Cardiovascular System Flashcards

Question

Which organs require high, constant flow of blood to them?

Answer 1

Brain Kidneys Heart

Answer 2

Heart Brain Skeletal muscle

Answer 3

Normal-5 litres per minute | Exercise-25 litres per minute

Answer 4

Excess fluid building up relatively rapidly in the pericardial space. The heart becomes compressed due to the inextensible fibrous pericardial layer Compression of the heart leads to cardiac tamponade Pressure of the fluid means that the heart cannot fully fill during diastole leading to a smaller stroke volume and smaller cardiac output.

Answer 5

Fluid from pericardial space to be removed for testing | Fluid from pericardial space to be removed to relieve compression after a cardiac tamponade

Answer 6

Posterior to the pulmonary trunk and the ascending aorta, superior to the left atrium and anterior to the superior vena cava. A clamp can be placed here during a heart lung bypass so that there is no blood leaving the heart without damaging the pericardium. The heart lung bypass machine receives blood from the inferior and superior vena cava, oxygenates the blood and transfers it to the aortic arch.

Answer 7

Small concavity in the pericardium, posterior to the heart bound by pulmonary veins on either side.

Answer 8

Myocardial infarction

Answer 9

Incomplete valves Inferior vena cava - eustachian valve Coronary sinus - thebesian ring

Answer 10

The entrance of the left atrium into the left ventricle is smaller than the entrance of the right atrium into the right ventricle.

Answer 11

750ml per minute

Answer 12

``` Heart- pump Arteries - distributing vessels Arterioles - resistance vessels- restricting blood flow to easily perfused areas so that blood can flow to those often vulnerable parts that are not easily perfused Capillaries- exchange vessels Veins - capacitance vessels ```

Answer 13

Veins store blood (without an increase in pressure) to cope with temporary imbalances between the amount of blood returning to the heart and the amount that is required to pump out. This gives the cardiovascular system the ability to cope with changes in cardiac output.

Answer 14

The intervening region in the thoracic cavity between the right and left pleural cavities occupied by the lungs.

Answer 15

Resistance vessels restrict blood flow to drive supply to areas that are difficult to perfuse.

Answer 16

In exercise, more blood needs to flow to the heart muscle, skeletal muscle and cardiac muscle Resistance vessels restrict flow to other organs by constricting and dilate to allow blood to flow to these organs Cardiac output increases so there is less blood stored in capacitance vessels.

Answer 17

Neither- its the same. Any difference would cause oedema.

Answer 18

Left ventricle 120 systole / 10 diastole Right ventricle 25 systole/ 4 diastole

Answer 19

Contraction and ejection of blood from ventricles

Answer 20

Relaxation and filling of ventricles

Answer 21

70 beats per minute

Answer 22

Splanchnic Mesoderm

Answer 23

Resistance vessels restrict blood flow to drive supply to hard to perfuse areas

Answer 24

Enable CVS to vary amount of blood pumped around the body

Answer 25

Blood supply must change to meet demand and this is achieved by a balance between blood in these vessels.

Answer 26

Left atrium= 8-10 mm Hg | Right atrium = 0-4 mm Hg

Answer 27

Aorta- 120 systole/ 80 diastole mm Hg | Pulmonary artery- 25 systole/ 10 diastole mm Hg

Answer 28

It is relatively longer because it lasts for the duration of a single contraction (beat) of the heart. Duration of cardiac action potential = 280 ms Duration of skeletal muscle action potential = 2-5 ms

Answer 29

They prevent inversion of the cusps of the mitral and tricuspid valves.

Answer 30

Phase 2: Isovolumetric contraction Phase 3: Rapid ejection Phase 4: Reduced ejection

Answer 31

Phase 5: Isovolumetric relaxation Phase 6: Rapid filling Phase 7: Reduced filling Phase 1: Atrial contraction

Answer 32

0.35 seconds

Answer 33

0.55 seconds

Answer 34

Each cardiac cycle is shorter. | Systole stays the same length but diastole shortens.

Answer 35

Diastole Phase 6: Rapid filling Phase 7: Reduced filling Phase 1: Atrial contraction

Answer 36

Could be in systole. Phase 2: Isovolumetric contraction Could be in diastole. Phase 5: Isovolumetric relaxation

Answer 37

When pressure in the atria exceeds pressure in the ventricles. Pressure in the atria gradually rises due to venous return until it exceeds pressure in the ventricles after phase 5-Isovolumetric relaxation. This marks the beginning of Phase 6: Rapid filling

Answer 38

Atrial pressure rises due to atrial systole during phase 1 (atrial contraction) of the cardiac cycle.

Answer 39

Atrial pressure increases slightly due to closing of the mitral valve during phase 2 (Isovolumetric contraction) of the cardiac cycle.

Answer 40

Atrial pressure initially decreases as the atrial base is pulled downward as the ventricle contracts during phase 3 (rapid ejection) of the cardiac cycle.

Answer 41

Atrial pressure gradually rises due to continued venous return from the lungs during phase 4 (reduced ejection) of the cardiac cycle.

Answer 42

There is a slight rise in aortic pressure as the aortic valve closes during phase 5 (isovolumetric relaxation) of the cardiac cycle.

Answer 43

Atrial pressure decreases after opening of the mitral valve during phase 6 (rapid filling) of the cardiac cycle.

Answer 44

Signifies onset of atrial depolarisation on an electrocardiogram.

Answer 45

Signifies onset of ventricular depolarisation on an electrocardiogram.

Answer 46

Signifies ventricular repolarisation on an electrocardiogram.

Answer 47

Phase 4: Reduced ejection

Answer 48

Phase 1: Atrial contraction

Answer 49

Beginning of Phase 2- Isovolumetric contraction, as the mitral/tricuspid valves close.

Answer 50

Beginning of phase 5- isovolumetric relaxation as the mitral/pulmonary valves close.

Answer 51

During phase 6- rapid ventricular filling. This is usually silent but can sometimes be heard in children and is a sign of pathology in adults.

Answer 52

10% | Passive filling driven by venous pressure accounts for 90% of the filing of the ventricles.

Answer 53

It increases because venous pressure in the elderly decreases so there is less passive filling of the ventricles.

Answer 54

NONE - they are caused by the closing of valves.

Answer 55

At the apex of the heart

Answer 56

Aortic valve- 2nd intercostal space, right sternal edge Pulmonary valve- 2nd intercostal space, left sternal edge

Answer 57

Tricuspid valve 4th intercostal space, left sternal edge Mitral valve 5th intercostal space, mid-clavicular line

Answer 58

Valve does not open enough. There is an obstruction to blood flow when the valve is usually open.

Answer 59

Valve does not open fully. Back leakage when valve should be closed.

Answer 60

Degenerative (senile calcification/fibrosis) Congenital (bicuspid form of valve) Chronic rheumatic fever- inflammation - commissural fusion

Answer 61

Less blood can get can get through valve. > increased left ventricle pressure--> LV hypertrophy > left sided heart failure--> syncope, angina

Answer 62

Blood flows back into left ventricle during diastole Increases stroke volume Systolic pressure increases Diastolic pressure decreases Bounding pulse (head bobbing, Quinke's sign- beds of nails flush in colour with each heart beat) LV hypertrophy

Answer 63

Aortic root dilation- leaflets pulled apart | Vlavular damage- endocarditis rheumatic fever

Answer 64

99.9% cases caused by rheumatic fever (autoimmune) Commissural fusion of valve leaflets Harder for blood to flow from left atria to the left ventricle

Answer 65

REMEMBER Chordae tendinae and papillary muscles normally prevent prolapse in systole -Myxomatous degeneration can weaken tissue leading to prolapse Other causes: -Damage to papillary muscle after heart attack -Left sided heart failure leads to LV dilation which can stretch valve -Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation

Answer 66

Less blood can get through the valve. This causes left sided heart failure leading to angina.

Answer 67

Insufficient blood flow to the CNS

Answer 68

Red blood cells are damaged as blood is transported under very high pressure through a very narrow gap.

Answer 69

Aortic valve regurgitation

Answer 70

Crescendo-decrescendo murmur

Answer 71

Early decrescendo diastolic murmur

Answer 72

Snap as valve opens | Diastolic rumble

Answer 73

Holosystolic murmur

Answer 74

The load the heart must eject blood against (roughly equivalent to aortic pressure).

Answer 75

Amount the ventricles are stretched (filled) in diastole- related to the end diastolic volume or central venous pressure.

Answer 76

Sometimes referred to as systemic vascular resistance- resistance to blood flow offered by all the systemic vasculature

Answer 77

The pressure that the blood exerts drops as it flows through 'a resistance'.

Answer 78

Arterioles. Constriction of the arterioles increases resistance.

Answer 79

Venous pressure decreases | Arterial pressure increases

Answer 80

Arterial pressure decreases | Venous pressure increases

Answer 81

Arterial pressure increases | Venous pressure decreases

Answer 82

Arterial pressure increases | Venous pressure decreases

Answer 83

Arterial pressure

Answer 84

Tissues require more blood. Arterioles and pre-capillary sphincters dilate. Peripheral resistance decreases so more blood flows to these tissues. To counteract arterial pressure decreasing and venous pressure increasing cardiac output increases as this increases arterial pressure and decreases venous pressure. Cardiac output increases by intrinsic and extrinsic mechanisms.

Answer 85

EXTRINSIC MECHANISMS Greater activity of sympathetic nervous system: Increase in heart rate Increase in stroke volume by increasing contractility (changing the slope of the frank starling curve) INTRINSIC MECHANISMS Increase in stroke volume by: Increased preload- increased end diastolic volume and increased venous pressure Decreased afterload (aortic impedance) - decreased end systolic volume

Answer 86

The greater the venous pressure, the more the heart fills.

Answer 87

The ventricle fills until the walls stretch enough to produce an intraventricular pressure equal to venous pressure.

Answer 88

Compliance curve X axis = LV volume (ml) Y axis = LV pressure (mmHg)

Answer 89

In lungs - pulmonary oedema | In peripheries- peripheral oedema

Answer 90

``` EDV = 120ml Pressure = 10 mm Hg ```

Answer 91

More difficult to stretch Therefore, decreased compliance. Pressure increases to a higher value with the same value of end diastolic volume.

Answer 92

Simple dilatation- the walls do not materially decrease in thickness, but the cavities of the heart are enlarged Hypertrophic dilatation-the cavities enlarge and the walls increase in thickness. Atrophic dilatation-the cavities are enlarged and the walls of the heart become thin Hypertrophy-the walls increase in thickness

Answer 93

Dilated left ventricles causes increased compliance as the ventricle stretches more. The pressure in the ventricle is lower with the same value of end diastolic volume than in a healthy ventricle.

Answer 94

Hypertrophy. Less room for blood. Decreased compliance. As venous pressure increases, LV end-diastolic pressure increases to a greater extent than usual. As LV end-diastolic pressure increases, stroke volume increases up to a certain point after which the actin and myosin filaments are too far apart from one another and stroke volume decreases (Frank-starling law).

Answer 95

Decreased compliance. As venous pressure increases, LV end-diastolic pressure increases to a greater extent than usual. As LV end-diastolic pressure increases, stroke volume increases up to a certain point after which the actin and myosin filaments are too far apart from one another and stroke volume decreases (Frank-starling law).

Answer 96

Increased compliance. More room for blood. As venous pressure increases, LV end-diastolic pressure increases to a lesser extent than usual. Decreased end-diastolic pressure results in a lower stroke volume due to less stretching of the actin and myosin filaments. (Frank-starling law).

Answer 97

Increasing venous return in diastole, increases LV end diastolic pressure and causes an increase in stroke volume up to a certain point.

Answer 98

X axis = left ventricular end diastolic pressure/ left ventricular volume/ venous pressure Y axis = stroke volume

Answer 99

In both cardiac and skeletal muscle, an increased sarcomere length decreases overlap between the actin and myosin filaments and increased the force of contraction. In cardiac muscle, there is also an increase in calcium sensitivity as the muscle fibres are stretched.

Answer 100

As stroke volume on the right side of the heart increases, venous pressure to the left side of the heart increases so stroke volume on the left side of the heart increases...

Answer 101

More blood pumped to lungs than returns to the heart---> pulmonary oedema More blood pumped to the peripheries than returns to the heart---> peripheral oedema

Answer 102

Increased peripheral resistance

Answer 103

Increased afterload decreases stroke volume as the heart has to pump out against a higher pressure. Caused by increased peripheral resistance which decreases venous pressure causing a decrease in stroke volume. Cardiac output decreases. Eventually causes left ventricle hypertrophy as ventricle has to contract against a high pressure.

Answer 104

Contractility | Heart rate

Answer 105

``` Vasodilation in the gut Peripheral resistance decreases Arterial pressure decreases Venous pressure increases Stroke volume increases so cardiac output increases ``` The fall in arterial pressure suppresses the parasympathetic nervous system and stimulates the sympathetic nervous system. Heart rate increases Contractility increases Cardiac output increases Cardiac output increases Increases arterial pressure Decreases venous pressure Returns system back to normal

Answer 106

Venous pooling Venous pressure decreases. Decreased stroke volume. Decreased cardiac output. Arterial pressure decreases

Answer 107

Both venous and arterial pressures are lowered Intrinsic mechanisms would normally increase peripheral resistance to increase arterial pressure and decrease venous pressure. This would further decrease venous pressure. Therefore, the autonomic nervous system is involved with the baroreceptor reflex. This increased heart rate and increases total peripheral resistance so that arterial pressure increases and venous pressure does not fall further.

Answer 108

Postural hypotension

Answer 109

Initially muscle pumping and venoconstriction increases venous pressure and returns more blood to the heart, increasing stroke volume. Later, decreased total peripheral resistance increases venous pressure further. Very early response of increased heart rate via decreased parasympathetic drive and increased sympathetic drive. Increased contractility due to increased sympathetic drive - without this, increased venous pressure alone would move ventricular function to the top part of the Starling curve.

Answer 110

If only venous return increased, then ventricular function would be shifted to the flat part of the frank starling curve. Increasing contractility couples with increased venous return to cope to prevent this from occurring.

Answer 111

Turbulent flow

Answer 112

Disturbed flow through a valve due to stenosis | Back flow through an incompetent valve due to regurgitation

Answer 113

Unclotted whole blood Plasma Buffy coat Red blood cells Clotted whole blood Serum Clot

Answer 114

Add an anti-coagulant eg. Heparin

Answer 115

Clotting factors | Particularly fibrinogen

Answer 116

Sludging of blood in peripheries. Peripheries feel colder.

Answer 117

Multiple myeloma Cancer of plasma cells- a malignant clone of plasma cells produces immunoglobulins in large quantities which increases the viscosity of the blood.

Answer 118

Multiple myeloma- increased plasma cells Polycythaemia- increased red blood cells Thrombocythaemia- increased thrombocytes Leukaemia- increased white blood cells

Answer 119

Minor changes in plasma viscosity can result from raised levels of acute phase proteins (eg. Fibrinogen, complement factors and C-reactive protein). Acute phase proteins increase in response to inflammation. Therefore, minor changes in plasma viscosity can be used to measure the inflammatory response. In recent years, we have been able to measure C-reactive protein (CRP) and this is more commonly used to measure inflammation

Answer 120

Turbulent flow- blood flowing in all directions in the vessel and continually mixes within the vessel. Laminar flow- blood flows in streamlines with each layer of blood remaining the same distance from the wall.

Answer 121

``` Increased blood flow and the rate of blood flow becomes too great Blood passes an obstruction in a vessel Blood makes a sharp turn Blood passes over a rough surface Increased resistance to flow ```

Answer 122

Limited number of red blood cells. Heart rate to increase cardiac output so oxygen can be transported around the body quick enough Results in turbulent flow which can be heard as a murmur

Answer 123

Increased T3 and T4 Causes increased sensitivity to catecholamines Increased chronotropy and inotropy Turbulent flow

Answer 124

Psi (pounds per square inch)

Answer 125

Volume per unit time ml/min or l/hour

Answer 126

1/2 x m x v squared ``` M= mass V= velocity ```

Answer 127

Volume does not change in response to pressure.

Answer 128

Proximal to the stenosis, flow is less, pressure is greater, velocity is lower and kinetic energy is lower Distal to the stenosis, flow is less, pressure is less, velocity is higher and kinetic energy is higher

Answer 129

A thrill | Blood vessel vibrates due to the high velocity and kinetic energy.

Answer 130

Peripheral artery Bruit - sounds like a plane taking off Heart valve Murmur

Answer 131

Narrowing of a blood vessel

Answer 132

Distal to the stenosis, blood hits the wall of the artery at high velocity and high kinetic energy. This causes a post stenotic dilatation of the blood vessel as the wall of the artery dilates. Bursting of this is an aneurysm.

Answer 133

One stenosis followed by another stenosis. | Distal to the second stenosis, flow is further decreased and may stop flowing completely.

Answer 134

As people age, arteries often calcify and become less compliant. Volume does not increase in response to an increase in pressure so a pulse cannot be felt.

Answer 135

Flow and pressure decreases | Velocity increases

Answer 136

Flow and pressure increases | Velocity decreases

Answer 137

Systolic uptake Pressure in the descending aorta increases rapidly during systole as blood is ejected out of the ventricles as they contract and the elastic walls of the aorta stretches. Peak systolic pressure This is the highest pressure in the descending aorta.

Answer 138

Systolic decline Pressure decreases as the ventricles relax and less blood is ejected from the ventricles Dicrotic notch The pressure in the aorta exceeds that in the left ventricle and the aortic valve closes. This is the end of systole. There is a slight increase in pressure as blood collects in the aorta. Diastolic run off Pressure decreases as blood flows down the aorta and the aortic wall recoils End diastolic pressure This is the lowest pressure in the aorta as there is no flow of blood from the ventricles

Answer 139

Pulse pressure = peak systolic pressure - end diastolic pressure

Answer 140

120 - 80 = 40 mm Hg

Answer 141

Sphygomanometer

Answer 142

Diastolic pressure + 1/3 pulse pressure

Answer 143

80 + 13 = 93 mm Hg

Answer 144

Organ perfusion is impaired

Answer 145

Cuff must go around at least 80% of the arm. | An undersized cuff can give a false reading of blood pressure.

Answer 146

The height at which blood pressure is measured due to the effect of gravity. Venous and arterial pressure is greater at a lower height when standing up. The size of the cuff. An undersized cuff can give a false reading of blood pressure.

Answer 147

Retrograde flow is when the blood bounces back slightly. It can occur in the arterial system and is greatest when peripheral resistance is high.

Answer 148

Greater peripheral resistance---> greater retrograde flow

Answer 149

1. The force with which the left ventricle is able to eject the blood into the arterial system to develop a normal shock wave. Weaker force ---> reduced pulse volume---> thready pulse 2. Pulse pressure. This is the major determinant of how strong the pulse is. Greater pulse pressure---> increased pulse volume---> bounding pulse Pulse pressure= peak systolic pressure - end diastolic pressure

Answer 150

Pulse volume is lower than usual

Answer 151

LV failure Aortic valve stenosis Hypovolaemia (severe dehydration/bleeding)

Answer 152

Bradycardia- greater amount of time spent in diastole than usual. End diastolic pressure reaches a smaller value than normal. Pulse pressure increases and pulse volume increases

Answer 153

Low peripheral resistance caused by vasodilation- diastolic run off occurs more quickly as blood rushes out of the aorta to the peripheries. End diastolic pressure reaches a smaller value within the same period of time. Pulse pressure increases and pulse volume increases

Answer 154

Genetic Downs, turner's syndrome, marfan's syndrome Environmental Teratogenicity from drugs, alcohol etc. Maternal infections Rubella, toxoplasmosis etc.

Answer 155

``` Left atrium- 99% Left ventricle- 99% Aorta- 99% Right atrium- 67% Right ventricle- 67% Pulmonary arteries- 67% ```

Answer 156

``` Right atrium- 0-4mmHg Right ventricle- 25/3 mmHg Pulmonary arteries- 25/10mmHg Left atrium - 8-10 mmHg Left ventricle- 120/7mmHg Aorta-120/80mmHg ```

Answer 157

A communication between two sides of the circulation.

Answer 158

Bluish discolouration skin, nail beds and mucous membranes due to unsaturated haemoglobin entering the systemic circulation

Answer 159

In the 3rd week of development because nutrient and gas exchange needs of the rapidly growing embryo can no longer be met by diffusion alone so the developing cardiovascular system is formed to deliver these substances over long distances.

Answer 160

The endocardial tubes are brought together during embryonic folding and fuse in the midline.

Answer 161

Cranial end ``` Aortic roots (2 vessel outlet) Truncus arteriosus Bulbus cordis Ventricle Atrium Sinus venosus (4 vessel inlet) ``` Caudal end

Answer 162

The roots and proximal portions of the pulmonary trunk and aorta

Answer 163

Part of the right ventricle

Answer 164

The left ventricle

Answer 165

Most of the right atrium and some of the right ventricle

Answer 166

A zone within the mesoderm consisting of blood pools and tiny vessels. There is a space which will be the pericardial cavity.

Answer 167

Right atrium

Answer 168

The tube elongates. It runs out of room. Twists and folds up placing the inflow cranially and dorsally to the outflow.

Answer 169

Most of the primitive atrium Sinus venosus This recieves venous drainage from the body (venue cavae) and the heart (coronary sinus)

Answer 170

A small portion of the primitive atrium Absorbs proximal parts of pulmonary veins Receives oxygenated blood from the lungs

Answer 171

The left atrium mainly develops from proximal parts of the pulmonary veins which has a smooth inner surface whereas the right atrium mainly develops from the primitive atrium which has a rough inner surface.

Answer 172

Looping in the fourth week of embryonic development

Answer 173

There is a double circulation in series in an adult but in a foetus, the lungs do not work so there is no requirement for this double circulation. Oxygenation and removal of carbon dioxide occurs at the placenta for a foetus. Shunts are required to maintain foetal life but these must be reversible at birth

Answer 174

Ductus venosus- between inferior vena cava and the liver to prevent all blood entering the liver Ductus arteriosus- between the aorta and pulmonary trunk which is right to left to ensure all highly oxygenated blood is pumped to the foetus Foramen ovale-between the atria which is right to left to ensure that blood enters the left atria and hence the left ventricle so that blood can enter the systemic circulation

Answer 175

The inferior vena cava which comes from the placenta

Answer 176

Ductus venosus-physiological closure Placental support is removed Ductus arteriosus Ductus arteriosus undergoes a muscular spasm and closes Ductus venosus and ductus arteriosus become fibrotic and close. Foramen ovale-mechanical closure Left atrial pressure increases Septum primum closes firmly against septum secondum

Answer 177

Arch 4 LHS = arch of the aorta | Arch 6 RHS = pulmonary artery

Answer 178

Left recurrent laryngeal nerve

Answer 179

Neural crest cells migrate into the developing heart making a shaft of tissue called endocardial cushions. Endocardial tissues create a crescent shaped wedge down the roof of the atria towards the atrioventricular canal called the septum primum. The hole is the Ostium primum which allows right to left shunt. Septum secundum forms and the foramen ovale forms. This forms a right to left shunt.

Answer 180

There is a complex process in producing the atrial septum. Atrial septal defect can arise due to problems in forming either septum primum or septum secondum.

Answer 181

Muscular | Membranous

Answer 182

The muscular portion of the septum which forms the majority of the septum grows upwards towards the fused endocardial cushions.

Answer 183

The interventricular foramen is the gap formed when the muscular portion of the septum grows upwards towards the endocardial cushions. This is closed by the membranous portion of the interventricular septum formed by connective tissue derived from endocardial cushions to fill the gap.

Answer 184

Endocardial cushions appear in the truncus arteriosus. As they grow towards each other, they twist around each other to form a spiral septum. This connects the left ventricle to the aorta and connects the right ventricle to the pulmonary trunk

Answer 185

The aorta arises from the right ventricle. | The pulmonary trunk arises from the left ventricle.

Answer 186

Large ventricular septal defect Overriding aorta Right ventricular outflow tract obstruction (pulmonary stenosis) Right ventricular hypertrophy

Answer 187

They migrate to from the endocardial cushions which are the foundation of atrial septation, ventricular septation and septation of the outflow tracts.

Answer 188

Low concentrations of alcohol can kill or damage these cells

Answer 189

Right to left shunting

Answer 190

Narrowing of the aortic lumen in the region of the former ductus arteriosus.

Answer 191

The condition of severe pulmonary vascular obstruction that results from chronic left to right shunting through a congenital heart defect. The elevated pulmonary vascular resistance causes reversal of the original shunt and systemic cyanosis.

Answer 192

Takes on significance if the right atrial pressure becomes elevated (due to pulmonary hypertension or right heart failure) leading to right to left shunting since the higher left atrial pressure causes functional closure of the flap valve.

Answer 193

Because vessels to the head and upper limbs usually emerge proximal to the coarctation, the blood supply to these regions is not compromised. However, blood flow to the rest of the body is reduced.

Answer 194

Compatible with life in uterus because flow through ductus arteriosus and foramen ovale allows communication between the two circulations. After birth, without any intervention, TGA is not compatable with life because oxygenated blood does not reach systemic tissues.

Answer 195

Femoral pulses are weak and delayed. | An elevated blood pressure in the upper body is common.

Answer 196

``` Left to right shunts: Atrial septal defect (ASD) Patent foramen ovale (PFO) Ventricular septal defect (VSD) Patent ductus arteriosus (PDA) Obstructive lesions: Aortic stenosis (Hypoplasia) Pulmonary stenosis (Valve, outflow, branch) Coarctation of the aorta Mitral stenosis ```

Answer 197

``` Complex, right to left shunts Tetralogy of Fallot Tricuspid Atresia Transposition of the great arteries Hypoplastic left heart ```

Answer 198

Left ventricle and ascending aorta fail to develop properly.

Answer 199

Caudal shift of the development heart and expansion of the developing neck region The need for a foetal shunt between the pulmonary trunk and aorta

Answer 200

Cardiomyocytes = Na+ influx via the opening of fast type Na+ channels due to depolarisation. Pacemaker cells = Ca2+ influx via the opening of L-type Ca2+ channels due to depolarisation.

Answer 201

Cardiomyocytes Fast type Na+ channels-responsible for upstroke in AP Pacemaker cells Slow type Na+ channels- responsible for 'pacemaker potential'

Answer 202

Slow Na+ channels slowly open and the resting membrane potential depolarises steadily from its most negative value of -60mV in pacemaker cells. They activate more with hyperpolarisation.

Answer 203

Plateau phase in cardiomyocytes | Ca2+ influx and K+ outflux

Answer 204

Phase 0 --> Na+ influx Phase 1 --> transient K+ efflux Phase 2 --> Ca2+ influx and K+ efflux Phase 3 --> K+ efflux

Answer 205

Slow Na+ influx Fast Ca2+ influx K+ outflux

Answer 206

False Activated by hyperpolarisation They are HCN channels Hyperpolarisation activated cyclic nucleotide gated channels

Answer 207

SA node- therefore, this sets the rhythm

Answer 208

SA node and AV node

Answer 209

No they have slow type Na+ channels that allows Na+ to continuously leak in. But does not depolarise as fast as SA node

Answer 210

Those which do not have a stable resting potential due to continuous influx of Na+ : SA node AV node Purkinje fibres

Answer 211

Asystole- action potentials fail | Fibrillation- electrical activity becomes random

Answer 212

3.5-5.5 mmol/L

Answer 213

>5.5mmol/L of K+ in the blood

Answer 214

Their resting membrane potential is very close to Ek (-90mV) There are many different kinds of K+ channels

Answer 215

<3.4mmol/L of K+ in the blood

Answer 216

EK is less negative Inactivates some of the voltage gated Na+ channels Slow upstroke Narrows action potential

Answer 217

Asystole- the heart can stop because of the slower upstroke of the action potential May initially get an increase in excitability Depends on extent of hyperkalaemia and how quickly hyperkalaemia develops

Answer 218

Calcium gluconate Insulin + glucose These won't work if the heart has already stopped

Answer 219

Mild hyperkalaemia = 5.5-5.9mmol/L Moderate hyperkalaemia = 6.0-6.3 mmol/L Severe hyperkalaemia> 6.5mmol/L

Answer 220

Calcium makes the heart less excitable because it is a bivalent cation.

Answer 221

To prevent hypoglycaemia If you gave insulin alone, this would increase uptake of glucose from the blood and would cause hypoglycaemia. Insulin increases uptake of K+ into cardiac myocytes

Answer 222

Decreased plasma K+ concentration Allosteric effect reducing the conductance of voltage gated K+ channels so downstroke of AP is slower Leads to a longer action potential Early reactivation of some voltage gated Ca2+ channels as some of the membrane repolarises Leads to early after depolarisations (EADs) and hence oscillations in membrane potential Ventricular fibrillation

Answer 223

Oscillations in membrane potential--->Ventricular fibrillation

Answer 224

In patients - with existing heart problems - people on anti-arrhythmic drug

Answer 225

Depolarisation open L-type Ca2+ channels in the T-tubule system Localised Ca2+ entry opens CICR channels in the sarcoplasmic reticulum Close link between L-type channels and Ca2+ release channels (but they're not directly connected) 25% enters across the sarcolemma, 75% released from SR

Answer 226

Ca2+ in the cardiac myocytes is returned to resting levels Most is pumped back into the SR as 75% of Ca2+ came from here, some exits across the membrane Ca2+ ATPase is activated (high affinity)

Answer 227

Tunica media

Answer 228

Opening of voltage gated Ca2+ channels due to depolarisation allows Ca2+ to enter A1 adrenoreceptors activate and Ca2+ is released from SR via activation of phospholipase C and creation of iP3 which binds to SR Ca2+ binds to calmodulin. Ca2+ activates myosin light chain kinase which phosphorylates the myosin light chain to permit activation with actin. DAG stimulates PKC which inhibits myosin light chain phosphatase. This allows sustained vasoconstriction.

Answer 229

No. Ca2+ binds to calmodulin. This activated myosin light chain kinase Myosin light chain kinase phosphorylates the myosin light chain to permit interaction with actin

Answer 230

Myosin light chain phosphatase dephosphorylates the myosin light chain

Answer 231

Ca2+ binds to calmodulin which activates myosin light chain kinase in smooth muscle Ca2+ binds to troponin C in cardiac muscle

Answer 232

Autonomic nervous system

Answer 233

Can change: Rate Force of contraction of heart Peripheral resistance of blood vessels (arteriolar/venous constriction)

Answer 234

Anatomical grounds

Answer 235

Cranial and sacral origin

Answer 236

Thoracic and lumbar origin

Answer 237

Network of neurones surrounding GI tract | Normally controlled via sympathetic and parasympathetic fibres

Answer 238

Parasympathetic nervous system

Answer 239

Smooth muscle of blood vessels- vasoconstriction Pupil of eye. Dilation Sweat glands - increased sweat release

Answer 240

No, sympathetic drives to different tissues is independently regulately

Answer 241

It beats at a faster rate to about 100 beats per minute because parasympathetic nervous system dominates at rest

Answer 242

Vagus nerve-10th cranial nerve

Answer 243

Decreases heart rate (negative chronological effect) | Decreases AV node conduction velocity

Answer 244

Increases heart rate (positive chronograph) | Increases force of contraction (positive inotropy)

Answer 245

Sympathetic Innervates: SA node, AV node, myocardium Parasympathetic Innervates: SA node, AV node

Answer 246

Sympathetic Post ganglionic nerves come from the paravertebral disc/sympathetic trunk Parasympathetic Post ganglionic nerves are within the epicardium or within walls of heart at SA node and AV node

Answer 247

Baroreceptors which are sensitive to stretch in: Carotid sinus of internal carotid artery - arterial pressure Aortic arch - arterial pressure Atrial receptors - venous pressure Sensory (afferent neurones) from the baroreceptors/atrial receptors go to the cardiovascular centre in the medulla oblongata The cardiovascular centre in the medulla oblong at a acts as a control centre and alters the activity of the efferent preganglionic nerves which go to the heart and vessels

Answer 248

Action potentials in the sa node | Slow depolarising pacemaker potential eventually causing the opening of Ca2+ channels responsible for upstroke

Answer 249

Sympathetic effect mediated by beta 1 adrenoreceptor GPCR Increase cAMP Speeds up pacemaker potential--->Increases slope

Answer 250

Parasympathetic effect mediated by M2 GPCR Increase K+ conductance and decrease cAMP Decreases slope of pacemaker potential

Answer 251

Noradrenaline B1 adrenoreceptors in myocardium cAMP ---> activates PKA -phosphorylation of Ca2+ channels increases Ca2+ entry during the plateau of the AP -increased uptake of Ca2+ in sarcoplasmic reticulum -increased sensitivity of contractile machinery to Ca2+ All lead to increased force of contraction

Answer 252

Sympathetic innervation

Answer 253

Activating beta 2 adrenoreceptors causes vasodilation

Answer 254

a1 adrenoreceptors Coronary, skeletal and liver vasculature also have b2 adrenoreceptors

Answer 255

Vasoconstriction

Answer 256

Vasodilation

Answer 257

Alpha 1 - noradrenaline from sympathetic nervous system and circulating adrenaline at high plasma concentrations of adrenaline (higher affinity of a1) Beta 2 - circulating adrenaline at physiological concentration (higher affinity for b2)

Answer 258

B2 - only some tissues eg. Skeletal muscle, myocardium and liver Usually vasodilation is just a lack of sympathetic tone

Answer 259

Increases cAMP Activates PKA Opens K+ channels and inhibits myosin light chain kinase and phosphorylates myosin light chain kinase Relaxation of smooth muscle

Answer 260

Stimulates ip3 production Increase of intracellular calcium from stores and via influx of extracellular calcium Contraction of smooth muscle

Answer 261

Active tissue produces more metabolites eg. Adenosine, K+, H+, increased co2 Local increases in metabolites has a strong vasodilator effect

Answer 262

False It is a sensory and motor neurone Sensory - from baroreceptors in aortic arch Motor - to AVN and SAN

Answer 263

When maintaining blood pressure over short term | Compensates for moment to moment changes in arterial blood pressure

Answer 264

Baroreceptors re-set to higher levels with persistent increases in blood pressure

Answer 265

It is a non-selective B1/B2 antagonist Slows heart rate and reduces force of contraction (b1) Acts on bronchial smooth muscle to cause bronchoconstriction (b2)

Answer 266

A1 antagonist B1-selective antagonist

Answer 267

Glaucoma | Activates constriction papillae muscle- agonises m3 receptor

Answer 268

Asthma, antagonises m3 receptors | Dilation of pupils for examination, antagonises m3 receptors

Answer 269

Total peripheral resistance Distribution of flow Cardiac output - heart rate and force of contraction

Answer 270

Increases return of blood to the heart

Answer 271

``` LV dilation More room for blood Increased compliance Stretched mitral valve Mitral valve regurgitation ```

Answer 272

``` Blood leaks back into left atrium Increases preload More blood enters left ventricle in subsequent cycles Causes left ventricle hypertrophy Left ventricle failure ```

Answer 273

The walls of the atria stretch and there is more room for blood. Pacemaker cells become 'irritated'. Leads to atrial fibrillation

Answer 274

Individual fibrils contract not in synchrony with one another. Blood remains stagnant in the atria. Leads to thrombus formation

Answer 275

Increase LA pressure LA dilation Oesophagus compression Dysphagia

Answer 276

Increased left atrial pressure Pulmonary hypertension Right ventricle hypertrophy

Answer 277

Mechanical stress which is usually distributed over three leaflets is now only distributed over two leaflets.

Answer 278

Repeated inflammation and repair leads to fibrosis of valves and hence stenosis

Answer 279

``` Less blood can get through valve Increase left ventricle pressure Left ventricle hypertrophy Left sided heart failure Insufficient blood flow to CNS = syncope Insufficient blood flow to heart = heart ```

Answer 280

Damage to red blood cells as blood is being transported under a very high pressure through a very narrow gap

Answer 281

Aortic valve regurgitation Blood flows back into LV during diastole Increases stroke volume Systolic pressure increases and diastolic pressure decreases

Answer 282

Bounding pulse - head bobbing and quinke's sign (nail beds change colour with pulse)

Answer 283

Ductus arteriosus | Foramen ovale

Answer 284

Works well to control acute changes in blood pressure Does not control sustained increases because the threshold for baroreceptor firing resets after a short period- it responds to changes

Answer 285

Short term- heart rate, TPR, force of contraction To cause: vasoconstriction/dilation, changes in CO Long term-sodium concentration in extracellular fluid To cause: increase/decrease in blood volume

Answer 286

Juxtaglomerular apparatus in kidney

Answer 287

- Reduced NaCl concentration in distal tubule - Reduced perfusion pressure in the kidney detected by baroreceptors in afferent arteriole (going into the kidney- reflects peripheral arteriole blood pressure) - Sympathetic stimulation to juxtaglomerular apparatus increases release of renin

Answer 288

Mean arterial BP = CO x TPR Mean arterial BP = diastolic pressure + 1/3 pulse pressure

Answer 289

Controls and produces a rapid response to acute changes in blood pressure by: - adjusting sympathetic and parasympathetic inputs to the heart to alter CO - adjusting sympathetic input to peripheral resistance vessels to alter TPR

Answer 290

Renin-angiotensin-aldosterone system Sympathetic nervous system Antidiuretic hormone Atrial natriuretic peptide (ANP)

Answer 291

Stimulates the conversion of angiotensin I to angiotensin II Kininase enzyme that breaks down the vasodilator bradykinin into peptide fragments so causes vasoconstriction

Answer 292

Angiotensin II receptor 1 (AT1) = | GPCR

Answer 293

1. Vasoconstriction 2. Stimulates Na+ reabsorption 3. Stimulates release of aldosterone 4. Increases noradrenaline released 5. Stimulates ADH release, increasing thirst sensation

Answer 294

Principal cells of collecting ducts

Answer 295

- activates apical Na+ channel and apical K+ channel | - increases basolateral Na+ extrusion via Na+/K+ ATPase

Answer 296

Low potassium levels Aldosterone stimulates basolateral Na+/K+ ATPase to promote extrusion of Na+ into capillaries but in turn decreases K+ concentration in capillaries

Answer 297

The inhibit ACE so - prevent the conversion of angiotensin I to angiotensin II (so all the effects of this including release of aldosterone are inhibited) - prevent the conversion of bradykinin into peptide fragments by ACE.

Answer 298

High levels of sympathetic activation causes: -reduced renal blood flow: Vasoconstriction of arterioles to kidneys Decreased glomerular filtration rate-decreased Na+ excretion - activation of apical Na+/H+ exchanger and basolateral Na+/K+ ATPase in proximal convolutions tubule - stimulates renin released from juxtaglomerular renal cells

Answer 299

Produced in hypothalamus but secreted by pituitary gland by neurocrine secretion

Answer 300

- formation of concentrated urine by retaining water by leading to increased transcription of aquaporins - stimulates Na+ reabsorption by acting on the thick ascending limb and stimulating the Na+/K+/Cl- co-transporter - vasoconstriction

Answer 301

Plasma osmolarity | Severe hypovolaemia

Answer 302

Hypervolaemia

Answer 303

Atrial myocytes

Answer 304

High level of stretching by low pressure volume sensors in the atria

Answer 305

Vasodilation of afferent arterioles Increased blood flow to kidneys to increase glomerular filtration rate Inhibits Na+ rebasorption along the nephron

Answer 306

Natriuretic peptides- ANP and BNP

Answer 307

Stage 1 hypertension = 140/90mmHg Stage 2 hypertension = 160/100 mmHg Severe hypertension > or equal to 180 systolic > or equal to 110 diastolic

Answer 308

A rapid increase in blood pressure which causes damage to blood vessels

Answer 309

Primary- cause cannot be defined | Secondary-cause can be defined

Answer 310

Occlusion of the renal artery Fall of perfusion pressure in that kidney Increased renin production Activation of RAAS Vasoconstriction and Na+ retention at other kidney Hypervolaemia Hypertension

Answer 311

Cushing's syndrome- excess secretion of glucocorticoid cortisol from adrenal cortex Conn's syndrome- mineralocorticoid aldosterone secreting adenoma in adrenal cortex Tumour of the adrenal medulla-secretes catecholamines adrenaline and noradrenaline

Answer 312

Exercise Diet Reduced Na+ intake Reduced alcohol intake

Answer 313

``` Brain Eyes Heart Kidneys Arteries ```

Answer 314

Hypertension causes arterial damage Leading to weakened vessels Leading to retinopathy

Answer 315

Increased afterload Left ventricular hypertrophy Heart failure

Answer 316

Increased afterload Increased myocardial oxygen demand Myocardial ischaemia Myocardial infarction

Answer 317

Acute condition of general inadequate blood flow throughout the body

Answer 318

A drop in arterial blood pressure

Answer 319

Cardiogenic shock Mechanical shock Hypovolaemic shock

Answer 320

Anaphylactic shock | Septic shock

Answer 321

MI---> damage to left ventricle Serious arrhythmias---> profound bradycardia/tachycardia Acute worsening of heart failure---> at rest, BP cannot be maintained

Answer 322

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply to cells because the ventricle cannot eject enough blood.

Answer 323

Heart failure is a chronic condition. With heart failure, patients have an adequate blood pressure which may change if they exert themselves but at rest, they are not in an acutely life threatening condition. Cardiogenic shock refers to acute failure of the heart to maintain cardiac output so blood pressure can no longer be maintained for vital organs to be adequately perfused, making it acutely life threatening.

Answer 324

Unresponsiveness associated with lack of pulse | The heart has stopped or ceased to pump effectively

Answer 325

Yes- cardiac arrest can be due to a loss of electrical and/or mechanical activity Pulseless Electrical Activity= presence of electrical activity but loss of mechanical activity

Answer 326

Loss of electrical and loss of mechanical activity of the heart

Answer 327

Electrical current delivered to the heart Depolarises all of the cells Puts them into a refractory period Allows coordinated electrical activity to restart

Answer 328

Enhances myocardial function | Vasoconstriction--->increases peripheral resistance

Answer 329

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply to cells because: - there is a restriction on filling of the heart - there is obstruction to blood flow through the lungs

Answer 330

Mechanical shock

Answer 331

Embolus occludes a large pulmonary artery – Pulmonary artery pressure is high – Right ventricle cannot empty – Central venous pressure high – Reduced return of blood to left heart – Limits filling of left heart – Left atrial pressure is low – Arterial blood pressure low – Shock

Answer 332

• Typically due to deep vein thrombosis • Potion of thrombus breaks off • Travels in venous system to right side of the heart • Pumped out via pulmonary artery to lungs • The effect of this will depend on the size of the embolus

Answer 333

Amount and speed of blood loss

Answer 334

Haemorrhage Severe diarrhoea Vomiting Excessive loss of Na+

Answer 335

Vasoconstriction (increased TPR) reduces capillary hydrostatic pressure and there is a net movement of fluid into capillaries This occurs when there is peripheral vasoconstriction because low arterial pressure is detected by baroreceptors

Answer 336

– Peripheral vasoconstriction to increase blood pressure impairs tissue perfusion – Tissue damage due to hypoxia – Release of chemical mediators – vasodilators – TPR falls – Blood pressure falls dramatically – Vital organs can no longer be perfused – Multi system failure

Answer 337

Septic shock

Answer 338

Fluid resuscitation to maintain BP | Vasosuppressants required due to peripheral vasoconstriction and leaky capillaries

Answer 339

TPR Vasodilation--->reduced arterial pressure SV Capillaries become leaky resulting in reduced blood volume

Answer 340

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply of cells due to loss of circulating fluid volume.

Answer 341

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply to cells due to uncontrolled falls in peripheral resistance ie. sepsis or anaphylaxis

Answer 342

- consists of specialised cells (lost their contractile ability) - able to generate action potentials - conduct impulses very rapidly to all subendocardial regions of the ventricles - results in depolarisation of myocytes and coordinated contraction of atria and ventricles

Answer 343

From endocardium to epicardium (His-purkinje system is in the endocardium) Starts with the interventricular septum, following rapidly by the apex and free wall of the ventricles. Last part to be depolarised is the base of the ventricles.

Answer 344

Sinoatrial node Fastest rate of depolarisation so sets sinus rhythm At junction between right atrium and superior vena cava

Answer 345

Atrioventricular node At base of right atrium Slow rate of depolarisation so electrical activity is delayed here by about 120-200ms This allows time for atrial contraction

Answer 346

Bundle of His Continuous with AV node Atrial impulse cannot travel from atria to ventricles due to the fibrous non-conductive connective tissue separating them

Answer 347

Left bundle branch because the left ventricular muscle wall is thicker.

Answer 348

Fine branches of Bundle of His Rapid spread of depolarisation throughout ventricular myocardium to allow synchronised contraction (4 metres/sec)

Answer 349

1. The electrical events start with depolarisation of the sinoatrial node and is followed by depolarisation of the myocytes of the right and left atria. 2. The wave of depolarisation is delayed by about 100-200ms at the AV node, allowing time for atrial contraction. 3. Depolarisation can only spread from the atria to the ventricles via the Bundle of His. It is thereafter rapidly conducted to all parts of the ventricles by the His-Purkinje system.

Answer 350

The overall direction of the wave of depolarisation. This is directed towards the apex somewhat to the left of the inter-ventricular septum in the normal heart.

Answer 351

All of the ventricular myocardial cells depolarise before any start to repolarise. Repolarisation does not follow the same sequence across the heart, as the cells at the outside of the ventricle (epicardium) repolarise first, so the direction of spread of repolarisation is opposite to that of depolarisation. (Therefore, the duration of the action potential of the cells in the epicardium is short)

Answer 352

An ECG records changes on the extracellular surface of cardiac myocytes during a wave of depolarisation and repolarisation From the surface of the body Using electrodes pasted on the skin

Answer 353

Upward deflection

Answer 354

Downwards deflection

Answer 355

Downward deflection

Answer 356

The amplitude (height) of the deflection depends on • the size of muscle changing potential • how fast depolarisation occurs • how directly the wave of activity is travelling towards the electrode ◦ directly towards /away yields a large signal ◦ obliquely towards/away yields a smaller signal ◦ spread at right angles yields no signal

Answer 357

Peak to peak of R-waves Shorter interval - faster heart rate

Answer 358

Start of Q wave to end of S wave Wider QRS complexes are associated with ventricular depolarisations that are not initiated by the normal conductance mechanism. Normal QRS is less than or equal to 3 small boxes

Answer 359

Start of P-wave to start of Q wave Longer P-R intervals indicate slow conduction from the atria to the ventricle (first degree heart block) Normal PR interval = 3-5 small boxes

Answer 360

End of S wave to start of T wave The ST segment should be isoelectric. If it is raised or depressed, this indicates myocardial infarction or ischaemia.

Answer 361

Start of Q-wave to end of T-wave A prolonged Q-T interval suggests prolonged repolarisation of the ventricles. This can lead to arrhythmias as occur in long QT syndrome. Varies with heart rate. Upper limit of corrected QT interval: 11-12 small boxes

Answer 362

Start of the P wave is SA node depolarisation Majority of it is atrial depolarisation

Answer 363

Depolarisation of the myocardium in intraventricular septum Septum depolarises from left to right Produces a small downward deflection because it is moving obliquely away.

Answer 364

Depolarisation of apex and free ventricular wall upward because depolarisation moving directly towards electrode Large because large muscle mass – more electrical activity If left ventricle was hypertrophies – Then R wave will be correspondingly taller

Answer 365

End of depolarisation as depolarisation has spread to the base of the ventricles. Downwards because moving away Small because not moving directly away

Answer 366

Ventricular repolarisation Upward because it is repolarisation moving away from the electrode

Answer 367

QRS complex

Answer 368

Flat line segment

Answer 369

10 electrodes 4 on the limbs 6 on the chest 12 views of the heart

Answer 370

Lead II, III, aVF

Answer 371

Lead I and aVL | V5 and V6

Answer 372

Leads II, III, aVF - inferior view Leads I, aVL - LHS view Lead aVR - mirror image of lead II Vertical plane

Answer 373

V1 and V2 - septal leads face the right ventricle and septum V3 and V4 - anterior leads face the apex and anterior wall of ventricles V5 and V6 - lateral leads face the left ventricle

Answer 374

Sinus rhythm = depolarisation initiated by sinus node - is the rhythm regular? - heart rate? (60-100bpm) - are there p waves? - are p waves upright in leads I, II? -Is PR interval is normal (3-5 small boxes)? - is every p wave followed by QRS? - every QRS preceded by a p wave? - normal QRS width (≤3 small boxes)

Answer 375

No. Sinus rhythm changes with respiration so small irregularity is not seen as pathological, it is good because it shows the sympathetic nervous system is working.

Answer 376

Heart rate = 300/how many large squares there are between each R wave

Answer 377

Find number of QRS complex in 6 seconds (30 large squares) | Then x 10

Answer 378

- abnormal impulse formation | - abnormal conduction

Answer 379

Supraventricular rhythms - sinoatrial node - ectopic atrial foci - atrioventricular node Ventricular rhythms -ventricle

Answer 380

Conducted into and within ventricles by His-Purkinje system Normal ventricular depolarisation Normal (narrow) QRS complex Depending on origin of impulse, P wave will vary

Answer 381

- from a focus/foci in ventricle - conduction not via normal His-purkinje system - depolarisation takes longer - wide (> 3 small boxes) QRS complex - rhythms from different foci will have different shapes - depending on the origin of the impulse, the P wave and QRS complex will vary allowing us to diagnose the arrhythmia

Answer 382

Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above. However, if an ectopic focus depolarises early enough, prior to the arrival of the next sinus impulse, it may “capture” the ventricles, producing a premature contraction. Premature contractions (“ectopics”) are classified by their origin — atrial (PACs), junctional (PJCs) or ventricular (PVCs).

Answer 383

60-100 beats per minute

Answer 384

< 60 beats per minute

Answer 385

>100 beats per minute

Answer 386

* Multiple atrial foci (supraventricular escape rhythm) * Impulses are random and chaotic * Atria quiver rather than contract * Impulses arrive at AV node at rapid irregular rate * Only some conducted to ventricles at irregular intervals when the AV node is not refractory * Ventricles depolarise and contract normally

Answer 387

* Absence of isolectric baseline (Wavy baseline) * No p waves * Irregular R-R intervals * QRS complex normal (narrow) * Irregularly irregular rhythm

Answer 388

• CO maintained in most cases as atrial contraction only accounts for 10% of filling in diastole • Blood remains stagnant in the appendage of the atria • Clots form in the atria ◦ Left atria- embolism in peripheral arteries eg. cerebral arteries ---> stroke ◦ Right atria- embolism in the pulmonary artery

Answer 389

Heart block = AV conduction block | Delay or failure of conduction of impulses from the atria to the ventricles via the AV node and Bundle of His

Answer 390

When an alternative pacemaker takes over the role of the SAN in initiating the heart beat.

Answer 391

- most commonly, acute MI | - degenerative changes

Answer 392

Complete heart block/third degree heart block

Answer 393

What happens? • Delay at AV node and Bundle of His Presentation on ECG? • P wave normal • PR interval prolonged > 5 small squares (0.2 seconds) • QRS normal

Answer 394

What happens? -Delay at AV node and one beat is not transmitted to allow the AVN to repolarise Presentation on ECG? - progressive lengthening of PR interval > 5 small squares - until one P is not conduced - cycle begins again

Answer 395

Ischaemic damage

Answer 396

What happens? -AV node fails to conduct heart beat with no warning Presentation on ECG? - PR interval normal (3-5 small squares) - sudden absent QRS complex

Answer 397

Mobitz type 2

Answer 398

What happens? • Atrial depolarisation is normal • Impulses are not conducted to ventricles at all • Ventricular pacemaker (slower to depolarise) takes over (ventricular escape rhythm) • Heart rate is often too slow to maintain blood pressure and perfusion Presentation on ECG? • P waves present • P-P intervals constant (about 93 bpm) • R-R intervals constant and much slower (about 37 bpm) • P-R intervals variable from beat to beat- P waves have no relationship with QRS complex • Wide QRS complexes • Very slow rate (30-40 beats per minute)

Answer 399

False Atrial fibrillation doesn't usually result in a significant loss of cardiac output as atrial contraction only accounts for the final 10% of filling of the ventricles.

Answer 400

* Ectopic focus in ventricle muscle which randomly produces a beat (this is not a ventricular escape rhythm which would occur after a pause and is regular- it is ONE random beat initiated in the ventricles in between normal beats which are conducted by the SAN which occurs as cells in the ventricle have been able to depolarise before conduction of depolarisation from the SAN- usually due to ischaemia) * Impulse not spread via fast His-purkinje system * Slower depolarisation of ventricle

Answer 401

Wide QRS complex (> 3 small boxes) in the middle of sinus rhythm QRS complex different in shape to usual QRS

Answer 402

An ectopic beat is one random beat initiated somewhere other than the SAN in between normal beats conducted by the SAN An escape rhythm occurs after a pause and is regular

Answer 403

Usually asymptomatic and normal

Answer 404

What happens? • Run of 3 or more ventricular ectopics • It is a broad complex tachycardia Presentation on ECG? • Run of 3 or more abnormally shaped, wide QRS complexes

Answer 405

* Persistent ventricular tachycardia is a dangerous rhythm that requires urgent treatment * High risk of ventricular fibrillation

Answer 406

Use defibrillator to depolarise all of the heart muscle cells and put them into a refractory period so that the SAN depolarises first and a sinus rhythm is established

Answer 407

What happens? • Abnormal, chaotic, fast ventricular depolarisation • Impulses from numerous ectopic sites in ventricular muscle • No co-ordinated contraction • Ventricles quiver • No cardiac output Presentation on ECG? - no recognisable QRS complexes - no heart beat/pulse

Answer 408

Cardiac arrest

Answer 409

Use defibrillator to depolarise all of the heart muscle cells and put them into a refractory period so that the SAN depolarises first and a sinus rhythm is established CPR

Answer 410

Atrial depolarisation is where impulses are conducted irregularly to ventricles. - ventricular depolarisation occurs - coordinated ventricular contraction occurs - cardiac output is present - pulse and heart rate is irregularly irregular Ventricular fibrillation is where ventricular depolarisation is chaotic - no coordinated ventricular contraction - no cardiac output - no pulse or heart beat - require CPR and immediate defibrillation to restore rhythm

Answer 411

Atrial fibrillation

Answer 412

-reduced perfusion of myocardium due to coronary atherosclerosis -major coronary arteries lie on epicardial surface so subendocardial muscle is furthest away and most vulnerable to ischaemia • Flow is during diastole- if diastole is short (rapid heart rate), there is less time for flow when arteries are narrowed (atherosclerosis) • Does not affect all parts of the heart • Changes may only be seen during exercise (STABLE ANGINA) . If severe reduction of lumen size, there are ischaemic changes at rest (UNSTABLE ANGINA)

Answer 413

• Changes seen in leads facing affected area • Need to look at P-QRST in all 12 leads • Ischaemia of subendocardial region---> ◦ leads facing affected area show ST segment depression ◦ T wave inversion - due to abnormal current during depolarisation

Answer 414

* Complete occlusion of lumen by thrombus * Muscle injury extends full thickness from endocardium to epicardium * If perfusion is not re-established, muscle necrosis will follow which can be detected using blood tests

Answer 415

• Changes shown on leads facing affected area • Need to look at P-QRST for all 12 leads • Ischameia of full thickness from endocardium to epicardium---> ◦ Leads in affected area show ST segment elevation - abnormal repolarisation

Answer 416

Pathological large Q wave > 1 small square wide > 2 small squares deep Depth more than a quarter of the height of the subsequent R wave

Answer 417

A previous myocardial infarction

Answer 418

Ischaemia of subendocardial region | NSTEMI

Answer 419

Ischaemia of full thickness from endocardium to epicardium | STEMI

Answer 420

plasma potassium >5.5mmol/L

Answer 421

>5.5 mmol/L plasma potassium More K+ in extracellular environment than usual Ek is less negative Resting membrane potential is less negative Cardiomyocyte action potential: -is narrower -slower upstroke - Na+ channels are inactivated Heart is less excitable as hyperkalaemia worsens Conduction problems

Answer 422

7mmol/L - high T wave 8 mmol/L - prolonged PR interval, depressed ST segment, high T wave 9mmol/L - P wave absent, AV block 10mmol/L - ventricular fibrillation

Answer 423

< 3.5 mmol/L

Answer 424

Less K+ in extracellular environment than usual Ek is more negative than usual Resting membrane potential is more negative Effect on action potentials in cardiomyocytes: -downstroke slower - allosteric effect of K+ channels so K+ enters more slowly -wider action potential -early after depolarisations - some cells repolarise more quickly than others Early after depolarisations can lead to ventricular fibrillation

Answer 425

``` 3.5mmol/L = low T wave 3mmol/L = low T wave, high U wave 2.5mmol/L = low T wave, high U wave, low ST segment ```

Answer 426

P-R interval Start of P wave to beginning of Q wave P-R segment End of P wave to beginning of Q wave

Answer 427

The overall direction of ventricular depolarisation is upward and to the left.(

Answer 428

1. Conduction block of the anterior branch of the left bundle 2. Inferior MI (left anterior descending artery affected) 3. Left ventricular hypertrophy

Answer 429

When the overall direction of ventricular depolarisation is downwards and to the right (>+90degrees)

Answer 430

1. Right ventricular hypertrophy | 2. RHS MI (right anterior descending artery affected)

Answer 431

Look at leads I, III, aVF If QRS is positive in lead I and negative in aVF, it is left axis deviation Lead I and Lead aVF are leaving each other (start with lead I)

Answer 432

Look at QRS in leads I, III, aVF QRS in lead I is negative and positive in lead III or aVF Lead I and aVF are reaching for each other (start with lead I)

Answer 433

QRS complexes positive in both

Answer 434

Left cardiac axis deviation

Answer 435

Right cardiac axis deviation

Answer 436

Respiratory problem. Probably... Pneumonia (Inflammation of the tissue in one or both of the lungs usually caused by bacterial infection)

Answer 437

Pulmonary embolism (DVT has broken off, entered the right atrium and lodged in the pulmonary artery causing a blockage in the pulmonary circulation)

Answer 438

Ischaemic damage to the heart | Lack of blood supply to the heart secondary to ischaemic heart disease

Answer 439

Pericarditis Inflammation of pericardial sac often secondary to a viral illness Pericardial rub may be heard on auscultation

Answer 440

Pericarditis

Answer 441

Aortic dissection Tear in the wall of the aorta so blood flows in between the layers of the blood vessel leading to aortic rupture and decreased blood flow to organs

Answer 442

Acid reflux from stomach into oesophagus

Answer 443

Rib fracture or costochondritis

Answer 444

Pleural/pericardial pain is somatic. -there are sensory impulses through somatic spinal nerves Pleura - intercostal and phrenic nerves Pericardial - phrenic nerves -It is well localised and sharp -it is aggravated by movement of the chest wall (inspiration and coughing) Ischaemic chest pain is visceral. - there are sensory impulses through autonomic nerves with pain in organs - it is poorly localised and dull - it is aggravated by exertion

Answer 445

- Begins with atherosclerosis - Build up of fat in the walls of the arteries over time. - Coronary arteries are small so does not take long for this fatty deposit to narrow the lumen. - Fibrous cap forms on top of this fatty deposit - This fibrous cap can rupture

Answer 446

``` Modifiable risk factors: • Smoking • Hypertension • Hypercholesterolaemia • Diabetes • Obesity • Sedentary lifestyle ``` Non-modifiable risk factors: • Advanced age • Family history • Male

Answer 447

Pathophysiology? Fixed narrowing of coronary artery due to atherosclerosis. What? Heart tissue ischaemia only when metabolic demands of cardiac muscle are greater than what can be delivered via coronary arteries.

Answer 448

Stable angina Fixed narrowing of coronary artery due to atherosclerosis. Heart tissue ischaemia only when metabolic demands of cardiac muscle are greater than what can be delivered by coronary arteries.

Answer 449

GTN spray - relieves pain

Answer 450

Pathophysiology Narrowing of coronary artery due to atherosclerosis. What? Heart tissue ischaemia at rest as usual metabolic demands cannot be delivered by coronary arteries.

Answer 451

Unstable angina Risk of deteriorating further ---> NSTEMI/STEMI Heart may fail and CO may be compromised

Answer 452

GTN spray does not relieve pain | Patient admitted to hospital for surgical intervention

Answer 453

Myocardial infarction

Answer 454

Acute myocardial ischaemia caused by atherosclerotic coronary artery disease. Atheromatous plaques rupture with thrombus formation causing an acute increased occlusion in an already partially occluded lumen leading to ischaemia. It is a spectrum of increasing occlusion from a common pathophysiological mechanism.

Answer 455

All except stable angina

Answer 456

ECG -look at ST segments, T waves, pathological Q waves Blood tests -troponin - indicates cardiac myocyte death (NSTEMI/STEMI)

Answer 457

STEMI has occurred minutes-hours ago

Answer 458

STEMI has occurred hours-1 day ago

Answer 459

Presentation on ECG? • ST segment depression • T wave flattening or inversion Check troponin • NSTEMI = positive because there is cardiomyocyte death • STEMI = negative because there is no cardiomyocyte death

Answer 460

Heart failure is a state ‘in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure’. In heart failure the heart can no longer produce the same amount of force (or cardiac output) for a given level of filling

Answer 461

It is often the final and most severe manifestation of nearly every form of cardiac disease • Ischaemic heart disease (coronary artery disease) is the primary cause • Hypertension • Non-ischaemic dilated cardiomyopathy ◦ Infectious- viral, bacterial, myobacterium ◦ Alcohol/drugs/poisoning ◦ Pregnancy ◦ Idiopathic • Valvular heart disease/congenital • Restrictive cardiomyopathy eg. Amyloidosis • Hypertrophic cardiomyopathy • Pericardial disease • High-output heart failure - heart cannot keep up with CO required • Arrhythmia

Answer 462

Heart beat is irregular, too fast or too slow.

Answer 463

1. Increase preload (venous capacity). Increase end diastolic volume to increase stroke volume. 2. Decrease afterload (aortic and peripheral impedance. Decrease end stroke volume to increase stroke volume. 3. Increase contractility. Decrease end stroke volume to increase stroke volume. 4. Increase heart rate

Answer 464

``` Increase preload (venous capacity). Increase EDV. Increase stroke volume. The force developed in the myocardium depends on the degree to which the fibres are stretched (or the heart is filled). Within a physiological range, the greater the venous pressure, the larger the ventricular volume during diastole, the more the fibres are stretched before stimulation and the greater the force of the next contraction. (Frank-Starling Law) ``` PROOF Muscle is passively stretched and then stimulated to contract while its ends are held at fixed positions (isometric contraction). The total tension, generated by the fibres is proportional to the length of the muscle at the time of stimulation as stretching causes there to be greater overlap between actin and myosin.

Answer 465

``` Decrease afterload (aortic and peripheral impedance) . Decrease ESV. Increase stroke volume. The pressure generated by the ventricle and the size of the chamber at the end of each contraction depends on the load against which the ventricle contracts but is independent to the stretch on the myocardial fibres before contraction. ``` PROOF Fibres are allowed to shorten during stimulation against a fixed load (isotonic contraction). The final length of the muscle at the end of contraction is determined by the magnitude of the load and is independent of the length of the muscle before stimulation.

Answer 466

Increase contractility. Decrease ESV. Increase stroke volume. Contractility reflects chemical and hormonal influences on cardiac contraction. The sympathetic nervous system affects contractility by the release of adrenaline/noradrenaline Increased contractility increases the cycling rate of actin-myosin cross bridge formation. PROOF When contractility is enhanced, the relationship between initial fibre length and force is shifted upwards so that a greater total tension develops with isometric contraction at any given preload. When contractility is enhanced, the fibre contracts to a greater extent and achieves a shorter final fibre length with isotonic contraction at any given afterload.

Answer 467

``` CO = 5 litres/min SV = 75ml LV end systolic volume = 75ml LV end diastolic volume = 150ml Ejection fraction = 50% + ```

Answer 468

``` Diastolic dysfunction (decreased EDV)- preserved ejection fraction 1. Impaired ventricular relaxation and filling ``` Systolic dysfunction (increased ESV)- reduced ejection fraction 2. Increased afterload 3. Impaired ventricular contractility Many patients demonstrate both systolic and diastolic abnormalities.

Answer 469

1. Advanced aortic stenosis 2. Uncontrolled severe hypertension This chronic pressure overload causes an increased resistance to flow.

Answer 470

1. Coronary artery disease (MI, transient myocardial ischaemia) 2. Chronic volume overload (mitral regurgitation, aortic regurgitation) 3. Dilated cardiomyopathies These cause destruction of myocytes, abnormal myocyte function or even fibrosis resulting in reduced ability of the myocytes to contract.

Answer 471

Impaired diastolic filling: 1. Left ventricular hypertrophy 2. Restrictive cardiomyopathy 3. Myocardial fibrosis 4. Transient myocardial ischaemia 5. Cardiac tamponade These either impair early diastolic relaxation which is energy dependent or increase the stiffness of the ventricular wall.

Answer 472

A decrease in contractility is seen as a shallower slope on the frank starling curve.

Answer 473

End diastolic volume increases. Stroke volume decreases. Normal venous return is added to the increased end systolic volume that has remained in the ventricle due to incomplete emptying. End diastolic volume increases above normal End systolic volume remains elevated. Reduced ejection fraction There is a compensatory rise in stroke volume to remain cardiac output End diastolic volume increases further and there is a high end diastolic pressure. During diastole, pressure is transmitted to the atrium through the open mitral valve/tricuspid valve to Pulmonary veins and capillaries from the left ventricle ---> pulmonary oedema Systemic veins and capillaries from right ventricle ---> systemic oedema To cope with the increased volume, hypertrophy of the ventricle occurs. Eccentric hypertrophy - synthesis of new sarcomeres in series with the old causing the myocytes to elongate. The radius of the ventricular wall enlarges proportional to the increase in wall thickness.

Answer 474

* High end diastolic volume ---> increased LV capacity (capacity>150ml) * Reduced end systolic volume and reduced ejection fraction---> Reduced cardiac output (compensatory mechanism to increase CO by increasing end diastolic volume is not sufficient)

Answer 475

Dilation of the left ventricle via thinning of the myocardial wall ◦ Fibrosis and necrosis of myocardium ◦ Activity of matrix proteinases

Answer 476

* Further loss of muscle---> loss of contractility * Conductive tissue may affected ---> uncoordinated or abnormal myocardial contraction ---> cardiac arrhythmias • Changes to the extracellular matrix Increase in collagen (I, III) from 5% to 25% Slippage of myocardial fibre orientation • Changes of cellular structure and function ◦ Myocytolysis and vacuolation of cells ◦ Myocyte hypertrophy ◦ Sarcoplasmic reticulum dysfunction ◦ Changes to calcium availability and receptor regulation * Mitral valve incompetence * Greater exposure to neuro-hormonal activation

Answer 477

In diastole, filling of the ventricle is dependent on higher than normal pressures. Pressure transmitted to the atrium through open mitral/tricuspid valves to Pulmonary veins and capillaries capillaries from left ventricle ---> pulmonary oedema Systemic veins and capillaries from right ventricle ---> systemic oedema To cope with the increased pressure, the myocardium hypertrophies. Concentric hypertrophy - synthesis of new sarcomeres in parallel with the old so the wall thickness increases without proportional chamber dilatation.

Answer 478

Elderly and female | Often history of hypertension/diabetes/obesity

Answer 479

Left ventricle as it is this ventricle that is under higher pressure so more likely to be less compliant due to left ventricle hypertrophy, myocardial fibrosis, transient myocardial ischaemia etc. Left ventricle filling becomes dependent on high left atrial pressure. Right ventricle systolic dysfunction can result from high left atrial and pulmonary artery pressure

Answer 480

• Dyspnea = breathlessness on exertion due to pulmonary venous congestion and decreased cardiac output • Dulled mental status reduced cerebral perfusion • Impaired urine output decreased renal perfusion • Orthopnea = laboured breathing while lying flat relieved by sitting upright (how many pillows do you use when you sleep?) redistribution of intramuscular blood from lower portions of the body to the lungs after lying down • Paroxysmal nocturnal dyspnoea = severe breathlessness that awakens the patient from sleep gradual resorption into the circulation of lower extremity interstitial oedema after lying down with expansion of intravascular volume and increased venous return to heart and lungs • Lethargy decreased cardiac output

Answer 481

• Tachycardia increased sympathetic nervous system activity • Basal pulmonary crackles popping open of small airways during inspiration that had been closed off by oedema fluid • S3 or S4 S3= in adults with systolic heart failure caused by abnormal filling of the dilated chamber S4= late diastolic sound from forceful atrial contraction into a stiffened ventricle common where there is increased LV compliance in diastolic dysfunction

Answer 482

``` S3= in adults with systolic heart failure caused by abnormal filling of the dilated chamber S4= late diastolic sound from forceful atrial contraction into a stiffened ventricle common where there is increased LV compliance in diastolic dysfunction ```

Answer 483

It is a thin-walled highly compliant chamber that accepts blood at low pressures and ejects against a low pulmonary vascular resistance.

Answer 484

Acute pulmonary embolism | It has a thin wall that's relatively less muscular.

Answer 485

Left sided heart failure increases pulmonary vascular pressure. This increases afterload for the right ventricle. Leads to right sided systolic heart failure.

Answer 486

Diseases of the lung parenchyma or pulmonary vasculature.

Answer 487

Relate to distension and fluid accumulation in areas drained by the systemic veins: - fatigue, dyspnoea, anorexia, nausea - increased jugular vein pressure - tender, smooth hepatic enlargement - dependent pitting oedema - ascites - pleural effusion

Answer 488

Long term control of blood pressure is via neurohormonal alterations: 1. Sympathetic nervous system 2. Renin-angiotensin-aldosterone system 3. Increased production of ADH 4. ANP However, these have the effect of making an already struggling heart work harder.

Answer 489

Increases TPR but decreases CO BP = TPR x CO

Answer 490

Chronic sympathetic release of noradrenaline causes: • down-regulation of cardiac β-adrenergic receptors and up-regulation of inhibitory G proteins, contributing to a decrease in the myocardium's sensitivity to circulating catecholamines and a reduced inotropic response • Induces cardiac hypertrophy myocyte apoptosis and necrosis • Stimulates RAAS • Reduction in heart rate variability---> increased risk of cardiac arrhythmias

Answer 491

Chronically elevated levels of AII and aldosterone have additional detrimental effects. They provoke the production of cytokines (small proteins that mediate cell–cell communication and immune responses), activate macrophages, and stimulate fibroblasts, resulting in fibrosis and adverse remodeling of the failing heart.

Answer 492

Secreted by vascular endothelial cells. Causes local vasoconstriction There are increased levels in patients with heart failure so is used as a prognostic sign as it correlates with indices of severity.

Answer 493

Elevated ANP/BNP demonstrates there is a high level of stretching of the heart. This is caused by increased stroke volume which occurs in systolic heart failure. Therefore, ANP/BNP can be used to diagnose heart failure along with other factors.

Answer 494

They increase in concentration as their production is stimulated by noradrenaline and RAAS They act as vasodilator on the afferent renal arterioles to attenuate effects of noradrenaline and RAAS Taking NSAIDS blocks synthesis of these and reduces vasodilation.

Answer 495

It is a potent vasodilator produced by endothelial cells via NO synthase. In heart failure, NO synthase may be blunted There is a loss of vasodilation balance

Answer 496

Promotes natriuresis Vasodilation Stimulates production of prostaglandins

Answer 497

Increased in heart failure | It depresses myocardial function and has a role in cachexia

Answer 498

* Increased sympathetic output * RAAS * Reduced NO * Increased endothelin

Answer 499

- reduction of skeletal muscle mass - renal failure - anaemia

Answer 500

Afterload increases and this decreases stroke volume decreasing cardiac output further.

Answer 501

It increases the metabolic demand of the heart

Answer 502

Net filtration pressure = hydrostatic pressure - osmotic pressure

Answer 503

Peripheral oedema occurs due to right-sided heart failure. Failure of the right side of the heart to pump effectively raises venous pressure and therefore capillary pressure. An increased capillary hydrostatic pressure favours the movement of water out of the capillaries.

Answer 504

Pulmonary oedema occurs due to left sided heart failure Failure of the left side of the heart to pump effectively raises left atrial pressure and thus the pressure of vessels in the pulmonary system. Since these vessels have a low resistance this also causes an increase in pulmonary artery pressure. Presentation: -breathless

Answer 505

Diuretics • Promote elimination of Na+ and water through the kidney • Reduce intravascular volume • Reduce venous return to heart • Reduced end-diastolic volume without a significant decrease in SV. Preload is decreased • Diastolic pressure of left ventricle falls out of the range that causes pulmonary congestion Limitations Only used where there is peripheral oedema or pulmonary congestion due to the risk of decreasing stroke volume too much that cardiac output will be compromised (especially in a patient operating on the steep portion of the frank-starling curve- best used when on flat portion where it is moved towards the steep portion)

Answer 506

--->Venous vasodilators - nitrates • Increase venous capacitance • Decrease venous return to the heart • Decrease end-diastolic volume and decrease preload • Diastolic pressure of left ventricle falls out of the range that causes pulmonary congestion Limitations Only used where there is peripheral oedema or pulmonary congestion due to the risk of decreasing stroke volume too much that cardiac output will be compromised (especially in a patient operating on the steep portion of the frank-starling curve- best used when on flat portion where it is moved towards the steep portion)

Answer 507

Diuretics Vasodilators Inotropic drugs Beta blockers Aldosterone antagonist therapy

Answer 508

- ectopic pacemaker activity - afterdepolarisations - atrial flutter/atrial fibrillation - re-entry loop

Answer 509

- sinus bradycardia (sick sinus syndrome, extrinsic factors such as drugs) - conduction block (problems at AV node or bundle of His, extrinsic factors such as drugs)

Answer 510

Malfunction of the sinus node Normally, the sinus node produces a regular, steady pattern of signals. With sick sinus syndrome, the pattern is irregular - they may have a heart rhythm that is too low or too fast Typically occurs in elderly people

Answer 511

Tachycardia which originates from the Bundle of His, purkinje fibres or ventricular myocytes (ectopic pacemaker activity, afterdepolarisations)

Answer 512

Tachycardia which arises from the atria or AV node (atrial fibrillation/atrial flutter, re-entry loop)

Answer 513

Can lead to ventricular fibrillation Cardiac output cannot be maintained in ventricular fibrillation and this is a life-threatening situation which must be reversed.

Answer 514

Ectopic pacemaker activity is activated in damaged area of ischaemic myocardium as it becomes constantly depolarised and spontaneously active. This dominates over the SA node.

Answer 515

After depolarisations (triggered activity) following an action potential

Answer 516

There should be approximately a 700ms pause between one action potential and another in a cardiomyocyte. In delayed, after-depolarisations there are delayed after-depolarisations before this 700ms pause. This is likely to happen when intracellular Ca2+ is high. Eg. Drugs such as cardiac glycosides

Answer 517

Early after-depolarisations occur during the plateau phase of the ventricular action potential They are more likely to happen if the action potential is prolonged (longer QT interval) eg. Hypokalaemia, certain drugs

Answer 518

Incomplete conduction damage (unidirectional block) Excitation can take a long route to spread the wrong way through the damaged area setting up a circus of excitation

Answer 519

Conditions which put extra stretch or pressure on the atria eg. Mitral stenosis

Answer 520

Atrial flutter - regularly irregular rhythm (sawtooth pattern) Atrial fibrillation - irregularly irregular rhythm (wavy baseline)

Answer 521

Atrial fibrillation

Answer 522

Fast and slow pathways in the AV node create a re-entry loop.

Answer 523

An accessory pathway between the atria and ventricles creates a fixed re-entry loop

Answer 524

1. Na+ channel blockers 2. Beta-adrenoreceptor antagonists 3. K+ channel blockers 4. Ca2+ channel blockers

Answer 525

Class 1 - blocks voltage gated Na+ channels Damaged area of myocardium has sustained depolarisation and more Na+ channels open. Lidocaine binds to Na+ channels in open or inactive state during the phases of the refractory period of the action potential when Na+ channels should be inactive or closed. It is use-dependent (the degree of block is proportional to the rate of nerve stimulation) so preferentially blocks damaged depolarised tissue It dissociates rapidly so has little effect in normal cardiac tissue. It blocks depolarisation but dissociates in time for the next action potential.

Answer 526

Sometimes used following MI because damaged areas of myocardium may be depolarised and fire automatically (risk of ectopics leading to VF) Because... More Na+ channels are open in depolarised damaged tissue. Lidocaine blocks these Na+ channels that are in open or inactive form and is use-dependent. BUT not used prophylactically following MI, people showing ventricular tachycardia generally use other drugs.

Answer 527

The degree of block is proportional to the rate of nerve stimulation.

Answer 528

Beta adrenoreceptor antagonists

Answer 529

Block sympathetic action by acting on beta adrenoreceptors on the heart - decrease slope of pacemaker potential in SA node - decreases heart rate - slow conduction in AV node - prevents supraventricular tachycardias and slows ventricular rate in patients with atrial fibrillation - reduces inotropy - reduces oxygen demand and hence reduces myocardial ischaemia which is beneficial for patients following an MI

Answer 530

A myocardial infarction can cause increased sympathetic input to the heart to maintain cardiac output Beta blockers decrease this sympathetic input to the heart, reducing heart rate to prevent ventricular arrhythmias from arising due to this increased sympathetic activity. Beta blockers reduce heart rate and the force of contraction which reduces the workload and hence the oxygen demand of the heart. This reduces the chance of further myocardial ischaemia.

Answer 531

Prolongs action potential by blocking K+ channels so prevents repolarisation. This lengthens the absolute refractory period (time during which Na+ channels are in inactive state) In theory, it was thought this should prevent another action potential from occurring too soon. However, it causes early after depolarisations which can lead to arrthymias.

Answer 532

K+ channel blockers are not usually used because they prolong the action potential and increase the risk of early after depolarisations leading to arrhythmia. Although amiodarone is a type III anti-arrhythmic, it has other actions in addition to blocking K+ channels. Therefore, it is effective in treating supraventricular tachycardia associated with Wolff-Parkinson-White syndrome It is also effective at suppressing arrhythmias post-MI.

Answer 533

Opening of voltage gated Ca2+ channels Ca2+ influx

Answer 534

Class IV - blocks L-type Ca2+ channels Decreases slope of action potential at SA node Decreases AV nodal conduction Decreases force of contraction (negative inotropy) (Blocks L-type Ca2+ channels in plateau phase in ventricular myocytes and this prevents high intracellular Ca2+ triggering further Ca2+ release from SR) Some coronary and peripheral vasodilation

Answer 535

L-type Ca2+ channel blocker Acts on vascular smooth muscle so causes vasodilation (Does not act on L-type Ca2+ channels in the heart because these are a different sub-type)

Answer 536

Doesn't fit into any of the classes Administered intravenously Useful for terminating supraventricular tachycardia

Answer 537

Acts on A1 receptors (purinergic receptors) at AV node (GPCR) Has a very short half-life (10 seconds) Beta-gamma subunit binds to potassium channels and increases K+ conductance This hyperpolarises cells of the conducting tissue to prevent re-entry loops and hence atrial fibrillation/flutter.

Answer 538

-positive inotropes to increase cardiac output (not routinely used) Cardiac glycosides - improves symptoms but not long-term outcome B-adrenergic agonists -drugs which reduce workload of the heart Reduce afterload and preload

Answer 539

Cardiac glycoside

Answer 540

Na+/K+ exchanger blocked Intracellular Na+ concentration increases Rise in extracellular Na+ leads to decrease in activity of NCX Intracellular Ca2+ concentration increases More Ca2+ stored in SR This results in an increased force of contraction Increased vagal activity which: - slows heart rate initiated at SA node - slows AV conduction

Answer 541

Heart failure when there is an arrhythmia such as atrial fibrillation

Answer 542

Beta adrenoreceptor agonists eg. Dobutamine Increases myocardial contractility

Answer 543

Beta 1 adrenoreceptor agonists eg. Dobutamine Increase myocardial contractility

Answer 544

Diuretics eg. ACE inhibitors (reduces preload and afterload) Beta adrenoreceptor antagonists (reduce heart rate and contractility)

Answer 545

ACE inhibitor inhibits ACE. Functions of ACE: • Breaks down bradykinin which has vasodilatory effects (causes dry cough) • Converts angiotensin I to angiotensin II so blocks the effects of angiotensin II Angiotensin II antagonist only blocks the effects of angiotensin II which includes: • Vasoconstriction • Aldosterone release

Answer 546

-reduce afterload Decrease vasomotor tone --> decrease blood pressure -reduce preload Reduce fluid retention ---> reduce blood volume Reduces workload of the heart

Answer 547

-reduce workload of the heart Beta adrenoreceptor blocker Ca2+ antagonists Organic nitrates -Improve blood supply to the heart Organic nitrates Ca2+ channel antagonists

Answer 548

Diastole - backflow of blood as aortic valve closes | During systole there is pressure of the left myocardium that prevents filling

Answer 549

Glyceryl trinitrate (GTN) Isoorbide dinitrate

Answer 550

Reaction of organic nitrates with thiols in vascular smooth muscle causes NO2- to be released NO2- is reduced to NO NO a powerful vasodilator: NO activates guanylate cyclase. This increases cGMP which lowers intracellular Ca2+ causing relaxation of vascular smooth muscle MAINLY Venodilation - primarily works by dilating the veins decreasing preload Dilation of collateral coronary arteries - improving blood supply to the heart

Answer 551

False (arterioles are fully dilated in the ischaemic region)

Answer 552

Atrial fibrillation Acute myocardial infarction Mechanical prosthetic valves

Answer 553

Anticoagulants: Heparin - activates antithrombin III which inhibits thrombin. Used acutely for short term action) Warfarin - antagonises action of vitamin K which is a co-factor for many clotting factors (2, 7 9 10) Anti-platelet drugs: Aspirin - inhibits cyclo-oxygenase from forming prostaglandins and thromboxane. Thromboxane causes platelet aggregation.

Answer 554

``` Heparin (IV) Fractionated heparin (subcutaneous injection) ```

Answer 555

Aspirin - clots that form in the arterial system tend to be platelet rich

Answer 556

ACE inhibitors | Reduce afterload and preload

Answer 557

Lower blood volume Lower cardiac output Lower peripheral resistance

Answer 558

``` ACE inhibitors Ca2+ channel blockers selective for vascular smooth muscle Diuretics Beta blockers Alpha 1 adrenoreceptor antagonist ```

Answer 559

Velocity and direction of flow

Answer 560

No, flow is volume per unit time Doppler can be used to measure velocity. This can be used to infer flow.

Answer 561

In muscles

Answer 562

Within subcutaneous fat

Answer 563

Connect superficial veins to deep muscles

Answer 564

Superficial to deep

Answer 565

Deep fascia is tightly attached to muscles in one compartment. When the muscles contract, pressure increases in a compartment so blood is forced to flow in through the veins. (Calf pump)

Answer 566

External iliac vein Femoral vein Popliteal vein

Answer 567

Long saphenous vein | Short saphenous vein

Answer 568

Anterior to the medial malleolus

Answer 569

Varicose veins are tortuous, twisted or lengthened veins

Answer 570

The vein wall is inherently weak in varicose veins, which leads to dilatation and separation of valve cusps so that they become incompetent.

Answer 571

Heaviness Tension Aching Itching

Answer 572

Result from vein itself: - haemorrhage - thrombophlebitis Result from venous hypertension: - oedema - skin pigmentation - varicose eczema - lipodermatosclerosis - venous ulceration

Answer 573

Venous thrombosis - produces inflammatory response including pain

Answer 574

Venous hypertension

Answer 575

Calf muscle pump failure

Answer 576

‘Failure’ of calf muscle contraction - immobility, obesity, reduced hip, knee and/or ankle movement Deep vein incompetence Volume overload - superficial vein incompetence

Answer 577

Abnormality of the lining of vessel wall (eg. Atherosclerosis)

Answer 578

Abnormality of flow - stasis

Answer 579

In reality, it is usually stasis plus another factor eg. Surgery Oral contraceptive pill Dehydration Cancer

Answer 580

FALSE Arterial thrombosis in response to bleeding involves platelets, extrinsic and then intrinsic pathways. Arterial thrombi are platelet rich Venous thrombosis does not involve platelets in a major way, initially the intrinsic pathway is involved and then the extrinsic. Venous thrombi are fibrin rich

Answer 581

Initially vasoconstriction Platelets Extrinsic and then intrinsic pathways (Arterial thrombi are platelet rich)

Answer 582

Venoconstriction Particular the intrinsic pathway and then both pathways (Venous thrombi are fibrin rich)

Answer 583

Sympathetic drive increases Heart rate increases Diastole decreases Filling of coronary arteries is during diastole, so filling of coronary arteries decreases.

Answer 584

- failure of calf muscle contraction - immobility, obesity, reduced hip, knee and/or ankle movement - deep vein incompetence - volume overload - superficial vein incompetence

Answer 585

Incompetence of valve in saphenous vein resulting in backflow in the saphenous vein. Blood flows through perforating veins from this superficial vein into deep veins every time blood is ejected by the calf pump. This results in calf pump failure due to volume overload.

Answer 586

Usually caused by decreased end diastolic pressure Eg. Bradycardia

Answer 587

Carotid pulse

Answer 588

Produces inflammatory response: - calor - skin warmth, pyrexia - dolor - pain, calf tenderness - functio laesa - cannot walk - rubor - blue-red discolouration - tumor - oedema Others: - muscle induration - increase in the fibrous elements in muscle resulting in reduced elasticity - distended, warm superficial veins

Answer 589

Capillary hydrostatic pressure falls Pressure drop across the system is greater as you increase the resistance.

Answer 590

Arterial pressure increases Venous pressure decreases

Answer 591

In hypertension, arterioles are constricted. This increases arterial pressure but decreases capillary hydrostatic pressure and decreases venous pressure, if pumping remains the same. In heart failure, there is decreased venous return to the heart. This increases venous pressure and increases hydrostatic pressure in the capillaries. Increased capillary hydrostatic pressure results in more fluid leaving the capillaries than returns. This results in oedema due to a build up of tissue fluid.

Answer 592

- left ventricle cannot empty so well - left atrial pressure is higher - higher pressure in pulmonary veins and pulmonary capillaries - higher pulmonary capillary pressure causes pulmonary oedema

Answer 593

- increased pressure in pulmonary veins (left sided heart failure) - pulmonary hypertension

Answer 594

Elastic recoil

Answer 595

Hypoxic pulmonary vasoconstriction ensures optimal ventilation/perfusion ratio. (Alveolar hypoxia results in vasoconstriction of pulmonary vessels - opposite to what normally happens in systemic circulation) - in chronic lung disease, there are poorly ventilated alveoli. These are less perfused by vascular resistance to optimise gas exchange. - this increases pressure in the pulmonary artery. Increases afterload - harder for right ventricle to pump ---> right sided heart failure

Answer 596

Chronic hypoxia in the lungs causes smooth muscle cells in arterioles to contract. This results in vasoconstriction. (Hypoxia pulmonary vasoconstriction ensures optimal ventilation/perfusion ratio) In the systemic circulation, hypoxia triggers vasodilation to increase blood flow and hence oxygen delivery to the hypoxic region.

Answer 597

- poor pumping of right ventricle - right ventricular end systolic volume is increased (systolic dysfunction) - more difficult to fill right ventricle - increased right atrial and systemic venous pressure - increased capillary hydrostatic pressure in systemic circulation ---> systemic oedema

Answer 598

-reduce peripheral resistance by preventing production of Ang II HF - reduced preload BP - reduced blood pressure - reduce blood volume through preventing production of AngII - HF - heart has to work less hard

Answer 599

Adrenaline/noradrenaline binds to beta 2 adrenoreceptors and changes its conformation. The change in conformation on the activated adrenoreceptor increases its affinity for the G-alpha q protein. The GPCR-G protein interaction causes the GDP on the alpha sub-unit of the G protein to change to GTP. Once GTP binds to the alpha sub-unit, the alpha sub-unit loses affinity for the beta-gamma sub-unit so they seperate The alpha-subunit binds to phospholipase C and stimulates it. Phospholipase C converts PiP2 to IP3 and DAG. IP3 binds to IP3 receptors on the SER/SR inducing the release of Ca2+ in the cytosol from the SER/SR. Ca2+ binds to calmodulin. The Ca2+-calmodulin complex stimulates myosin light chain kinase. Myosin light chain kinase phosphorylates myosin light chain so that actin binding sites are exposed. DAG stimulates protein kinase C. Protein kinase C inhibits myosin light chain phosphatase, preventing the phosphate from being removed from myosin light chain, maintaining contraction and hence vasoconstriction.

Answer 600

- immobility prior to surgery - no calf muscle pump during surgery - immobility after surgery - surgery is trauma, the body's response to trauma includes a pro-thrombotic state

Answer 601

Peripheral artery disease is a disease which results in stenosed peripheral arteries. It can be acute or chronic.

Answer 602

Collateral circulation develops in response to a stenosis.

Answer 603

Across joints such as elbow and knee.

Answer 604

Acute limb ischaemia Fixed mottling Gangrene

Answer 605

Acute peripheral artery disease - the limb goes from a normal blood supply to a greatly impaired blood supply over a period of minutes. There is no chance for collateral vessel development (which takes weeks/months). Chronic peripheral artery disease - the limb goes from a normally blood supply to an impaired blood supply over months. There is a chance for collateral vessel development.

Answer 606

Embolism (from heart or abdominal aortic aneurysm)

Answer 607

Dead tissue releases intracellular potassium Hyperkalaemia - makes Ek less negative, inactivates Na+ channels, slower upstroke, narrower action potential Leads to asystole

Answer 608

6 P's ``` Pain Paralysis Paraesthesia Pallor Perishing cold Pulseless ``` (These are the 6 P's of compartment syndrome)

Answer 609

Spotting with patches of colour that won't blanch It is a sign of irreversible ischaemia (dry gangrene is a late sign of irreversible ischaemia >2 weeks)

Answer 610

-intermittent claudication (equivalent to stable angina) - critical ischaemia - --> rest pain (equivalent to unstable angina) - --> ulceration/gangrene (equivalent to myocardial infarction)

Answer 611

Pain in the muscles of the lower limb elicited by walking and exercise Pain relieved rapidly by stopping exercise for a few minutes even whilst standing up

Answer 612

Calf muscles - gastrocnemius - soleus - plantaris

Answer 613

Mid-inguinal point Mid-way between the pubis symphysis and ASIS (REMEMBER THIS IS DIFFERENT TO THE MIDPOINT OF THE INGUINAL LIGAMENT WHERE THE FEMORAL NERVE IS)

Answer 614

Deep in the popliteal fossa and is difficult to feel.

Answer 615

Dorsal pedis artery - lateral to the tendon of extensor hallucis longus Posterior tibial artery - just behind the medial malleolus

Answer 616

Anterior tibial artery

Answer 617

Femoral pulse - mid-inguinal point Popliteal pulse - popliteal fossa Dorsalis pedis pulse - lateral to tendon of EHL Posterior tibial pulse - behind medial malleolus

Answer 618

Aortoilliac occlusion

Answer 619

Common iliac occlusion

Answer 620

Right thigh and calf claudication Absent right femoral pulse, popliteal pulse, dorsalis pedis pulse, posterior tibial pulse

Answer 621

Superficial femoral artery occlusion

Answer 622

Superficial femoral artery occlusion

Answer 623

- gravity is not forcing blood to feet as it would if patient was standing - metabolic activity of feet is high to keep feet warm - cardiac output is reduced when sleeping

Answer 624

Ischaemia = hypoxia due to reduced blood supply The ischaemia is so severe that at rest the foot, skin, muscles, bones are ischaemic at rest. This means that there is not enough oxygen to provide for the cells basic metabolic requirements.

Answer 625

Ulceration/gangrene

Answer 626

Blood supply to the anterior shin is poor

Answer 627

Acute ischaemia

Answer 628

Substance P is a neuropeptide that is released locally when there is ischaemia. It increases the sensitivity of pain afferents in muscle.

Answer 629

Critical ischaemia - rest pain

Answer 630

Low pH Substance P (neuropeptide)

Answer 631

Degree of ischaemia depends on whether you have enough blood supply to meet metabolic demands.

Answer 632

Ischaemia - reversible damage due to lack of oxygen Infarction - irreversible damage due to lack of oxygen with cell death (necrosis)

Answer 633

Stable angina Unstable angina Myocardial infarction

Answer 634

-increased heart rate Decreasing time for diastole Reduced filling of coronary arteries -increases metabolic rate Increased metabolic demand Blood supply may not be sufficient to meet this metabolic demand

Answer 635

Ischaemia - reversible damage due to lack of oxygen Infarction - irreversible damage due to lack of oxygen with cell death (necrosis)

Answer 636

Visceral and somatic afferents synapse in similar place in spinal cord. The brain cannot tell if the pain is coming from the skin or heart.

Answer 637

- diaphoresis (sweating) - nausea - systemic vasoconstriction (Pallor) - tachypnoea

Answer 638

- reduced cardiac output due to MI. Decreased arterial pressure - pain and anxiety from MI

Answer 639

- sinus tachycardia - increased awareness of normal heartbeat - arrhythmias

Answer 640

Dyspnoea - difficulty breathing Orthopnoea - shortness of breath when lying flat Paroxysmal nocturnal dyspnoea - shortness of breath that wakes the patient up at night

Answer 641

When lying flat, increased venous return to right side of the heart. More blood is in the lungs so there is increased hydrostatic pressure and more oedema is formed.

Answer 642

Drop in systolic pressure over 20mmHg when standing

Answer 643

``` Venous pooling Impaired vasomotor tone eg. Diabetic autonomic neuropathy Reduced muscle tone Hypovolaemia Drugs antihypertensives Addison's disease ```

Answer 644

Decreased aldosterone ---> aldosterone increases transcription and activity of Na+/K+ ATPase. This increases Na+ retention and hence water retention Decreased cortisol ---> increases blood pressure

Answer 645

-elevation pallor In an ischaemic leg, elevation to less than 20 degrees may cause pallor -rubor of dependency Hang leg off edge of bed Leg reverts to pink colour more slowly than normal Goes through normal pinkness to reddish colour Dilation of arterioles in an attempt to get rid of metabolic waste 'reactive hyperaemia'

Answer 646

Foot becomes parodoxically pink - becomes hyperaemic due to lactate causing vasodilation Can take six weeks of ischaemia to develop

Answer 647

Moveable mottling Press and the spots blanch because there is still some blood supply Fixed mottling Press and spots will not blanch because there is nowhere for the blood to move - capillaries are thrombosed - no blood supply

Answer 648

2nd degree heart block - intermittent failure of conduction between atria and ventricles

Answer 649

Variable filling time of the ventricles

Answer 650

There is a longer time in diastole. Ventricles are able to fill to a larger volume in diastole and pump a larger volume of blood than usual in systole End systolic pressure has increased because the ventricles are pumping a larger volume.

Answer 651

Poor cardiac output eg. Hypovolaemia

Answer 652

Low peripheral resistance - causes lower diastolic blood pressure Bradycardia

Answer 653

Increased pulse pressure as blood falls away more profoundly.

Answer 654

In inspiration: Chest wall moves out Diaphragm flattened Decreased (negative) pressure so air rushes into lungs and more blood drawn into right side of heart Pulmonary valve closes after aortic valve – giving a split second heart sound

Answer 655

Chest wall moves out Diaphragm flattened Decreased pressure so air rushes into lungs and more blood drawn into right side of heart Blood flowing through tricuspid and pulmonary valves increases, therefore can hear right sided murmurs better

Answer 656

Chest wall moves in Diaphragm moves up Increases pressure so air rushes out of lungs and more blood pushed out of heart Blood flowing through mitral and aortic valves increases, therefore can hear left sided murmurs better

Cardiovascular System Flashcards

(707 cards)