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cardiology > cardiovascular principles > Flashcards

cardiovascular principles Flashcards

1
Q

how is a regular spontanous action potential generated in the SA node

A
  • the spontaneous pacemaker potential takes the membrane potential to a threshold
  • every time the threshold is reached an action potential is generated
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2
Q

what is vagal tone

A
  • the vagus nerve (parasympathetic supply to the heart) exerts a continuous influence of the SA node under resting conditions.
  • vagal tone dominates under resting conditions
  • the vagal tone slows the intrinsic heart rate from 100bpm to produce a normal resting heart rate of 70bpm
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3
Q

what is the normal resting heart rate and what is the term for a heart rate above it and below it

A
  • 60-100bpm
  • tachycardia = resting heart rate above 100bpm
  • bradycardia = resting heart rate below 60bpm
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4
Q

what effect does the vagal stimulation have on the SA and AV node

A
  • Slowed rate of firing from the SA node

- Increase in AV nodal delay

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5
Q

what are the phases of ventricular muscle action potential

A 
0 = fast Na2+ influx 
1 = closure of Na2+ channels and transient K+ efflux 
2 = mainly Ca2+ influx 
3 = closure of Ca2+ channels and K+ efflux 
4 = resting membrane potential
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6
Q

what are the standard limb leads

A
  • lead 1 = RA-LA
  • lead 2 = RA-LL
  • lead 3 = LA-LL
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7
Q

what does the P wave show

A

atrial depolarisation

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8
Q

what does the QRS complex show

A

ventricular depolarisation

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9
Q

what does the T wave show

A

ventricular repolarisation

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10
Q

what does the PR interval show

A

largely AV node delay

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11
Q

what does the ST segment show

A

represents the interval between ventricular depolarization and repolarization.

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12
Q

what does the TP interval show

A

diastole

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13
Q

what is the refractory period on an ECG

A

the period following an action potential in which it isn’t possible to produce another action potential

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14
Q

how are the cardiac monocytes electrically coupled

A

gap junctions - these protein channels form low resistance electrical communication pathways between neighbouring monocytes

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15
Q

what provides mechanical adhesion between cardiac cells

A

desmosomes - they ensure that the tension developed by one cell is transmitted to the next

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16
Q

what produced muscle tension

A

sliding of actin filaments on myosin filaments

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17
Q

define stroke volume

A

the volume of blood ejected by each ventricle per heart beat

-SV=EDV(end diastolic volume)-ESV(end systolic volume)

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18
Q

what affects the stroke volume

A
  • Cardiac preload
  • Cardiac afterload
  • Myocardial contractibility
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19
Q

what is blood pressure

A

the outwards hydrostatic pressure exerted by the blood on the blood vessels

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20
Q

what is the ideal blood pressure for an adult under 80 yrs

A

120/80 to 90/60mmHg

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21
Q

what bp is hypertension

A

140/90mmHg and day time average of 135/85mmHg

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22
Q

what is pulse pressure

A

difference between the systolic and diastolic blood pressures

  • normally between 30 and 50 mmHg
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23
Q

what is the mean arterial blood pressure

A

the average arterial blood pressure during a single cardiac cycle which involves contraction and relaxation of the heart

  • MAP = [(2X diastolic) + systolic] divided by 3
  • MAP = CO X SVR
  • a MAP of at least 60mmHg is needed to perfuse vital organs like the brain, heart and kidneys
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24
Q

what factors can change the mean arterial blood pressure

A
  • heart rate
  • stroke volume
  • systemic vascular resistance
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25
Q

what do baroreceptors respond to

A

acute changes in arterial blood pressure

  • baroreceptor firing decreases if high arterial blood pressure is sustained
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26
Q

what hormones regulate extracellular fluid volume

A
  • the renin angiotensin aldosterone system (RAAS)
  • natriuretic peptides
  • antidiuretic hormone
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27
Q

where is renin released

A

Juxtaglomelular apparels in the kidneys

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28
Q

what are natriuretic peptides

A
  • released in response to cardiac distension
  • cause excretion of salt and water in the kidneys,
  • reduce blood volume and blood pressure
  • decrease renin release and hence decrease blood pressure
  • act as vasodilators, decrease SVR and blood pressure
  • they are a counter regulatory system for RAAS
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29
Q

what is shock

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

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30
Q

what causes hypovolaemic shock

A

caused by loss of blood volume

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31
Q

what causes cariogenic shock

A

caused by sudden severe impairment of cardiac function - heart suddenly unable to pump sufficient blood to provide adequate tissue perfusion

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32
Q

what causes obstructive shock

A

caused by physical obstruction to circulation either into or out of the heart

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33
Q

what causes distributive shock

A

caused by excessive vasodilation and abnormal distribution of blood flow

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34
Q

what is the cardiac cycle

A

all events that occur from the beginning of one heart beat to the beginning of the next

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35
Q

how long is diastole and systole at a heart rate of 75bpm

A 
diastole = 0.5 seconds 
systole = 0.3 seconds
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36
Q

what are the events during the cardiac cycle

A 
1 = passive filling 
2 = atrial contraction 
3 = isovolumetric ventricular contraction 
4 = ventricular ejection 
5 = isovolumetric ventricular relaxation
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37
Q

explain passive filling in the cardiac cycle

A
  • pressure in atria and ventricles at 0
  • AV valves open
  • aortic valve is closed
  • ventricles become 80% passively filled
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38
Q

explain atrial contraction of the cardiac cycle

A
  • P wave of ECG signals atrial depolarisation
  • the atria contracts between the P wave and the QRS complex
  • atrial contraction complete the end diastolic volume
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39
Q

explain isovolumetric ventricular contraction of the cardiac cycle

A
  • starts after QRS complex
  • ventricular pressure rises
  • when the ventricular pressure exceed atrial pressure the AV valves shut = first heart sound (Lub)
  • the tension rises around a closed volume “isovolumetric contraction”
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40
Q

explain ventricular ejection of the cardiac cycle

A
  • when ventricular pressure exceeds the aortic/pulmonary pressure the valves open
  • stroke volume is ejected
  • T wave signals ventricular depolarisation
  • the ventricular pressure will start to fall and will fall below the aortic/pulmonary pressure so they shut = second heart sound (dub)
  • the valve vibration produces the dicrotic notch in aortic pressure curve
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41
Q

explain isovolumetric ventricular relaxation in the cardiac cycle

A
  • closure or aortic/pulmonary valves signals the start of isovolumetric ventricular relaxation
  • ventricle becomes a closed box
  • when the ventricular pressure falls below atrial pressure, AV valves open
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42
Q

what causes the S1 heart sound

A
  • closure of metric and tricuspid valves = Lub
  • beginning if systole
  • occurs during isovolumetric contraction
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43
Q

what causes the S2 heart sound

A
  • closure of the aortic and pulmonary valves

- occurs ding isovolumetric relaxation

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44
Q

what causes the S3 heart sound

A
  • early ventricular filling

- normal in children but in adults is associated by ventricular dilation

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45
Q

what causes the S4 heart sound

A
  • atrial contraction

- associated with stiff, low compliant ventricle ie ventricular hypertrophy

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46
Q

what are the 4 cardiac auscultation points to auscultate the heart valves

A
  • aortic area = 2nd right intercostal space beside the right sternum
  • pulmonary area = left side in the 2nd intercostal space
  • tricuspid area = 4th intercostal space
  • mitral area = 5th intercostal space on the mid clavicular line
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47
Q

the estimation of jugular venous pressure is an indirect estimate of what

A

right atrial pressure

  • normally JVP is no more than 3cm vertically above the sternal angle
  • an elevated JVP is a sign of heart failure
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48
Q

what occurs when adrenaline acts on alpha receptors

A

vasoconstriction

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49
Q

what occurs when adrenaline acts on beta 2 receptors

A

vasodilation

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50
Q

what does angiotensin II cause in relation to vascular smooth muscle

A

vasoconstriction

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51
Q

what hormones affect control of vascular smooth muscles

A

Adrenaline
Angiotensin II
Antidiuretic hormone

52
Q

what effect does antidiuretic hormone have on vascular smooth muscle

A

vasoconstriction

53
Q

what local metabolites cause the relaxation of artery smooth muscles resulting in vasodilation and metabolic hyperaemia

A
  • decreased local PO2
  • increased local PCO2
  • increased local [H+] ie decreased pH
  • increased extracellular [K+]
  • increased osmolatiry of ECF
  • adenosine release
54
Q

what effect does nitric oxide have on vascular smooth muscles

A
  • produced by vascular epithelium from the amino acid L-arginine through the enzymatic action of Nitric Oxide Synthase
  • potent vasodilator
  • NO diffuses from the vascular endothelium into the adjacent smooth muscle cells where it activates the formation of cGMP that serves as second messenger for signalling smooth muscle relaxation
55
Q

what are some endothelial produced vasodilators

A
  • anti-thrombotic
  • anti-inflammatory
  • anti-oxidants
56
Q

what are some endothelial produced vasoconstrictors

A
  • pro-thrombotic
  • pro-inflammatory
  • pro-oxidants
57
Q

what causes venous return to increase

A
  • increased venomotor tone
  • increased blood volume
  • increased skeletal muscle pump
  • increased respiratory pump
58
Q

which vessel contains the most of the blood volume under resting conditions

A

the veins are capacitance vessels that contain most of the blood volume under resting conditions

59
Q

what does increased venomotor tone cause

A
  • increased venous return
  • increased stroke volume
  • increased mean arterial pressure
60
Q

what is the effect of noradrenaline of pacemaker cells

A
  • slope of pacemaker potential increases
  • pacemaker potential reaches threshold quicker
  • frequency of action potentials increases = positive chronotropic effect
61
Q

where are beta 1 adrenoceptors found

A
  • nodal cells (ie AV node)

- myocardial cells

62
Q

explain the autonomic regulation of cardiac rate and force of the sympathetic system

A

Noradrenaline or adrenaline activate the beta 1 adrenoceptors. Coupling through Gs protein alpha subunits stimulates adenylyl cyclase to increase the intracellular concentration of cyclic AMP. By signalling through Gs, beta 1 adrenoceptor activation causes:

  • increased SA node action potential frequency and heart rate
  • initiation by enchanted Ica,l.
  • increased contractility
  • increased condition velocity in AV node
  • increased automaticity
  • decreased duration of systole
63
Q

explain the autonomic regulation of cardiac rate and force of the parasympathetic system

A

Acetylcholine activates M2 muscarinic cholinoceptors, largely in nodal cells. By signalling through Gi, M2 muscarinic receptor activation causes

  • decrease SA node action potential frequency and heart rate
  • decrease in the slope of phase 4 depolarisation
  • an increase in the threshold for AP initiation by reduced Ica,l
  • hyperpolarisation during phase 4 via GIRKS
  • decrease in contractibility
  • decrease in conduction of AV node
  • may cause arrhythmias to occur in the atria
64
Q

explain the excitation contraction of coupling in cardiac muscle contraction

A
  • Ventricular action potential
  • Opening of voltage activated Ca2+ channels during phase 2
  • Ca2+ influx into the cytoplasm
  • Ca2+ release from the sarcoplasmic reticulum
  • Ca2+ binds to troponin C and shifts tropomyosin out of the action cleft
  • Cross bridge formation between actin and myosin resulting in contraction via the sliding filament mechanism
65
Q

explain the excitation contraction coupling in cardiac muscle relaxation

A
  • Depolarisation in phase 3 to 4
  • Voltage activated Ca2+ channels return to closed state
  • Ca2+ influx ceases. Ca2+ efflux occurs by the Na+/Ca2+ changer 1 (NXC1)
  • Ca2+ release from the sarcoplasmic reticulum ceases. Active sequestration via Ca2+-ATPase (SERCA) of Ca2+ from the cytoplasm now dominates
  • Ca2+ dissociates from troponin C
  • Cross bridges between actin and myosin break resulting in relaxation
66
Q

what are examples of beta adrenoceptor agonists

A

Dobutamine, Adrenaline and noradrenaline

67
Q

what are examples of beta adrenoceptor antagonists

A

Propanolol, Atenolol, Bisprolol

68
Q

what are some clinical uses of beta adrenoceptor antagonists (beta blockers)

A
  • treatment of disturbances of cardiac rhythm ie excessive sympathetic activity, atrial fibrillation
  • treatment angina
  • treatment of heart failure
  • treatment of hypertension
69
Q

what are some adverse effects of beta blockers

A
  • Bronchospasm
  • Aggravation of cardiac failure - but low dose is used in compensated heart failure
  • Bradycardia
  • Hypoglycaemia
  • Fatigue
  • Cold extremities
70
Q

what are the effects of non selective muscarinic ACh receptors

A

Decreased heart rate. Bronchial constriction (makes it hard to breath in asthmatics) Enhanced urination (by relaxing the sphincter and contracting the bladder)

71
Q

how does digoxin increase contractability

A

by inhibiting the sarcolemma ATPase

72
Q

what are the pharmacodynamics of digoxin

A
  • indirectly increases vagal activity
  • slows SA node discharge
  • slows AV node conduction; increases refractory period
  • directly shortens the action potential and refractory period in the atrial and ventricular myocytes
73
Q

what is the effect of organic nitrates on vasculature

A
  • venorelaxation at smaller doses
  • arteriolar dilatation at larger doses
  • increased coronary artery blood flow in angina as blood is redirected towards the ischaemic zone
  • used to relieve pain in angina
74
Q

what are examples of organic nitrates in angina

and what are there side effects

A
  • glyceryltinitrate (GTN)
  • isosorbide mononitrate (ISMN)

side effects = headaches, hypotension and fainting, reflex tachycardia

75
Q

what is the function of calcium channel blockers

A
  • block or prevent the opening of L type channels in excitable tissues in response to depolarisation and hence limit an increase in ca2+ concentration
  • used for hypertension - reduced Ca2+ entry into vascular smooth muscle cells causes generalised arteriolar dilatation, reducing TPR and MABP. The major effect is on the arteries with little effect on veins
  • cause coronary vasodilation
  • Often used in combination with GTN
  • cause peripheral arteriolar dilatation decreasing afterload and myocardial oxygen requirement
76
Q

what are examples of calcium channel blockers

A
  • Verapamil - block the pore
  • Amlodipine - acts allosterically to prevent channel opening
  • Diltiazem
77
Q

what does the RAAS system cause

A
  • increased MABP
  • increased blood volume
  • increases release of noradrenaline from sympathetic nerves
  • cell growth in heart and arteries
  • aldosterone secretion from adrenal cortex
  • tubular Na+ reabsorption and salt retention
78
Q

what is the function of an ACE inhibitor

A

blocks the conversion of angiotensin 1 to angiotensin 2

79
Q

what is the function of AT1 receptor antagonists

A

block the agonist action of angiotensin 2 at AT1 receptors in a competitive manner

80
Q

what are the effects of ACE inhibitors

A
  • causes venous dilatation and arteriolar dilatation
  • decreases preload
  • no effects of cardiac contractability
  • reduce the release of aldosterone - promotes loss of Na+
81
Q

what is an ECG lead

A

an imaginary line, the lead axis, between 2 or more electrodes

82
Q

what are the 3 standard limb leads

A

I, II, III these are termed bipolar

I = Right arm to Left arm 
II = RA to Left leg - inferior direction
III = LA to LL
83
Q

what are the 3 augmented voltage leads

A

aVR, aVL, aVF these are termed unipolar

aVR leads are negative as predominant vector is depolarisation moving away from the recording electrode

84
Q

what are the vertical or frontal coronal leads

A

lead I, II, III, aVR, aVL and aVF

85
Q

what are the 6 chest leads

A

V1-V6

86
Q

what are the horizontal or transverse leads

A

V1-V6

87
Q

what are the lateral leads

A

I and aVL - each have a recording electrode on the left arm and views the heart from the left

88
Q

what are the inferior leads

A

II, III and aVF - each has a recording electrode on the left foot and views the heart from an inferior direction

89
Q

what are… looking at:

  1. V1 and V2
  2. V3 and V4
  3. V5 and V6
A
  1. coming from the right and looking at the inter ventricular septum
  2. anterior of the heart
  3. lateral aspect (left ventricle) of the heart
90
Q

what are the standard ECG chest electrode positions

A

V1- 4th intercostal space immediately right of sternum
V2-4th intercostal space immediately left of sternum
V3-mid way between V2 and V4
V4-5th intercostal space on midclavicular line
V5-same horizontal level as V4 on anterior axillary line
V6-same horizontal level as V4 at the mid axillary line

91
Q

what is the paper speed on an ECG

A

25mm/sec

92
Q

how do you calculate the heart rate for a regular and irregular rhythm

A

regular =Count the number of large squares present within one R-R interval. Divide 300 by this number to calculate heart rate.

irregular = Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long). Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute).

93
Q

what are the 3 layers of a blood vessel

A

inner layer - tunica intima
middle layer - tunica media
outer layer - tunica adventitia

94
Q

what is the vascular supply to large vessels called

A

vasa vasorum

95
Q

what are pericytes

A

connective tissue cells with contractile properties often found in capillaries outside the basal lamina

96
Q

what are the 3 layers that make up the heart

A
  1. endocardium
  2. myocardium
  3. epicardium
97
Q

what are the 3 types of cardiac muscle cell

A
  1. contractile cells
  2. pacemaker cells
  3. conducting cells
98
Q

what are anti cholesterol drugs examples

A

statins, fibrates, PCSK 9 inhibitors

99
Q

what are some anti hypertensive drugs

A

Thiazide diuretics, beta blocker, vasodilators ( calcium antagonists, alpha blockers, ACE Inhibitors, angiotensin receptor blockers)

100
Q

what are common drugs for hyperlipedemia

A
  1. anti cholesterol - statins, fibrates, PCSK 9 inhibitors

2. anti hypertensive drugs - thiazide diuretics, beta blocker, vasodilators

101
Q

what are common drugs for hypertension

A
  1. anti hypersensitive drugs - thiazide diuretic, beta blockers, vasodilators , spironolactone
102
Q

what is the effect of diuretics

A

blocks Na reabsorption in kidneys

  • thiazide diuretic is mid and used in hypertension
  • loop diuretic is stronger and used in heart failure

side effects

  • hypokalaemia = tired
  • arrhythmias
  • hyperglycaemia = diabetes
  • increased uric acid = gout
103
Q

side effects of ACE inhibitors

A
  • cough
  • renal dysfunction
  • angioneurotic oedema
104
Q

what are common drugs used in coronary artery disease

A
  1. vasodilators = nitrates, nicorandil, calcium antagonists
  2. slow heart rate = beta blocker, calcium antagonists, ivabradine
  3. metabolic modulator = Ranolazine
105
Q

what is Nicorandil

A

anti anginas drug that acts as a vasodilator

  • K ATP channel activator
  • side effects = headache, mouth/GI ulcers
106
Q

what is Ivabradine

A
  • lowers heart rate only in sinus rhythm

- If channel modulator in the sinus nose

107
Q

what are examples of anti platelet agents

A

Aspirin, Clopidogrel, Ticagrelor, prasugrel

side effects = haemorrhage, peptic ulcer, asthma

108
Q

what are examples of anti coagulant drugs

A

Heparin, Warfarin, Rivaroxaban, Dabigatran

109
Q

what is transient loss of consciousness

A

A state of real or apparent loss of consiousness with loss of awareness, characterised by amnesia for the period of unconsiousness, loss of motor control, loss of responsiveness and a short duration

110
Q

what is syncope

A

transient loss of consciousness due to cerebral hypo perfusion, characterised by rapid onset, short duration and spontaneous complete recovery

111
Q

what is reflex syncope

A

brief loss of consiousness due to a neurologically induced drop in blood pressure

  • when activated the reflex causes cardioinhabition through vagal stimulation. This decreases heart rate and cardiac output
  • vasodepression through depression of sympathetic activity to blood vessels which decreases systemic vascular resistance, venous return, stroke volume and CO
  • There are 3 types of reflex syncope: vasovagal, situational, carotid sinus
112
Q

what is orthostatic hypertension

A

sudden drop in blood pressure when you stand from a seated or prone position

  • a positive result is indicated by a drop within 3 minutes of standing from lying position: in systolic BP of at least 20mmHg or a drop of 10mmHg in diastolic BP
113
Q

cardiac syncope

A

brief loss of consiousness characterised by rapid onset and spontaneous recovery. It is caused by decreased blood flow to the brain

can be caused by:

  • arrhythmias
  • acute MI
  • structural cardiac disease
114
Q

what is the vasovagal reflex syncope

A
  • most common type of syncope
  • faint is triggered by emotional distress or orthostatic stress
  • can be averted by horizontal gravity neutralisation position or leg crossing
115
Q

what is situational reflex syncope

A
  • faint during or immediately after a specific trigger

- treatment: treat the cause, avoid dehydration and excessive alcohol

116
Q

what is carotid sinus reflex

A
  • triggered by mechanical manipulation of the neck, shaving, tight collar
  • may occur after head and neck surgery or radiation
  • cardiac permanent pacing is generally recommended
117
Q

what is postural hypotension

A

results from failure of baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

118
Q

in terms of cholesterol what is cardiovascular (atherosclerosis) is strongly associated with

A
  • elevated LDL

- decreased HDL

119
Q

what are the 4 main classes of lipoproteins

A
  • HDL particles ( apoA-I and apoA-II)
  • LDL particles (apoB-100)
  • very low density lipoproteins (VLDL) particles
  • chylomicrons (apoB-48)
120
Q

what are chylomicrons

A

formed in the intestinal cells and transport dietary triglycerides - the exogenous pathway

121
Q

what are VLDL particles

A

formed in the liver cells and transport TAGs synthesised by that organ - the endogenous pathway

122
Q

why is LDL the bad cholesterol (timeline)

A
  1. Uptake of low density lipoproteins from the blood into the intima of the artery. LDL subsequently oxidised to atherogenic oxidised LDL
  2. Migration of monocytes across the endothelium into the intima where they become macrophages
  3. Uptake of OXLDL by macrophages converts them to cholesterol-laden foam cells that form a fatty streak
  4. Release of inflammatory substances from various types of cells causes division and proliferation of smooth muscle cells into the intima and the deposition of collagen
  5. The formation of an atheromatous plaque consisting of lipid core and fibrous cap
123
Q

why is HDL the good cholesterol

A
  • key role in removing excess cholesterol from cells by transporting it in plasma to the liver. Only the liver has the capacity to remove cholestrol from the body
  • formed mainly in the liver, initially as apoA-I in association with a large amount of surface phospholipid and unesterfied cholesterol
  • disc like pre- beta-HDL matures in the plasma to spherical alpha-HDL as surface cholesterol is enzymatically converted to hydrophobic cholesterol ester that migrates to the core of the particle
  • mature HDL accepts excess cholesterol from the plasma membrane of cells and delivers cholesterol to the liver, known as reverse cholesterol transport
124
Q

how do statins lower LDL

A

act as competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase - rate limiting step in cholesterol synthesis in hepatocytes

  • decrease in hepatocyte cholesterol syntheses causes a compensatory increase in LDL receptor expression and enhanced clearance of LDL
125
Q

wha is a drug that inhibits cholesterol absorption

A

Ezetimibe - acts to inhibit NPC1L1 transport protein in enterocytes of the small intestine, reducing the absorption of cholesterol. It causes a reduction of LDL with little change in HDL. Used in combination with statins when the latter alone doesn’t achieve sufficient response

cardiology (13 decks)

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