cardiovascular Flashcards
(277 cards)
1
Q
define AF
A
irregular atrial contraction caused by chaotic impulses
2
Q
causes of AF
A
hypertension,
ischaemic heart disease, MI,
cardiomyopathy
rheumatic heart disease
3
Q
clinical signs in atrial fibrillation
A
left atrial thrombus
apical+radial pulse defect
palpitation
4
Q
2 main types of atrial fibrillation treatment
A
rate control: first line. control fast ventricular rate
rhythm control: acute onset, restore sinus rhythm
5
Q
examples of rate control drugs
A
beta blockers (metoprolol, bisoprolol) rate limiting calcium channel blockers (verapamil, diltizem) digoxin: bed bound patients
6
Q
when is rhythm control used for Atrial fibrillation?
A
new- onset
HF exacerbated by AF
atrial flutter
identifiable reversible cause
7
Q
2 types of rhythm control methods
A
- pharmacological: amiodarone, flecainide, beta blockers
2. electrical: DC cardioversion
8
Q
treatment for AF onset of 48hours +
A
increase thromboembolism risk, need minimum of 3 weeks of anticoagulant to reduce risk before cardioversion
9
Q
treatment for AF onset less than 48hours
A
low risk of thromboembolism, immediate electrical or pharmo cardioversion
10
Q
when and why is anticoagulant given for AF
A
CHA2DS2-VASc score 2 or more
AF leads to stasis of blood in left atrial appendage forming thrombus
clot could move to cerebral, limb, abdominal causing stroke/ ischemia
11
Q
how is AF confirmed
A
ecg: absent p wave, fibrillation baseline
12
Q
mechanism of aspirin
A
antiplatelet: Irreversible inhibition of cyclooxygenase and thromboxane A2
13
Q
unstable vs stable angina
A
unstable pain at rest, relieved by GTN
stable pain while running or excercise
14
Q
heparin/ LWMH mechanism
A
anticoagulant: increase the action of anti-thrombin III to inhibit factor Xa
15
Q
mecahnsim of clopidogrel
A
antiplatelet: Inhibition of the adenosine diphosphate (ADP) receptor.
16
Q
anticoagulant vs anti platelet
A
Anticoagulants slow down your body’s process of making clots.
Antiplatelets, prevent blood cells called platelets from clumping together to form a clot, ie, after heart attack or stroke or prevention
17
Q
immediate/ initial management for all ACS patient
A
MOAN morphine oxygen (94) nitrates (GTN) aspirin + ticagrelor/clopidogrel
18
Q
site and artery for V1-V4
A
anterior
LAD
19
Q
site and artery for I, aVL V3-V6
A
anterolateral
circumflex, LAD
20
Q
site and artery for I, aVL, V5-V6
A
Lateral
circumflex
21
Q
STEMI management
A
PCI (w/ anitplatelet)
Thrombolysis
ACEi (prevent cardiac remodelling)
BB (reduce mortality)
22
Q
2 main treatments for NSTEMI and UA
A
dual antiplatelet
antithrombotic: fondaparinux (2.5mg)
BB
23
Q
post MI management
A
dual antiplatlet therapy (asparin + clopidogrel) for 1 year
High dose atorvastatin for high cholesterol
No alcohol
24
Q
ACS diagnostic
A
ECG
raised troponin T & I (STEMI & NSTEMI, myocardial necrosis)
25
examples of tachycardia
Atrial fibrillation, atrial flutter, SVT (AVNRT, AVRT)
| Ventricular Tachycardia
26
causes for tachycardia vs bradycardia
increase vs decrease automaticity
tachy: triggered activity & reentrant circuit
Brady: conduction block
27
causes of increased automaticity
increase sympathetic trunk tone
| increase metabolic activity
28
examples of increased sympathetic tone
hypovolemia
hypoxia
sympathomimetic drugs
pain/ anxiety
29
examples of increase metabolic activity
fever
| hyperthyroidism
30
causes of hypoxia
decrease in RBC
lung disease
PE
31
slow/ block AV conduction drugs
bb, ccb, digoxin
32
causes of decreased automaticity
```
increase parasympathetic/vagal tone
slow AV conduction drugs
decrease metabolic activity
hyperkalemia
Cushing triad
```
33
examples of decreased metabolic activity
hypothermic
| hypothyroidism
34
what is the cushing's triad
bradycardia
irregular respiration
hidden pulse pressure
35
2 types of triggered activity/ after depolarization (main cause of ventricular tachycardia)
early(EAD): phase 3 of electrical potential
| late (LAD): phase 4 of electrical potential
36
causes of early after depolarization EAD
decrease in K+, Ca+, magnesium
37
causes of late after depolarization LAD
tachycardias
| overload of intracellular calcium
38
EAD vs LAD physiology
trigger occurs on polarization of myocardial cells
EAD: early trigger of during depolarization, increase QT interval
DAD: late trigger after depolarization is complete
39
physiology of AVRT(atrioventricular reentry tachycardia)/ Wolff Parkinson white
contain bundle of Kent: bi direction accessory pathway
normal: AV node-> bundle of his & Purkinje fibres-> ventricule depolarize
abnormal: AV node-> bundle of Kent-> comes back down= re-entery circuit
40
physiology of AVNRT
reentry due to 2 SA->AV node pathways
path 1: slow w/ short refractory
path 2: fast w/ long refractory
2 electrical signal travel and refract at different speed causing electrical conduction to travel back from AV-> SV node = problematic
41
causes of conduction block
```
RCA occlusion causing inferior MI
fibrosis of AV node
hyperkalemia
drugs (BB, CCB, digoxin)
amyloidosis & sarcoidosis
```
42
tachycardia treatment: regular rhythm+ narrow QRS
1. vagal manoeuvre
| 2. adenosine
43
ventricular tachycardia ecg
wide QRS + regular rhythm/ broad complex tachycardia
44
ventricular tachycardia treatments
1. amiodarone+ procanimide
| 2. DC shock cardioversion (do this first if they have symptoms of shock, chest pain, HF)
45
ventricular fibrillation ECG
wide QRS with irregular rhythm
46
ventricular fibrillation treatment
VERY dangerous
| CPR+defibrillation and repeat
47
Common death cause in first hour inferior wall MI
Arrhythmia: ventricular fibrillation
48
presentations of aortic stenosis
ejection systolic murmur radiates to carotid
| soft/ absent S2, narrow pulse pressure
49
presentation of pulmonary stenosis
ejection systolic, crescendo descendo
| ventricular thrill/ heave
50
presentation of mitral regurgitaion
pansystolic murmur radiates to axilla
| soft s 1 with s 3
51
what is ventricular septal defect
congenital opening causing blood flowing from left to right ventricle
pansystolic murmur
may occur post MI
52
where is VSD heard
louder at the left sternal edge
53
infective endocarditis symptoms
fever, splinter, haemorrhages, splenomegaly
54
pathophysiology of infective endocarditis
innerlining/ endothelial/ valve infection
| infection of platelet fibrin complex by posited bacteria-> vegetation-> break off and migrate to other parts of body
55
what is vegetation during infection
vegetation: collection of fibrin, platelets, WBC, RBC debris and bacteria
56
mutation change in Down's syndrome
trisomy 21: three copies of 21st chromosomes
57
cardiac defect asso w/ Down syndrome
atrioventricular septal defect
other: VSD, tetralogy of fallot, patent ductus arteriosus
58
clinical signs of tricuspid regurgitation
prominent, pulsatile, large CV wave in JVP
59
clinical signs of tricuspid stenosis
af, hepatomegaly, peripheral oedema
60
what is a early diastolic murmur heard loudest on lower left sternal edge
aortic regurgitation with high risk of aortic dissection
61
murmur asso w/ Marfan's syndrome
aortic regurgitation
62
2 murmurs during hypertrophic cardiomyopathy
ejection systolic: left ventricular outflow obstruction
| mid late systolic: systolic anterior motion of mitral valve
63
causes of aortic stenosis
calcification
congenital bicuspid valve
rheumatic heart disease
64
causes of pulmonary stenosis
Noonan syndrome
tetralogy of fallot
congenital rubella syndrome
65
pathology of hypertrophic cardiomyopathy
mutation of B-myosin heavy chain or myosin binding protein C
66
murmur best heard on expiration leaning forward and lying on left side
aortic regurgitation and mitral stenosis
67
causes of hypertrophic cardiomyopathy
pulmonary/ aortic stenosis-> ventricle pump harder-> ventricular hypertrophy
mitral/ tricuspid stenosis-> aorta pump harder-> atrial hypertrophy
68
causes of dilated cardio myopathy
pulmonary/ aortic regurg-> blood flow back and stretch-> ventricular dilatation
mitral/ tricuspid regurg-> blood flow back and stretch-> atrial dilatation
69
infective endocarditis murmurs
aortic/ mitral regurgitation
70
symptoms of murmur
SAD
syncope
angina
dyspnea
71
complication of mitral regurgitation
HF and pulmonary oedema
72
aortic regurgitation clinical signs
Displaced apex (chronic)
Soft S1
HF
Corrigan's pulse/collapsing pulse
73
clinical signs of mitral stenosis
mallar flush
| tapping apex
74
murmur during pericarditist
triphasic systolic and diastolic rub
75
general causes for AV block
increased vagal tone
normal variant
drugs
mitral valve surgery
76
define 1st degree AV block
delayed in conduction through av node
| ecg pr interval 200ms+
77
causes of 1st degree AV block
coronary artery disease
hypokalemia
hypomagensium
78
treatment of 1st degree AV block
no treatments unless symptomatic
| pacemakers considere due to risk of AF
79
define 2nd degree AV block (Mobitz I)
non constant, progressively longer PR due to fatigue of AV cells
ie, every 4 P, 3 QRS
80
causes of Mobitz I
myocardial infarction
| hyperkalemia
81
treatments of Mobitz I
may cause bradycardia + hypotension
| atropine if needed
82
define 2nd degree AV block (Mobitz II)
constant pr interval with intermittent non conducted P wave
83
causes of Mobitz II
structural heart disease
| myocardial ischemia/ firbosis
84
symptoms of Mobitz II and complete heart block
syncope, fatigue, chest pain, death
85
treatment for Mobitz II
pacemaker
| DON'T use atropine may lead to complete block
86
define 3rd degree/ complete heart block
no association between atria and ventricles/ P and QRS
| junctional ventricular escapee rhythm
87
causes of 3rd degree/ complete heart block
inferior myocardial infarction
av blocking agents
degeneration of conduction system
88
treatment for 3rd degree/ complete heart block
transcutaneous/ transvenous pacemaker
89
why is mobitz 2 more dangerous than mobitiz 1
risk of becoming haemodynamic unstable
severe bradycardia
progression to 3rd degree heart block
syncope, sudden cardiac death
90
Define stroke volume
Amount of blood pumped out of the heart from each contraction
91
Define cardiac output
The amount of blood pumped out of the heart in one minute
| CO=HR x SV
92
Preload vs after load
Preload: stretching of cardiomyocytes at the end of diastole
After load: pressure ventricles need to exert against to eject blood out during systole
93
Inotropy, what cause positive inotropic effect
Myocardial contractility/ force of muscular contraction
| stimulation of beta 1 adrenergic receptor leads to positive inotropic effect
94
How is preload increased
Increase venous pressure-> increased venous return-> increase end diastolic volume-> increase cardiomyocyte stretch/ preload
95
What is the frank starling law
Increased preload/ Cardiac muscle stretch = increase force of contraction/ stroke volume
96
How does afterload and Inotropy (contractility) affect stroke volume
Decreased after load with increased Inotropy= increased SV
| Increase after load with decreased Inotropy = decreased SV
97
3 determinants of Stroke volume
Preload
Myocardial contractility
After load
98
What are the 2 determinants of Mean arterial Pressure (MAP)
1. Cardiac output
| 2. Systemic vascular resistant
99
MAP formula
diastolic pressure + 1/3 (systolic pressure- diastolic pressure)
100
Define systemic vascular resistance
Resistance to blood flow offered by all systemic vasculature excluding pulmonary vasculature
Determined by vasodilation and vasoconstriction
101
2 factors that influence preload
1. Venous return
| 2. Filling time: longer = more blood in ventricles
102
2 factors that influence after load
1. Vascular resistance: increased pressure from vasoconstriction= harder for heart to pump against= decrease SV
2. Valvular disease: stenosis valves
103
3 factors that Effect of Inotropy/ contractility
1. Muscular function: hypertrophy
2. Autonomic nervous system
parasympathetic vs sympathetic (beta 1 adrenergic)
3. drugs
104
Compensatory mechanisms for decreased cardiac output
baroreceptor
| RAAS
105
what is compensatory mechanism for?
When decreased in cardiac output is detected
106
How does increase preload as a compensatory mechanism effect the heart and body during heart failure
Increase EDV, compensate for reduced ejection fraction to maintain CO
Large increase: pulmonary oedema, ascites, peripheral oedema
107
How may increase heart rate as a compensatory mechanism effect the heart and body during heart failure
Sinus tachycardia
| CO= SV x HR
108
describe function of chemoreceptors during decreased tissue perfusion
poor tissue perfusion= increased lactic acid.=decreased pH / increase artery PCO2
activates chemoreceptors=^ resp rate, leads to more CO2 being ‘blown off’ =resp compensation in metabolic acidosis.
109
What is the function of BNP
Protein released by cardiomyocytes during excessive stretching
Good negative predictive Used to measure likelihood of HF (excludes HF if normal amount)
110
Causes of acute HF
Acute myocardial dysfunction
Acute valvular disease
Pericardial tamponade
111
Causes of chronic HF
Cardiomyopathy
Ischaemic heart disease
Aortic stenosis
AF
112
Define systolic HF
ejection fraction below 40% :
decreased stroke volume,
increased preload + decreased contractility
eccentric remodelling
113
Define diastolic HF
decreased stroke volume and total volume= ejection fraction remained.
Impaired ventricular filling/ preload
usually due to ventricular hypertrophy
concentric remodeling
114
Define cardiac remodeling
Changes in cardiac size, shape, function in response to cardiac injury or increased load
115
Define congestive cardiac failure
Combination of left and right failure
116
What leads to left sided HF
systolic: ischemic heart disease, hypertension, dilated cardiomyopathy
diastolic: hypertension, hypertrophy, aortic stenosis, hypertrophic + restrictive cardiomyopathy
117
how does RAAS mechanism activation work?
reduced CO-> activate RAAS-> increase venous pressure/vasoconstriction, water and sodium reabsorption-> increased preload-> increase contraction strength
118
what are heart failure cells
so much fluid in capillaries-> rupture leaking blood to alveoli-> alveolar macrophages eat up RBC (hemosiderin laden macrophages)
119
how does left HF cause pulmonary oedema
decreased CO-> back up in left atrium-> pulmonary circulation-> increase pressure in pulmonary capillaries-> pulmonary odema-> decrease gas exchange-> dyspnea
120
how is systemic circulation effected during right HF
blood backs up in the body for right HF
| JVP distention, splenomegaly, hepatomegaly, ascites, pitting edema
121
What leads to right sided HF
caused by left HF: Pulmonary hypertension
Pulmonary/ tricuspid valve disease
cor pulmonale
ventricular septal defect (blood flow from left to right )
122
Cause of cor pulmonale
Alteration of right ventricular structure/ dysfunction due to pulmonary hypertension
COPD, PE, interstitial lung disease
123
What is high output HF
CO> 8L/min
| Heart can’t meet increased demand for perfusion despite normal cardiac function
124
Causes of high output HF
```
Increase metabolic demand (hyperthyroidism)
Reduced vascular resistance (thiamine deficiency, sepsis)
Significant shunting (large arteriovenosu fistula)
```
125
Diagnostic of HF
TTE when BNP is raised, murmur present, abnormal ecg
| Cardiac MRI if TTE is non-diagnostic
126
What does TTE measure for in HF and how is it classified
Ejection fraction
HF with reduced ejection fraction: <40%
HF with minimally reduced ejection fraction: 40%-49%
HF with preserved ejection fraction: 50% or more
127
What does echocardiogram looks for
Evidence of previous MI
ventricular/ valve hypertrophy
Conduction abnormalities/ AF
128
What does CXR look for
```
Cardio megaly
alveolar shadowing oedema
Kerley B lines (fluid in lobules)
Pleural effuction
Upper lobe diversion
```
129
Management for HF with preserved ejection fraction
Loop diuretic: furosemide 20 mg OD
130
Treatment for HF due to left ventricular systolic dysfunction
1. ACEi (rampiril1.25mg) + beta blocker (bisoprolol 1.25 mg)
loop diuretic (fureosemide 20mg)
2. Spironolactone
3. digoxin
131
Mechanism of spironolactone
antagonist of mineralcortisone receptor of aldosterone dependent Na/ K+ exchange site at distal convoluted renal tubule
(hypertension and HF)
132
Symptoms of congestive heart failure
Orthopnoea, paroxysmal nocturnal dysponoea, ankle swelling
133
Treatment for acute pulmonary oedema secondary to acute left ventricular dysfunction
```
FOND
Furosemide
Oxygen
Nitrates
Diamorphine IV
```
134
Symptoms of hypertension
Palpitations
Angina
Headaches
Blurred vision
135
What are the four grades of Keith wage et barker system for hypertension
1: generalized arteriolar narrowing
2: focal narrowing and arteriovenous nipping
3: retinal haemorrhages, cotton wool spots
4: papilloedema
136
Diagnostic of stage 1 & 2 hypertension
If clinical BP is 140/90 mmHg->Ambulatory BP measurements, 2 measurements an hour during waking hours and confirm with average value
137
Confirm Hypertension diagnosis other than ABPM
home BP monitoring:
evening & night for 4-7 days
Seated, taken twice each time 1 min apart
Average without day 1
138
Stage 1 hypertension measurement
ABPM: 135/85 or more
| Clinic BP 140/90 or more
139
Stage 2 hypertension measurement
ABPM: 150/95 or more
Clinical: 160/100 or more
140
Stage 3 hypertension measurement
Clinic BP: 180/120 or more
141
Define malignant hypertension
BP> 190/120 with signs of papilloedema/ retinal haemorrhage
142
treatments of hypertension for diabetic + younger than 55
ACEi
ARB
BB
143
treatments of African + older than 55
CCB
| Diuretic
144
Treatments for malignant hypertension
IV nitroprusside, labetalol, glyceryl trinitrate
| Phentolamine
145
What are the 2 mechanism allowing exchange between capillaries and extracellular fluids
1. Diffusion: net movement of solutes (O2, CO2) down their respective concentration gradients due to random motion of individual molecules
2. Bulk flow: movement of water and solutes together due to pressure gradient
146
What are the 2 pressure gradients in bulk flow
1. Hydrostatic pressure push fluid out of blood capillaries (arteriolar to venous 37-17)
2. Oncotic pressure push fluid into blood capillaries (25 through out )
Net outward pressure on fluid at arterioles side, net inward pressure at venous side
147
Function of alpha 1 adrenergic recpetor
Located in vascular smooth muscle, induce vasoconstriction
148
What are the 2 barorecptor that maintain blood pressure
Carotid sinus baroreceptor - glossopharngyngeal nerve
| Aortic arch baroreceptors - vagus nerve
149
Phase 0 of cardiac action potential
Rapid depolarization
Rapid sodium influx
-96mv to +52 mV
150
Phase 1 of cardiac action potential
Early repolarization
| Efflux of potassium
151
Phase 2 of cardiac action potential
Plateau
| Slow influx of calcium
152
Phase 3 of cardiac action potential
Final repolarization
| Efflux of potassium
153
Phase 4 of cardiac action potential
Restoration of ionic concentration
Na+ / K+ ATPase
Slow entry of Na+ to decrease potential difference until threshold is reached
154
Inotropic vs chronotorpic vs dromotropic vs lusitropic
inotropic (contractility), chronotropic (heart rate), dromotropic (rate of conduction through AV node) and lusitropic (relaxation of myocardium during diastole) effects
155
Class I antiarrhythmitics
Inhibit fast sodium channels, phase 0
Quinidine, flecainide, procainimide
Many side effects, Nausea vomiting, negative Inotropic effect
156
Class II antiarrthythmics
Beta blockers
Negative inotropic and chronotorpic
Phase 4/ refractory period
SE: bronchocontriction (dont use for asthmatics), bradycardia, heart block
157
Mode of action of beta blockers
Competitive antagonist of catecholamines, bind to beta receptors without activating them
158
Class iii antiarrhythmics
Block potassium channels K+
Phase 3
amiodarone
159
Class iiii antiarrhythmics
Non-dihydropryidine CCB, block conduction at AV node
Verapamil, diltizem
Phase 2
160
Non-dihydropyridines vs dihydropyridines
Antiarrhythmics: verapamil, diltizem
| Anti-hypertensive: nifedipine, amlodipine
161
Mode of action for digoxin
Cardiac glycosides, increase intracellular Na+, Ca2+, contractility through inhibiting Na+/ATPase pump on
162
Mode of action for adenosine
Acts on SA node to reduce heart rate and AV node to slow conduction
163
Mode of action for atropine
M2 antagonist blocks acetylcholine effect, inhibits vagal activity to increase heart rate
164
three types of infective endocarditis
native valves
prosthetic valve
IV drug
165
organisms that cause native valve endocarditis
streptococcal: alpha-haemolytic, strep. bovis
| enterococci
166
organism causing prosthetic valve endocarditis
early: coagulase negative staphylococcus (more common)
late: streptococcus
167
iv drug and dental related infective endocarditis organisms
staphylococcus aureus
| streptococci viridans
168
complications of infective endocarditis bacterial vegetation
break off-> embolic event-> formation of abscesses
| activation of immune system->clustering of immune complexes in the vegetation-> immune mediated vasculitis
169
IE diagnostic
3 sets of blood culture
| TTE/ TOE
170
dukes major criteria for IE
1. microbiological criteria: microorganism found in 2 blood cultures
2. evidence of endocardial involvement: vegetation/ abscess evidence on echo
171
5 of the dukes minor criteria for IE
```
predisposing heart condition/ IVDU
fever
vascular phenomenon
immunological phenomenon
microbiological evidence
```
172
staph aureus treatment
flucloxacillin 12g/day
| vancomyocin for penicillin allergy
173
oral streptococci/ streptococcus bovis treatment
4 weeks:
penicillin/ amoxicillin/ ceftriaxone
vancomycin for penicillin allergy
2 weeks:
add gentamicin
174
empirical Treatment for IE (highly suspected but organism not known yet)
native: vancomycin and gentamicin
| prosthetic valve: vancomycin, gentamicin, rifampin
175
define cardiac tamponade
accumulation of pericardial fluid in the pericardial space between parietal and visceral pericardium
176
what is the beck's triad
classical feature of cardiac tamponade
| hypotension, raised JVP, muffled heart sounds
177
causes of cardiac tamponade
pericarditis
tuberculosis
injury, stabbing
178
cardio tamponade diagnostic
ECHO
| see pericardial effusion and haemodynamic impact on the heart
179
cardiac tamponade treatment
needle pericardiocentesis
180
what are the 3 wave and 2 descents of JVP
3 wave
A,C,V
2 descent
X, Y
181
what is the A wave in JVP, when is it large or absent?
atrial contraction
large: tricuspid & pulmonary stenosis, pulmonary hypertension
absent: atrial fibrillation
182
define cannon 'a' wave
atrial contraction against closed tricuspid valve
| ie, complete heart block, ventricular tachycardia
183
what does C wave of JVP represent
closure of tricuspid valve
| not normally visible
184
what does V wave of JVP represent, when is it large?
passive filling of blood into atrium against closed tricuspid valve
large: tricuspid regurgitation
185
what does x and y descent represent
x: fall in atrial pressure during ventricular systole
y: opening of tricuspid valve
186
cyanotic heart disease
tetralogy of fallot
transposition of great arteries
tricuspid atresia
187
when does tetralogy of fallot appear
1-2 months
188
four characteristics of tetralogy of fallot
ventricular septal defect
right ventricular hypertrophy
pulmonary stenosis
overriding aorta
189
x ray finding of TOF
boot shaped heart
190
ecg of left ventricular hypertrophy
increased QRS amplitude
191
treatment of TOF
surgical repair in two parts
| beta blockers for cyanotic episodes
192
causes of ventricular septal defect
chromosomal disorders (down, Edwards, patau syndromes)
congenital infections
post MI
193
VSD symptoms
failure to thrive
HF symptoms (hepatomegaly, tachypnoea, tachycardia, pallor)
pan systolic murmur
194
complications of VSD
aortic regurgitaiton
infective endocarditis
eisenmenger's complex
right HF
195
what is esienmenger's complex
high right ventricular pressure from hypertrophy exceed left pressure-> reversal of blood flow
heart-lung transplant
196
AVNRT ecg
no p wave, fast rate, regular rhythm
197
treatments of AVNRT/ paroxysmal supraventricular tachycardia
carotid sinus massage and adenosine administed
198
murmur likely heard in rheumatic heart disease
opening snap on S2 followed by rumbling mid-diastolic murmur
199
causes of pericarditis
viral/ bacterial infection
respiratory infection
tuberculosis
post MI: Dressler's syndrome
200
presentation of pericarditis
pleuritic Chest Pain aggrevated by breathing deeply and improved by leaning forward, mild fever and nausea
201
ecg of pericarditis
global saddle-shaped ST elevation with PR depression
202
treatment of pericarditis
NSAID/ analgesia
| aspirin, ibuprofen
203
main cause of death during 4-7 days post MI
myocardial wall rupture
| papillary muscle rupture
204
ecg for hyperkalemia
peaked T wave
prolonged PR
p wave flatted
widen QRS
think of it as: when is potassium present the most in an action potential? phase 3 and 1, 3= t wave, 1-QRS, too much potassium exaggerates those phases making it longer and more prominent
205
ecg for hypokaelmia
U wave
ST depression
absent T wave
206
ecg: p wave
P-waves: atrial depolarisation
207
ecg: QRS
QRS complexes (<120 ms): ventricular depolarisation.
208
ecg: t waves
T-waves: ventricular repolarisation.
209
ecg: U waves
U-waves: sometimes seen, origin disputed. May be pathological if follows abnormal T-wave
210
treatments for stable angina
1. BB + GTN
2. long acting nitrate (ie, isosobride)
3. non urgent/ out patient angiogram
211
what is the erb's point for?
third intercostal space
| S3 and S4
212
another type of irregular irregular rhythm
ventricular ectopics
213
how is amiodarone administered
use central line or large bore peripheral cannula in large vein
214
grades of murmur
1: Difficult to hear
2: Quiet
3: Easy to hear
4: Easy to hear with a palpable thrill
5: Can hear with stethoscope barely touching chest
6: Can hear with stethoscope off the chest
215
what is 2: 1 heart block
P waves remain normal
QRS complex occurs after alternative P wave (after every second P wave)
150 bpm for ventricular rate
ie, atrial flutter
216
where does RCA supply
Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area
217
where does left circumflex supply
Left atrium
| Posterior aspect of left ventricle
218
where does LCA supply
Anterior aspect of left ventricle
| Anterior aspect of septum
219
normal QRS time
<0.12s
220
treatments for hypertension
55+, non-black patient A or B OR 55- or black then C.
221
what are FBC, U+E, LFT important for in regards to cardiovascular
FBC (anaemia)
U+E (prior to ACEi and other meds)
LFTs (prior to statins)
222
medication for angina
GTN spray
Aspirin (e.g. 75mg once daily)/clopidogrel is an alternative
Atorvastatin 80mg once daily
Calcium channel blocker (e.g. amlodipine 5-10mg once daily) or;
Beta blocker (e.g. bisoprolol 5mg once daily)
223
normal cardio thoracic ratio
<0.5 or <1:2
224
complications of prothetic valves
Thrombus formation
Infective endocarditis
Haemolysis causing anaemia
A click replaces S1 for metallic mitral valve
A click replaces S2 for metallic aortic valve
225
medication for chronic HF
ACEi, BB
| loop diuretics
226
What lung disease does left HF correlate to?
Pulmonary oedema
227
typical presentation of Wolff Parkinson white
syncope+ palpation
slurred upstroke/ wide QRS and short PR
delta wave in V1
228
risk of post MI
```
dressler's: pericarditis (autoimmune phenomenon/leukocytosis)
papillary rupture (CHF, mitral regurgitation symptoms)
```
229
side effect amiodarone
dizziness
visual disturbance
unco-ordination
230
function of CCB
angina, hypertension, negative inotropic effect
| stop for HF
231
which congenital defect is Turner and Marfan's syndrome asso w/
turner: coarctation of aorta (part of aorta is more narrow)
| marfan's: aortic dissection
232
hyperkalemia treatment
calcium glutinate
233
what is the function of baroreceptors
when decreased blood pressure/ cardiac output is detected: they increase sympathetic & decrease paraysympathtic stimulation
achieve: increase BP, HR, vasocontriction, adrenaline and noradrenaline is released from medulla
234
where are baroreceptors located
aortic arch and carotid sinus
| act on the medulla
235
what does increase in blood pressure to do sympathetic discharge
baroreceptor activity will also increase -> decrease sympathetic discharge:
ventricular muscle causing decrease contractility /fall in stroke volume
venous system causing increased compliance
236
what does increase in blood pressure do to parasympathetic discharge
baroreceptor activity will also increased which send signal to increased parasympathetic discharge to the SA node so decrease firing/ HR can be achieved
237
ECG changes during hypocalcemia
prolong QT
238
mode of action/ purpose of thiazide diuretic
inhibit sodium reabsorption by blocking Na+ CI symptorer at distal convoluted tubule (step 3 hypertension treatment)
239
mode of action: DOAC (ie, rivaroxaban)
direct inhibition of clotting factor Xa
240
LVEF formula
(SV/EDV) x 100%
241
mode of action: loop diuretic (ie, furosemide)
inhibit Na-K- Cl cotransporter in thick ascending loop of Henle
242
five steps of atherosclerosis
1. endothelial dysfunction + proinflammatory changes
3. fatty infiltration by LDL and oxidize
4. macrophage phagocytose LDL then turn into foam cells
5. foam cells release growth cytokines encouraging SMC proliferation and migration from tunica media inward to intima
243
progression of atherosclerosis from SMC proliferation to thrombus formation
1. SMC proliferation synthesize collagen-> hardening of atherosclerotic plaque
2. at the same time, foam cells die lipid content release (plaque rupture)
3. thrombosis from rupture causes blood coagulation forming thrombus (dangerous, stops blood flow)
244
mode of action: atorvastatin
HMG-CoA reductase inhibitor dug reducing plasma cholesterol lvl
HMGCoA: in mevalonate pathway occurs in liver hepatocytes
245
pathophysiological mechanism for leg oedema during RIGHT HF
increased venuole hydrostatic pressure because blood backs up into venous system as they can't get in
246
mode of action: GTN
relax smooth muscles via activating guanylate cyclase
247
treatment for leg claudication
1. exercise program
| 2. angioplasty
248
side effect of amlodipine (ccb)
ankles swelling
| headache
249
pulmonary oedema from left HF but not congestive HF symptoms
SOB when lying down
needs pillow at night to breathe
no limb swelling
250
oncogene tested during biopsy for breast cancer
HER2
251
route parasympathetic stimulation causing negative chronotropic effect
from release of Acetylcholine onto M2 receptors in SA node, acts to reduce slope fo pacemaker potential
(parasympathetic only acts on SA node)
252
route of sympathetic stimulation causing positive chronotropic effect
mediated by noradrenaline onto B1 receptors, increase slope of pacemaker potential, rate of conduction through AV node, rate of myocardial relaxation
(sympathetic acts on SA, AV, ventricle)
253
how is force generated in the heart
calcium and ATP dependant cross bridge cycles, making plateau phase important bc it allow calcium induced calcium release allowing enough calcium to be present.
254
define blood pressure
outward hydrostatic pressure exerted against the vessels by blood
product of CO and SVR
90-105mmHg
255
causes of arterioles smooth muscle constriction
serotonin
| thomboxane A2
256
causes of arterioles smooth muscle dilation
acidosis, hypoxia, hypercapnia
| fever, inflammation, nitric oxide
257
sympathetic effect of arteriole smooth muscle
Alpha: skin, gut, kidneys-> contraction and reduce flow
Beta: cardiac and skeletal muscle-> dilatation and increase flow
258
how does angiotensinogen become angiotensin 2
Renin catalyzes conversion angiotensinogen into angiotensin I. angiotensin-converting enzyme (ACE) converts angiotensin I into an angiotensin II
259
describe renin
hormone related from granular cells in juxtamedullary apparatus of kidney in response to reduced BP, low sodium , sympathetic stimulation
260
effects of angiotensin 2
stimulates thirst
vasoconstriction
aldosterone release
261
describe aldosterone
hormone that increase sodium reabsorption in the kidney which results in increased fluid reabsorption, blood volume, and BP
262
treatment for stable angina
stop smoking
aspirin+ statin (modify risk)
GTN (symptomatic relief)
263
layers of the heart inner to outer
```
endocardium
myocardium
visceral layer of serous pericardium (epicardium)
pericardial space
parietal layer of serous pericardium
fibrous pericardium
```
264
define TIA (transient ischaemic attack)
brief disruption of blood supply to the brain caused by embolism, thrombus that will resolve, if not and worsen-> ischaemic stroke
265
what are the 2 types of stroke
ischaemic
| haemorrhages
266
describe ischaemic stroke
occlusion of blood vessels that supply brain parenchyma leading to infection (necrosis secondary to ischaemia)
267
procedure after stroke is detected, diagnostic and treatments
send to stroke unit
CT head
thrombolysis if needed
268
describe haemorrhages stroke
bleeding w/ in brain parenchyma, ventricular system, subarachnoid space
269
causes of ischemic stroke
1. thrombosis (local blockage due to atherosclerosis from hypertension/ smoking)
2. emboli (propagation of blood clot that leads to acute obstruction and ischeamia from AFib, carotid artery disease)
270
cause of haemorrhages stroke
hypertension
brain tumour
trauma
271
define sepsis
dysregulated host response to infection leading to life-threatening organ dysfunction-> may lead to septic shock
272
what is sepsis 6 / bufalo
```
blood cultures
urine output
fluids
antibiotics
lactate
oxygen
```
273
define shock
circulatory failure resulting in inadequate tissue perfusion and insufficient delivery of oxygen.
274
four types of shock
hypovolemic
distributive (septic, anaphylactic, neurogenic)
cardiogenic
obstructive
275
define hypovolemic shock
occurs secondary to a reduction in intravascular volume.
| decrease blood pressure, poor tissue perfusion (^ lactic acid)
276
define distributive shock
peripheral vasodilatation leading to abnormal volume distribution and inadequate perfusion.
277
symptoms of shock
hypotension, decrease oxygen, low cardiac output
| fast resp rate, fever
