Cardiology Flashcards
(157 cards)
1
Q
Define Thrombosis
A
- Exaggeration of normal haemostatic mechanisms that lead to
- formation of a solid mass within
- the circulating vascular system during life
- made from the blood constituents
2
Q
Predisposing factors for thrombosis (3)
A
NB stasis -> turbulence
3
Q
Mechanism of thrombus formation
A
- Stasis -> turbulence -> vessel wall damage
- Platelets recruited -> adhere, aggregate+ secrete factors to -> coagulation
- Vascular endothelium controls platelets + coagulation (protect blood)
4
Q
Features of arterial/cardiac thrombi
A
- Mainly platelets = pale
- Mural or occlusive depending on vessel size
- Lines of Zahn
5
Q
Features of venous thrombi
A
- Mainly blood clot = red
- Usually occlusive
- Lines of Zahn
6
Q
Lines of Zahn
A
Light lamination layers - platelet + fibrin
Dark layers - blood
7
Q
3 locations for cardiac thrombi and precipitating factors
A
- Atria - appendanges
a) HF = stasis
b) AF = stasis - Valves -> vegetation
a) Rheumatic fever
b) Infective endocarditis
c) Thrombotic endocarditis (Nonbac eg malignancy, SLE) - Ventricles -> mural
a) MI = stasis
b) Cardiomyopathy = stasis
8
Q
3 precipitating causes of ARTERIAL thrombi
A
- atherosclerosis -> ruptutre -> mural thrombus = wall
- aneurysms = stasis
- inflammation, vasculitis
9
Q
Precipitating causes of VENOUS thrombosis
A
- trauma
- post op (muscle relax, breath pain)
- immobility
- MI
- HF
- pelvic mass inc pregnancy
- thrombophlebitis(rare)
10
Q
Natural clot resolution sequence
A
- Resolution = fibrinolysis within clot
- Organisation = ingrowth of granulation tissue (fibroblasts->collagen, phagocytes, capillaries)
- Recanalisation = restore lumen, organised thrombus
- Fibrosis to reconstruct
11
Q
Main complication of arterial thrombus
A
ischaemia/infarction
12
Q
Main complication of venous thrombosis
A
Embolism
13
Q
Define embolism
A
- Passage of an insoluble mass
- within the blood stream
- impaction at a site distant from origin
14
Q
Commonest places of emboli impaction and origin
A
- Pulmonary arteries when thrombus is R side of heart
- Systemic arteries when thrombus is from Lheart/aorta
15
Q
Define ischaemia
A
- reduced blood supply to tissue/organ
- leading to harm effects due to hypoxia
16
Q
3 mechanisms of ischaemia. think pipe
A
- Internal vessel disease
- Occlusion bc thrombus/emboli
- External compression of vessel
17
Q
Define infarction
A
- Tissue death due to ischaemia
- usually caused by arterial occlusion
18
Q
Clinical complications of PE
A
- Sudden death
- Pulmonary infarction
- Pulmonary hypertension
- Asmptomatic
19
Q
Coronary artery network
A
LAD = apex, ant LV, ant IVS
LC = lat LV
RA = post inf LV, post IVS, RV
20
Q
2 main types of MI
A
1.Transmural (majority)
- full wall thickness infarct
- usually bc main CA for that area occluded (atherosclerosis)
- sometimes caused by vasopasm/emboli
- see ST elevation + Q waves (STEMI)
2.Subendocondrial
- involves diffuse infarction, least perfused region
- usually due to critical stenosis, without plaque change event (eg triple vessle atheroma)
- see ST depression (NSTEMI)
21
Q
What is haemopericardium and when does it usually develop
A
Rupture of LV wall post MI
4-10 days
consider in MI pxs who are having HF symptoms
NB myocardial rupture on free wall -> tamponade
septum -> shunt
pap muscle -> acute severe MR
22
Q
What is a late >3 month complication of MI due to fibrosis of wall
A
Cardiac aneurysm
23
Q
Define Gangrene
A
Necrosis
w bacterial infection
24
Q
Rare things that can be emboli
A
- Fat
- Air/gas
- Tumour
- Amniotic fluid
- Infective material
25
Layers of arterial wall
Intima - thin, where atherosclerotic plaque lesions occur
Media- full of smooth muscle or elastic
Adventitia - blood supply to artery itself
26
Constituents of atherosclerotic plaque
Fibrous cap
Lipid core
CT, ECM
smooth muscle and inflamm cells
27
clinical consequences of atherosclerosis
1. stroke
2. Mi, CHD, sudden death
3. AAA
4. Gut ischaemia
5. Gangrene of leg
28
Modifiable and non modifiable RF for atherosclerosis
_Non modifiable:_
1. Age
2. male
3. FH
4. Genetics
_Modifiable:_
1. Hyperlipidaemia
2. Hypertension
3. Smoking
4. Diabetes
NOT exercise
29
Response to injury hypothesis
Continuous endothelial damage -\> inflammation -\> plaque formation
30
Precipitating factors of ischaemic heart disease
1. Atherosclerosis (majority)
2. Hypertrophy, inc demand
3. Inc HR, inc demand
4. Hypotension, dec supply
5. Hypoxoemia
31
MI vs Angina
Angina = episodic ischaemia -\> pain
MI = prolonged ischaemia -\> myocyte necrosis
= raised CrK, Trop
both rise within 4-8 hours of MI
Crk stays for 3 days
trop 10
32
Define critical stensosis
Atleast **75%** cross sectional area of vessel occluded
**compensatory vasodilation** is **insufficient** to meet demand
NB less than this w unstable plaque, don't produce angina but dangerous bc no pre-conditioning
33
Explain the terms:
1. **Reperfusion Injury**
2. **Stunned myocardium**
3. **Pre-conditioning**
in the context of MI
1. Ischaemic tissue gets ox for 1st time = free radical release = 2nd hit
2. Saved ischaemic myocytes takes days to recover function
3. Rep'd ischaemic hits may prepare tissue to protect from infarction eg via bv formation
34
Complications post-MI
1. Cardiogenic shock (pump failure)
2. **Arrhythmias -\> sudden death**
3. **Late heart failure**
**4. post infarct unstable angina**
5. Cardiac rupture (MR, tamponade)
6. Pericarditis
7. Mural thrombus over scarred infarct
8. Ventricular aneurysm
35
Body's natural compensatory mechanisms for HF
1. Hypertrophy SIZE.
2. Dilation to inc preload
3. Fluid retention -\> inc BP + HR -\> CO
NB hypertensive hypertrophy -\> AF bc inc stiffness -\> atrial load inc
36
LHF
1. organ ischaemia
2. pulmonary oedema
37
RHF
1. Peripheral oedema
2. congestion of organs
3. ascites/ PE
usually secondary to LHF
Cor pulmonale is RHF due to pulmonary hypertension
Cor pulmonale **can** be acute - straight dilation eg due to PE (LHF cant)
or chronic = hypertrophy -\> dilation
38
Define Valve Stenosis
Failure of valve to open comletely
impedes forward blood flow
39
Define Valve Regurg/Incompetence + functional regurg
Failure of valve to close completely
due to valve OR environmental abnormality
leads to backward flow
functional regurg - due to ventricle dilation
can be acute OR chronic
40
Which valve is normally bicuspid
Mitral
41
Causes and consequences of mitral stenosis
1. **RHEUMATIC FEVER (99%)**
minority congenital
Consequences:
1. Inc atrial pressure -\> dilatation -\> AF -\> thromboemboli
2. inc atrial pressure -\> pul hypertension -\> oedema
3. Pul hypertension -\> RH dilation + failure
42
What is rheumatic fever and relevance in cardio
**Systemic inflammatory disease** caused by **group A** **strep** infection
usually few weeks after throat infection
multiple infections = cumulative damage = **chronic rheumatic heart disease** :
* Mitral stenosis (fish mouth, button hole sten)
* Pancarditis
*
43
symptoms of mitral stenosis
* Exertional dyspnoea
* Fatigue
* Haemoptysis
* Emboli - stroke, PE, cyanosed face
44
Signs of mitral stenosis
AF
Raised JVP
Malar flush (low CO)
Others - palpable + loud S1 (snap)
RV heave + loud P2 bc pul hypertension
rumbling diastolic
45
Malar Flush
Indicitave of mitral stenosis because of Co2 retention
NB more commonly because of rosacea, SLE, COPD
46
Mitral Stenosis
Mid diastolic murmur
Rumbling
slight click after s2 (opening) before wooshing sound
NB can have presystolic murmur if sinus rhythm
47
Mitral Stenosis
Descending, ascending
Mid diastolic murmur, rumbling
loud S1, open snap
ACCENTUATE IT
48
Causes of Mitral Regurg (4,4)
PRIMARY (degen) : 1. **Valve prolapse ( may be congenital)**
2. **Rheumatic** heart disease
3. **Infective** endocarditis
4. Collagen diseases
SECONDARY(func): IHD or cardiomyopathy
4. Papillary/chordae **rupture**
5. Papillary muscle dysfunction (**post MI**)
6. functional = LV dilation due to **HF**
7. Dilated **cardiomyopathy**
49
ACUTE MR presentation
No time for LV dilation to compensate so LA pressure inc -\> pulmonary hypertension + oedema
SOB
Fatigue
RHF signs
50
CHRONIC MR presentation
Same as acute (SOB, fatigue)
+ palpitatons (dilation)
LHF
51
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MR
Pan systolic
soft S1
Loudest at apex, radiates to axilla
accentuate by expiration, NOT move
may hear S3 w bell, lower pitch than S2
52
Signs of MR
Displaced apex beat, thrusting
if get LVF -\> S3 sound
if get pul hypertension -\> RV heave and loud S2
53
INV for MR
Transthoracic echo
ECG
54
Medical + surgical management of MR
IF LVF -\> diuretics and ACEI
IF AF -\> anti-coag + digoxin
treat any systemic hypertension and prophylaxis for infective endocarditis. Observe
**Surgical**
- valve replacement prosthetic or bioprosthesis (donate or animal)
- valve repair/ring
- mitraclip
- issue: emboli (anticoag), deterioration, infective endocarditis
55
Causes of AS
1. **Calcification** (most common, elderly \> 70)
2. Calcification of **congenital bicuspid** valve (middle age)
3. **Rheumatic** heart disease
56
Presentation of AS
1. Angina
2. Breathlessness/HF (LVH on ecg)
3. Collapse/syncope
4. Death
ABCD
57
Signs of AS
1. Slow rising carotid pulse
2. Thrusting apex beat
3. Soft/absent S2
4. May have LVF (S3), LVHeave
5. PP small
58
AS
Ejection Systolic murmur
loud S1
soft/absent S2
59
Early AS
Ejection systolic
soft S2
60
Causes of aortic regurgitation
**ACUTE:**
1. Infective endocarditis
2. Aortic dissection (usually due to aortic root dilation)
**CHRONIC:**
1. Rheumatic fever
2. Congenital bicuspid aortic valve
3. Other eg syphylis, hypertension, CT disorder (lead to dilation of aortic root)
61
Presentation of AR
1. SOB (sudden if acute cause)
2. LVF signs
3. Fatigue, chronic
62
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**AR**
End diastolic murmur
flat woosh after S2
63
Signs of AR
Collapsing pulse
Wide PP
displaced apex
Quinke
Head nodding (de mussets)
Visible carotid pulsation (corrigan's)
64
Layers of heart
65
Define infective endocarditis and complications
Usually **bacterial infection of endocardium** of heart
can be acutem (on normal valve) or chronic (on congenital or acquired valve defect)
Usually -\> bulky, **friable,** mitral/aortic valve (L sided) -\> **L sided thromboemboli, kidney**
IF IV drug user -\> tricuspid (R sided-\> **PE**
emboli may be **septic**
**can lead to myocardial abscess**
**valve rupture**
circulating immune complexes **-\> golemrular nephritis**
66
Risk factors for infective endocarditis
1. Abnormal valve
2. IV drug abuse
3. Immunosuppresion
4. DM
5. Alcohol
67
Symptoms and signs of infective endocarditis
1. Systemic features of infection: fever, sweats, acheetc
2. Murmurs and heart failure signs
3. Immune complex deposits -\> vasculitis:
Skin petechial haemorrhages
Oslers nodes (finger tender)
Janeway lesions (painless palm)
Splinter haemorrhages (nails)
68
Organisms and their virulence for infective endocarditis
69
Non- bacterial thrombotic endocarditis define, clinical relevance and risk
deposition of **small** **sterile**, fibrin/platelet **thrombi** on any **normal** heart valve
does NOT destroy the heart valve but can -\> **emboli**
WHY: **hypercoaguable** state:
- pregnancy
- cancer
- DIC
70
Define Myocarditis and causes
**inflammatory** process of myocardium -\> cardiac myocyte **injury**
usually caused by **viral infection**
can be caused by immune response:
- post infection
- rheumatic
- SLE
- drug sensitivity
- transplant
OR unknown cause : sarcoidosis
71
Complications of myocarditis
1. Asymptomatic -\> dilated cardiomyopathy later
2. Arrythmias
3. Acute HF (present w this + fever)
4. sudden death
72
Define pericarditis and causes
**inflammation** of pericardium typically post **viral** infection or **MI**
other causes:
cardiac, thoracic, systemic, mets
73
Pericarditis symptoms and signs
1. sharp, **pleuritic** chest pain, relieved when **sit forward**
**NB** pain can mimic MI in being dull and radiating to shoulder and back
also get ST elevation but its in ALL leads
2. May have fever
SIGNS:
1. **pericardial rub** because fibrosed layers
74
Pericardial rub
75
What is Erb's point
3rd ICS MCL
loudest S2
76
What is cardiomyopathy and the 3 types
Cardiomyopathyis heart disease resulting from primary abnormality in myocardial tissue.
1. **dilated (90%)**
**2. hypertrophic**
**3. restrictive**
77
Dilated cardiomyopathy characteristics
1. Hypertrophy
2. Dilation
3. Cardiac dysfunction -\> (arrythmias + thromboembolism + HF)
78
Causes of dilated cardiomyopathy
1. Idiopathic mostly ( can be in young people)
2. alcohol
3. peripartum - pregnancy reveals it about 5 months before
4. Genetic
5. Myocarditis
6. Haemochromotosis
7. chronic anaemia
8. drugs - doxorubicin, adriamycin
9. Sarcoidosis
79
Characteristics of hypertrophic cardiomyopathy
1. Hypertrophed myocardium (may inc septum) -\> **angina, AF, HF**
2. Impaired ventricle filling
3. Obstruction to outflow
**NB there is NO ventricle dilation**
**can lead to ventricular arrhythmia -\> sudden death**
80
Causes of hypertrophic cardiomyopathy
1. Genetic (50%)
4 contraction genes can have many mutate (aut dominant):
* cardiac troponin T
* B myosin heavy chain
* A tropo-myosin
* Myosin binding C protein
2. Sporadic (50%)
81
What is restrictive cardiomyopathy
Primary impairment of ventricular **compliance** -\> impaired ventricular **filling**
so have normal sized atria and ventricles, both atria dilated but actual myocardium is **firm**
82
Causes of restrictive cardiomyopathy
1. Idiopathic
2. Fibrosis secondary to radiotherapy (cancer)
3. Tumour mets
4. Amyloidosis (deposition of protein)
5. Sarcoidosis
6. Endomyocardial fibrosis and fibroelasticosis (tropical, young)
7. Congenital
83
Most common type of heart tumour + location
1. L atrial myxoma -\> mitral valve damage
most common primary heart tumour, but still rare
84
3 main categories of congenital heart disease
1. L-\>R shunt (abnormal connection, flow from high -\> low P)
2. R-\> L shunt
3. Obstructive
85
CONGENITAL : R-\> L shunts = **T**'s
= de-ox blood in systemic circulation -\> **CYANOTIC** **CONGENITAL HEART DISEASE**
1. Tetralogy of fallot
2. Transposition of great arteries
3. Persistent truncus arteriosus
4. Tricuspid atresia
5. Total anomalous pulmonary venous connection
86
**L-\>R = D's**
systemic -\> pulm = inc flow -\> **pul hypertension**
**TYPES:**
1. AS**D**
2. VS**D** = congenital, most common
3. P**D**A (patent ductus arteriosus)
4. AV septal **d**efect
over time the pul P\> systemic = reversal of flow = R-\> L shunt
**Eisenmenghers syndrome = late cyanosis**
87
CONGENITAL : Obstructive
Abnormal narrowing of chambers, valves or vessels
usually **congenital coarctation of aorta**
88
# Define hypertension
Stages of hypertension + limits
Persistently raised arterial BP
Stage 1- 140/90
Stage 2- 160/100
Stage 3- 180/110
89
BP drugs
Under 55: ACEi/ARB
55+ or Afro-carribean: CCB or D
stage 2 treatment: A+C
stage 3 : A+C+D
stage 4 (resistant): ACD + D + alpha/beta blocker
NB may need to give statins, antiplatelts etc to reduce CV risk if high
90
How ACEi work and why not useful in afro/carrib
1. Inhibits conversion of angiotensin 1-\>2
2. Black ppl have low plasma renin
91
ACEi indication, examples, SE, contraindications
1. **First line antihypertensive** in non black under 55. ALSO in CKD, HF, post MI
2. **-pril** eg ramipril, preinidopril, lisinopril, enalapril
3. SE
* **dry cough** (ACE mediated break down of bradykinin in lungs is inhibited)
* **hypotension** with first dose
* **AKI** reversible
* **hyperkalaemia**
* normal cr release
* angiodema - lip and airway
**CONTRAINDICATION**: pregnancy, breastfeeding, bilateral RAS
92
ARBs mechanism, indication, example, SE, contraindication
Inhibit the receptor of angiotensin 2 (AT1)
Indication: Alternative 1st line antihypertensive non black, CKD, HF, post MI
Example: - sartan, candesartan ,losartan, valsartan, irbesartan
SE: similar to ACEi other than cough ( rare)
CI: same as ACEi
NB dont use with ACEi = \> risk of AKI
93
CCB two types
1. Dihydropyridines = preferential action on **vascular** smooth muscle
- **dipine**
2. Non-dihydropyridines = act on **heart** and **vascularture (rate limiting)**
94
CCB: Dihydropyridine indication, mechanism, examples, SE, contraindications
Indications: First line antihypertensive in obver 55/afrocar. ALSO raynauds, angina
Mechanism: block L type calcium channels to block vasoconstriction, vasoselective so not rate limit
Examples: amlodipine, filodipine, nifedipine (short acting)
SE: ankle swelling, acid reflux, flushing, gingival hyperplasia
95
CCB: Non-dihydropyridines mechanism, indication, example, SE, contraindication
Rate limiting CCB (heart and vasculature Ca2+ block)
Indication: can use in hypertension but also: tachy's, angina, migraine + cluster headaches
Example: Verapamil(cardioselective), Diltiazem (heart + bv)
SE: worsens HF, cause bradychardia, heart block
verapamil = constipation
dont use in HF or px on beta blockers
96
Thiazide like diuretics mechanism, examples + SE
Block Na/Cl channel on DCT -\> Na + water loss
Examples: **indapimide**, chlortalidone. og thiazides -\> dm
SE: gout, erectile dysfunction,electrolyte disturbance,impaired glucose tolerance, hypercalcaemia (dont give in px with hyperparathyroidism)
97
Loop diuretics mechanism of action, examples, se
Block Na+K+CL- channel on ascending limb of LoH = block water and na reabsorption
indication: hypertension but longer diuretic than antihypertensive
other indications: pulmonary oedema,HF,nephrotic syndrome, ascites
Examples: furosemide, bumetanide
SE: elecrolyte disturbance, polyuria, dehydration
98
Potassium sparing diuretics AA mechanism, examples, SE, other indications
Aldosterone antagonists - block aldosterone mediated Na absoprtion and K+ excretion in CD eg spironolactone
eplerenone - primary aldosteronism or post MI
low dose in hypertension
SE: gynaecomastea, erectile dysfunction, hyperkalaemia
Other indications: HF, ascites
99
Potassium sparing diuretics NOT AA mechanism, examples, Se
Blocks epithelial Na+ channels and K+ excretion in CD, not via aldosterone
Eg. amiloride , triamterene
Indication: in combo with stronger diuretic eg furosemide
SE: hyperkalaemia
100
Alpha blockers mechanism of action, indications, examples, side effects
blocks alpha adrenoreceptor mediated vasoconstriction -\> vasodilation
Indication: men w BPH (tamsulosin), add on to other treatments
End in -**zosin** eg doxazosin, terazosin, prazosin
101
Beta blockers mechanism and selectivity examples
B1 = HR inc + force
B2 = smooth muscle dilation (vaso, broncho, muscle)
Beta blockers refer to **beta 1**
MOA: reduce HR and renin release
-**olol**
Cardioselective BAMN: bisoprolol, atenolol, metoprolol, nebivolol
Non selective : propranolol for anxiety etc
102
Beta blockers indications, adverse effects, CI
Indications: HF, IHD, arrhythmias, anxiety, migraine, oesophageal varices, glaucoma, thyrotoxicosis, essential tremor
SE: Bradycardia, tiredness, bronchoconstriction, cold extremities, depression, hypoglycaemia(may be masked) + depression
CI: **absolute in asthma**
relative in acute HF, peripheral arterial disease
103
Direct renin inhibitor MOA, Eg, SE
Renin secreted by juxtaglomerular cells to convert angiotensin 1-\>2
eg Aliskiren but limited clinical use
SE: diorrhoea, AKI
104
Postural hypotension - define and causes
Drop in SBP of \>=20, diastolic \>=10 from sitting to standing
Causes:
* drugs (doxazosin/a blockers)
* adrenal insufficiency
* DM
* alcohol
* PD
105
Management of postural hypotension
1. fludrocortisone
2. Midrodine (alpha agonist, opp of doxazosine)
3. droxydopa
nb can -\> hypertension
106
Define HF and 2 types
CO inadequate to perfuse organs
1. HF w reduced LVEF: systolic HF
2. HF w preserved LVEF: diastolic HF
107
Management of systolic heart failure
* ACEi or ARB (pril or sartan to reduce preload/afterload = work, slow disease progression)
* NB can combine with neprylisin inhibition = natriuresis -\> diuresis. **sacubitril-valsartan**
* Aldosterone antagonist (spironolactone, epleronone to reduce mortality)
* B blocker (olol, reduce HR/work = long term survival)
* Diuretic (thiazide or loop=reduce preload, doesn't reduce mortality)
* Digoxin (if HF caused by AF, inc force of contraction)
* Ivabridine (if B blocker not tolerated)
* Hydralazine w nitrate = dilate
108
Diastolic HF
Usually cuased by hypertension so control bp
symptomatic treatment
no evidence of systolic treatment reducing mortality here
109
Sinus bradycardia define, causes + treat
Regular heart beat, reduced rate.
ECG normal P-P increased
Causes:
* Young healthy, athletes (physiological)
* Increased vagal tone (psymp = slows)
* Hypoxia, hypothermia
* Drugs - beta blockers, calcium channel blockers
* post Mi ISCHAEMIA
* Sick sinus syndrome
Treat symptomatic: Atropine, block vagal tone
110
Heart Block define, types and describe ECG
**Impaired A-\>V conduction**
1. **First degree** - dont treat
heart rate consistent (P-P), P-QRS delay (\>0.2)
**2. Second degree**
* **Mobitz type 1 -** P-P gets bigger until QRS drops
* **Mobitz type 2-** P-P stays same, random QRS drop
**3. Complete heart block -** AV node sets pace
30-55bpm
111
RBBB
112
LBBB
113
Atrial tachy
114
Atrial flutter
115
Atrial fibrillation
116
Ventricular tachy
117
Ventricular fibrilation
118
Secondary hypertension causes
NB only 5% of hypertension is secondary
1. Primary hyperaldosteronism (and other endocrine disorders)
2. Renal disease
3. Vascular disorders like aortic coarctation
4. Drugs like alcohol and cocaine
119
Hypertension increases your risk of:
1. Stroke, haemorrhage
2. Retinopathy
3. CHD, LVH, HF
4. Aortic dissection/aneurysm
5. CKD, renal failure
6. peripheral vascular disease
(causes atherosclerosis)
120
Direct vasodilators for hypertensive emergencies
1. Nitrates
2. Hydralazine
3. Minoxidil
4. Sdium Nitroprusside
121
Centrally acting antihypertensives
1. Methyldopa
2. Moxonidine
3. Clonidine
122
Causes of angina
1. Narrowing or occlusion of major CA
2. AS, hypertrophic cardiomyopathy, severe anaemia = angina without CAD
3. CAD w anaemia, tachy, uncontrolled hypertension, hyperthyroidism
123
Diagnosis and treatment of stable angina
Present: chest pain on exertion/stress, relieved onr est/by GTN, lasting a few minutes
INV: resting ECG (normal or with ST dep or Q waves), FBC (anaemia) HbA1c (DM, silent), lipid profile
Manage: lifestyle, GTN, Bblock or CCB 1st line anti-angina, prevent CV event: aspirin (antiplatelet), statins (lipid), ACEi (bp, dm)
MAY decide to revasculate
124
Diagnosis and treatment of ACS (Unstable, NSTEMI, STEMI)
**PRES**: chest pain \>20min at rest/new onset/inc freq/severity, radiating to jaw/neck/arm, dyspnoea
**INV:** ECG (normal or ST depression), Trop, CrK, FBC (anaemia precipitate), U+E (baseline), Hba1c, lipid profile, INR (baseline), CXR (rule out DDs), coronary angiography (CAD)
**Manage**: MONAC - morphine, oxygen, nitrates, aspirin, clopidogrel + statin + betablocker
may have reperfusion therapy
**NOTE distinguish from NSTEMI by troponin- only raised with infarction not ischaemia. ie normal troponin in unstable angina.**
125
Treatment of STEMI
1. Reperfusion - PCI may have thrombolysis (fondaparinux)
2. MONAC
3. Long term:
* Beta blocker (reduce ox demand, inc diastole)
* ACEi
* Clopidogrel (12m) + Aspirin for life
* Statin
* BP control
* Lifestyle
* GTN prn
126
What is ACS
Unstable angina, NSTEMI + STEMI going from ischaemia -\> necrosis
Mostly caused by atherosclerosis but can have normal CA with other problems (See causes of agina flashcard)
127
Reperfusion therapy for ACS
1. PCI- requires angiography then angioplasty done where stent is inserted, balloon inflated
2. CABG- where there is anatomical indication
128
What is shock?
Clinical syndrome categorised by drop in mean arterial bp -\> tissue **hypoperfusion** and **hypoxia**
BP = CO X R
CO = SV X HR
SV = EDV-ESV
129
4 types of shock and eg
1. Cardiogenic - pump failure eg MI
2. Hypovolemic - reduced vol eg bleed,burn,diorrhoea
3. Obstructive - filling or after failure eg tamponade, PE
4. Distributive - widespread vasodilation eg sepsis, anaphylaxis
CHOD
All ead to tissue death
130
Physiological compensation for shock
1. Inc CO - symp stim = inc HR (SV) + vasoconstrict (R)
2. Inc Ox - symp stim = bronchodilate, inc resp
3. Redistribute to vital organs - vasoconstriction, ADH, renin (reduce urine)
4. Cortisol
5. Glucagon
6. Complement + inflamm cascade
131
Clinical signs of shock
1. tachy, hypotensive
2. inc resp rate
3. cold, mottled skin unless septic
4. reduced urine output
5. reduced consciousness
Other depending on cause: fever, SOB, chest pain etc
132
Management of shock
* A- stabilise airway even if GCS \<8
* B- oxygen (15L non-rebreathe), position
* C- 2 large bore (OG) cannulas, control haemorrhage, Cross match, fluid (crystalloid or colloid), Catheter
* D- manage blood sugar, monitor GCS
* Treat cause
* Analgesia
133
Crystalloid vs Colloid fluids and examples
Crystalloid = replace, maintain
* Dextrose, Saline, Hartmanns
Colloid = haemorrhage
* Gelofusine, hydroxyethyl starch
134
Types of blood product
1. Packed RBC = RBC + SAGM
2. FFP
3. Cryoprecipitate
4. Platelets
135
Universal blood donor and recipient
**donor:** O negative, no antigens, RHD-
**recipient:** AB (no antibodies)
136
4 classifications of haemorrhagic blood loss
1. \<15%(750ml) HR may inc, no change BP
2. 15-30%(750-1.5L), HR inc, no change bp
3. 30-40% (1.5-2L) HR inc, BP dec
4. 40+% (\>2L) HR inc, BP inc
137
Treatment of AR
1. Valve repair
2. Replace w tissue valve
xenograft: pig
autograft: ross kids
homograft: autopsy
3. TAVI
4. Mechanical valce:
bileaflet
138
Causes of AF
PIRATES
1. PE
2. IHD
3. Resp problems
4. Anaemia
5. Thyroid disease
6. Ethanol
7. Sepsis
139
Management of AF
1. Haem unstable -\> DC cardioversion
2. Rate control = beta blockers, CCB diltiazem, verapamil
3. Rhythm control - flecainide, procainamide pill in pocket or DC
4. Anticoagulation - assess risk of stroke w AF via CHA2DS2VAS score and risk of bleeding via HAS BLED score . start on lifelong **warfarin or doac**
140
What is CHA2DS2VAScore stand for
CHF
Hypertension
Age
Diabetic
Stroke history
Vascular disease
Age
Sex (female)
141
**ACEi**
SE's
CI
**SE:**
First dose hypotension
Dry cough
RAS (reversible AKI)
Angiodema
**CI:**
Bilateral RAS
Pregnancy/breastfeeding
142
Can an ARB be used with ACEi
No, risk of severe AKI
143
**CCB - dihydropyridines**
Uses: 1st line antiHTN for black + over 55. Also in raynauds, angina
**preferential for vascular smooth muscle, not rate limiting**
SE: **ankle swelling,**flushing, gingival hyperplasia, acid reflux
144
**CCB : non dihydropyridines**
**verapamil, diltiazem (AF) because rate controlling**
SE- verapamil = constipation
SE: slow HR in HF, brady pxs = bad
145
Name 2 diuretics that work in PCT , descending LoH respectively
PCT - acetazolamide (CA inhibitor, glaucoma)
descending LoH - mannitol (osmotic diuretic, ICP reduction)
146
MoA of loop diuretics, SE, examples
**Loop = ascending LoH block NaKCl**
SE- polyuria, dehydration, hypoelectrolytes inc calcium
Eg: furosemide, bumetanide
147
Thiazide diuretics + Thiazide like
Thiazide : bendroflumethiazide
Thiazide LIKE: indapamide
MoA block NaCL channels in DCT
SE - diabetes, gout, erectile dysfunction, electrolyte disturbed (hyponatraemia, hypercalcaemia)
148
Name some K sparing diuretics and moa
spironolactone - AA
amiloride, triamterene- block ep NaK channels in CD
149
MoA and SE of spironolactone
competitive antagonist for aldosterone in collecting ducts
SE - gynaecomastia, erectile dysfunction, hyperkalaemia
150
What is tamsulosin
alpha blocker used in BPH
SE - orthostatic hypotension
Alpha blockers can be used as last resort in hypertension but don't reduce mortality
151
SVT management
Narrow complex, regular rhythm tachy
Manage with:
1) vagal manouvers (syringe, carotid sinus massage)
2) Adenosine
If sinus rhythm does not return ?atrial flutter and start rate control = beta blocker
152
How does adenosine work (drug for SVTs) + SE
what drugs do the opposite
Works on receptors in AVN to cause K efflux, hyperpolarise cells, reduce HR
SE - impending doom transiently, flushing
Opp - theophylline, caffeine
153
Side effects of digoxin and how to treat OD
rate controller
can cause **hypokalaemia in a px on a diuretic already**
**toxicity (OD) can cause hyperkalaemia, arrhythmias,** NVDiorrhoea, yellow tingue to vision, fatigue, confusion
OD digoxin = atropine (blocks vagal tone to heart)
154
Name a few things that increase INR
interact with p450 - slows warfarin metabolism
INC: cranberry juice, ciprofloxacin, clarithromycin, metranidazole
155
Name a few things that decrease INR
Dietary vitamin K
Rifampicin
Carbamezapine
St Johns Wort
156
2 types of DOACs and examples
1. Direct thrombin inhibitors - dabigatran
2. Factor Xa inhibitors - apixaban, rivaroxaban
157
Name ways to support a px with smoking cessation
1. Behavioural
2. Nicotine replacement therapy - patches, lozynges, vape
3. Nicotine receptor partial agonist- Varenicline
4. Buproprion - helps with withdrawal symptoms
