemaker.
261
What is LAD syndrome and what can it cause ?
Left anterior descending syndrome from severe stenosis/occlusion of LAD.
Can cause NSTEMIs
262
What are px sx with NSTEMIs and what tx plan would you advise ?
Sx; Chest pain (at rest) breathless, sweating, syncope
Tx; Antiplatelets (aspirin+clopidogrel) , B blockers , pain (morphine) , check troponin for myocardial damage, coronary angiogram for PCI if needed.
263
What condition shows a fixed PR interval with an intermittent QRS on an ECG ? What are the causes ?
2nd degree heart block (type 2).
| Causes; age related conduction degeneration, MI, electrolyte imbalance
264
What are the px sx for 2nd degree heart block and how would you advise tx?
Sx; bradycardia, syncope, haemodynamic instability
| Tx; correct underlying cause, cardiac monitoring, permanent pacemaker insertion
265
How would a 3rd degree heart block be displayed on ECG ?
Ventricular rate <40bpm , atrial rate uncoupled from ventricular. Looks like random squiggles.
266
What are the cause of 3rd degree heart block?
Degeneration of AVN, inf MI, AVN blocking drugs, hyperkalaemia
267
What are the key features of BCT?
broad complex tachycardia
| assume VT until proven otherwise. Regular monomorphic rhythm. QRS >120ms , HR>100.
268
What are the px sx of BCT?
Hypotension, pulmonary oedema, palpitations, syncope, chest pain, cardiac arrest
269
What investigations would you do for BCT?
DCCV if unstable, anti arrhythmic drugs, echocardiography/angiography to determine cause.
270
How is pulse pressure defined ? (2)
Systolic bp - diastolic bp
| Delta V / Compliance
271
What are the systolic and diastolic pressures ?
Systolic, max pressure in aorta when heart contracts and ejects blood into aorta from LV
Diastolic, min pressure in aorta when heart relaxes before ejecting blood into LV
272
How does compliance vary through the human arterial system ?
Aorta is most compliant (so Pp is low) , compliance gradually down until min in saphenous and femoral arteries
273
What are the parameters for narrow and wide Pp ?
```
Narrow = <25% of systolic
Wide = Pp of >100
```
274
What are the 3 layers to a typical artery ?
Tunia intima, tunic media, tunica adventitia (externa)
275
What are the components of the tunica intima ?
endothelial layer, subendo layer, internal elastic lamina
276
Which layer of an artery has longitudinally orientated type 1 collagen ?
Tunica adventitia
277
What is the tunic media made up of ?
concentric layers of helical SM cells, elastic and reticular fibres, proteoglycans.
278
What type of artery regulates blood flow and how is it adapted?
Muscular artery, thin intimal layer with well developed internal elastic lamina. Regulates blood flow through adjustment of caliber.
279
Apart from muscular, name another type of artery and state how it's adapted for its function?
Elastic artery. Tunica media shows elastic fibres between SM cells. They store kinetic energy to smooth out surge in BP during systole
280
What are 3 main ways in which pulse pressure can be ^ ?
```
Endurance athletes (total peripheral resistance down, SV/CO ^)
^ Age (compliance low, less elastin, ^ type 1 collagen , ^ calcification (stiff wall))
Valvular disease (aortic; stenosis, regurgitation)
```
281
What is the action of class 1 drugs ?
Inhibit fast Na channels during depolarisation (phase 0) decreases conduction velocity and depolarisation.
282
What is the difference between 1A, B and C drugs ?
a, prolonged AP duration
b, decrease AP duration
c, no effect on AP
283
Give examples of 1 a, b and c drugs ?
A; Quinidine, Procainamide
B; Lignocaine, pheytoin
C; Flecainide, Encainide
284
What is propranolol and what effect does it have ?
Class 2 b-adrenoreceptor antagonist. ^AVN ERP (phase 4) to decrease HR and O2 consumption.
285
Which class of VW drug effect phase 3 of AP ?
Class 3 (inhibit K channels) to prolong cardiac depolarisation, AP duration and ERP.
286
Give two examples of Class 3 drugs ...
Amiodarone, Bretylium
287
What is Diltiazem, give two more examples of its class ?
Class 4 VW drug
| Verapamil, Nifedipine
288
What are class 4 drugs ?
Inhibit inward slow Ca (L type) current that would contribute to VT. Impairs pacemaker activity (phase 0/4 in pacemaker). Phase 2 in cardiac AP.
