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Medicine COPY > Phase 1 - Week 7 (Autonomic Nervous System, Autonomic Dysreflexia), Phase 3 - Week 1 (Heart, Murmurs) > Flashcards

Phase 1 - Week 7 (Autonomic Nervous System, Autonomic Dysreflexia), Phase 3 - Week 1 (Heart, Murmurs) Flashcards

1
Q

List the functions of the autonomic nervous system

A
  • Digestion
  • Defecation
  • Cardiorespiratory
  • Stress response
  • Genitourinary
  • Sexual
  • Exercise ability
  • Maintain electrolytes
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2
Q

Is the autonomic nervous system under voluntary or involuntary control?

A

Generally subconscious, element of conscious control - can be overridden consciously (e.g. breathing rhythm)

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3
Q

Describe the divisions of the autonomic nervous system

A
  1. Sympathetic nervous system
  2. Parasympathetic nervous system
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4
Q

Sympathetic nervous system

A
  • Accelerator
  • Fight and/or flight (stress response)
  • Origin - thoracolumbar origin
  • Ganglia = next to spinal cord
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5
Q

What are the neurotransmitters of the sympathetic nervous system?

A

Acetyl choline at pre-ganglionic synapse Noradrenaline at post-ganglionic synapse

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6
Q

List the effects brought about by the sympathetic nervous system

A
  1. Vasoconstriction of vessels in the skin and gut
  2. Bronchodilation
  3. Increased heart rate and myocardial contractility
  4. Increased blood pressure
  5. Pupil dilation
  6. Inhibition of the bladder
  7. Vasodilation of vessels to skeletal muscles
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7
Q

Give the exceptions to the origin and neurotransmitters of the sympathetic nervous system

A

Origin = cervical ganglia (head + arms) Neurotransmitters = post ganglionic acetyl choline at sweat glands + deep muscles

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8
Q

List the types of post-ganglionic receptors of the sympathetic nervous system

A

Alpha receptors: - Alpha 1 = arteriole constriction - Alpha 2 = coronary + venous vasoconstriction Beta receptors: - Beta 1 = heart, some in brain - Beta 2 = everything else - smooth muscle relaxation, uterus, gut, bladder, lungs, eye

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9
Q

Parasympathetic nervous system

A
  • Brake - Rest/digest - Origin = craniosacral outflow - Ganglia = diffusion near site of action
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10
Q

What are the neurotransmitters of the parasympathetic nervous system?

A

Acetyl choline pre and post-ganglion

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11
Q

List the effects of the parasympathetic nervous system

A
  1. Constrict pupils 2. Mucous membranes engorge 3. Increase salivation 4. Increase gastric secretions 5. Increase intestinal blood flow 6. Decrease heart rate/blood pressure
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12
Q

List the origins of the parasympathetic nervous system

A

Cranial - - 3 = pupillary constriction - 7 = mucous membranes - 9 = salivation - 10 = vagus nerve Sacral - - 2 - 3 - 4

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13
Q

Describe the receptors of the parasympathetic nervous system

A

Muscarinic receptors: - M1,4,5 = brain - M2 = heart - M3 = salivary glands, gut, bladder, blood vessels Nicotinic receptors: - N1, N2 - motor end plate (near skeletal muscle)

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14
Q

List the functions of the brain stem

A
  • Cranial nerve function - Respiration, cardiovascular, sleep, arousal, consciousness - Conduit function - spinothalamic, corticospinal
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15
Q

List the cranial nerves and their functions

A
  1. Olfactory nerve - smell 2. Optic nerve - visual 3. Oculomotor nerve - eye movement 4. Trochlear nerve - eye movement 5. Trigeminal nerve - face sensation + muscles of mastication 6. Abducens nerve - eye movement 7. Facial nerve 8. Vestibulocochlear nerve - hearing and balance 9. Glossopharyngeal nerve - oral sensation, taste and salivation 10. Vagus nerve - parasympathetic 11. Accessory nerve - shoulder elevation, head turning 12. Hypoglossal nerve - tongue movement
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16
Q

Describe the parasympathetic sensory pathway

A
  1. Sensory interoceptors 2. CNS 3. Preganglionic motor neurone
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17
Q

Describe the parasympathetic motor pathway

A
  1. Preganglionic motor cell body 2. Preganglionic motor neuron 3. Automatic ganglion 4. Postganglionic neuron 5. Effector
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18
Q

Describe the sympathetic pathway

A
  1. Preganglionic motor cell body 2. Preganglionic motor fibres 3. Autonomic ganglion 4. Postganglionic motor fibres
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19
Q

What is the chemical formula for adrenaline

A

C9H13NO3

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20
Q

Where is adrenaline produced?

A

Adrenaline and noradrenaline are produced in the medulla of the adrenal glands and in some neurones of the CNS

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21
Q

What triggers the production of adrenaline?

A

The sympathetic nervous system

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22
Q

Describe tissue specificity of adrenaline

A

Different action depending on tissue it is acting on due to different receptors e.g. smooth muscle relaxation in airways, smooth muscle contraction in arterioles

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23
Q

What is the overall effect of adrenaline

A
  • Response to acute stress, ‘fight or flight’ - Stimulatory effect on alpha and beta adrenic receptors (adrenoreceptors) of sympathetic nervous system - agonist
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24
Q

List the actions of adrenaline

A
  1. Increase HR 2. Increased BP 3. Expanding bronchi 4. Pupil dilation 5. Increased blood flow to skeletal muscle 6. Alters metabolism - maximise blood glucose levels esp. in brain, + fatty acids
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25
Q

Describe the production of adrenaline

A

Tyrosine -> noradrenaline -> adrenaline (methylation, + of methyl group)

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26
Q

How is the action of adrenaline halted?

A

Metabolic breakdown, re-uptake into nerve endings or diffusion from action sites

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27
Q

Define heart rate

A

Number of heartbeats per unit time, usually beats per minute

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28
Q

What is the normal resting heart rate?

A

70-90 BPM

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29
Q

How is heart rate controlled?

A

Sympathetic control: - Release of adrenaline and noradrenaline increases HR Parasympathetic control: - Release of acetyl choline decreases HR

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30
Q

What is responsible for controlling heart rate?

A

Cardiorespiratory centre in the medulla oblongata

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31
Q

Define blood pressure

A

Pressure exerted by the blood on the walls of blood vessels

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32
Q

Define systolic and diastolic pressure

A

Systolic = max arterial pressure during ventricular systole Diastolic = min arterial pressure during dilation of ventricles

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33
Q

What is normal blood pressures?

A

120/80 -> 140/90

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34
Q

How is blood pressure regulated?

A
  • Baroreceptors - medulla, ANS changes pressure by changing force/speed of contractions + systemic vascular resistance - Baroreceptors regulate secretion of ADH, changing blood volume therefore pressure - Aldosterone (steroid hormone) stimulates sodium retention/potassium secretion by kidneys to change the blood volume - Renin secretion by the kidneys
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35
Q

Define autonomic dysreflexia

A

A condition occurring primarily in patients with spinal cord injury above T6 in which an external or bodily stimuli causes an imbalanced reflex sympathetic discharge, leading to potentially life-threatening hypertension.

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36
Q

What is the effect of untreated autonomic dysreflexia?

A
  • Seizures - Retinal haemorrhage - Pulmonary oedema - Renal insufficiency - MI - Cerebral haemorrhage - Death
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37
Q

Describe the development of autonomic dysreflexia

A
  1. Strong sensory input - intact peripheral nerves -> spinal cord (common origins = bladder, bowel) 2. Reflex sympathetic surge from thoracolumnar sympathetic nerves 3. Widespread vasoconstriction - hypertension 4. Brain attempts to resolve - inhibitory impulses to sympathetic surge, decrease HR to decrease BP through vagus nerve - spinal cord damage doesn’t allow
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38
Q

Describe the measures taken to prevent autonomic dysreflexia

A
  • Bladder and bowel care (catheterisation etc.) - Education - recognise early symptoms - Home blood pressure monitoring
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39
Q

List the symptoms of autonomic dysreflexia

A
  • Anxiety and apprehension - Palpitations - Hypertension - Pounding headache - Flushing of the skin - Lightheadedness - Confusion - Dilated pupils
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40
Q

List the triggers of autonomic dysreflexia

A
  • Distended bladder - Blocked catheter - Urinary retention - Urinary tract infection - Bladder stones - Constipation - Bowel impaction - Hemorrhoids - Skin irritation - Pressure stones - Tight clothing
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41
Q

Describe the treatment of autonomic dysreflexia

A
  • Removing stimulus (tight clothing, blocked catheter, faecal impaction) - Administering antihypertensive drugs to decrease blood pressure e.g. nitrates + nifedipine
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42
Q

List the functions of the cardiovascular system

A
  • Transport of nutrients, oxygen and waste products around the body - Transfer of heat (generally core->skin) - Buffer body pH - Transport of hormones - Assist in response to infection - Assist in formation of urine - filtration + circulation
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43
Q

Describe the heart sounds

A

1 = AV valves closing 2 = Pulmonary and aortic valves closing

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44
Q

Describe a cardiac cycle

A
  • Systole (contraction) and diastole (relaxation) of the atria then ventricles - Blood flow controlled by valves and sequences of diastole and systole - Blood flows from area of higher pressure to one of lower pressure
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45
Q

Explain the differences between the left and right ventricles

A

Left has much thicker more muscular wall - right has to pump blood smaller distance (to lungs) than right (whole body)

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46
Q

Stroke volume

A

Volume of blood ejected from the heart per beat

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47
Q

Starling’s Law

A

The stroke volume increases in response to an increase in volume of blood in the ventricles

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48
Q

Equation for cardiac output

A

CO = SV x HR (each side)

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49
Q

What makes the heart contract?

A
  • Impulses generated within the SA node spread over the atria the ventricles - SA has fastest intrinsic rate so determines heart rate - pacemaker - Atria and ventricles on left and right sides of heart contract at same time - AV node slows conduction and can act as secondary pacemaker if required - Purkinje fibres interdigitate with myocytes to spread impulse across ventricles - excitation-contraction coupling
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50
Q

How do ECGs work?

A
  • Detects phasic change in potential difference between two electrodes: on surface of heart and on limbs - Recorded on oscilloscope/computer/paper
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51
Q

What are ECGs used for?

A

Diagnosis of arrhythmias, post MI damage, congenital/iatrogenic abnormalities

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52
Q

Describe the sections of a typical ECG

A

P wave = atrial depolarisation QRS complex = ventricular depolarisation T wave = ventricular repolarisation P-R interval = delay through AV node S-T interval = plateau phase of AP

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53
Q

Describe the process of cardiac muscle contraction

A
  • Calcium entry into cardiac muscle cells triggers contraction - Exterior of the myocyte - Sarcoplasmic reticulum inside cell - ‘Calcium-induced calcium release’ - Allows a greater contraction for a small calcium movement - amplifier
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54
Q

How are changes in cardiac output detected and modulated?

A
  • Detected by baroreceptors, information on blood pressure fed back to CVS control centre in medulla of brain - HR increased by binding of noradrenaline from sympathetic nerves and circulating adrenaline - HR decreased by action of the vagus nerve which terminates on the nodal tissue, acetyl choline released
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55
Q

List the types of blood vessels in the cardiovascular system

A
  1. Large arteries 2. Arterioles 3. Capillaries 4. Venules 5. Veins
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56
Q

Which cells line all blood vessels ?

A
  • Endothelial cells line all blood vessel and inside of heart chambers
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57
Q

List the functions of endothelial cells

A
  • Prevent platelet aggregation and blood clot formation - Permeability barrier for nutrients/fluid between plasma and interstitial fluid - Angiogenesis + vessel remodelling - Release constrictors - endothelin, thromboxane and dilators - nitric oxide, prostacyclin - Influence proliferative state if smooth muscle cells
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58
Q

What is the role of vascular smooth muscle?

A
  • Present in all vessels except small capillaries - Determine vessel radius by contracting and relaxing - Secrete ECM giving vessel elastic properties
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59
Q

Mean arterial pressure (MAP)

A

Average pressure pushing blood around the system, MAP = diastolic pressure + 1/3 (systolic pressure - diastolic pressure)

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60
Q

Why is it important that arteries are elastic?

A

To allow stretching by raised blood pressure in systole

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61
Q

Explain how the structure of arteries and the aorta are adapted to their function

A
  • Contain a small volume of blood at high pressure - Very thick walled/elastic
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62
Q

What is the function of arterioles?

A
  • Variable resistance system which distributes the blood - Dissipates most of the pressure
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63
Q

Explain how the structure of capillaries is adapted to their function

A
  • Large surface area where interchange of substances with the extracellular fluid of the tissue occurs - As little as one cell thick - Exchange of nutrients/waste products - Just wide enough for an erythrocyte to squeeze through
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64
Q

Explain how the structure of venules, veins and the vena cavae are related to their function

A
  • A collecting and reservoir system containing most of the blood at low pressure - Very distensible - Veins have valves to stop back-flow due to low pressure
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65
Q

List the factors which control blood flow

A
  1. Length of the vessel 2. Viscosity of the blood 3. Pressure gradient across the length of the vessel 4. Cross sectional area of the vessel 5. Resistance of the vessel - proportional to diameter
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66
Q

What happens to blood flow as branching increases down the arterial tree?

A

Arteries -> arterioles -> capillaries, resistance increases, flow is reduced

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67
Q

How is blood flow maintained in the veins

A
  • Valves direct blood towards heart - Skeletal muscle pump - Respiratory movements aid venous return - Sympathetic nerves - noradrenaline constricts veins = increased venous return to the heart
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68
Q

Preload

A

Venous return to the right ventricle - if preload increases the heart has to work harder to pump blood out

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69
Q

How can preload be reduced?

A

Nitrates

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70
Q

List the functions of the nervous system

A
  1. Communication 2. Regulating internal events 3. Organising behaviour (external) 4. Information storage (memory) 5. Sensations, perceptions, emotions
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71
Q

List the cells of the nervous system

A
  • Neurones - Glia
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72
Q

Glia

A
  • More numerous than neurones - Supportive, nutritional role - Myelin formation
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73
Q

List the types of glial cells

A
  • Schwann cells (PNS) - Oligodentrocytes (CNS)
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74
Q

Neurones

A
  • Excitable cells - Generation and transmission of signals - Synaptic processing - Various types with structure related to function
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75
Q

Describe the structural organisation of the nervous system

A
  • Central nervous system - brain + spinal cord - Peripheral nervous system - spinal nerves + cranial nerves
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76
Q

Describe the functional organisation of the nervous system

A
  • Sensory - afferent - Motor - efferent
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77
Q

List the parts of the brain

A
  1. Cerebral hemispheres 2. Cerebellum 3. Brainstem
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78
Q

Telencephalon

A

Cerebrum

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79
Q

Diencephalon

A

Thalamus,, hypothalamus

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80
Q

Forebrain

A

Telecephalon + diencephalon

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81
Q

Mesencephalon

A

Midbrain - vision, hearing, motor function, arousal state

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82
Q

Hindbrain

A

Rhombencephalon

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83
Q

List the parts of the cerebral hemispheres

A
  1. Frontal lobes - executive functions, long-term memory 2. Parietal lobe - integration of sensory functions 3. Occipital lobe - visual processing 4. Temporal lobe - primary auditory cortex
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84
Q

List the sulci of the cerebral hemispheres

A
  1. Central sulcus 2. Lateral sulcus 3. Parieto-occipital sulcus
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85
Q

Describe the arrangement of the spinal cord

A
  • Dorsal roots - sensory - Ventral roots - motor - One pair of spinal nerves from each segment - Dorsal root ganglia contain cell bodies of primary sensory neurones
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86
Q

Nerve plexus

A

Peripheral nerves that supply specific body regions

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87
Q

Describe the functional divisions of the nervous system

A
  • Somatic nervous system - motor and sensory - Autonomic nervous system - visceral afferent and visceral efferent (sympathetic and parasympathetic)
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88
Q

Afferent peripheral nerves

A
  • Carry information to the CNS - Afferent signals in somatic nerves are associated with sensations/perceptions - Afferent signals from internal organs do not usually give rise to sensations
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89
Q

Efferent peripheral nerves

A
  • Carry information away from the CNS - Cause actions e.g. muscle contraction - Somatic efferents control voluntary muscle - Visceral efferents constitute the autonomic nervous system (controlling cardiac muscle and some glands)
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90
Q

Describe the function of the heart

A
  • 2 pumps, one for systemic and one for pulmonary circulation - Transporting oxygen to cells of the body and removal of waste products - Deoxygenated blood to lungs an oxygenated blood around the whole body - Must continuously beat, so is composed of cardiac muscle and myocardium made of specialised cardiac muscle cells which have their own contractile rhythm
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91
Q

Describe the anatomical position of the heart

A
  • Above and on superior surface of the diaphragm - Posterior to sternum - Lies in middle mediastinum - Base is superior and to the right, apex is inferior and to the left (close to 5th intercostal space) - Anchored to diaphragm, back of sternum and great vessels by pericardium
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92
Q

List the great vessels

A
  • Aorta - Pulmonary arteries - Pulmonary veins - Vena cavae
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93
Q

Mediastinum

A

Space covered with connective tissue behind the sternal body, divides the thoracic cavity into two pleural cavities

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94
Q

Describe the structure of the pericardium

A
  • Two serous membrane layers - Each has epithelial lining with underlying connective tissue
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95
Q

What is the function of the pericardium?

A
  • Keeps heart in place, limits motion, prevents over-expansion - Pericardial fluid between layers functions to reduce friction
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96
Q

Describe the layers of the pericardium

A
  1. Serosal pericardium - visceral layer and parietal layer 2. Fibrous pericardium
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97
Q

Serosal pericardium

A
  • Visceral layer on outer surface of the heart wall - Parietal layer on deep surface of the fibrous pericardium - Between layers is pericardial cavity, filled with pericardial fluid
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98
Q

Fibrous pericardium

A
  • Superficial layer of the pericardium - Composed of dense irregular connective tissue - Attaches to parietal layer of serous pericardium, encloses the heart - Attached below to diaphragm and above to the great vessels of the heart - Function = limits motion of the heart, resists stretch to stop heart from over expanding
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99
Q

List the layers of the heart wall

A

From inside -> outside 1. Endocardium 2. Myocardium 3. Epicardium

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100
Q

Endocardium

A
  • Smooth, thin membrane lining the inner surface of the heart chambers - Composed of a layer of endothelial cells, lies over a layer of connective tissue - Covers valves of the heart - Helps prevent resistance as blood passes through heart
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101
Q

Myocardium

A
  • Heart muscle - Varies in thickness depending on location - thin in atria, thick in ventricles - Composed of cardiac muscle fibres, exhibit striations diagonally across heart
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102
Q

Epicardium

A
  • Outer serous membrane of heart wall - Same as inner layer of serous pericardium (visceral pericardium) - Composed mainly of connective tissue mesothelial cells - Gives a smooth texture on the outer surface of the heart
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103
Q

List the chambers of the heart

A
  1. Right atrium 2. Right ventricle 3. Left atrium 4. Left ventricle
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104
Q

Right atrium

A
  • Small, thin walled chamber - Receives deoxygenated blood from entire body via superior and inferior vena cava - Receives blood from myocardium through the coronary sinus
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105
Q

Describe the function of the right atrium

A

Pumps deoxygenated blood from the atrioventricular (tricuspid) valve into the right ventricle

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106
Q

Left atrium

A
  • Small, thin walled chamber - Forms the base of the heart - Receives oxygenated blood from the lungs via the four pulmonary veins
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107
Q

Describe the function of the left atrium

A

Pumps oxygen-rich blood from the atrioventricular (bicuspid) valve into the left ventricle

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108
Q

Atria

A
  • Two upper chambers of the heart, positioned near its base - Have small semi-elastic pouches called auricles, that expand when filled with blood - Auricles ensure there is sufficient blood volume to permit maximal contraction of the ventricles - Atrial walls are thin as they only have to squeeze blood past the AV valves into their corresponding left or right ventricles
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109
Q

Ventricles

A
  • Two lower chambers of the heart positioned near its apex - Walls are thicker than atria and wall of left ventricle is especially thick - has to push blood at high pressure around the entire body
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110
Q

Right ventricle

A
  • Thick walled chamber that forms most of the anterior surface of the heart - Receives deoxygenated blood through tricuspid valve from right atrium
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111
Q

Describe the function of the right ventricle

A

Pumps deoxygenated blood into the the lungs from the pulmonary valve and trunk

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112
Q

Left ventricle

A
  • Thickest walled chamber - Cone-shaped - Forms most of back and lower surface of the heart - Receives oxygenated blood through the bicuspid valve into left atrium
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113
Q

Describe the function of the left ventricle

A

Pumps oxygenated blood to the entire body through the aortic valve via the aorta

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114
Q

Septum of the heart

A

Muscular septum - divided into interatrial septum and interventricular septum

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115
Q

Interarterial septum

A

Separates the left and right atria

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116
Q

Interventricular septum

A

Divides the left and right ventricles

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117
Q

Fossa ovalis

A

Small depression on the interatrial septum, the embryonic remnant of the foramen ovale - an opening in the fetal heart which closes shortly after birth

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118
Q

What separates the atria from the ventricles?

A

Shallow grooves on the external surface of the heart called sulci

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119
Q

List the sulci of the heart

A
  • Coronary sulcus - Anterior interventricular sulcus - Posterior interventricular sulcus
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120
Q

Coronary sulcus

A
  • Groove on the external surface of the heart - Marks the division between the superior atria and inferior ventricles - Contains the trunks of the coronary vessels and coronary sinus
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121
Q

Anterior interventricular sulcus

A
  • Shallow groove on sternocostal, anterior surface of the heart - Marks the division between right and left ventricles - Contains the branch of the left coronary artery
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122
Q

Posterior interventricular sulcus

A
  • Shallow groove on the diaphragmatic, posterior surface of the heart - Marks the division between right and left ventricles - Contains the posterior interventricular artery and the middle cardiac vein
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123
Q

Cardiac skeleton

A

Dense layer of connective tissue which connects the atria and ventricles. Serves as an insertion point for cardiac muscle fibres, provides electrical insulation through the atrioventricular node from right atria to right ventricle. Gives structural stability in the form of rings of connective tissue that surround the valves of the heart.

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124
Q

List the valves of the heart

A
  1. Pulmonary valve 2. Aortic valve 3. Right atrioventricular valve (tricuspid valve) 4. Left atrioventricular valve (bicuspid valve)
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125
Q

How do the valves of the heart work?

A

Open and close in response to pressure created by the volume of blood as it is pumped into each chamber as the heart contracts

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126
Q

What is the function of the atrioventricular valves?

A

Located between the atria and ventricles and prevent the blood in the ventricles from flowing back into the atria. Closing of the AV valves creates the first heart sounds - ‘lub’.

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127
Q

Right atrioventricular valve (tricuspid)

A
  • Lies between the right atrium and right ventricle - Also known as tricuspid valve - because it has three cusps - Chordae tendinae attached to inferior portion of the cusps
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128
Q

Chordae tendinae

A
  • Thin, string like structures attached to the inferior portion of the atrioventricular valves - Attached to the ventricular wall or papillary muscles - They prevent the valve prolapsing into the atria - Prevent the back-flow of blood from the ventricles into the atria during ventricular systole
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129
Q

Left atrioventricular valve (biscuspid)

A
  • Lies between the left atrium and left ventricle - Known as mitral valve or bicuspid valve because it has two cusps - Chordae tendinae attached to inferior portion of cusps
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130
Q

Semilunar valves

A
  • Prevent the back flow of blood from the pulmonary trunk and the aorta to the right ventricle and left ventricle - Have three crescent-shaped cusps - When ventricles contract, cusps of valves are pushed flat against the walls of the vessels, keeping the valves open - When the ventricles stop contracting, the blood immediately tries to flow back in the opposite direction - into ventricles - Returning blood flows into the cusps of the valves, opening them out and blocking the flow of blood back into the ventricles
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131
Q

Pulmonary valve

A
  • Lies between the right ventricle and pulmonary trunk - Cusps are attached partly to the wall of the right ventricle and partly to the walls of the pulmonary trunk
132
Q

What is the function of the pulmonary valve?

A

After the ventricle has contracted, pressure from blood trying to rush back into the ventricle from the pulmonary trunk fills the cusps and closes the valves

133
Q

Aortic valve

A
  • Lies between the left ventricle and aorta - Cusps are attached partly to the wall of the left ventricle and partly to the walls of the aorta
134
Q

What is the function of the aortic valve?

A

After ventricle has contracted, pressure from blood trying to rush back into the ventricle from the aorta fills the cusps and closes the valve. Just above cusps are the openings to the coronary arteries - back-flowing blood supplies the myocardium

135
Q

What is the origin of the coronary arteries?

A

Left and right coronary arteries arise from the ascending aorta just above the cusps of the aortic valve

136
Q

Describe the path of the coronary arteries

A
  • Left and right coronary arteries and their main branches follow the atrioventricular an interventricular grooves on the surface of the heart - Are often embedded in pericardial fat - Branches communicate by anastomosing together around the heart to from continuous loops
137
Q

Why is the anastomosis of coronary arteries important?

A

If one of the vessels becomes blocked, it proves an alternative route for blood to get to the myocardium

138
Q

What is supplied by the branches of the left coronary arteries?

A
  • Both ventricles - Interventricular septum - Left atrium
139
Q

List the main branches of the left coronary artery

A
  1. Anterior interventricular artery 2. Circumflex artery 3. Left marginal artery
140
Q

Anterior interventricular artery

A

Lies in the anterior interventricular groove and descends along the groove to the apex of the heart

141
Q

Circumflex artery

A

Passes along the atrioventricular groove to the crux of the heart

142
Q

Left marginal artery

A

Runs along the margin of the heart

143
Q

What is supplied by the branches of right coronary artery?

A
  • Right atrium - Right ventricle - Variable portions of the left atrium and left ventricle
144
Q

List the main branches of the right coronary artery

A
  1. Posterior interventricular 2. Right marginal artery
145
Q

Posterior interventriclar artery

A

Runs along the posterior interventricular sulcus to the apex of the heart

146
Q

Right marginal artery

A

Travels along the inferior surface of the heart to the apex

147
Q

Describe the path of the coronary veins and their branches

A
  • Follow the coronary arteries - Merge to form the coronary sinus which empties into the right atrium
148
Q

List the main branches of the coronary sinus

A
  1. Great cardiac vein 2. Middle cardiac vein 3. Small cardiac vein
149
Q

Great cardiac vein

A

Begins at the apex of the heart and ascends along the anterior interventricular groove

150
Q

Small cardiac vein

A

Extends from the apex of the heart, runs along the posterior atrioventricular groove between the right atrium and right ventricle

151
Q

Middle cardiac vein

A

Extends from apex of heart and continues along base of the heart

152
Q

How many heart sounds are there in each cardiac cycle?

A

4 - in a healthy heart only 2 can be heard through a stethoscope

153
Q

First heart sound

A

S1 = ‘lub’ - Longer and louder than the second - Caused by blood turbulence generated as the atrioventricular valves close at the beginning of ventricular systole

154
Q

Second heart sound

A

S2 = ‘dub’ - Shorter and softer - Caused by sudden block of blood flow as the semilunar valves at the beginning of ventricular diastole

155
Q

Third heart sound

A

Cannot usually be heard, produced during the rapid filling of blood into the ventricles from the atria

156
Q

Fourth heart sound

A

Cannot usually be heard, produced by the forceful contraction of the atria

157
Q

List the events of the cardiac cycle

A
  1. Right atrial systole 2. Right ventricular systole 3. Right atrial diastole 4. Right ventricular diastole 5. Left atrial systole 6. Left ventricular systole 7. Left atrial diastole 8. Left ventricular diastole
158
Q

Right atrial systole

A
  • De-oxygenated blood from superior and inferior vena cavae enters the relaxed right atrium - Blood flows passively through tricuspid valve into right ventricle - During atrial systole, right atrium contracts, pushes remaining blood into right ventricle
159
Q

Right ventricular systole

A
  • Right ventricle contracts, forcing blood through the pulmonary valve into the pulmonary trunk - Pulmonary trunk divides into right and left pulmonary arteries which carry deoxygenated blood to the lungs, where gas exchange occurs
160
Q

Right atrial diastole

A

While heart is undergoing ventricular systole atrium relaxes during atrial diastole + pressure increases in the right ventricle causing the tricuspid valve to close

161
Q

Right ventricular diastole

A
  • When blood is ejected from the ventricle, it relaxes during ventricular diastole - Atrium and ventricle fill with the blood and the cycle begins again - Simultaneously, oxygenated blood produced during gas exchange enters the left side of the heart from the pulmonary veins
162
Q

Left atrial systole

A
  • Oxygenated blood enters the heart from the pulmonary vein allowing blood to flow through the bicuspid valve into the left ventricle - During atrial systole, left atrium contracts pushing the remaining blood into the left ventricle
163
Q

Left ventricular systole

A
  • Left ventricle contracts during ventricular systole forcing aortic valve to open, pushing blood into the ascending aorta - Ascending aorta continues to split into a number of branches, which carry the oxygenated blood to the entire body
164
Q

Left atrial diastole

A

Atrial diastole and ventricular systole occur simultaneously, causing the atrium to relax and the bicuspid valve to close

165
Q

Left ventricular diastole

A
  • Ventricular diastole occurs and the ventricles relax - Blood flowing into the heart causes the aortic valve to close - Atrium and ventricles then fill with blood and the cardiac cycle will begin again
166
Q

What are the cells of the myocardium?

A

Cardiac myocytes

167
Q

List the prominent structural features of cardiac myocytes

A
  • Oval nuclei - Abundant mitochondria for a constant energy supply - Sarcolemma (plasma membrane) - Transverse tubules for co-ordinated muscle contraction - Sarcoplasmic reticulum - reservoir of calcium ions needed for contraction - Contractile elements arranged into sarcomeres and myofibrils
168
Q

Describe the nucleus of cardiac myocytes

A
  • One nucleus located centrally within the cell - Pale, oval shaped - Largest organelle
169
Q

Describe the function of the nucleus of cardiac myocytes

A

Regulates gene expression and therefore controls the activities of the cell

170
Q

Describe the mitochondria of cardiac myocytes

A

Large and abundant

171
Q

Describe the function of the mitochondria of cardiac myocytes

A

Provide the cardiac muscle with a constant supply of energy. Energy is transferred by ATP. Can self-replicate when demand for ATP increases.

172
Q

Describe the sarcolemma of cardiac myocytes

A

Plasma membrane, invaginates into the cytoplasm, creating the membrane-bound tunnels called transverse tubules.

173
Q

Describe the function of the sarcolemma of cardiac myocytes

A

Transverse tubules ensure the spread of excitation deep into the muscle fibres for co-ordinated muscle contraction

174
Q

Describe the transverse tubules of cardiac myocytes

A

Invaginations of the sarcolemma which run from the surface of the sarcoplasmic reticulum into the central portions of the muscle fibre. Filled with interstitial fluid.

175
Q

Describe the function of the transverse tubules of cardiac myocytes

A

Critical role in excitation-contraction coupling, transmitting electrical impulses from the sarcoplasm to the core of the muscle fibre

176
Q

Describe the myofibrils of cardiac myocytes

A

Cylindrical bundles of thick and thin filaments, run from one end of a cardiac myocyte to the other. Vary in diameter and branch extensively, interspersed with numerous mitochondria

177
Q

Describe the function of the myofibrils of cardiac myocytes

A

Contain the contractile elements of the myocytes and are responsible for contraction

178
Q

Describe the sarcoplasmic reticulum of cardiac myocytes

A

Smooth endoplasmic reticulum of a muscle cell, made of a network of fluid-filled, membrane-bound tubular sacs that surround each myofibril

179
Q

Describe the function of the sarcoplasmic reticulum of cardiac myocytes

A

Reservoir for calcium ions, has gated ion channels distributed throughout its membrane, which allow the sudden influx of calcium into the cytosol, triggering muscle contraction.

180
Q

Define heart murmur

A

An unusual heart sound produced by blood flow across a heart value

181
Q

Describe the types of heart murmurs

A
  1. Innocent heart murmurs - present in a normal healthy heart 2. Abnormal heart murmur - due to congenital heart disease or acquired heart valve defects
182
Q

Describe the classification of heart murmurs

A
  1. Timing - systolic or diastolic 2. Shape - intensity over time, crescendo or decrescendo 3. Location - where it is heard best 4. Radiation - where the sound radiates 5. Intensity - loudness of the murmur 6. Pitch - low, medium or high 7. Quality - blowing, harsh, rumbling or musical
183
Q

List the anatomical causes of systolic heart murmurs

A
  1. Aortic valve stenosis 2. Mitral regurgitation 3. Mitral valve prolapse 4. Pulmonary valve stenosis 5. Tricuspid valve regurgitation 6. Hypertrophic obstructive cardiomyopathy 7. Atrial septal defect 8. Ventricular septal defect
184
Q

List the anatomical causes of diastolic heart murmurs

A
  1. Aortic valve regurgitation 2. Mitral stenosis 3. Tricuspid valve stenosis 4. Pulmonary valve regurgitation
185
Q

List the anatomical causes of continuous and combined systolic/diastolic heart murmurs

A
  1. Patent ductus arteriosis 2. Severe coarctation of the aorta 3. Acute severe aortic regurgitation
186
Q

Give examples of pathological causes of heart murmurs

A
  1. Valve calcification 2. Endocarditis 3. Rheumatic fever
187
Q

What to pathological problems caused by valve abnormalities result from?

A
  • Valvular stenosis = valves become thickened or calcified and obstruct the normal flow of blood into a chamber or vessel - Valvular incompetence = valves lose their normal function and fail to prevent the reflux of blood after contraction of an individual chamber - Vegetations = valve leaflets develop either infective of thrombotic nodules that impair normal valve mobility and can fragment and embolise
188
Q

Explain the pathological cause and clinical features of mitral stenosis

A

Caused by rheumatic vascular disease Features: - Pulmonary hypertension - Left atrial dilation - Right ventricular hypertrophy

189
Q

Describe the heart murmur caused by mitral stenosis

A

Opening snap and diastolic murmur

190
Q

Explain the pathological causes and clinical features of mitral incompetence

A

Caused by infective endocarditis or rheumatic valvular disease Features: - Variable haemodynamic effects dependent on rate of development

191
Q

Describe the heart murmur caused by mitral incompetence

A

Pansystolic murmur, mid-systolic click and late systolic murmur in mitral prolapse

192
Q

Explain the pathological causes and clinical features of aortic stenosis

A

Caused by rheumatic valvular diseases Features: - Left ventricular hypertrophy - Angina - Syncope - Left ventricular failure - Sudden death

193
Q

Describe the heart murmur caused by aortic stenosis

A

Ejection systolic murmur

194
Q

Explain the pathological causes and clinical features of aortic incompetence

A

Caused by infective endocarditis, rheumatological disorders e.g. rheumatoid arthritis, ankylosing spondylitis Features: - Wide pulse pressure - Collapsing pulse - Angina - Left ventricular failure

195
Q

Describe the heart murmur caused by aortic incompetence

A

Diastolic murmur

196
Q

Give examples of common congenital heart defects

A
  1. Aortic valve stenosis 2. Ventricular septal defect 3. Patent ductus arteriosis
197
Q

Define congenital heart defect

A

A problem in the structure of the heart present at birth

198
Q

List the causes of congenital heart defects

A
  • Often unknown - Due to infection in pregnancy e.g. rubella - Use of drugs such as alcohol/tobacco - Poor nutritional status or obesity in mother - Congenital conditions e.g. Down syndrome, Marfan syndrome - Genetic - parent with congenital heart defect
199
Q

What is the foramen ovale?

A
  • Structure present in the foetal heart - Allows blood to flow from right to left atrium - Blood bypasses pulmonary circulation - Closes at birth in healthy individuals - Forms the fossa ovalis
200
Q

What is the ductus venosus?

A
  • Structure which shunts part of the left umbilical vein blood flow directly to the inferior vena cava - Allows oxygenated blood from the placenta to bypass the liver - Closes during the first week of life in healthy neonates - Forms the ligamentum venosum
201
Q

List the anatomical features of the circulation unique to developing foetuses

A
  1. Ductus arteriosus 2. Foramen ovale 3. Ductus venosus
202
Q

What is the ductus arteriosus?

A
  • Vessel connecting the main pulmonary artery to the proximal descending aorta - Allows most of the blood from the right ventricle to bypass the foetus’s lungs - Closes at birth, becomes ligamentum arteriosum
203
Q

Patent foramen ovale

A
  • Failure of closure of the foramen ovale at birth - Blood is able to flow between the atria (from right to left) - Can lead to low oxygenation in arterial blood supplying the systemic tissues
204
Q

List the standard types of cardiac imaging

A
  1. Echocardiography 2. Chest X-ray 3. CT 4. MRI 5. Types of radionuclide imaging e.g. SPECT
205
Q

Describe the steps involved in a cardiovascular examination

A
  1. General inspection 2. Hands 3. Pulses 4. Jugular venous pressure 5. Face 6. Inspection of chest 7. Apex beat 8. Heaves/thrills 9. Auscultation
206
Q

Describe the clinical signs which may be present during the general inspection of a CV examination

A
  • Bedside - O2, GTN spray, motility aids - Check patient is comfortable at rest - Malar flush - plum red discolouration of cheeks, may suggest mitral stenosis - Obvious scars/pulsations - Legs - Scars from saphenous vein harvest for CABG, peripheral oedema, missing limbs/toes
207
Q

Describe the clinical signs which may be present during inspection of the hands of a CV examination

A
  • Splinter haemorrhages - red/brown streaks on nail bed, infective endocarditis - Finger clubbing - infective endocarditis, cyanotic congenital heart disease - Cyanosis suggests hypoxia - Temperature, cold suggests poor CO/hypovolaemia - Sweaty/clammy associated with coronary syndrome - Janeway lesions - non-tender maculopapular erythematous palm pulp lesions (infective endocarditis) - Osler’s nodes - tender red nodules on finger pulps/thenar eminence - infective endocarditis - Tar staining (smoker) - Xanthomata - raised yellow lesions - hyperlipidaemia - Capillary refill time - prolonged may suggest hypovolaemia
208
Q

List the pulses taken during a CV examination

A
  • Radial pulse - Brachial pulse - Carotid pulse
209
Q

What is assessed when taking the radial pulse during a CV examination?

A
  • Radial rate and rhythm - Radio-radial delay - may suggest aortic coarctation - Collapsing pulse - aortic regurgitation
210
Q

What is assessed when taking the brachial pulse during a CV examination?

A
  • Volume and character assessed - Blood pressure also taken - narrow pulse pressure = aortic stenosis, wide pulse pressure = aortic regurgitation
211
Q

What is assessed when taking the carotid pulse during a CV examination?

A

Character and volume - slow rising character = aortic stenosis

212
Q

What is assessed when observing the jugular venous pressure during a CV examination?

A
  • Raised JVP = fluid overload, right ventricular failure, tricuspid regurgitation - Positive hepatojugular reflux sign = right-sided heart failure and/or tricuspid regurgitation
213
Q

Describe the clinical signs which may be present during examination of the face in a CV examination

A

Eyes: - Conjunctival pallor = anaemia - Corneal arcus (yellow/grey ring around iris) = hypercholesterolaemia - Xanthelasma (yellow raised lesions around eyes) = hypercholesterolaemia Mouth: - Central cyanosis - blue discolouration of lips/tongues = hypoxaemia - Angular stomatitis - inflammation of corners of mouth = iron deficiency - High arched palate - Marfan’s syndrome = risk of aortic aneurysm/dissection - Dental hygiene - source of infective endocarditis

214
Q

Describe the clinical signs which may be present during close inspection of the chest during a CV examination

A

Scars: - Thoracotomy = valve surgery - Sternotomy = CABG/valve surgery - Clavicular = pacemaker - Left mid-axillary line - subcutaneous implantable cardioverter defibrillator Chest wall deformities: - Pectus excavatum - Pectus carinatum Visible pulsations: - Forceful apex beat = hypertension/ventricular hypertrophy

215
Q

Describe the clinical signs which may be present during palpation of a CV examination

A

Apex beat: - Lateral displacement = cardiomegaly Heaves: - Parasternal heave = right ventricular hypertrophy Thrills: - Heart murmurs = heart valve defect

216
Q

Describe the clinical signs which may be present during auscultation of a CV examination

A

Murmurs due to stenosis/regurgitation of valves - (mitral, tricuspid, pulmonary, aortic)

217
Q

Where is the thorax?

A

Neck -> abdomen

218
Q

What organs are contained within the thorax?

A

Lungs and heart

219
Q

What is the thoracic wall composed of?

A

Cartilage, bone, vessels

220
Q

List the bones of the thoracic wall

A
  1. Sternum 2. 12 ribs 3. Thoracic vertebrae - 1-12
221
Q

List the parts of the sternum

A

Superior -> inferior: 1. Manubrium 2. Body 3. Xiphoid process

222
Q

Describe the muscles which of the thoracic wall

A

Intercostal muscles in intercostal spaces: 3 layers - external, internal + innermost

223
Q

Describe the locations of the vessels and nerves of the thoracic wall

A

Intercostal vessels and nerves between internal + innermost intercostal muscle layers

224
Q

Explain the importance of the costal cartilages

A
  • Allow for movement of intercostal muscles and diaphragm for respiration - Extends ribs anteriorly and attach them to the sternum
225
Q

Describe the structure of the ribs

A
  • 1st and 2nd ribs are smaller and narrower - True ribs - first 7 pairs, joint to sternum directly - False ribs - 8th, 9th and 10th pairs, costal cartilage attached to cartilage above - Floating ribs - 11th and 12th ribs, not attached to sternum
226
Q

Which structures pass through the diaphragm?

A
  • Oesophagus - oesophageal hiatus (T10) - Descending aorta - aortic hiatus (T12), surrounded by semilunar ligament - Inferior vena cava - caval opening (T8)
227
Q

Describe the structure of the diaphragm

A
  • 2 domes - higher on right than left due to liver - Inserts in intercostal region + spinal column
228
Q

Describe the innervation of the diaphragm

A

Phrenic nerve - origins = C3,4,5

229
Q

External intercostal muscles

A
  • From cartilage portion of ribs to vertebral column - Fibres go from anterior to inferior - Active during inspiration
230
Q

Internal intercostal muscles

A
  • From intercostal spaces to anterior angle of ribs - Fibres go from anterior to posterior - Active during expiration
231
Q

Intercostal neurovascular bundle

A
  • Nerves + BVs between internal and innermost intercostal muscles - Anterior rami of T1-11 form intercostal nerves - Anterior ramus of T12 = subcostal nerve - Arrangement = veins, artery, nerve - Intercostal arteries = posterior intercostal arteries from aorta
232
Q

Describe the vascular supply to the thoracic cavity

A
  • Internal thoracic artery - from subclavian artery - Bifurcates into musculophrenic and superior epigastric arteries
233
Q

Describe the compartments of the thoracic cavity

A
  • 2 pulmonary cavities for lungs - Mediastinum for heart
234
Q

List the surface anatomy landmarks of the thorax

A
  • Jugular (suprasternal) notch - Sternal angle - Anterior median line - Midclavicular lines - Axillary fossa - Anterior axillary lines - Midaxillary lines - Posterior axillary lines
235
Q

How can blood pressure be calculated?

A

BP = cardiac output x peripheral vascular resistance

236
Q

Describe the hierarchy of pacemakers in the heart

A
  1. SAN 2. AVN 3. Purkinje cells
237
Q

Define atherosclerosis

A

A disease of the larger arteries characterised by the deposition of fatty material on their inner walls

238
Q

Which arteries are most commonly effected by atherosclerosis?

A
  • Aorta - Coronary arteries - Internal carotid artery - Circle of willis
239
Q

Describe the formation of an atherosclerotic plaque

A
  1. Arterial wall thickened by intimal smooth muscle cell proliferation and deposition of fibrous connective tissue, forming hard fibrous cap. This projects into vascular lumen, restricting flow of blood - often causes ischaemia in tissue served by artery 2. Soft pool of extracellular lipid + cell debris accumulates beneath fibrous cap. This weakens the arterial wall so that the fibrous cap may fissure or tear away. As a result, blood enters the lesion + thrombi form. Thrombi or material leaking out of ruptured lesion may be carried to the upstream vascular bed to embolise smaller vessels. Larger thrombus may totally occlude artery at the site of the lesion (can cause MI/stroke if in coronary or cerebral artery). 3. Endothelium over lesion is partially/completely lost, can lead to ongoing formation of thrombi, causing intermittent flow occlusion (as in unstable angina). 4. Medial smooth muscle layer under lesion degenerates - weakens vascular wall which may distend and eventually rupture (aneurysm, especially common in abdominal aorta). May also exhibit spasms/reduced vasodilation - worsens restriction of blood flow + promotes thrombus formation
240
Q

List the risk factors associated with atheroslcerosis

A
  • Genetic predisposition - Age >40 - Gender (men at higher risk - protective affect of oestrogen) - Smoking - Hypertension - Diabetes - High serum cholesterol
241
Q

Describe the pathogenesis of atherosclerosis

A
  • Initiated by endothelial injury/dysfunction - Plaques tend to develop in areas of dynamic sheer stress (where arteries branch or bifurcate - endothelium susceptible to damage, as evidenced by increased endothelial cell turnover + permeability - Endothelial dysfunction promotes adhesion of monocytes (WBC which burrow beneath endothelial monolayer and become macrophages - normally have important role in inflammation, act as scavenger cells to remove dead cells/foreign material, release cytokines + GFs - Lipoproteins transport cholesterol + other lipids in the bloodstream, elevated levels of low-density lipoproteins are associated with atherosclerosis - LDL delivers cholesterol to cells from the liver, HDL takes excess cholesterol from cells to be stored in the liver - Native LDL is not atherosclerotic, oxidative modification of LDL by oxidants derived from macrophages and endothelial/smooth muscle cells can lead to generation of highly atherogenic oxidised LDL within the vascular wall
242
Q

Describe the effects of oxidised LDL

A
  • Oxidised LDL is chemotactic for circulating monocytes and increases expression of endothelial cell adhesion molecules to which monocytes attach - Monocytes penetrate the endothelial monolayer, lodge beneath it and mature into macrophages. Macrophages are unable to control their uptake of oxidised LDL, which occurs via scavenger receptors - Once within the vascular wall, macrophages accumulate large quantities of oxidised LDL, becoming cholesterol-laden foam cells forming the fatty streak - Stimulation of macrophages and endothelial cells by oxidised LDL causes release of cytokines (+ released by platelets aggregating on the endothelium where it is damaged) - Cytokines act on vascular smooth muscle cells causing them to migrate into the intima, to proliferate and secrete abnormal amounts of collagen and other connective tissue proteins - Initial accumulation of smooth muscle cells and connective tissue forms fibrous cap on inner arterial wall - Ongoing foam cell formation + deterioration forms a layer of extracellular lipid (cholesterol + cholesteryl esters) and cellular debris - Underneath the lipid, the medial layer of smooth muscle cells is weakened and atrophied
243
Q

List the clinical consequences of advanced atherosclerosis

A
  1. Coronary stenosis, leading to cardiac ischemia, leading to stable or exertional angina 2. Advanced plaques have large areas of endothelial denudation - sites from thrombus formation 3. Lipid/foam cell lesions particularly unstable + prone to tearing - plaque rupture, allows blood to enter lesion resulting in unstable angina or MI 4. In cerebral arteries major cause of stroke 5. Stenosis of renal arteries major cause of renovascular hypertension
244
Q

Describe the causes of cardiac ischemia

A
  • Caused by coronary artery stenosis = narrowing of coronary arteries (e.g. due to atherosclerosis) - Narrowing leads to reduced blood supply, oxygen demand of myocardium not met, becomes ischemic - Can also be due to to pathological increase in oxygen demand e.g. due to ventricular hypertrophy
245
Q

Describe the symptoms associated with cardiac ischemia

A
  • Crushing, tight chest pain in central anterior chest - Radiation of pain to throat/jaw/arms - Pain exacerbated by exercise, emotion, cold - Pain relieved by rest or GTN (glyceryl nitrate) - Sweating - Breathlessness - Nausea
246
Q

Define angina pectoris

A

Crushing pain/discomfort felt in anterior chest, commonly radiating to left arm + jaw. Caused by coronary arterial insufficiency leading to intermittent myocardial ischemia

247
Q

What causes the pain which is typical of cardiac ischemia/angina?

A

Arterial insufficiency leads to build up of metabolites (adenosine, carbon dioxide, lactate, potassium etc.) which stimulate pain receptors of sensory nerves, causing tight, crushing pain across chest.

248
Q

List the classifications of angina

A
  1. Stable (predictable) angina 2. Unstable (unpredictable) angina 3. Variant (unpredictable) angina
249
Q

Describe the features of stable angina

A
  • Caused by temporary inadequacy of blood flow to myocardium - Lasts 1-15 mins - Provoked by exercise, emotional stress, extreme cold or heat, heavy meals, alcohol, smoking - Relieved by rest/anti-anginal drugs (GTN) - Constricting discomfort in front of chest, arms, neck, jaw
250
Q

Describe the features of unstable angina

A
  • Increase in frequency, severity or duration of previously stable angina, culminating in pain at rest - Requires immediate hospitalisation and often surgery - Similar pathology to MI - platelet-fibrin thrombus associated w/ atherosclerotic plaque, without complete occlusion of BV - Greatly increases risk of MI - Acute coronary syndrome
251
Q

Describe the features of variant angina

A
  • Uncommon - Caused by coronary artery spasm (often in artery affected by atherosclerotic disease) - Frequency/severity of attacks reduced by vasodilators e.g. organic nitrates + calcium antagonists - Beta-adrenoceptor antagonists may increase vasospasm + worsen pain
252
Q

Describe the investigations done when a patient presents with chest pain

A
  • 12-lead ECG to exclude acute coronary syndrome - Exercise ECG - sometimes abnormalities can only be seen during exercise. Patient attached to exercise machine. + ECG leads.
253
Q

Describe the lifestyle changes which would be encouraged in management of angina pectoris

A
  • Stop smoking - Weight loss - Reduced sodium intake - Increase exercise - Diabetics - tightly control blood glucose - Hypercholesterolemia should be treated (statin therapy)
254
Q

List the potential drug treatments for cardiac ischemia/angina

A
  1. Nitrates 2. Beta blockers 3. Calcium channel blockers 4. Anti-platelet therapy (aspirin)
255
Q

Describe how nitrates are used to treat angina

A
  1. Glyceryl trinitrate - Converts to nitric oxide - potent vasodilator - mimics effects of endothelial release of nitric oxide - Vasodilation of coronary arteries ensures myocardial perfusion, acts on arteries, reducing arterial pressure + veins - Given sublingually as spray/tablet, quickly absorbed into bloodstream - Used in prophylaxis of angina (e.g. before exercise) or as reliever during episode 2. Isosorbide mononitrate/dinitrate - Slower onset, more prolonged duration - Given as oral tablet
256
Q

Describe the pathway activated by GTN sprays

A
  • Acts on smooth muscle cells - Activates guanylate cyclase - has haem portion - Nitric oxide binds to haem receptor - Converts guanosine triphosphate -> cyclic guanosine monophosphate (cGMP) - Increase in cGMP causes vasodilation
257
Q

Describe the side effects associated with nitrates used to treat angina

A

Can cause headaches (dilation of cerebral arteries) and tolerance on prolonged use

258
Q

Describe the use of beta blockers to treat angina

A
  • Act directly on the heart - Competitive reversible antagonists of adrenaline + noradrenaline at cardiac beta-1-adrenoceptors - Cause decreased HR + force, decreased myocardial work, decreased myocardial oxygen demand - E.g. propranolol (non-selective beta 1 + 2), atenolol (beta 1 selective) - Used in all forms of angina
259
Q

List the side effects associated with beta blockers

A
  • Cold extremities - loss of beta receptor mediator vasodilation in cutaneous vessels - Fatigue - reduced cardiac output and muscle perforation - Bradycardia - Hypotension - Contraindicated with asthma - blockage of beta 2 receptors in bronchioles - Hypoglycaemia
260
Q

Describe the use of calcium channel blockers to treat angina

A
  • Block long type voltage operated calcium channels (open upon membrane depolarisation + allow calcium entry into cardiac + vascular smooth muscle) - When channels are blocked, reduced calcium entry resulting in reducing peripheral resistance and reduced cardiac output
261
Q

List the side effects associated with calcium channel blockers

A
  • Headache - Constipation - Cardiac dysrhythmias
262
Q

Describe the use of anti-platelet therapy (aspirin) in treating angina

A
  • Low dose aspirin reduces risk of MI - Prescribed to patients at risk indefinitely - Reduces platelet aggregation, risk factor for development + progression of atherosclerotic plaques
263
Q

List the treatments other than medication which are used to manage angina

A
  1. Percutaneous coronary intervention - angioplasty and stenting 2. Coronary artery bypass grafting
264
Q

Describe percutaneous coronary intervention

A
  • Fine guide wire passed across coronary stenosis under radiographic control - Ballon is positioned and inflated to dilate the stenosis - Coronary stent is a piece of coated metallic scaffolding that can be deployed on a ballon and used to maximise + maintain dilation of a stenosed vessel (re-vascularisation) - Common complication = re-stenosis
265
Q

Describe the use of coronary artery bypass grafting to treat angina

A
  • Achieve re-vascularisation by bypassing a stenotic lesion using grafts - Vein grafts harvested from saphenous vein or arterial grafts (radial artery or internal mammary arteries)
266
Q

Describe the progression of the treatments used in management of angina

A
  1. Short-acting nitrovasodilator (GTN) + beta blocker/calcium channel blocker/drugs for secondary prevention (e.g. anti-platelet) 2. Beta blocker + calcium channel blocker 3. Add long-acting nitrovasodilator 4. Consider surgical intervention: stenting or coronary artery bypass grafting
267
Q

Non-ST-elevation acute coronary syndrome (NSTEACS)

A

Includes non-ST-elevation MI and unstable angina pectoris (both produce same ECG, difference based on presences of raised cardiac enzymes e.g. troponin 8-12 hours after onset of chest pain).

268
Q

Describe the features of ECGs in NSTEACS

A
  • ST segment depression - up-sloping, down-sloping or horizontal - Depression >1mm = worse prognosis - Depression >2-3mm associated with high probability of MI + predicts significant mortality - T wave flattening or inversion - T wave inversion evidence of myocardial ischemia if at least 1mm deep, present in >2 continuous leads with dominant R waves (R/S ratio >1), dynamic - not present in old ECG or changing over time - Hyperacute (peaked) T waves or pseudo-normalisation of previously inverted T waves i.e. becoming upright - U wave inversion
269
Q

List the parts of a normal ECG

A

P wave = atrial depolarisation QRS complex = ventricular depolarisation T wave = ventricular repolarisation P-R interval = delay through AV node S-T interval = plateau phase of AP

270
Q

List the expected ECG changes in a normal heart during exercise

A
  1. RR interval decreases 2. P wave amplitude and morphology under minor changes 3. Septal Q wave amplitude increases 4. R wave height increases from rest to submaximal exercise + then reduces to minimum at maximal exercise 5. QRS complex experiences minimal shortening 6. J-point depression occurs 7. Tall, peaked T waves occur 8. ST segment becomes upsloping 9. QT interval experiences a rate-related shortening 10. Superimposition of P waves and T waves on successive beats may be observed
271
Q

What is the Bruce protocol used for?

A

A diagnostic test used in the evaluation of cardiac function - gives the maximal oxygen uptake (VO2)

272
Q

Describe the process of the Bruce protocol

A
  • Gradual increase in intensity of exercise on a treadmill/bicycle - 7 stages of 3 minutes - 21 minutes in total - Level of exercise measured in metabolic equivalents (METs) = amount of energy espended at rest (approx 3.5 ml oxygen per kg per minute) - Stage 1 = 1.7 mph at 0% incline - Full 21 minutes is rarely completed - 9-12 minutes/85% of max predicted heart rate is satisfactory - Patient connected to ECG machine, standard resting ECG performed - ECG repeated with patient standing - During test continuous record o heart rate is taken and 12 lead ECG is recorded intermittently - BP measured at end of each stage of exercise - Systolic BP should increase as exercise level rises - up to 225mmHg is normal (more for athletes) - Diastolic pressure falls slightly - Aim is for patient to reach target HR of 85% maximum
273
Q

List the cardiovascular changes which occur during exercise

A
  1. Increased heart rate 2. Increased stroke volume 3. Increased cardiac output 4. Increased blood flow 5. Increased blood pressure
274
Q

Describe the autonomic nervous changes which occur during exercise

A
  • Increased sympathetic action, decreased parasympathetic action - Increased firing rate of cardiac accelerator nerve due to stimulation from cardiorespiratory centre in medulla - Redistribution of blood flow to skeletal muscles, away from internal organs e.g. stomach, liver, kidneys, small intestines - Widespread release of adrenaline + noradrenaline to increase myocardial contractility, cause vasodilation of BV to skeletal muscles - Stimulates release of glucose from liver
275
Q

List the risk factors associated with atherosclerosis

A
  • Age - Male gender - Family history - Smoking - Hypertension - Hyperlipidaemia - Diabetes - Obesity - Ethnicity - Physical inactivity
276
Q

List the potential causes of chest pain

A
  1. Cardiac 2. Respiratory 3. Gastrointestinal 4. Musculoskeletal 5. Other
277
Q

List the cardiovascular causes of chest pain

A
  • Cardiac - ischemia - Aortic dissection - Pulmonary embolism - Aortic stenosis - Pericarditis - Myocarditis - Takotsubo cardiomyopathy
278
Q

Give examples of non-cardiovascular causes of chest pain

A
  • Pneumonia - Pneumothorax - Cancer - Musculoskeletal - Oesophagitis/reflux disease - Pancreatitis - Gallstones - Neuraglia - Psychogenic
279
Q

What is the primary symptoms associated with acute myocardial infarction

A

Sudden prolonged severe chest pain

280
Q

List the complications of an acute MI

A
  • Arrhythmia - Pericarditis - RV infarct - Mural thrombus - Heart failure - Mechanical damage - Expansion/aneurysm - Extension/ischemia
281
Q

Give examples of common cardiology presentations

A
  • Chest pain - Breathlessness (dyspnoea) - Palpitation - Syncope - Sudden cardiac death
282
Q

List common causes of breathlessness (dyspnoea)

A
  • Cardiac - angina, heart failure, valvular disease - Respiratory - multiple - Anaemia - Deconditioning
283
Q

List common causes of palpitations

A
  • Sinus rhythm - inappropriate sinus tachycardia, postural orthostatic tachycardia syndrome - Ectopics - supraventricular extrasystole, bigeminy, trigeminy - True arrhythmia - atrial fibrillation, atrial flutter, SVT, ventricular tachycardia
284
Q

List common causes of syncope

A
  • Cardiac = arrhythmia, valvular disease, outflow tract obstruction - Haemodynamic - postural hypotension, vasovagal syncope, autonomic dysfunction - Neurological - seizures
285
Q

List common causes of sudden cardiac death

A
  • Myocardial infarction - Arrythmia/channelopathies - Cardiomyopathy - dilated cardiomyopathy, hypertrophyic cardiomyopathy, arrhythmiogenic right ventricular cardiomyopathy - Pulmonary embolism - Aortic dissection
286
Q

List the symptoms/signs of a pulmonary embolism

A
  • Pleuritic chest pain - Breathlessness (dysponea) - Tachycardiac - Tachypneoic - Hypotensive - Hypoxic - Haemoptysis
287
Q

List the symptoms of aortic dissection

A
  • Tearing interscapular pain - Sudden onset - Severe - BP difference in each arm - Wide mediastinum on chest X-ray
288
Q

List the types of stroke

A
  1. Ischaemic stroke - thrombus, embolism 2. Haemorrhagic stroke - intracerebral, subarachnoid
289
Q

List the functions of cardiovascular imaging

A
  1. Define the structure/anatomy of the heart - normal and abnormal 2. Detail the function or physiology - valve function, ventricular function, coronary physiology 3. Image the heart during stress - provoke ischemia, assess valve function
290
Q

List the basic and advanced modalities of cardiovascular imaging

A

Basic: - Chest X-ray - ECG (image of the electrical activation of the heart) Advanced: - Ultrasound - transthoracic echocardiography, transoesophageal echocardiography - Ionising radiation - nuclear, CT, invasive angiography - MRI

291
Q

Describe the uses of chest X-rays in imaging the heart

A
  • Cardiac silhouette - size/position - Pulmonary vasculature - Great vessels - Pulmonary oedema - Pleural effusions
292
Q

Describe the uses of echocardiography in imaging the heart

A
  • Structure and function of the heart - Valve assessment - Pericardial assessment - Assess inducable ischemia (stress)
293
Q

List the pros and cons of echocardiography in imaging the heart

A

Pros: - Cheap - Available - Portable - No radiation Cons: - Requires good acoustic window - User dependent

294
Q

List the types of functional stress testing

A
  • Exercise stress testing - Nuclear stress testing - Echo stress testing
295
Q

Describe the uses of nuclear perfusion imaging in imaging the heart

A
  • Assess ischemia - Assess ejection fraction
296
Q

List the pros and cons of nuclear perfusion imaging in imaging the heart

A

Pros: - Availability Cons - Radiation - No structural assessment

297
Q

Describe the uses of cardiac CT scans in imaging the heart

A
  • Coronary artery anatomy - Great vessel anatomy
298
Q

List the pros and cons of cardiac CT scans in imaging the heart

A

Pros: - Good ‘rule out’ for coronary artery disease - Low risk Cons: - Radiation dose - Requires low heart rate - No functional assessment of ischemia

299
Q

Describe the uses of invasive angiography in imaging the heart

A
  • Ischemia - Primary percutaneous coronary indications - Valve assessment - Assessment of ventricular pressures
300
Q

List the pros and cons of invasive angiography in imaging the heart

A

Pros: - Gold standard - Option for intervention during same procedure - Availability Cons: - Radiation - Risks - cerebrovascular accident, MI, contrast reaction, bleeding, death

301
Q

Describe the uses of cardiovascular MRI in imaging the heart

A
  • Assess structure and function - Perfusion/stress - Assess great vessels - Tissue characterisation - infiltrative cardiomyopathies, previous infarction
302
Q

List the pros and cons of cardiovascular MRI in imaging the heart

A

Pros: - Gold standard left ventricular assessment - Reproducible - No radiation Cons: - Cost - Availability - Claustrophobia - Pacemakers

303
Q

Describe the mechanism of action of statins

A

E.g. Simvastatin, pravastatin, rosuvastatin - Competitive inhibitors of rate-limiting step in cholesterol biosynthesis - Marked decrease in cholesterol levels may stimulate LDL receptor up-regulation - Most effective at night, when most cholesterol biosynthesis occurs

304
Q

How is intravascular blood coagulation and platelet activation normally suppressed?

A
  • Non-thrombogenic surface of endothelium - Production by endothelium of prostacyclin and nitric oxide which inhibit platelet aggregation, nitric oxide also inhibits adhesion of platelets to vascular wall - Presence in plasma of natural anticoagulants e.g. antithrombin III
305
Q

List the types of leads used in ECGs

A
  1. Unipolar leads - measure potential variation at a single point 2. Bipolar leads - measure the potential difference between two points
306
Q

Which ECG leads are unipolar and which are bipolar?

A

Unipolar: Augmented limb leads aVR, aVL, aVF and chest leads V1-V6 Bipolar: Limb leads I, II and III

307
Q

How is heart rate determined from an ECG?

A

300 divided by the number of large squares between each QRS complex or number of QRS complexes across ECG (10 sec) x 6

308
Q

List the normal ranges for an ECG

A

PR interval - <1 large square, <200ms QRS - <3 small squares, <120ms QT - <11 small squares, <440ms

309
Q

List in vitro and in vivo anticoagulants

A

In vitro: 1. Heparin 2. Calcium chelators e.g. citrate and ethylenediamine tetra-acetic acid In vivo: 1. Heparin or low molecular weight heparin 2. Oral anticoagulants - e.g. vitamin K antagonists

310
Q

Describe the mechanism action of heparin

A
  • Heparin binds to and enhances the action of the endogenous anticoagulant, antithrombin III - The heparin-antithrombin II complex binds to inhibits the action of clotting factors IIa, IXa, Xa, XIa, XIIa - Immediate inhibiton of clotting - Low MW heparin inhibits factor Xa (predominantly)
311
Q

Describe the administration of heparin/LMWH

A
  • Not orally active (absorption prevented by high MW and charge) - Given intravenously or sub-cutaneously - Does not cross placenta or blood-brain barrier
312
Q

Describe the uses of heparin + LMWH

A
  • Deep venous thrombosis - Can be used safely in pre-eclampsia of pregnancy (foetus unaffected) - In vitro anticoagulant
313
Q

List the side effects associated with heparin

A
  • Allergic reactions - Haemorrhage - Heparin-induced thrombocytopaenia
314
Q

Describe the mechanism of action of oral anticoaglants

A

E.g. warfarin - Structural analogue of vitamin K - Blocks synthesis of coagulation factors (in the liver)

315
Q

List the uses of warfarin

A
  • Venous thrombosis - Prevent pulmonary embolism - Prevent embolism in patients with atrial fibrillation - Prophylaxis of thrombosis after insertion of prosthetic heart valves etc.
316
Q

Describe the administration of warfarin

A
  • Orally active (more convenient than heparin) - 99% bound to plasma albumin
317
Q

List the side effects of warfarin

A
  • Haemorrhage - Crosses placenta and blood-brain barrier (should not be used in pre-eclampsia of pregnancy - haemorrhage in foetus)
318
Q

Give examples of anti-thrombotic agents

A
  1. Low dose aspirin 2. Dipyridamole 3. Epoprostenol 4. Clopidogrel 5. Abciximab
319
Q

Give examples of fibrinolytic (thrombolytic) agents

A
  1. Tissue plasminogen activator (t-PA) 2. Streptokinase
320
Q

Define absolute risk

A
  • Incidence of disease in a given population - Number of new cases per population over specified time
321
Q

Relative risk

A
  • Want to know if having the exposure/risk factor changes the risk - Compare the two groups of people - 1. have exposure/risk factor, 2. do not expose/risk factor - Determine the absolute risk in each group, then compare - Expresses risk as how many times greater or smaller among exposed
322
Q

Explain how to interpret relative risk

A

RR = 1 - Risk in exposed = risk in not exposed - No association RR > 1 - Risk in exposed > risk in not exposed - Positive association RR < 1 - Risk in exposed < risk in not exposed - Negative association

323
Q

Attributable risk

A

Incidence of cases among those exposed that are due to the exposure/risk factor = incidences of disease in exposed - incidence of disease in un-exposed

324
Q

Attributable risk percentage (AR%)

A

Percentage of cases among those exposed that are due to the exposure/risk factor = AR x 100/incidence of disease in exposed

325
Q

Population attributable risk

A

Incidence of case among the whole population (exposed and not exposed) that are due to the exposure = AR x prevalence of exposure

326
Q

Population attributable rise percent

A

Proportion/percentage of cases in whole population (exposed and unexposed) that are due to the exposure/risk factor = PAR x 100 / incidence of disease in population

Medicine COPY (18 decks)

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