Flashcards in Cardio W1 Deck (132)
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1
muscarinic receptors of the heart and what acts on them
M2 receptors, acetylcholine
2
inotropic
force
3
chronotropic
HR
4
Frank Starling
as EDV increases, the SV increases
5
beta receptors on the heart and what acts on them
B1 receptors, noradrenaline
6
what does the PR interval indicate
AV node delay
7
what are striation of cardiac muscle caused by
contractile fibres
8
four phases of action potential generation in pacemaker cells
phase 0: Na+ channels open
phase 1: Na+ close, transient K+ efflux
phase 2: Ca++ open (L-type channels)
phase 3: K+ efflux
phase 4: resting potential
9
what is the A band
myosin only
10
what is the I band
between myosin
11
what is the H zone
between actin
12
What is happening when muscle is relaxed
no cross bridge because the actin binding site is blocked by the troponin- tropomyosin complex
13
what is happening when muscle contracts
Ca++ binds to troponin and pulls the troponin-tropomyosin complex away to expose binding site and cross bridge forms
actin-myosin cross bridge forms, power stroke pulls actin inwards during contraction
14
time of pacemaker cell AP vs Ventricular muscle AP
250ms, 800ms
15
what happens to calcium after AP has passed
Ca++ influx ceases and Ca++ goes back into SR by Ca++ATPase (relaxation)
16
what effects the stroke volume?
preload, afterload, myocardial contractility
17
Effect of sympathetic stimulation on frank starling curve and shift?
greater contractility, so for every EVD, there is a greater SV
Frank starling curve shifts to the left
18
How to record BP using kortkoff sounds
record systolic BP when you hear the 1st heart sound, then record diastolic BP when the heart sounds disappear
19
Normal HR
60-100BPM
20
normal systemic BP
90/60mmHg to 120/80mmHg
21
Definition of hypertension
average clinical BP of 140/90mmHg or above and a daytime average of 135/85mmHg or above
22
What is MABP
average arterial BP during a single cardiac cycle involving contraction and relaxation of the heart
23
How to calculate MABP
(2D+S)/3 or DBP+ (PP/3)
24
Normal range for MABP
70-105mmHg
25
what systems regulate BP in long term and their effect on BP
RAAS (increase)
Naturetic peptides
ADH
26
Describe whole RAAS
fall in BP-kidney releases renin- renin causes conversion of angiotensinogen (liver) to angiotensin 1. angiotensin 1 is converted to angiotensin II by ACE (lung vascular endothelium). Angiotensin II causes vasoconstriction, vascular muscle hypertrophy, increased thirst, increased ADH and aldosterone release (adrenal cortex). Aldosterone increased plasma volume and increased BP, water and sodium reabsorption form the kidneys.
27
what is the rate limiting step in RAAS
renin release
28
what releases renin
granular cells
29
what monitors tubular Na+ in kidney tubules
macula densa
30
Physiological closing of S2
pulmonary valve closes before the aortic valve
31
contents of juxtaglomerular apparatus and their function
granular cells (renin release) and macula densa (monitors Na+ in kidney tubules)
32
Three stimuluses of renin release
1. Reduced renal BP due to reduced overall BP
2. Decreased Na+ in kidney tubules
3. Stimulation of renal sympathetic nerves
33
Function of Naturetic peptides and all its actions
To reduced BP by excretion of salt and water is response to cardiac distension or neurohormonal stimuli
also reduce renin release and act as vasodilators
34
Two types of naturetic peptide
ANP 28 AA (atria)
BNP 32AA (ventricles)
35
Name and describe the 4 types of shock
Hypovolaemic (non/haemorrhagic)
Obstructive (TPX, PE, tamponade)
Cardiogenic (eg MI)
Distributive (neurogenic- spinal cord injury, vasoactive-septic or anaphylactic shock)
36
until what point can body compensate for loss in blood volume
until loss of >30% blood volume
37
Amount of exercise adults should do weekly
150 minutes/week moderate exercise or 75 minutes per week of intense exercise
38
Amount of exercise children should do weekly
1h per day for 5 days a week
39
X ray features of heart failure
Alveolar oedema
B lines
Cardiomegaly
Diversion of vessels (upper zone vessel enlargement)
Effusion
40
Events during cardiac cycle
1. Passive Filling (80%)
2. Atrial Contraction
3. Isovolumetric ventricular contraction
4. Ventricular Ejection
5. Isovolumetric ventricular diastole
41
What is the average EDV
130ml
42
What causes the closure of AV valves
when ventricular pressure is greater than atrial pressure
43
when do aortic and pulmonary valve open
when ventricular pressure exceeds pressure in vessels
44
Average stroke volume
70ml
45
4 areas of cardiac auscultation
aortic- 2nd int space, right parasternal edge
pulmonary- 2nd, left parasternal edge
tricuspid- 4th int space, left parasternal edge
mitral- 5th int space, left midclavicular line
46
When does JVP occur and which waves are normal and abnormal
occurs after atrial contraction
a and c wave= normal
v wave= abnormal
a= atrial contraction
c= bulging of tricuspid into atria in ventricular contraction
v= rise in atrial pressure during atrial filling
47
Where is most blood in the body
peripheral veins
48
Diameter of arterioles
30-200 micrometers
49
Diameter in capillaries
4-8 micrometers
50
what are pericytes
connective tissue with contractile properties, outside of capillaries
51
describe the 3 types of capillaries
continuous- no gaps- skin, muscle, nerves, lungs, connective tissue
fenestrated- 50 nanometer pores- gut mucosa, kidney glomeruli, endocrine glands
discontinuous/sinusoidal- large gaps- spleen, bone marrow
52
Diameter of PCV
10-30 micrometers
53
When do PVC become venules
acquire intermittent smooth muscle and 50 micrometers diameter
54
what are valves
inward expansions of the tunica intima in veins
55
what is on the outer layer of the heart
mesothelium
56
core of heart valves
dense irregular connective tissue- the lamina fibrosa which is continuous with the fibrous skeleton of the heart
57
blood supply of the heart valves
valves have no blood vessels
58
Diameter of pacemaker cells and compare to contractile cells
4-8 micrometers
smaller than contractile cells
59
Appearance of pacemaker cells
small, pale
60
Location and Appearance of Purjunke fibres
subendothelial layer
larger than cardiac cells, clear area in the centre and pink in margins- myosin and actin at the periphery
61
Equation for resistance to blood flow
R=nL/r4
62
What regulates blood pressure in arterioles in the short term
Baroreceptor reflex
63
Nervous innervation of arterioles
Sympathetic- a1 adrenoceptors- noradrenaline
(vasomotor tone)
no parasympathetic innervation (except penis and clitoris)
64
Effect of adrenaline on alpha and beta receptors
alpha- vasoconstriction (skin, gut, kidneys)
B2- vasodilation (cardiac and skeletal muscle)
65
Effect of angiotensin II and ADH on vascular smooth muscle
vasoconstriction
66
can extrinsic control of VSM over ride intrinsic control?
No
intrinsic factors can over ride extrinsic factors
67
How in NO produced in vascular endothelial cells
L-arginine via NO synthase
68
why may NO be released
increased BP or chemical signalling
69
Chemicals that cause vasoconstriction of blood vessels
Serotonin, Thromboxane A2, Endothelin, Leukotrienes
70
Factors which increase venous return
blood volume
venomotor tone
respiratory pump
skeletal muscle pump
71
Effect of exercise on frank-Starling curve
Contractility of heart increases- FS curve shifts to the left
72
Describe depolarisation and repolarisation
Depolarisation is becoming more positive
Repolarisation is becoming more negative
73
What does an ECG provide information on?
Rate, Rhythm, Chamber size, axis
main test for MI and ischaemia
74
Contents of 12 lead ECG
3 limb leads ( L1, L2, L3)
3 augmented voltage lead (aVL, aVR, AVF)
6 chest leads (V1-6)
75
Horizontal leads
chest leads V1-V6
76
Vertical leads
AVL, AVR, AVF, L1, L2, L3
77
Which lead is used as the rhythm strip
Lead II
78
Normal Duration of P wave
less than 0.12s (120ms), 0.08-0.1s
79
what is an S wave
downward deflection after R wave
80
what is a q wave
downward deflection before R wave
81
What is a R wave
Upward deflection that does not have to come after Q wave
82
Normal duration of QRS complex
less than 0.1s (less than 100ms)
83
Why is the Twave an upward deflection
repolarisation moving away from seeing electrode
84
Normal duration of PR interval
0.12-0.2ms
85
Normal duration of QT interval
0.44s men, 0.46s in women
86
what are precordial leads
chest leads
87
what are unipolar leads and bipolar leads
augmented voltage leads, limb leads
88
Lateral leads
Lead I and AVL
89
Inferior leads
aVF, LII and LIII
90
what does each chest lead 'look at'
V1-V2- IV septum
V3-V4- anterior heart
V5-V6- lateral (left)
91
positions of each chest lead
V1 4th int space right parasternal
V2 4th int space left parasternal
V3 between V2 and V4
V4 5th int space, midclavicular line (left)
V5 same horizontal level as v4, anterior axillary line
V6 same horizontal level as V4, midaxillary line
92
Duration of one small ECG square
0.04s
93
Speed of ECG paper
25mm/s
94
Calculating HR with normal rhythm
300/no of small squares in R-R interval
95
Calculating HR with abnormal rhythm
no of QRS complex in 30 small squares
96
What is normal sinus rhythm
Normal sinus rhythm is characterized by P waves that are upright in leads I and II of the ECG
but inverted in the cavity leads AVR and V1
97
What can a normal ECG now exclude
MI
Intermittent rhythm disturbances (24h/7day ECG)
Stable angina
98
What investigation for stable angina
Exercise ECG- look for ST changes before/ after exercise (usually not shown at rest)
99
what is TLC
the real or apparent loss of consciousness with loss of awareness, loss of motor control, loss of responsiveness and amnesia for a short duration
100
what is syncope
TLC due to cerebral hypoperfusion which is short and rapid and results in spontaneous recovery
101
Types of syncope
Reflex syncope, Orthostatic hypoperfusion, cardiac syncope
102
Reflex syncope
when there is a fall in HR (cardioinhibition) or vasopressin which causes reduced CO due to neural reflexes via vagal stimulation
103
Types of reflex syncope
vasovagal reflex syncope
situational reflex syncope
carotid sinus reflex syncope
104
Postural hypotension defintion
when there in a change in BP within 3 minutes of standing from lying down by
20mmHg SBP with/without symptoms
10mmHg DBP with symptoms
105
Causes of cardiac syncope
- Arrhythmia (bradycardia or tachycardia)
- Acute MI
- Structural cardiac disease (aortic stenosis, hypertrophic cardiomyopathy)
- Other (PE, Tamponade, TPX)
106
Action of ivabradine and its use
Blocks HCN channels (reduced Na+ Influx/funny current) used in angina to reduce HR
107
What is calcium induced calcium release
when intracellular calcium acting on ryanodine II receptors causes Ca2+ influx from the SR
108
Two methods of calcium efflux
to extracellular space via Na+/Ca2+ exchanger 1 (NCXR)
to SR via Ca2+ATPase (SERCA)
109
Influence of PKA on relaxation
PKA phosphorylates phospholamban, increasing Ca2+ATPase activity therefore increased relaxation
110
Action of PDE
converts cAMP to 5AMP (inactive)
111
Name the catecholamines and describe their selectivity
Dobutamine (B1)
Adrenaline (b over a)
NA (a OVER B)
112
What is dobutamine used in
acute HF, but will cause early death if used in chromic HF
113
Uses of BB
Angina (1st line), HF (Carvedilol, start low, go slow), Hypertension, arrhythmia
114
What is atropine + its effect
Atropine is a non-selective muscarinic antagonist- increases HR
115
use of atropine
used in Bradycardia and ACh poisoning
116
What type of drug is digoxin, its action, and what is it used to treat
Inotropic drug (cardiac glycoside) which increases heart contractility
Na/K ATPase blockade increases Ca2+ influx from SR
used IV in acute HF, oral in chronic HF, HF with AF
117
side effects of digoxin
blurred yellow vision
effect of digoxin is increased in hypokalaemia
oscillatory after potentials (Ca2+ overload)
Arrhythmia
heart block (excessive AV depression)
N+V+D
Gynaecomastia
118
Contraction of VSM
calcium combines with calmodulin to make calcium-calmodulin complex, which activates MLCK.
MLCK phosphorylates MLC- contraction
119
Relaxation of VSM
MLC phosphatase will dephosphorylate MLC-relaxation
120
what activates MLC phosphatase
PKG
121
Action of organic nitrates
metabolism of ON to NO causes relaxation of smooth muscle. reduced preload and afterload. Redirects blood to areas of ischaemia. venodilation at low doses, arterial dilation at higher doses.
122
Types of ON and what they are used in
Isosorbide mononitrate- short term relief (spray/patch)
tablet in stable angina, IV in unstable
Glyceryl trinitrate- prophylaxis (need 8 hour nitrate free period)
used in all types of ANGINA
123
Side effects of ON
Hypotension, headaches, dizziness/syncope, Methaemoglobin (cyanide poisoning treatment), reflex tachycardia (px with BB)
124
types of CCB and what they are used in
Verapamil- heart (dysrhythmia)
amlodipine (vascular- used in hypertension)
diltiazem (heart and vascular)
also used in angina
125
Side effects of CCB
ankle oedema, flushing, hypotension
126
what is bradykinin
potent vasodilator inhibited by ACE
127
SE of ACEI
dry cough, angioneurotic oedema, hypotension, hyperkalaemia (less aldosterone)
128
who is ACEI contraindicated in? who are they good for?
Pregnant/child-bearing age women and bilateral renal stenosis
diabetic neuropathy
129
what are ACEI/ARB used in?
Hypertension (1st line for under 55 non-African/Caribbean, diabetic neuropathy)
Cardiac Failure
Post-MI
130
Use of nicorandil
type of drug
SE
used in refractory angina (NO activity)
K channel opener
mouth ulcer
131
Use of alpha antagonists
SE
Hypertension with prostatic hypertrophy
postural hypotension
132
