ZJ: cardiac clinical 🫀 Flashcards
1
Q
L: Arrhythmia and Anticoagulation
Whats an arrythmia? and 2 possible reasons for it
A
change in normal rate/rhythm of heart.
- altered impulse gen e.g. changes in automaticity of pacemaker cells in SAN/ APs from elsewhehre
- altered impulse conduction e.g. complete/ partial block of conduction pathways in myocardium
2
Q
3 types of arrhythmias?
A
- bradycardia: HR < 60bpm
- tachycardia: HR > 100bpm
- AF
3
Q
whats sinus bradycardia?
and what might bradyc. also be caused by?
A
slowed HR but rhythm unchanged.
heart block
4
Q
whats the differenc ebetween supra-ventricular tachycardia and ventricular tachycardia?
A
SVT: arise above level of ventricles wither within atria
VT: arise within ventricles themselves
5
Q
how may sinus tachycardia occur?
A
HR increased but rhythm unchanged
6
Q
affect of rapid atrial rate and disturbance of conduction pathways in atrial flutter?
A
increased risk of localised thrombus formation and secondary embolic events (i.e. thrombotic stroke)
7
Q
most common type of arrythmias and who is it more prevalent in/risk factors?
A
atrial FIBRILLATION
- older people
- hypertensive
- HF
- coronary artery disease
- valvular artery disease
- obesity
- DM
- CKD
- caffeine
- alcohol
- cardiac surgery
- stress
- pulmonary embolism
8
Q
complications of AF?
A
stroke
congestive HF
9
Q
AF symptoms
A
- breathless
- light headed
- fatigue
- palpitations- racing, pounding, thumping in chest
- chest pain
10
Q
how is AF diagnosed in prim care?
A
WatchBP: oscillometric BP monitor (microlife).
records BP and detects pulse irregularity that may be caused by symptomatic/asymptomatic AF.
11
Q
whats AF often associated with?
A
other arrhythmias: atrial flutter/ supraventricular tachycardia
12
Q
what may occur during treatment of AF with anti-arrhythmic drugs?
A
atrial flutter
13
Q
6 classes of antiarrhythmic meds:
A
Na+ channel blockers (and affect phase 0)
- IA
- IB
- IC
beta blocker
- II
K+ channel blocker
-III
Ca+ channel blcoker
- IV
14
Q
why monitor for bradycardia when using II anti-arrhythmic drugs.
A
have beta blocker mechanism of action.
block symp activity; reduce rate! and conduction
15
Q
AF diagnosis?
A
- ECG
- ECHO
- TFTs
- CXR.
also maybe thyoid function
16
Q
3 types of AF?
A
paroxysmal: spontaneous within 7 days
persistent: > 7 days
permanent: over a year. needs management
17
Q
how is AF managed?
A
arrhythmia control (by rhythm/rate control)
thromboprohylaxis: to prevent strokes
treat underlying caus
18
Q
NICE: rate control is offered as first line strategy in AF patients EXCEPT?
A
- if their AF has reversible cause
- have HF primarily caused by AF
- new onset AF
- rhythm control strategy more suited (clinical judgement)
19
Q
rate control guidelines: what is offered (2) as part of strategy? NICE
A
standard beta blcoker or
rate limiting calcium channel blocker as initial monotherapy
consider digoxin monotherapy for those with non-paroxysmal AF only if theyre sedentary.
if doesnt work, consider combination therapy with:
- beta blcoker
- diltiazem
- digoxin
20
Q
rate control guidelines: what must not be offered for long term rate control?
A
amiodarone
21
Q
what must be considered (2) for patients with AF?
A
pharmacological and/or electrical rhythm control
22
Q
what is offered as therapy for patients having cardioversion for AF, thats persisted longer than 48h?
A
- offer electrical (instead of pharmacological) cardioversion.
- consider: amiodarone starting 4wks before and contrinuing up to 12 months after: electrical cardioversion. maintaining sinus rhyhtm.
- discuss benefits/risks of amiodarone.
23
Q
long term treatment options for rhythm control
A
- standard beta blocker first line unless contraindicated: then assess comorbidities:
- dronedarone for maintenance of sinus rhythm after successful cardioversion in those with paroxysmal/persistent AF/
24
Q
what drugs to avoid in tretment of rhythm control in patients with known ischaemic/structural heart disease?
A
class 1c antiarrhythmic drugs e.g. flecainide/propafenone
25
what strategies should be considered in people with infrequent paroxysms and few symptoms/ where symptoms induced by known factors (alcohol/caffeine)?
'no drug treatment'/'pill in the pocket'
26
what is amiodarone and what type of effects does it have?
| whats its dominant effect?
- iodine containing. struc similar to thyroxine.
- complex effects.
- Clas I, II, III, IV actions.
- dominant effect = prolongation of AP and refractory period.
27
amiodarone pahrmacokinetics
- incompletely absorbed after oral admin
- unusual: prolonged half life of several wks and extensively distributed in adipose tissue
- full clinical effects after months of treatment start
28
common side effects of amiodarone
- interstitial pulmonary fibrosis
- hyper/hypothyroidism
- liver tox
- photosensitivity: affect skin. wear big hats, sunscreen
- blue skin discolour- iodine accumulation in skin
29
amiodarone counselling points
- possible phototox: shield skin from light during treatment and months after.
- use wide spectrum sunscreen
- blurred vision- counsel on driving and skilled tasks
- symptoms of bradycardia and heart block if taken with sofosbuvir- containing regiments.
- compliance
- dont drink grapefruit juice: higher chance of SE
- Do not take if allergic to iodine.
- Discuss with your pharmacist or doctor if you are intolerant to lactose
30
non drug treatment options (5)
- ablation (pulmonary vein)
- ablate and pace (AV node ablation)
- atrial defibrillators
- maze procedure
- removal of left atrial appendage
31
antithrombotic therapy:
- risk and benefits of anticoags
- place of NOACs in AF management
due to rhythm abnormalities with AF, what is there a risk of to patient? how is this risk assessed?
risk of blood clotting.
using CHA2DS2-VASc scale
32
with CHA2DS2-VASc scale, which patients dont require antithrombotic therapy?
patients with AF who are clearly low risk. (age<65 and lone AF).
= males with score 0
= females with score 1 (point for F sex)
33
CHA2DS2-VASc scale: score 0-9 with 9 as highest annual stroke rate.
what are each points assigned for?
The acronym CHA2DS2-VASc stands for
```
Congestive heart failure,
Hypertension,
Age ≥75 (doubled),
Diabetes,
Stroke (doubled),
Vascular disease,
Age 65 to 74 and
Sex category (female)
```
34
what scale/score is used to assess bleeding risk in patients started on anticoagulation
HAS-BLED:
```
Hypertension: Uncontrolled, >160 mmHg systolic
Absorbance renal/ liver function: 1/2
Stroke history
Bleeding
Labile INR
Elderly >65
Drugs/alcohol use: 1/2
```
score= 3: increased 1 year bleed risk
35
whats the other clinical prediction calcluator for decisions on non-VKA oral anticoag (NOAC) and a vitK antagonist (VKA)?
the SAMe-TT2R2 score
36
role of anticoagulant?
preventing stroke and arrhythmias consequences
37
5 examples of anticoag?
```
apixaban
dabigatran etexilate
rivaroxiban
edoxaban
vit K antag e.g. warfarin
```
38
warfarin is a well established VKA that requires...
regular blood tests and counselling as many interactions
39
what is warfarin indicated for and what 2 things done prior to starting therapy?
PE, DVT, AF, mechanical heart valves etc...
- rule out contrainds e.g. active bleeding (main SE)
- baseline international normalised ratio (INR) taken
40
effect of anticoagulant therapy e.g. warfarin on INR
normal INR = 1.
warfarin adjusts this to 2-4.
i.e. anti-coagulated blood taken 4x as long to clot
41
target INR for:
a) AF, DVT, PE
b) mechanic heart valve?
a) 2-3
| b) 2.3-3.5
42
how to initiate warfarin therapy for: patients requiring rapid anticoag?
- 5-10mg on 1st day (lower induction dose for elderly)- given with a heparin usually LMWH.
- continue for min. 5 days and until INR=2 for 2 consec days.
- subsequent doses depend on prothrombin time, reported as INR.
43
how to initiate warfarin therapy for: patients NOT requiring rapid anticoag?
-lower LD over 3-4wks
| daily maintence: 3-9mg. taken at same time each day. (-6pm)
44
in which situations is INR regularly/not reg monitored?
if patients on oral anticoags- monitor INR
| NOACS/DOACS- dont need to monitor INR
45
how do the following NOACS/DOACS work?
a) dabigatran etexilate
b) rivaroxiban and apixaban
c) edoxaban
a) direct thrombin inhibitor
b) inhibit activated factor Xa
c) reversive and direct inhib of activated factor X (factor Xa)
46
whats recommended as an alternative to warfarin and what used for?
NOACS= alternative.
| prevention of stroke, systemic embolism in patients with AF.
47
how do NOACS compare with warfarin in reduction of relative risk of stroke and systemic embolism in AF patients?
NOACS are as effective as warfarin :)
48
what patients is anticoagulation offered to?
people with CHA2DS2-VASc score of 2 or more.
| taking bleeding risk into account
49
do not offer aspirin therapy solely for....
stroke prevention to people with AF
50
() when may idarucizumab (PRAXBIND) be used?
when rapid reversal of anticoag effects of DABIGATRAN is needed for emergency surgery/urgent procedures / in life threatening/uncontrolled bleeding
but studies of efficacy and safety are ongoing.
51
noacs side effects
bleeding,
minor (e.g., slight bruising/ occasional bleeding from the gums when bruising teeth) --> serious (e.g., vomiting blood, blood in stools/urine/ bleeding inside head).
52
2 types of heparin and the differences?
UFH- unfractioned: conventional heparin
- large mucopolysacc mols
- immediate anticoag properties
LMWH- low MW hep
- smaller polysacc chains
- longer and more predicatble half life than UFH
53
what does UFH do and how does it compare with LMWH?
UFH
prevents production of fibrin from fibrinogen
also has effects on inhibition of production of activated clotting factors.
LMWH
anticoag effect by inactivating factor Xa
54
which heparin more suitable for renal impairment?
UFH as short half life than LMWH- which also exreted renally.
55
how is UFH administered?
IV/ SC
56
adverse effects of the heparins?
UFH: major= haemorrhage
LMWH: potential= heparin induced thrombocytopenia. smaller risk
57
when is APTT coag monitoring required and when is it not?
req for high dose heparin
| no need for LMWH
58
whats Fondaparinux and when used?
synthetic pentasacc - inhibits activated factor X.
use: prophylaxis of VTE and treatment of DVT, PE.
used in acute management of MI.
59
what has a greater risk of intracranial haemorrhage: warfarin/DOACS?
warfarin
60
time to get to peak effect (Tmax) for DOACS?
immediate anticoag effect: 1-4hrs
61
is effect of missed doses greater for warfarin or DOACs and why?
greater loss of anticoag from missed doses for DOACS and they have a shorter half life
62
3 points to do before prescribing doacs/ warfarin?
- view patient holistically- comorbidities, indications for use of DOACS for appr treatment
- review compliancee
- review all meds, check inetractions.
63
clincially: whats checked before prescribing warfarin/doacs?
- renal function and consider cautions and dose adjustments
e. g. apixaban risk of bleeding if eGFR <15ml/min/1.73m2...
- monitor renal func annually esp in elderly w age relaed decline in kidney func
- review hepatic impairment, avoid in severe impairment
- account for patient weight if needed.
64
L: cardiac clinical pharmacy
how can drugs affect heart function? 2
direct: force of contraction or rate/rhythm
indirect: vasculature or BV/composition- diuretics
65
whats CO? and eqn?
CO= HR x SV
vol of blood ejected for each vent contraction
66
2 things SV is determined by?
preload/ LV EDP
afterload: pressure in wall of LV during ejection
inotropy: contractility
67
What determines contractility?
the myocardial striated muscle, involving Ca2+
68
What do inotropic drugs affect?
the force of the heart contractions
69
What do positive inotropic drugs do and how?
Increase force of heart's contraction by increasing calcium, therefore increase heart rate
70
What do negative inotropic drugs do? give example drug
decrease the force of the heart's contraction and therefore decrease heart rate
Verapamil
71
What are 3 inotropic drug classes?
- Cardiac glycosides
- Sympathomimetics
- Phosphodiesterase inhibitors
72
How does digoxin work?
| image p46 s1 w9
- inhibits cell memb Na+/K+ATPase -> reversal of usual Na/Ca exchange
- normally, ⬆ intracellular Ca -> enhanced strength of contraction (+ inotropism)
- also affects elec physiology of heart, blocking (AV) conduction and ⬇ HR by enhancing vagal nerve activity
⬆Ca, contraction, HR
73
What is the principal indication of digoxin?
permanent/persistent Atrial Fibrillation (AF) with a fast ventricular rate - but not preferred first-line
74
What does NICE guidance suggest digoxin should be used as first-line in?
patients with AF who also have co-existing HF
75
Digoxin is reserved for patients where the heart failure is due to... and has worsened despite the use of...
- due to left ventricular dysfunction
- despite the use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and diuretic therapy (No impact on mortality).
76
Is the therapeutic index of digoxin low or high? What action should be taken?
low, so patients should be reviewed for clinical signs
77
What are the signs and symptoms of digoxin toxicity?
- Bradycardia
- Arrhythmia
- Nausea, vomiting
- Confusion
- Visual disturbances, blurred or yellow vision
78
Digoxin toxicity is more pronounced with what types of disturbances? What action should be taken consequently?
with metabolic or electrolyte disturbance (potassium levels?) - electrolyte monitoring is important
79
What might be required when treating digoxin-toxicity in an emergency?
Digoxin-specific antibody fragments
80
What is the inital dosing of digoxin for patients with AF and atrial flutter?
high dose as initial LD (rapid digitalisation)
15mcg/kg lean body weight
LBW= total body mass-fat mass
81
The maintainance dose of digoxin is calculated as a fraction of the XX and is adjusted for renal function based on XX
fraction of the effective loading dose..
| ..based on creatinine clearance (mL/min)
82
Monitoring for digoxin is important to prevent factors that can provoke toxicity. Name two of these factors?
renal dysfunction and hypokalaemia
83
How often should urea and electrolytes be measured in patients taking digoxin?
anually but more regularly if change in dose or clinical status
84
inotropic drug receptors position and action.
Where are alpha receptors expressed?
vasculature
85
Do alpha receptor agonists cause vasoconstriction or vasodilation?
vasoconstriction
86
Where are beta 1 receptors expressed?
in the heart
87
Are beta 1 agonists positively or negatively chronotropic?
positively
88
Where are beta 2 receptors predominantly expressed?
vasculature
89
Do beta 2 receptor agonists cause vasodilation or vasoconstriction?
vasodilation
90
Sympathomimetics are mostly limited to hospital use. What is the route of admin of them?
IV
91
medium dose of dopamine is associated with what?
b1 tachycardia and increased force of contraction
92
whats large dose dopamine predominanty assoc with?
alpha effects causing peripheral vasoconstriction
93
Which receptors does dobutamine act on?
predominatly b1 and some b2
94
Does dobutamine cause more or less tachycardia than dopamine?
less
95
Why is dobutamine used in cardiogenic shock?
b2 action offloads heart and b1 action increases force of contraction
96
which receptors does adrenaline act on?
b1 and b2
97
What is the rationale behind using adrenaline for cardiac arrest?
attempts to save brain and myocardium from ischaemia by causing mass peripheral vasoconstriction (alpha effects) and strong positive chronotropia (B1 effects)
98
Noradrenaline is an alpha adrenoceptor.
| Does it cause vasoconstrictor or vasodilator action?
vasoconstrictor
99
Why are phosphodiesterase inhibitors rarely used now and only in severe heart failure as adjunctive therapy?
risk of mortality
100
Give two adverse effects of phosphodiesterase inhibitors associated with chronic use?
arrhythmias and increased mortality
101
give two examples of phospdiesterase inhibitors?
enoximone and milrinone
102
affect of phosphodiesterase inhibs?
⬆ contractility + ⬆ HR
103
What is the mechanism of action of phosphodiesterase inhibitors?
- ⬆ CAMP via coupling with other intracellular messengers
- ⬆ inotropy and chronotropy
(contractility and HR)
- cyclic AMP broken down by cAMP dependant PDE enz
- so inhibitors inhibit degradation of intracellular conc of cAMP
104
What is the difference between inotropy and chronotropy?
inotropy is contractility and chronotropy is heart rate
105
What are the 3 different types of HF?
LVSD
HFPEF
HF caused by diseased/damaged heart valves
106
Which type of heart failure is due to the left ventricle which pumps blood around the body becoming weak?
LVSD
107
which type of HF is due to the left ventricle becoming stiff and therefore it becomes difficult for the heart chamber to fill with blood?
HFPEF
108
Give 6 signs of heart failure?
rapid weight gain, shortness of breath, increased swelling in lower body, trouble sleeping, frequent dry hackign cough and loss of appetite
109
What thought should be given to medicines adherence in the general principles of management of HF?
keep dosing regimens as simple as possible and fully inform patients and carers
110
What are the 3 components of the general principles for the treatment of HF?
medicines adhrenece, multidisciplinary approach to care and comorbidities
111
first thing given to HF patients diagnosed (before checked for hefref/ hefpef)?
offer diuetics- relief of congestive symptoms + fluid retention
112
What is the first line treatment offered to patients with HF with reduced ejection fraction?
HFrEF
ACEi and BB
| MRA if symptoms continue
113
How should acei be introduced in the first line treatment of HF?
start at low dose and titrate upwards at short intervals until target or max tolerated dose is achieved
114
Give two counselling points that it would be important to tell patients who are about to start ACEi therapy?
take first dose at night to avoid dizziness caused by low blood pressure
report a persistent/ troublesome dry cough
115
what to monitor- first line ACEi for HF?
serum Na, K and renal function before and 1/2 wks after starting
and after each dose increment
116
```
What is the first line drug class that should be offered to all HF patients due to left ventricular systolic dysfunction?
LVSD
```
beta blockers
117
How should beta blockers be introduced in the first line treatment of LVSD?
start low go slow
118
What should be assessed after each titration of beta blockers in the treatment of LVSD?
HR, BP and clinical status
119
What counselling would you give to someone who has just started beta blockers for LVSD? 3
do not stop taking unless doctor advises
may experience SE: fatigue, cold hands and feet and dizziness.
Doctor will gradually increase dose so regular check ups required
120
What is the first line drug class that should be considered in HF patients due to LVSD who have intolerable effects such as a dry cough?
ARB
121
If a patient is intolerant to both an ACEi and an ARB, would would be the next step in the treatment plan?
seek specialist advice and consider hydralazine with a nitrate
122
What two drugs classes are usually the first line used together for HF patients?
acei and bb
123
What should be offered to patients who have heart failure with reduced ejection fraction who continue to have symptoms after using ACE/ARB and BB?
MRA:
| mineralocoricoid recp antagonist
124
What should be measured and when in relation to MRAs?
serum K and Na and renal function before and after starting MRA and after each dose increment
125
which ethnic group of patients may benefit from hydralazine in combination with a nirate for second line treatment of uncontrolled HF with moderate to severe HF?
afro caribbean
126
specialist treatment of HF:
Sacubitril valsartan is used for treating symptomatic chronic HF with REF only in which groups of patients?
NYHA 2 to 4 symptoms, and w
LV ejection fraction 35% or below and
taking a stable dose of ACEi/ARB
should be started by HF specialist w access to multidisciplianry HF team
127
Where digoxin tox/ non adherence is suspected, serum levels should not be monitored routinely. How should they be monitored?
within 8-12 hrs of last dose
128
whens digoxin recommended for use in HF?
worsening/ severe HF due to :VSD despite first and second line treatment for HF/
129
whats a big problem w digoxin and what does this mean for monitoring?
toxicity can occur in therapeutic range, so interpret in cinical context and monitor
130
Name a drug that inhibits the If channel in the sinus node?
ivabradine
131
What is the only known pharmacological effect of ivabradine?
slow heart rate in patients sinus rhythm
132
Who should initiate ivabradine?
HF specialist
133
What are some of the benfits of Ivabradine?
shown to reduce CV death or hospitalisation for HF. Improved left ventricular function and quality of life
134
What food product should be avoided by patients that are taking ivabradine?
grapefruit juice
135
Why should people taking ivabradine be careful driving or using machines at times where there could be a sudden change in light intensity especially driving at night?
may cause temporary luminous visual phenomena
temp brightness in field of vision
136
Give 3 side effects that patients taking Ivabradine may experience?
breathlessness, fatigue and irregular heartbeat
137
Why are loop diuretics such as furosemide commonyl used in HF patients?
treat fluid that accumulates in the body due to heart not pumping blood around the body as well as it should
138
Apart from furosemide name two other loop diuretics?
bumetanide and torasemide
139
who to avoid CCBs in and why?
| verapamil, diltiazem, short acting digydropyridine agents
ppl w HF and reduced ejection fraction as they reduce cardiac contractility
140
L: Acute Coronary Syndromes and Stable Angina
Define Acute Coronary Syndrome
any group of syndromes attributed to obstruction of coronary arteries
inc:
NSTEMI
STEMI
unstable angina
141
common cause of MI (heart attack)?
blood clot- stops blood flowing to part of heart muscle
, commonly clot formed inside coronary artery/ branch
may form if theres atheroma (plaques) that develop inside lining of arteries
142
in MI, a rise in what can be seen? and whne do levels become detectable?
cardiac enzyme troponin
- inc when cells are damaged
Toponin I and T: detectable in serum 3-6hrs after infarction.
peak: 12-24hrs
remain raised for up to 14 days
143
with MI, when are troponins (enz) testsed?
5-12 hrs after onset of pain as thats when become detectable and reaching peaks
144
2 types of MI?
```
ST elevated (STEMI)
- elevation on ST segment - after peak- of 12 lead ECG
```
Non ST elevated (NSTEMI)
- no change in 12 lead ECG
145
why are death rates higher in first few hours of cardiac event?
heart muscle starts to die within 80-90 minutes after it stops getting blood, and within six hours, almost all the affected parts of the heart could be irreversibly damaged.
get abnormal heart rhythms called arrhythmias!!!
146
MI caused by atherosclerotic plaque formation- what does this do?
- stable plaque
- unstable
stable plaques: can obstruct arterial blood flow and = symptoms of angina
unstable plaques: prone to rupture and can form thrombus
147
modifiable risk factors for MI?
```
tobacco smoke
high cholesterol
high BP
physical inactivity
obese
diabetes
```
148
non-modifiable risk factors for MI?
age: over 65
male
family history
race
149
symptoms of MI?
suddent onset crushing chest pain
starts in centre chest, radiates to arms, neck, jaw
sweating +shortness breath
150
MI symptoms often similar to..?
sometimes diff to distinguish: heart related chest pain and GORD
151
STEMI treatment?
| aspirin 300mg + ..... (4)
coronary reperfusion therapy
- prim percutaneous coronary intervention (PCI) with antiplatelet (ticagrelor/ prasugrel)
- or fibrinolysis (reteplase/ tenecteplase)
coronary angiography- find blockage w dye
med management and sec prevention
pain relief, anti-emetics, glycaemic control
152
3 antiplatelet examples used in STEMI treatment?
Prasugrel
Ticagrelor
Cangrelor
153
how does prasugrel anti-platelet inhibit platelet activation and aggregation?
through irreversible binding of its metabolite to P2Y12 class of ADP receptors on platelets
154
when prasugrel prescribed in MI?
with aspirin- prevntion of atherothrombotic events in STEMI having primary/ delayed PCI
155
whens ticagrelor (antiplatelet) used in MI treatment and what is it?
STEMI: PCI,med management
- ADP rec antagonist
156
Ticagrelor: SE?
dyspnoea, haemorrhage
PLATO-trial
advantage may lie in faster onset of action
157
when/hows cangrelor given in STEMI treatment?
with aspirin, to reduce thrombotic CV events in patients w coronary artery disease undergoing perc coronary intervention (PCI).. whove not had treatment w oral clopidogrel, prasugrel, ticagrelor prior... and cant take oral drugs.
give under expert supervision only
158
secondary prevention of STEMI?
aspirin low dose (75mg) lifelong +....
+ dual antiplatelet therapy (clopidogrel) if had stent
+ ticagrelor with aspirin for up to 12 months
- PPI to reduce GI SE
- BB to reduce mortality after MI
- lipid lowering treatment
- ACEi
- aldosterone antogonist (epleronone) w HF post MI
-low dose rivaroxaban w aspirin/ aspirin + clopidogrel- preventn of atherothrombotic events after STEMI. anticoag
159
rational for using factor Xa inhibitor: rivaroxaban as sec prevtnion of STEMI?
low dose rivaroxaban w aspirin/ aspirin + clopidogrel
| prevention of atherothrombotic events after STEMI.
160
whats Unstable Angina?
patient has symptoms of MI but not sufficient/no troponin rise
may/ may not have changes on ECG
161
treatment of STEMI and Unstable Angina?
| Aspirin LD 300mg +....? (5)
- Ticagrelor (180mg LD)
- eptifibatide/tirofiban (diff antiplatelet mechs) for patients undergoing coronary angioplasty/ abciximab as ajunct to PCI
- antithrombin therpay w fondaparinux/ unfractioned heparin
- coronary angiography w/wout PCI/ CABG
- pain relief and anti-emetics
162
treating NSTEMI, unstable angina: consider eptifibatide/tirofiban (diff antiplatelet mechs) for what patients?
undergoing coronary angioplasty/ abciximab as adjunct to PCI
163
individual risk of future adverse CVE after NSTEMI/ unstable angina?
low: up to 3%
inter: 3-6%
high: <6%
164
secondary prevention of NSTEMI and unstable angina? (4)
- dual antiplatelet therpay
- lipid lowering med statins
- ACEi
- beta blockers
165
lifestyle changes - cardiac rehab services for sec prevention?
stress management
physical activity
- healthy eating: meditt diet: more bread, fruit, veg
- less alcohol (14 units wk max)
- 20/30min activity a day
- stop smoking
- BMI
166
cardiac rehabilitation- when offered to patients?
to px soon after cardiac event
highlight benefits of program
start within 10 days of hospital discharge
diet, meds, exercise, therapy
167
Understand what stable angina is
| - what does it result from?
chest pain/ discomfort caused when heart muscle doesnt get enough blood
- demands of myocardum being unstable to be met by blood supply
168
what happens to coronary arteries in stable angina? and when?
narrowing of one/more
| occur when heart has to do work- exercise/ emotional stress
169
stable angina= imbalance in what?
myocardial O2 sypply... and O2 demand.
| need more O2!!
170
when does stable angina pain occur and what should it be managed as form of?
precipitated by predicatable factors- exercice
any time,
consider as acute coronary syndrome
171
aim of management of stable angina?
manage as acute coronary syndrome...
- stop/minimise symptoms
- imporve quality of life + long term morbidity + mortality
172
where does anginal pain occur and how is it relieved?
constricting discomfort in fron of chest, neck, shoulders, jaw, arms
precip by physical exertion
relief by rest/ GTN in about 5 mins
173
Describe the management of stable angina
- GTN for rapid symptom relief
- bb/ CCB as first line
symptoms not adequately controlled/ tolerated... switch to other/ use combo of both
174
Describe the _monotherapy_ management of stable angina
| IF bb/CCB not adeq controlled symptoms/ contraindicated/ not tolerated (3)
- long acting nitrate
- Ivabradine (selective inhib of sinus node pacemaker activity)
- Ranolazine (⬇ MIscaemia by acting on intracellular Na+ currents)
175
management of stable angina: what to use if using ccb with bb/ ivabradine?
slow release nifedipine, amlodipine, or felopdipine
176
management of stable angina: when can third anti-angina drug be added?
px symptoms inadequately controlled w 2 drugs
| px waiting for revascularisation/ not appropriate/ not acceptable
177
management of stable angina: when only to consider nicorandil?
other meds unsuitable bc risk of ulceration.
178
management of stable angina: whats nicorandil- MoA?
properties of nitrate but also activates ATP-dpeendant K+ channels.
opens them -> muscle cells in blood vessel walls relax -> widen -> more blood flow ☺
179
whens coronary revascularisation required?
in px at high risk
| those who have failure to be controlled by medical therapy
180
coronary revascularisation: nitrates- types and what do they protect against?
problem with them?
short vs long acting
- protect against exercise induced ischaemia
can get tolerance after certain timings in day
181
what to remember when how to prescribe nitrates?
| SE?
adjunctive therapy not monotherapy
headache and cutaneous flushing...
also maybe post hypotension and reflex tachycardia
182
how do nitrates work? to cause vasodilation and relax vasc SM?
- mimic endogenous NO (release it)-> vasodil by relaxing smooth muscle
- improve coronary blood flow,
⬇ pre load- dilate veins and afterload- dilate arteries
183
main limitation of nitrates?
| how to resolve/help
tolerance!
develops rapidly
nitrate free period of few hrs each 24hrs
should coincide w period of lowest risk- usually night time
184
DDI between nitrates and phosphodiesterase-5 (PDE5) inhibitor sildenafil?
dont combine... can -> severe hypotension and death
185
patient care after MI?
- diet, exercise, smoking cessation
- cardiac rehab
- med adherance
- divide med:
* presc to ⬇ reinfaction and mortality
* presc for symtpom control
- what to do if SE happen
- identify concerns openly-encourage
186
common problems to dicuss w patients after MI. patient care
- use of nitrates
- use of NSAID, ACEi
- SPEED! if fibrinolytic drugs needed after MI
- aspirin and GIT bleeding. take w food and water
- unpleasant bb SEs
187
whats are some unpleasant beta blocker SEs
| common
feeling tired, dizzy or lightheaded (slow heart rate)
cold fingers or toes (blood supply affected)
difficulties sleeping or nightmares
feeling sick
188
how are stents placed into artery?
| Coronary angioplasty and stent insertion
- coronary artery on surface on heart.
- balloon catheter put in with a closed stent around it
- balloon is inflated and stent expands and plaque around it is compressed= widened artery, inc blood flow
When the operation is finished, the cardiologist will check that your artery is wide enough to allow blood to flow through more easily. This is done by monitoring a small amount of contrast dye as it flows through the artery.
The balloon, wire, catheter and sheath are then removed and any bleeding is stopped with a dissolvable plug or firm pressure. In some cases, the sheath is left in place for a few hours or overnight before being removed.
189
meds usually taken with a stent (NHS site)
aspirin – taken every morning for life
clopidogrel – taken for 1 to 12 months depending on whether you have had a bare metal or drug-eluting stent, or whether you have had a heart attack
prasugrel or ticagrelor – used as alternatives to clopidogrel in people who have been treated for a heart attack
190
4 types of antiplatelet drugs
cox inhib: aspirin
P2Y12 receptor blockers: irreversible/reversible
GP IIb IIIa inhibitors
phosphodiesterase inhibitors
191
examples of:
- irreversible P2Y12 receptor blocker antiplatelets
- reversible P2Y12 receptor blocker antiplatelets
- ticlopidine, clopidogrel, prasugrel
| - ticagrelor, cangrelor
192
examples of: GP IIb IIIa inhibitors antiplatelets
- monoclonal antibody ones
- synthetic molecules
- abciximab
- eptifibatide, tirofiban
... prevent platelet aggregation
193
2 examples of antiplatelet: phosphodiesterase inhibitors?
dipyridamole, cilostazol
194
how does aspirin (cox inhib) prevent platelet recruitment and activation?
inhib cox, key enzyme in TXA2 generation
potent antiplatelet for inhibiting TXA2
195
how do P2Y12 receptor inhibitors inhib platelet recruitment + activation?
through irreversible binding of its active metabolite to P2Y12 class of ADP rec on platelets
196
how do GPIIb/IIIa inhibitors prevent platelet aggregation?
block GP... receptors on platelet surface
| - most abundant rec on surface, and are final common pathway of platelet aggregation
