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CVS Flashcards

1
Q

Diffusion is affected by what 3 factors

A

Surface Area

Diffusion Distance

Concentration Gradient

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2
Q

Arteries and Veins have 3 layers, what are they and what are they made from

A

Tunica Intima (Endothelium)

Tunica Media (Smooth Muscle Cells + Elastic Lamina)

Tunica Adventitia (Connective Tissue with vasa vasorum)

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3
Q

What are the vasa vasorum

A

Blood vessels that supply blood vessels

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4
Q

As arteries decrease in size what happens to the layers of the artery wall

A

the Tunica media decreases in thickness and the number of smooth muscle cells decreases

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5
Q

What are the main features of cardiac muscle

A

Striated

Branching

Centrally located nuclei

Intercalated Discs

Gap Junctions

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6
Q

Length of systole and diastole

A

Systole: 280ms

Diastole: 500ms

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7
Q

How long does thew AV node delay the action potential for

A

120ms

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8
Q

How does the action potential spread through the heart

A

From the SA node

To the AV node (120 ms delay)

Down the IV septum (Bundle of His)

Up the surface of the heart

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9
Q

What are the 1st and 2nd heart sounds caused by

A

1st: AV valves closing
2nd: Semilunar valves closing

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10
Q

Difference between acyanotic and cyanotic heart defects

A

Acyanotic defects do not result in a lower O2 saturation where as cyanotic defects do.

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11
Q

What are the common acyanotic heart defects

A

ASD (Atrial Septal Defect)

PFO (Patent Foramen Ovale)

VSD (Ventricular Septal Defect)

PDA (Patent Ductus Arteriosus)

Coarctation of the Aorta

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12
Q

What can happen regarding embolisms with a patent foramen ovale

A

Paradoxical embolism, when a venous embolism reaches the systemic circulation.

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13
Q

Where does the coarctation usually occur in coartctation of the aorta and how does this relate to it’s signs.

A

After the L. Subclavian Artery

Weak femoral pulse as blood cannot easily flow through the aorta after the l. subclavian artery.

Upper body hypertension as the coarctation causes LV hypertrophy.

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14
Q

What are the signs of a patent ductus arteriosus

A

Mechanical murmur (constant)

As pressure in aorta is always higher than that in the pulmonary a. so blood is always flowing through it.

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15
Q

Why don’t acyanotic heart defects affect the O2 saturation

A

Because the blood is shunted from the left side to the right side there is never any deoxygenated blood being pumped around the circulation.

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16
Q

how can cases of left to right shunting progress to something more serious.

A

Eisenmenger Syndrome

Long term left to right shunting can cause right sided hypertrophy which can increase the pressure in the right side of the heart. Eventually the pressure can increase above that in the left side of the heart which cause the shunt to reverse direction.

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17
Q

Name the common cyanotic heart defects

A

Tricuspid Atresia (No tricuspid valve)

Transposition of the great arteries (2 unconnected parallel circuits)

Hypoplastic Left heart (No Left Ventricle)

Tetralogy of fallot

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18
Q

What do patients with Tricuspid Atresia require and why?

A

Patent foramen ovale and a ventricular septal defect, this allows blood from RA to flow into the LA and blood in the LV to flow into the RV

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19
Q

What do patients witch Transposition of the great arteries require and why?

A

A shunt to be maintained or created to allow blood from the 2 circuits to cross over.

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20
Q

In Hypoplastic left heart how does the blood flow through the heart.

A

Blood reaches the aorta through the ductus arteriosus from the pulmonary artery

Blood reaching the LA passes through a patent foramen ovale back into the RA.

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21
Q

What are the 4 abnormalities present in tetralogy of fallot

A

VSD

Overriding Aorta

Pulmonary Stenosis

RV hypertrophy

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22
Q

Where does the blood mix in tetralogy of fallot to cause the cyanotic effects.

A

Oxygenated and deoxygenated blood mix in the VSD which then enter the aorta as it is overriding, meaning it sits directly above the VSD causing partially deoxygenated blood to enter the systemic circulation.

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23
Q

Describe the Sympathetic Outflow of the autonomic nervous system

A

Thoraco-Lumbar outflow

Short pre-ganglionic / Long post-ganglionic fibers

Pre ganglionic fibers are cholinergenic (Ach) (Nicotinic)

Post ganglionic fibers are adrenergic (NA) (α1,2 / β1,2)

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24
Q

Which post-ganglionic sympathetic pathways are cholinergenic

A

Perspiration and Ejaculation Pathways

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25
Q

What receptors do post-ganglionic fibers express

A

Nicotinic to detect the Ach from the pre ganglionic fibers

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26
Q

Describe the Parasympathetic Outflow of the autonomic nervous system

A

Cranio-sacral outflow

Long pre-ganglionic / Short post-ganglionic fibers

Pre and Post ganglionic fibers are cholinergenic (Ach) (Nicotinic)

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27
Q

Fill in the table

A
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28
Q

What mneumonic is used to remeber which G coupled protein is linked to which receptor

A

QISS QIQ

α1 Q

α2 I

β1 S

β2 S

M1 Q

M2 I

M3 Q

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29
Q

Describe vasomotor tone

A

The constant activity of the sympathetic nervous system through α1 receptors that maintain a medium level of vasoconstriction.

It can be increased or reduced to constrict or dilate blood vessels

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30
Q

In the skin, gut and skeletal muscles is the resting vasomotor tone high or low?

A

Resting vasomotor tone is high

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31
Q

When is the vasomotor tone to the skin, gut, skeletal muscle and brain is reduced and what is the effect

A

Skin: Due to thermoregulation, increasing blood flow helps to radiate heat more easily

Gut: After a meal, increasing blood flow enabling quicker nutrient absorption

Skeletal Muscle: During excercise, increasing blood flow helps deliever more oxygen to the tissues

Brain: Trick question, vasomotor tone remains constant.

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32
Q

What controls vasomotor tone

A

Medulla Oblongata

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33
Q

Where are the baroreceptors located

A

Carotid Sinus

Arch of the aorta

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34
Q

What are the equations of flow and velocity

A

Flow = Volume / Time

Velocity = Distance /Time

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35
Q

What is the difference between laminar and turbulent flow

A

Laminar flow is normal and healthy, it has a low resistance and occurs when the blood at the centre of the lumen moves the fastest

Turbulent flow is pathological, it has a high resistance and occurs when the blood tumbles over itself.

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36
Q

What is viscosity?

A

The extent to which pluids resist sliding over one and other. The higher the viscosity the slower the fluid will flow.

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37
Q

What is the formula for calculating pressure?

A

Pressure = Flow * Resistance

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38
Q

What is resistance dependent on?

A

Resistance in dependent on viscosity and the 4th power of the radius of the tube

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39
Q

What effect does decreasing the diameter of a tube have on the resistance

A

Dramatically increases the resistance (4th power)

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40
Q

How is resistance calculated for systems in series and parallel?

A

Resistance for vessels in series are summed

Resistance for vessels in parallel is lower as the is more than 1 path for the blood to flow down

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41
Q

What is total periperal resistance

A

The sum of all the resistance across the whole body

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42
Q

Do the following vessels have high or low resistance?

Arteries

Veins

Arterioles

A

Arteries : Low

Veins : Low

Arterioles: High

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43
Q

How does the elastic nature of arteries affect the resistance of the vessels

A

As the vessel is exposed to higher pressures it stretches. This increases the diameter of the vessel which causes the resistance to fall allowing the flow to increase.

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44
Q

What happens to vessels if the pressure falls too low?

A

The vessel will collapse causing the flow and pressure to drop to zero

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45
Q

Explain capacitance in regards to circulation and why it occurs most in the venous circulation

A

When veins stretch more blood enters them than leaves. This allows them to store a certain amount of blood (capacitance).

This mainly happens in veins as they are the most distensible vessel

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46
Q

What is normal blood pressure

A

120/80 mmHg

Systolic / Diastolic

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47
Q

How do you calculate mean arterial pressure?

A

2/3 diastolic + 1/3 systolic

This is because the heart spends 2/3 of it’s time in diastole

(80*0.66) + (120*0.33) = 93 mmHG

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48
Q

What action do local vasodilator metabolites exert and give examples of common ones

A

Cause local vasodilation, lowering resistance and increasing flow.

They include: H+, K+ and adenosine

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49
Q

Explain Reactive Hyperaemia

A

When the circulation to an organ or limb is cut off local vasodilator metabolites start to build up. If circulation is then restored relatively quickly this build up causes the arterioles to dilate to their maximum extent flooding the organ/limb with blood.

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50
Q

Define Central Venous Pressure?

A

Pressure in the great veins that supply the heart

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51
Q

Define Venous Return?

What does this limit?

A

Flow of blood back to the heart

Limits cardiac output

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52
Q

What happens to Arterial and Venous pressure if either TPR or CO fall?

What happens if TPR or CO rise?

A

Arterial pressure will fall

Venous pressure will rise

If TPR or CO rise then vica versa

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53
Q

Define End diastolic/systolic Volume

A

Volume of blood in the ventricles at the end of diastole/systole

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54
Q

Define stroke volume (2 different ways to define it)

A

Difference between end diastolic and systolic volume

Volume of blood pumped out of the heart

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55
Q

Define Pre-load

A

The higher the venous pressure the more the heart fills during diastole

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56
Q

Define after load

A

The force necessary to expel the blood from the ventricles into the arteries.

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57
Q

What is starling’s law.

When does starling’s law stop applying

A

The higher the pre load the higher the after load will be (more in, more out)

When the pre load becomes to high the heart becomes over filled and the myocardium is damaged by over stretching meaing after load is reduced.

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58
Q

Define Contractility, how is it represent on this graph?

A

The stroke volume for a given venous pressure, shown as the gradient of the curve.

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59
Q

What affects the contractility of the heart

A

Increased Sympathetic Activity

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60
Q

How does postural hypotension occur?

What are the signs?

A

When the baroreceptors are too slow to detect the drop in arterial pressure the occurs due to gravity when you stand up.

It can causes dizziness and fainting when standing up to quickly

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61
Q

Explain the change in ion concentrations that occur during the course of contraction of a cardiac myocyte.

Draw a graph of voltage throughout this process.

A

1) Intial depolarisation iccurs due to the spread of electrical activity from the pacemaker cells through gap junctions
2) Once threshold is reached, fast voltage gated Na+ channels open causing rapid depolarisation due to inlfux of Na+
3) Brief Repolarisation occurs as Na+ channels close causing unopposed K+ efflux
4) Ca2+ channels eventually open balancing the K+ efflux with Ca2+ influx
5) Ca2+ channels close causing repolarisation as K+ efflux is once again unopposed
6) Na+ / K+ ATPase exchanges Na+ for K+ resetting the ion concentrations in preparation for the next action potential.

62
Q

Explain the change in ion concentrations that occur during the course of contraction of a cardiac pacemaker cell.

Draw a graph of voltage throughout this process.

A

1) Spontaneous gradual deploarisation of pacemakes cells due to “funny” pacemakes currents (If) due to slow Na+ channels that allow a small amount of Na+ influx.
2) Once the threshold is reached Ca2+ channels open causing depolarisation that spreads throughout the rest of the heart.
3) Ca2+ channels then close and the cell repolarises due to K+ efflux
4) Na+ / K+ ATPase exchanges Na+ for K+ resetting the ion concentrations in preparation for the next action potential.

63
Q

Describe how sympathetic activation of the Sino Atrial Node occurs and it’s effect

A

NA acts on α2 receptors in the SAN speeding up the HR by increasing the gradient of the funny currents.

64
Q

Describe how parasympathetic activation of the Sino Atrial Node occurs and it’s effect

A

Ach acts on M3 receptors in the SAN slowing down the HR by drecreasing the gradient of the funny currents.

65
Q

What are the 3 causes of arrythmias and explain each one briefly

A

Ectopic Pacemaker Activity: Mycardium develops it’s own pacemaker following ischeamic damage.

After depolarisation: Abnormal depolarisation due to increased intracellular Ca2+

Re-entry loop: Abnormal spread of excitation

66
Q

Explain how atrial over stretching causes Atrial Fibrilation

A

Atrial over stretching causes several small re-entry loops to form causing atrial fibrilation

67
Q

Name the 4 classes of anti-arrhythmic drugs an example drug in each class

Which class is no longer used and why?

A

1) Na+ channel blocker (Lidocaine)
2) β blockers (Propranolol)
3) Ca2+ channel blockers (Amlodipine)
4) K+ channel blockers (Not used as can be pro-arrhythmic)

68
Q

Describe how β bockers work

A

Block β1 receptors which has 2 effects

Decreases the slope of the funny currents decreasing the HR

Inhibit adenyl cyclase leading to a decrease in contractility.

This reduces workload and O2 requirment of the heart

69
Q

Describe how Na+ channel blockers work

A

Prevent APs from firing too close together helping prevent arrhythmias from forming

70
Q

Describe how Ca2+ channel blockers work

A

Decrease funny current gradient at the SAN

Decrease AVN conduction

Decrease force of contraction in the myocardium

Reduce Aldosterone Production lowering BV

Vasodilation in arteries (CCB do not cause vasodilation in veins)

71
Q

Which endogenously produced substance has anti-arrhythmic properties

A

Adenosine

(Used to treat Wolff-Parkinson-White Syndrome)

72
Q

What do inotropic drugs affect

A

The force of contraction in the heart

73
Q

When would you give a negatively inotropic drug

A

After an MI to reduce workload and O2 requirment of the heart

74
Q

When would you give a positively iontropic drug

What class of drugs are they?

A

Cardiogenic Shock / Reversible Heart Failure, when you want the heart to beat stronger

β adrenoreceptor agonist

75
Q

Explain how ACE inhibitors work and their effects

A

Prevent the conversion of Angiontensin I to Angiotensin II. Angiotensin II has 2 effects

1) It is a powerful vasoconstrictor
2) Promotes aldosterone release from the adrenal cortex.

Therfore by inhibiting its formation ACE inhibitors cause vasodilation and diuresis

76
Q

Give examples of common β adrenoreceptor agonists

A

Digoxin.

Amiodarone.

Dopamine

Dobutamine

Dopexamine

Epinephrine (adrenaline)

Isoprenaline (isoproterenol)

Norepinephrine (noradrenaline)

Angiotensin II

77
Q

Why are diuretics used to treat heart problems

A

Diuretics reduce blood volume and therfore pre load on the heart. This means the after load is also reduced and the heart has to work less hard requiring less oxygen.

78
Q

Describe the effect of organic nitrates.

A

Organic Nitrates cause Nitric Oxide to be released which is a powerful vasodilator. NO activates guanylate cyclase increasing cGMP and lowering intracellular Ca2+ causing relaxation of SMC.

It acts on veins and coronary arteries to simultaneously reduce the after load and increase O2 delivery to the myocardium

79
Q

What can Atrial Fibrilation increase your risk of and how is this prevented?

A

Thrombus formation

Prevented using prophylactic anti-thrombotic medication such as warfarin.

80
Q

Why is aspirin given after an MI

A

Aspirin helps prevent platlet rich clots from forming as it is an anti-platlet drug.

81
Q

What do P, Q, R, S and T waves represent on an ECG

A

P wave: Atrial Depolarisation

Q wave: Septal Depolarisation

R wave: Main Ventricular Depolarisation

S wave: End Ventricular Depolarisation

T wave: Ventricular Repolarisation

82
Q

How many leads does a 12 lead ECG have, how many of these are chest leads and how many are limb leads?

A

10 Leads

6 Chest and 4 Limb

83
Q

What is the mneumonic for rembering which limb leads go where

A

Starting with the right hand and working Anticlockwise

Ride (Red) : Right Arm

Your (Yellow) : Left Arm

Green (Green) : Left Leg

Bike (Blue) : Right Leg

84
Q

Which of the limb leads is earthed and does not contribute to the ECG

A

Blue lead connected to the right leg

85
Q

Where do the 6 chest leads go in a 12 lead ECG?

A

V1: 4th Intercostal space to the right of the sternum

V2: 4th Intercostal space to the left of the sternum

V3: Midway between V2 and V4

V4: 5th Intercostal space at the midclavicular line

V5: Anterior axillary line at the same level as V4

V6: Midaxillary line at the same level as V4 and V5

86
Q

What angle is the normal cardiac axis between?

What does this represent?

A

-30° to +90°

The mean direction of the action potentials traveling through the ventricles during depolarization.

87
Q

What degrees are the following leads located at?

I, II, III, VL, VF and VR

A

I : 0° (3 o’clock position)

II: 60°

VF: 90°

III: 120°

VR: 210°

VL: 330°

88
Q

How do you calculate the HR by looking at an ECG?

A

300/ No. of big squares between the R-R interval

89
Q

What length of time do the big and little squares represent on an ECG

A

Big squares 200ms

Little Squares 40ms

90
Q

Explain how ventricular ectopic beats occur and how they present on an ECG

A

When ventricular contraction occurs before it is meant to resulting in an abnormal ORS complex that is taller and wider than normal

91
Q

Explain how Atrial Fibrilation occurs and what it looks like on an ECG

A

When the atrium does not contract in a co-ordinated fashion resulting in irregular fibrilation waves instead of normal P waves.

92
Q

Explain how Ventricular Fibrilation occurs and what it looks like on an ECG

A

When the ventricles do not contract in a co-ordinated fashion. The ecg trace is very chaotic

93
Q

Broadly explain what heart block is?

(Dont go talk about the different types)

A

Failure of action potential conduction from the atrium to the ventricles.

94
Q

Explain 1st degree heart block?

A

All impulses pass though but they are delayed increasing the P-R interval (>200ms)

95
Q

Explain the 2 types of 2nd degree heart block

A

In 2nd degree heart block only some impulses are conducted

Mobitz Type 1 (Wenckebach): P-R interval get progressively longer before a QRS complex is dropped and the system is reset.

Mobitz Type 2: P-R interval is constant but some QRS complexes are still lost

(Mobitz Type 1)

96
Q

Explain 3rd degree heart block

A

No impulses are conducted meaning the ventricles must generate their own ectopic beat. There is no correlation between the P waves and the QRS complex

97
Q

Does the pulmonary circulation have low or high resistance,

What features allow this?

Why is it important?

A

Low resistance

Due to the many short wide vessels all connected in parallel.

Allows the pulmonary circulation to accept the entire cardiac output.

98
Q

What is the optimal ventilation : perfusion ratio?

A

0.8

99
Q

How is the correct ventilation : perfusion ratio maintained?

A

By hypoxic pulmonary vasoconstriction.

This diverts blood away from poorly ventilated areas and towards well ventilated ones

When a certain area of alveolar become hypoxic they cause vasoconstriction of the pulmonary vessels that supply them. This decreases blood flow to this area, decreasing perfusion to match the reduced ventilation

100
Q

What does chronic hypoxic vasoconstriction cause

A

RV failure as the increase in pulmonary resistance puts a higher afterload on the RV

101
Q

What complication regarding the lungs can arise from increased venous pressure?

How does this occur?

A

Pulmonary Oedema

Hydrostatic pressure is reduced meaning less fluid is reabsorbed at the arterial end of the pulmonary circulation.

102
Q

How is pulmonary oedema affected by posture?

(Where does the water pool?)

A

When stood up the water pools in the base of the lungs

When lying down water is dispersed throughout the lungs

103
Q

Where do the R. + L. coronary arteries arise from?

When do the fill

A

R. + L. coronary sinuses.

Only fill during diastole as during systole the contraction of the heart prevents any filling from occuring.

104
Q

Why do the symptoms of angina get worse with excercise

A

When HR increases during excercise diastole gets shorter. This means there is less time for the coronary arteries to fill.

The heart is also beating faster so has an increased demand for blood.

105
Q

What causes angina

A

Narrowed coronary arteries

106
Q

What causes an MI

A

When a thrombus forms on an atheromatous plaque either occluding the vessel where it forms or breaking off to form an embolism which blocks a vessel further downstream.

107
Q

How is blood flow to the brain maintained

A

Myogenic Autoregulation

Increase in BP leads to vasoconstriction in an attempt to decrease blood flow

Decrease in BP leads to vasodilation in an attempt to increse blood flow

108
Q

How do the cerebral vessels respond to changes in PCo2?

A

Hypercapnia leads to vasodilation

Hypocapnia leads to vasoconstriction

109
Q

Why does hyperventilation cause dizziness and fainting?

A

Hyperventilation causes hypocapnia which causes vasoconstriction of the cerebral arteries reducing blood supply to the brain.

110
Q

Describe Cushing’s reflex

A

A rise in intracranial pressure impairs cerebral blood flow. This in turn causes increase sympathetic activty which increase arterial BP helping to maintain adequate blood flow to the brain.

111
Q

What effect does a change in body temperature have on the CVS

A

Decrease body temperature causes increased sympathetic activity causing vasoconstriction in the peripheries helping to conserve heat.

Increased body temperature causes decreased sympathetic activty cauing vasodilation in the peripheries helping to radiate heat by allowing more blood to flow through the skin close to the surface

112
Q

Common Causes of Chest pain

(Split them up based on system)

A
  • Pulmonary
    • Pneumonia
    • Pulmonary Embolism
    • Pneumothorax
  • GI System
    • Oesophageal Reflux
    • Peptic Ulcers
    • Cholecystitis
  • Chest Wall
    • Fractured ribs or metastasis
    • Muscle pain
    • Skin pain
  • CVS
    • Angina or MI
    • Pericarditis
    • Aortic Dissection
113
Q

What are the risk factors for MI

(Split into modifiable and non modifiable)

A

Modifiable:

Smoking, hypertension, Type 2 DM, Obesity and Hyperlipidaemia

Non modifiable:

Age, Gender and Family History

114
Q

Describe what ischeamic pain feels like?

A

Sense of impending doom

Heavy, crushing retrosternal pai.

Radiating to the arms, shoulders, neck and face

115
Q

What is stable angina

A

Ischeamic chest pain brought on by excercise, emotion, in cold weather and after meals.

116
Q

How is stable angina confirmed

A

During an ECG exercise stress test where there is an ST depression > 1mm

117
Q

How is angina treated acutely

A

Glyerol Trinitrate (GTN) Spray which causes the release of NO causing vasodilation of the coronary arteries.

118
Q

How does unstable angina differ from stable angina

A

In unstable angina the syptoms are present even at rest.

119
Q

How can patients differenciate angina from an MI

A

If the pain is not relieved by rest or GTN spray then they are having an MI.

120
Q

What are the 2 types of MI and how do they differ

A

Non ST elevated MI (NSTEMI) occurs when the infarct does not encompass the full thickness of the myocardium

ST elevated MI (STEMI) occurs when the infarct does encompass the full thickness of the myocardium.

121
Q

What are the two blood markers for MI

A

Creatine Kinase and Troponin.

It can be used clinically to distinguish between an NSTEMI and unstable angina as they both look very similiar on an ECG.

122
Q

How does Unstable Angina or a NSTEMI present on an ECG?

How does a STEMI present on an ECG?

A

NSTEMI / Unstable Angina: ST depression + T wave inversion

STEMI: ST elevation

123
Q

Describe how the ECG trace of a STEMI changes from the start to the end of the recovery process.

A

Mins: Hyperacute T waves

Hours: ST elevation

Day: Pathological Q wave + T wave inversion

Week: ST elevation normalises

Month: T wave normalises

(Pathological Q waves persist)

124
Q

How can previous MIs be detected on an ECG many years after the MI occured

A

Pathological (deepened) Q waves

125
Q

How can the site of an MI be localised using an ECG

A

Abnormalities will be seen in certain leads due to scarring over the top of the dead infarcted myocardium. (This occurs as scarred tissue does not condducted electrical impulses).

By examining which leads are affected the occluded artery and the region of dead myocardium it used to supply can be indentified

126
Q

Which leads are affected when the R. Coronary Artery is occluded

Which area of the heart is affected?

A

II, III and aVF

Inferior

127
Q

Which leads are affected when the proximal L. Anterior Descedning Artery is occluded

Which area of the heart is affected?

A

V1 + V2

Septal

128
Q

Which leads are affected when the Distal Left Anterior Descending Artery is occluded

Which area of the heart is affected?

A

V3 + V4

Anterior

129
Q

Which leads are affected when the L. Circumflex Artery is occluded?

Which area of the heart is affected?

A

I, aVL, V5 + V6

Lateral

130
Q

Which leads are affected when the Left Coronary Artery is occluded

Which area of the heart is affected?

A

I, aVL, V2 - V6

Extensive Anterior

131
Q

What 2 surgeries can angina patients undergo to help relieve symptoms.

A

Early Percutaneous Coronary Intervention (PCI) (Angioplasty) : A ballon with a wire mesh tube around it is placed in the artery and then inflated. This opens up the lumen increasing its size and allowing more blood to flow through it. The ballon is then deflated and removed while the wire mesh remains.

Coronary Artery Bypass Graft (CABG): Taking an artery from elsewhere in the body and grafting it to the heart.

132
Q

What are patients suffering from angina placed on to help prevent an MI from occuring

A

Anti-coagulants (Warfarin) and Antiplatlets (Aspirin)

133
Q

What is Angiography

A

X-ray using contrast that enables the coronary blood vessels to be examined and any occulsions identified.

134
Q

What is pericarditis pain characterised by?

A

Left sided chest pain that gets worse with inspiration andis relieved by leaning forward.

135
Q

What causes pericarditis

A

Infection

Inflamation post. cardiac surgery

Autoimmune

Malignancies

136
Q

What is heart failure?

A

When the heart fails to maintain adequate circulation despite adequate filling pressure.

137
Q

What is Heart Failure caused by?

A

Ischaemic Heart Disease

Hypertension

Cardiomyopathy (Dilated, Restricitve and Hypertrophic)

Congenital Valvular Disease

Pericardial Disease

Arrhythmias

138
Q

What are the differences between dilated, restricitve and hypertrophic cardiac myopathies?

A

Dilated: Ventricles enlarge and weaken

Restricitve: Ventricles stiffen

Hypertrophic: Ventricular walls enlarge and thicken

139
Q

How is the severity of Heart Failure assessed.

A

Grade 1-4

Grade 1: No symptoms

Grade 2: Slight limitations on physical activity

Grade 3: Marked limitations on physical activity

Grade 4: Symptoms at rest

140
Q

Draw a graph of End diastolic pressure against cardiac output for a normal heart and one with heart failure

A
141
Q

What is congestive heart failure and how does it occur

A

When both sides of the heart have failed.

Left sided heart failure raises the pulmonary arterial pressure. This increases the after load on the right side of the heart which also starts to fail

142
Q

What is the cause of right sided heart failure

A

Chronic lung diseases that raise the pulmonary pressure

143
Q

What are the signs and symptoms of heart failure

A

SOB upon excertion or when sleeping

Pitting oedema at ankles or sacrum

Raised JVP

Ascites

144
Q

What happens to RAAS during heart failure.

A

Heart Failure leads to a drop in BP which leads to RAAS activation. This increases Na+ absorption and water retention leading to increased blood volume. This means the already struggling heart has to work harder to pump more blood around he body.

145
Q

How is heart failure treated?

A

Treat underlying cause

Slow down progression of disease with medication

β-blockers, ACE inhibitors, Ca2+ channel blockers, organic nitrates and cardiac glycosides

146
Q

What is shock?

A

Acute circulatory failure resulting in generalised lack of oxygen supply to cells.

147
Q

What are the 4 types of shock

What is the mechanism by which they reduce the cardiac output

Give an example of a disease that may cause each type

A

Cardiogenic: Heart muscle is damaged meaning it cannot pump enough blood out (Myocardial Infarction)

Mechanical: Restriction on the filling of the heart (Pulmonary Embolism or Cardiac Tamponarde)

Hypovoleamic: Reduced blood volume (Haemorrhage)

Normovolaemic (Distributive): Decrease in TPR (Sepsis or Anaphylaxis)

148
Q

What are the nerve roots of the phrenic nerve

What does the phrenic nerve supply

A

C3, 4 and 5 keeps you alive

Motor and Sensory innveration to diaphragm

Sensory to pericardium

149
Q

Draw out the coronary arteries including:

Aorta

L. + R. Coronary Artery

L. + R. Marginal Artery

L. Anterior Descending Artery

L. Circumflex Artery

Posterior Interventricular Artery

(Mark the posterior and

A
150
Q

Where do the cardiac veins empty

A

Into the coronary sinus which drains straight into the R. Atrium.

151
Q

What are the 3 main cardiac veins and what are their course

A

Great cardiac vein: Follows the anterior IV grove from the apex to up round the L. side of the heart.

Middle cardiac vein: Accompanies the Posterior IV Artery

Small cardiac vein: Accompanies the R. Marginal Artery

152
Q

Fill in the blanks

A

Posterior Desceding Artery another name for the Posterior Interventricular Artery

Revision Cards (5 decks)

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