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Life Support > Cardiac Cycle and Hypertension > Flashcards

Cardiac Cycle and Hypertension Flashcards

1
Q

Where is electrical activity conducted from in the heart?

A

Sino atrial node

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2
Q

Why does the electrical activity slow down at the atrio ventricular node?

A

To allow correct ventricular filling

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3
Q

What side of the heart has a lower pressure?

A

Right

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4
Q

What is the path of blood flow through the heart?

A 
Venous return great veins (SVC, IVC) - Right atrium
Tricuspid valve
Right ventricle
Pulmonary semilunar valve
Pulmonary arteries
LUNG CIRCULATION
Pulmonary veins
Left atrium
Bicuspid (Mitral) valve
Left ventricle
Aortic semilunar valve
Aorta
SYSTEMIC CIRCULATION
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5
Q

What are the systolic/diastolic pressures in each chamber of the heart? (mmHg)

A 
RA: 1-15
RV: 25/5
LV: 120/8
LA: 8
Pulmonary circulation: 25/10
Systemic circulation: 120/80
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6
Q

What are the 4 phases of the cardiac cycle?

A
  1. Ventricular fillinf/atria contraction
  2. Isovolumetric contraction
  3. Isovolumetric relaxation
  4. Ejection
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7
Q

Ventricular filling/atria contraction

A

Higher pressure in atria > ventricles
tri/bi valves open - blood enters ventricles
Atrial contraction – extra filling

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8
Q

Isovolumetric contraction

A

Higher pressure in ventricles > atria so tri/bi valves close

Closed ventricle

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9
Q

Ejection

A

Higher pressure in ventricles > aorta/pulmonary artery
Valves open
Blood flows out of heart
Blood enters atria

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10
Q

Isovolumetric relaxation

A

Higher pressure in aorta/pulmonary artery > ventricles
Valves close
Closed ventricle
Relaxes, expands, ready to receive

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11
Q

Why is ventricular relaxation important?

A

Need them to be big enough and reduce pressure for valves to open and for adequate filling of blood otherwise amount of blood flow will be affected

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12
Q

What is cardiac output at rest?

A

5 litres (up to 20 w exercise)

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13
Q

After atrial systole what valve is closed?

A

Mitral (open during systole)

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14
Q

During atrial systole what happens to ventricular pressure?

A

Ventricle filling so pressure is lower than aorta as blood moves from high to low pressure, but as it fills pressure begins to increase

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15
Q

During isovolumetric contraction what happens to ventricular pressure?

A

Huge increase and then goes above aortic pressure

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16
Q

During ventricular systole what valve opens and closes?

A

Aortic valve opens due to increased ventricular pressure, once ejection occurs and pressure begins to decrease aortic valve closes

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17
Q

During isovolumetric relaxation what happens to ventricular pressure?

A

Decreases rapidly as blood has been ejected and chamber needs to have lower pressure and big space for filling of blood

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18
Q

After ventricular diastole what valve opens?

A

Mitral (allows filling of ventricles)

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19
Q

Why doesn’t the aortic valve close earlier?

A

Because during ejection blood has a lot of kinetic energy and can maintain ejection for longer to get enough out for good cardiac output (can keep ejecting even though pressure differences have dropped)

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20
Q

What is the volume in the ventricles during atrial systole?

A

Full volume

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21
Q

At the end of atrial systole what is the end diastolic volume?

A

EDV 120ml

mitral valve closes

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22
Q

What is end systolic volume?

A

Blood left after ejection
ESV 40ml
aortic valve closes

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23
Q

What is stroke volume?

A

EDV - ESV = 80ml

blood that is ejected

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24
Q

Ejection fraction

A

SV/EDV

eg. 80/120 = 66%
normal value 2/3 or more, lower values in heart failure

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25
Q

How is the ventricular pressure-volume loop affected by exercise?

A

Greater venous return -> increased heart rate -> greater end diastolic volume EDV -> greater stroke volume
(Starling’s law) more stretch so more blood ejected

loop gets wider, ejection fraction increases

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26
Q

How is the ventricular pressure-volume loop affected by hypertension?

A

Greater arterial blood pressure (afterload) -> greater isovolumetric contraction- lots of O2 used -> decreased stroke volume, greater ESV -> more energy used to eject less blood

loop taller and thinner, ejection fraction decreases

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27
Q

What happens to pressure in the right side of the heart during atrial contraction?

A

Pressure increases, tricuspid valve open (A wave)

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28
Q

What happens to pressure in the right side of the heart during ventricular systole?

A

Pressure drops and tricuspid valve closes as atria filling (X descent to V wave when atrium full)

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29
Q

What happens to pressure in the right side of the heart during diastole?

A

Pressure goes down then begins to gradually increase (Y descent to A wave)

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30
Q

What is the clinical significance of X and Y drops in pressure?

A

Seen as pulsatile collapse in neck veins

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31
Q

What would you see in jugular veins in right sided heart failure?

A

Pressures in right atria is raised

Therefore:
Less blood is ejected from right ventricle
More blood left in chamber after systole
Atria pumps against greater pressure

Height of venous distension is increased

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32
Q

What causes heart sounds?

A

Closure of cardiac valves (vibrations in ventriculr chambers)

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33
Q

What is S1 sound?

A

LUBB

Closing of tricuspid/mitral valves at beginning of ventricular systole

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34
Q

What is S2 sound?

A

DUPP

Closing of aortic/pulmonary valves at beginning of ventricular diastole

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35
Q

When would you hear S3 sound?

A

Occasional, turbulent blood flow into ventricles detecetd near end of first 1/3 diastole

common in young

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36
Q

When would you hear S4 sound?

A

Pathological in adults

Forceful atrial contraction against a stiff ventricle- potentially abnormal (just before ‘lubb’)

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37
Q

What is the extended edition of the cardiac cycle?

A
  1. Atrial contraction
  2. Isovolumetric ventricular contraction
  3. Rapid ventricular ejection
  4. Reduced ventricular ejection
  5. Isovolumetric ventricular relaxation
  6. Rapid ventricular filling
  7. Reduced ventricular filling
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38
Q

What constitutes cardiac output?

A

CO = Heart Rate (HR, beats per minute) x Stroke Volume (SV, volume ejected from heart per beat)

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39
Q

What constitutes blood pressure?

A

BP = CO (blood flow from the heart) x Total Peripheral Resistance (TPR, resistance to blood flow of the arterial circulation)

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40
Q

What parameters determine blood flow?

A

Blood Flow (CO) = Pa / TPR

Where Pa is arterial blood pressure

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41
Q

How does parasympathetic system control conductivity in the heart?

A

VIA VAGUS NERVE IN CNS: Sends long pre-ganglionic fibres to cardiac ganglion releasing Ach at nicotinic receptors, then short post-ganglionic fibres releasing Ach at M2 receptors acting on SA and AV node

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42
Q

How does sympathetic system control conductivity in the heart?

A

FROM THORACIC NERVES:
Sends short pre-ganglionic fibres synapsing with ganglia, Ach released at nicotinic receptors, and post-ganglionic fibres going to SA node, AV node and ventricles releasing NA acting on beta 1 receptors

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43
Q

Besides the heart where else does the sympathetic system send post-ganglionic fibres?

A

Blood vessels, releasing NA at alpha 1 adrenoreceptors

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44
Q

What is the role of the adrenal glands in the sympathetic system?

A

Act as a specialised post-ganglionic nerve, Ach from pre-ganglionic fibres acts at nicotinic receptors in adrenal glands = adrenaline and NA released in bloodstream -> act on blood vessels and heart

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45
Q

What 2 ways does sympathetic system control cardiac output?

A

Increase HR (chronotropic effect)

Contractility (inotropic effect)

Venoconstriction = greater venous return (preload) = increased CO via Starling’s Law

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46
Q

What 2 ways does sympathetic system control total peripheral resistance?

A

Vasoconstriction of arterioles = increased TPR

Vasodilatation of skeletal/coronary arteries during exercise = less TPR

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47
Q

Release of NA from post-ganglionic sympathetic nerves acts on which receptors of the heart?

A

Beta 1 adrenoreceptors

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48
Q

What is the name of the effect SNS has on the SA node and what does it do?

A

CHRONOTROPIC EFFECT

Increases frequency of pacemaker potentials which produces an increase in HR frequency

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49
Q

What is the name of the effect SNS has on the AV node and what does it do?

A

DROMOTROPIC EFFECT

Increases rate of impulses through atria to ventricles to maintain CO during increased HR

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50
Q

What is the name of the effect SNS has on atrial/ventricular myocytes and what does it do?

A

INOTROPIC EFFECT

Increases contractility to increase pumping force of the heart

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51
Q

What is the name of the effect the SNS has that increases relaxation in the heart and what does it allow?

A

LUSITROPIC EFFECT

Allows for increased heart rate

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52
Q

Sympathetic activity increases CO through…

A

Chronotropic effect on SA node
Dromotropic effect on AV node
Inotropic effect on atrial/ventricular myocytes

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53
Q

What channel is expressed in SA node?

A

sodium ion channel (If)

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54
Q

What is unusual about If?

A

Hyperpolarised and active, so unstable resting membrane potential

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55
Q

How does an action potential work at the SA node?

A

If sodium channel: hyperpolarised resting membrane potential -> sodium ions come into cell making it more positive so depolarising cell -> reaches threshold for voltage gated calcium channels -> upstroke more Ca+ coming in = more positive cell -> voltage gated potassium channels activated and potassium goes out cell -> cell repolarises due to K+ efflux -> If switched on again

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56
Q

How does stimulation of beta 1 adrenoreceptors induce an increase in HR via SNS?

A

In cardiac cell:

NA activates b1 receptor -> G-alpha-s pathway -> adenyl cyclase increases cAMP -> increases activity of If channels -> SPEEDS UP PACEMAKER POTENTIAL in SA node does not generate it

increased frequency = increased HR

57
Q

How does stimulation of beta 1 adrenoreceptors induce an increase in contractility via SNS?

A

In cardiac cell:

NA activates b1 receptor -> G-alpha-s pathway -> adenyl cyclase increases cAMP -> increases PKA which activates VGCCs increasing calcium ions in cell which binds to ryanodine receptors on calcium stores in cell causing CICR (Ca induced Ca release) -> increased Ca in cell engages with troponin -> causes increased crossbridge formation between actin and myosin proteins -> INCREASED CONTRACTION (inotropic)

CGCCs and Ryanodine receptors held open for longer = greater Ca influx = more calcium released = more contraction

58
Q

What two things does PKA phosphorylate in the G-alpha s pathway?

A

VGCCs and Ryanodine receptors

59
Q

How does stimulation of beta 1 adrenoreceptors induce an increase in relaxation via SNS?

A

In cardiac cell:

NA activates b1 receptor -> G-alpha-s pathway -> adenyl cyclase increases cAMP -> increases PKA -> phosphorylates K channels so potassium leaves hyperpolarising cell -> swithces off VGCCs -> so less calcium influx and calcium in cell is taken back up into stores via Ca+ ATPase much faster -> so calcium decreases faster -> INCREASES RELAXATION

60
Q

Why is speeding up relaxation period important?

A

So we can maintain diastolic time whilst hear rate is increasing, so chambers have time to fill with blood

61
Q

What drugs mimic sympathetic activity? What do they do?

A

Sympathomimetics, mimic SNS or activate B1 receptors to increase cardiac activity

62
Q

What do beta antagonists do to cardiac activity?

A

Reduce cardiac activity, inhibit B1 receptors

63
Q

How does SNS control TPR?

A

TPR is mainly controlled by the release of Noradrenaline (from sym nerves) and Adrenaline / Noradrenaline (from adrenal medulla via sympathetic nerves) acting at alpha 1-adrenoceptors on vascular smooth muscle cells in the walls of arterioles

64
Q

What do NA and Adrenaline do that is important in controlling venous return?

A

Vasoconstriction

65
Q

What does increased venous return do to stroke volume?

A

Increased venous return -> increased right atrium volume -> increased stroke volume (via Starling’s law)

increased SV = increased CO (CO = SV x HR)

66
Q

How does stimulation of alpha 1 adrenoreceptors produce contraction of arterioles and veins?

A

In vascular SM cell:

NA acts at a1 receptor activating Gq pathway -> stimulates PLC -> IP3 + DAG -> DAG stimulates PKC -> increases membrane excitability in ion channels so sodium influx causes depolarisation of cell -> activates VGCCs inducing Ca2+ influx -> increased Ca in cell

at same time IP3 -> opens calcium stores -> increased Ca in cell -> myosin light chain kinase (phosphorylates myosin heads = interaction between actin and myosin) -> CONTRACTION

67
Q

Where are vascular smooth muscle cells found?

A

Intermedia layer of blood vessels (so when they contract = reduce lumen, vasoconstriction, when they relax = increase lumen, vasodilatation)

68
Q

What causes contraction in cardiac cells vs smooth muscle cells?

A

Cardiac: Troponin
SM: Myosin light chain kinase

69
Q

Why are Ca2+ channel blockers effective at producing vasodilation and reducing blood pressure?

A

They block the VGCCs, stopping calcium influx therefore reducing contraction and reducing vasodilatation = reduced TPR

(BP = CO x TPR)

70
Q

What drugs increase vasoconstriction?

A

Sympathomimetics or alpha agonists

71
Q

What drugs reduce vasoconstriction?

A

alpha antagonists (inhibit a1 adrenoreceptors)

72
Q

alpha adrenoreceptor agonists

A

Adrenaline, noradrenaline, phenylephrine (selective)

73
Q

alpha adrenoreceptor antagonists

A

Prazosin, phenoxybenamine (for hypertension)

74
Q

Why is the baroreceptor reflex important?

A

Prevents postural hypertension and responds to haemorrhage

75
Q

What is the process of the baroreceptor reflex?

A

Reduced cardiac output -> sensed by threshold receptors -> less stimulation of afferent fibres -> less stimulation of inhibitory pathway in CVLM (nucleus tractus solitarus NTS and caudal ventral lateral medulla CVLM disinhbition, negative pathway switched off) -> so now RVLM (rostal ventral lateral medulla) stimulated bc CVLM no longer inhibiting it -> switches on pre-ganglionic nerves in spinal cord -> sympathetic nerve activity increases -> causes resistance vessel contraction so increases TPR -> vasoconstriction so increased venous return -> reflex also reduces parasympathetic innervation of heart

also increase heart rate, cardiac output and contractility (this will all be sensed by baroreceptors so no longer need to disinhibit CVLM when CO goes up)

76
Q

How does increased SNS activity affect the kidney?

A

Increased sympathetic nerve activity = kidney’s juxtaglomerular apparatus cells beta 1 = increased renin = increased angiotensin 2 via RAAS = vasoconstriction and aldosterone produced from adrenal glands -> causes more sodium and water retention to increase blood volume which can increase SV, CO and BP

77
Q

What drugs block the effect of SNS on the kidney?

A

ACE inhibitors, angiotensin blockers and beta blockers

78
Q

What effect do diuretics have on RAAS?

A

Action the increase of aldosterone and increased sodium + water retention to increase blood volume

79
Q

How does the PNS control cardiac output?

A

Post ganglionic fibres
Release of Ach from the vagus nerve controls CO byacting at M2 receptors
Decreased frequency of pacemaker potential at SA nodeleading to reduction in heart rate
Decreased conduction through AV node

CO = HR x SV -> Stimulation of vagus nerve ( HR) decreases CO

80
Q

Do blood vessels receive parasympathetic innervation?

A

Most blood vessels do not receive parasympathetic innervation

Exception is genitalia where release of NO (not Ach) causesdilatation of vessels to cause erection

81
Q

How does stimulation of M2 muscarinic induce a decrease in HR?

A

SA node: express M2 receptors for Gi pathway -> Ach released at receptor -> Gi pathway -> adenyl cyclase switches off -> decreased cAMP -> decreased activity of If channels -< less sodium coming into cell -> less depolarisation -> takes longer to reach threshold for VGGCs before upstroke -> PNS slowed down process to reduce pacemaker frequency -> reduce HR

82
Q

What drugs mimic parasympathetic activity? What do they do?

A

Parasympathomimetics decrease cardiac activity

83
Q

What do mus antagonists do?

A

Drugs that inhibit M2 receptors (mus antagonists)increase cardiac activity

84
Q

What potential side effects come with mus receptor antagonists?

A

constipation, dry mouth, blurred vision, potential tachycardia

85
Q

What potential side effects come with mus receptor agonists?

A

Bradycardia

86
Q

How is the PNS involved in erection of the penis?

A

Erection of the penis is produced by relaxation of arterioles (increased effect of parasym nerves) that supply blood to the corpus cavernosum

inflow resistance (arterioles) less than outflow resistance (venules, veins)

Stimulation of specialised parasympathetic nerves causes release of nitric oxide (NO)

87
Q

Hoe do viagra like drugs promote action of parasympathetic nerve stimulation on vascular smooth muscle?

A

Erectile dysfunction drugs (sildenafil) block action of phosphodiesterase type 5 (PDE 5) reducing breakdown of cGMP -> More cGMP is produced -> Increased blood flow -> Erection

88
Q

What contractile element is necessary for contraction?

A

Myocytes (cardiac cells) must be excited to contract

89
Q

What is the structure of cardiac muscle tissue?

A

Striated cells containing numerous mitochondria
Adjacent cells join at intercalated discs (provide physical integrity)

Intercalated discs:

  • Desmosomes - for strength
  • Gap junctions - for conduction

Forms 2 functional syncytia:

  • Atria
  • Ventricles.
90
Q

What are the characteristics of a cardiac myocyte?

A

Automaticity: ability to spontaneously initiate an impulse.
Excitability: indicates how well a cell responds to electrical stimuli.
Conductivity: ability of cell to transmit an impulse to another cell.
Contractility: ability to contract after receiving an impulse.

91
Q

What are the principle cation and anions intra and extracellularly in myocytes?

A

Intracellularly:
K+ is the principal cation
phosphate and the conjugate bases of organic acids dominant anion

Extracellularly:
Na+is the principal cation
Cl- is the dominant anion

92
Q

What is the resting membrane potential of a myocyte?

A

negative -90mV

93
Q

Summarise myocyte depolarisation, repolarisation and refractory period

A

Depolarisation:
Voltage-gated activation
Triggers release of sarcoplasmic reticular Ca++
Sarcomeric contraction

Repolarisation:
Restoration of resting membrane potential
Sarcomeric relaxation

Refractory:
Loss of excitability

94
Q

What are the two main cell types in the heart?

A
  1. Contractile cells:
    Atrial and ventricular tissue
    Different layers (epicardial, M-Cell and endocardial)
    Low automaticity (so they dont excite by themselves)
    High contractility and excitability
2. Automatic/ auto-rhythmic cells (pacemaker cells):
Pacemaker and conduction tissue
High automaticity (esp in SA node) and conductivity
95
Q

Pacemaker cells: Myocyte action potential phases

A

PHASE 4: Slow, inward diffusion of Na+ through If. This generates an unstable, slowly increasing resting membrane potential (around -60mV).

PHASE 0: Depolarisation occurs when threshold is reached (around -35mV), involving slow, and later rapid, influx of Ca2+.

PHASE 3: Repolarisation occurs due to outward diffusion of K+. Ca2+ influx terminates due to closing of channels.

96
Q

Contractile cells: Myocyte action potential phases

A

PHASE 0: RAPID DEPOLARISATION: Na+ entry causes rapid depolarisation. Some Ca2+ leaks slowly into the cell too

PHASE 1: EARLY REPOLARISATION: Na+ channels close and K+ channels open, causing partial repolarisation as K+ leaves the cell.

PHASE 2: Ca2+ enters (3Na+/Ca2+ exchanger and L-type Ca2+ channels) to prolong the depolarisation. K+ continues to leave the cell – plateau. Cardiac muscle contracts in response to Ca2+

PHASE 3: K+ rapidly leaves the cell to cause repolarisation. Ca2+ channels close.

PHASE 4: Resting membrane potential (-90mV) is established once again by active transport (through the Na+-K+ pump).

97
Q

What are the specialised areas for conduction?

A

Once action potential generated, resultant impulse propagates via conducting tissue.

Specialised areas for conduction:
SA node (highest automaticity)
Bundle of Bachmann
AV node
Bundle of His
R/L bundle branches
Purkinje fibres.
98
Q

Why does AV node have slow conduction?

A

To prevent too rapid contraction of ventricles

Also longer refractory period

99
Q

Why do impulses travel faster down the left bundle?

A

Thicker ventricular wall

100
Q

What is the funny current?

A

The pacemaker current (or If, or IKf, also referred to as the funny current) is an electric current in the heart that flows through the HCN channel or pacemaker channel. Such channels are important parts of the electrical conduction system of the heart and form a component of the natural pacemaker.

101
Q

What are the ECG values on paper?

A 
ECG recorded on standard paper 
time 25mm/s
voltage 10mm/mV
Large squares: 5mm = 0.2sec/0.5mV
Small squares: 1mm = 0.04sec/0.1mV
102
Q

What causes a positive and negative deflection on an ECG?

A

Wave travelling towards the lead = Positive deflection

Wave travelling away from leads = Negative deflection

103
Q

What are the limb leads and what plane do they look at?

A

I, II, III, aVL, aVF, aVR

104
Q

What are the chest leads and what plane do they look at?

A

V1, 2, 3, 4, 5, 6

105
Q

What gives the positions for leads 1, 2 and 3?

A

Einthoven’s triangle

106
Q

What phase equates to QRS in an ECG?

A

Phase 0

107
Q

What phases equate to the QT interval?

A

Phases 1, 2 and 3

108
Q

What would show decreased automaticity in the SA node?

A

Sinus bradycardia and pauses in sinus node disease, exit block so imulse struggling to leave node and when it does the pattern is irregular

109
Q

What is the most common basis for tachyarrythmia?

A

AV nodal re-entry (scar and fibrosis can form slow component re-entry circuit)

Supraventricular tachycardia

110
Q

How do we control BP?

A

Contraction of LV
Resistance of small blood vessels
Volume of blood

111
Q

BP = CO x TPR

A

Cardiac output = amount of blood pumped out by the heart per minute (=Stroke volume x Heart rate

Stroke volume = amount of blood ejected from the left ventricle per heart beat

Peripheral vascular resistance = resistance to flow in the peripheral vascular tree

112
Q

Low BP vs High BP

A

Low BP = low SV, slow/v fast HR, reuced TPR

High BP = high SV, high TPR

113
Q

Where is the majority of the blood volume?

A

Veins (81%)

114
Q

What is pressure naturesis?

A

A central component of the feedback system for long-term control of BP

Increasein renal perfusion pressure -> increase in renal interstitial hydrostatic pressure -> decrease in sodium reabsorption and increase in Na excretion

Exact mechanism not fully known but alterations in tight junctional Na permeability in proximal tubules, redistribution of apical Na transporters, and/or release of renal autacoids such as prostaglandin E2

115
Q

What is the importance of Poiseulle’s law?

A

R = 8 Ln/pi, r to the power 4
changes in radius ® will have a major effect on resistance

R = resistance
L = length of BV
n =  viscosity
r = radius

greater resistance in smaller blood vessels in peripheral circulation

116
Q

Which baroreceptors are activated when there is a fall in central blood volume?

A

Cardiopulmonary baroreceptors (SNS)

117
Q

Where do baroreceptors sense high and low pressure?

A

High-Pressure: Carotid sinus & Aortic arch

Low-Pressure: Heart & Pulmonary artery

118
Q

What is angiotensin 2?

A

Formed by the action of ACE on angiotensin I

Most powerful vasoconstrictor
Increases peripheral resistance
Increases arterial pressure
Stimulates the secretion of aldosterone resulting in salt & water retention

119
Q

What is epinephrine and how does it act on heart and smooth muscle of arterioles and veins?

A

Released by adrenal medulla in response to sympathetic activity
Increases mean arterial pressure

Acts on heart: Increases HR + Increases SV

Acts on smooth muscle of arterioles: Increases TPR

Acts on smooth muscle of veins: Increases venomotor tone

120
Q

What is vasopressin (ADH)?

A

Antidiuretic hormone
Enhances water retention
Causes vasoconstriction
Secretion increased by unloading of aortic Baroreceptors and atrial sensors

121
Q

What is Atrial Natriuretic Peptide?

A

Increases salt excretion via kidneys:
By reducing water reabsorption in the collecting ducts
relaxes renal arterioles
inhibits sodium reabsorption in the distal tubule

Released in response to stimulation of atrial receptors

122
Q

ADME

A
  1. Absorption – to get into the blood
  2. Distribution – around the body compartments
  3. Metabolism – chemical alteration
  4. Elimination – permanent removal from the body
123
Q

What are the modes of drug absorption?

A

Passive diffusion
Facilitated diffusion
Active transport
Endocytosis

124
Q

What are the modes of drug administration?

A

Enteral (via GI tract)

Parenteral (bypassing GI tract)

125
Q

What are the enteral modes of drug administration?

A

Oral
Buccal, sublingual
Rectal

126
Q

What are the parenteral modes of drug administration?

A 
Intravenous
Subcutaneous
Intramuscular
Intradermsal
Intra-arterial
Intrathecal
Epidural
Inhaled
Nasal mucosa
Topical/Transdermal
127
Q

What factors influence the mode of drug administration?

A

Patient preference
Timing
First pass metabolism (straight to liver)
Peak dose

128
Q

What does equilibrium (Kc) depend on?

A 
Permeability of barriers
pH of compartments
Binding capacity
Lipid solubility of drug
Blood flow
129
Q

What is bioavailability?

A

The proportion of a drug that enters the circulation after being introduced into the body.

130
Q

What is the volume of distribution?

A

The apparent volume into which a drug appears to be distributed to give a particular plasma concentration

VD = total amount of drug in body/plasma concentration of drug

131
Q

What factors affect the volume of distribution?

A

DRUG PROPERTIES
size
charge
lipid and water solubility

PATIENT FACTORS
protein levels
other drugs
total body water
pH
physiology and co-morbidities
132
Q

What can volume of distirbution values be used for?

A

Estimating drug dosage

e.g. VD morphine = 5L/kg body weight
Plasma concentration = 0.04mg/L
Dose = VD x plasma concentration = 5L/kg x 0.04mg/L
= 0.2mg/kg
= 14mg for a 70kg man
133
Q

What is pharmacokinetics?

A

The study of how the drug moves through the body

134
Q

Blood flow in cardiac cycle pt1

A

FILLING
In diastole, both the atria and the ventricles are relaxed. Blood flows from thevena cavaand pulmonary veins into the right and left atria respectively, before flowing directly into the ventricles. The ventricles fill with blood at a steadily decreasing rate, until the ventricles’ pressure is equal to that in the veins.
At the end of diastole, the atria contract, squirting a small amount of extra blood into the ventricles. This increases the ventricles’ pressure so that it is now higher than that in the atria, causing theatrioventricular valves(mitral/tricuspid) to close.

Isovolumetric Contraction
As contraction begins both sets of valves are closed, meaning that no blood can escape from the ventricles. Therefore, the start of systole increases the pressure within the ventricles, ready to eject blood into the aorta and pulmonary trunk. The stage of isovolumetric contraction lasts for approximately50ms,while the pressure builds up.

135
Q

Blood flow in cardiac cycle pt2

A

Outflow Phase
Once the ventricles’ pressure exceeds the pressure in the aorta/pulmonary trunk, theoutflow valves(aortic/pulmonary) open, and blood is pumped from the heart into the great arteries.
At the end of systole, around 330ms later, the ventricles begin to relax, decreasing the ventricular’s pressure compared to the aorta. The decrease in pressure causes the valves to close. As well as this, blood begins to flowbackwardsthrough the outflow valves, which also contributes to the valves’ closure.

Isovolumetric Relaxation
At the end of the outflow phase, both sets ofvalvesare closed once again. The ventricles begin to relax, reducing the pressure in the ventricles so that the atrioventricular valves open. The ventricles then begin to fill with blood, and the cycle begins once again.

136
Q

Where does the signal go after AV delay?

A

Bundle of His transmits signal to each ventricle via the Purkinje fibres -> they allow for rapid conduction of cardiac action potentials

137
Q

Hypertension stages

A

STAGE 1
140/90mmHg – 159/99mmHg
AND
ABPM average of 135/85mmHg – 149/94mmHg

STAGE 2
160/100mmHg – 180/120mmHg
AND
ABPM average of > 150/95mmHg

STAGE 3
> 180/120mmHg
RISK OF END ORGAN DAMAGE + COMPLICATIONS – refer for same day specialist assessment

138
Q

Why is ambulatory blood pressure offered?

A

To confirm hypertension diagnosis

139
Q

Hypertension drugs for:
Less forceful contraction
Less water reabsorption/more water excretion

A

Calcium channel blockers for less forceful contraction

Thiazide diuretics for less water reabsorption

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