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Cardiology > Mechanisms > Flashcards

Mechanisms Flashcards

1
Q

In an MI, what artery is most likely occluded?

A

Left anterior descending artery

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2
Q

Give 2 equations that can be used to calculate mean arterial pressure MAP

A

1.MAP=DP+(1/3PP)
(PP=SP-DP)

2.MAP=COxTPR

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3
Q

What 2 factors effect flow (volume passing in a certain time)?

A

Resistance (higher R, slower flow)

Pressure (higher P, faster flow)

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4
Q

Regarding haemodynamics, what does velocity mean?

What factor effects this?

A

Distance travelled in a given time

Area (larger the SA:V, higher the velocity)

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5
Q

Describe when in the cardiac cycle each valve in the heart opens
and closes.

Include when you will hear S1-lub and S2-dub sounds

A

DIASTOLE:
1) Atrial contraction - SLV: closed AVV: open

SYSTOLE: (ventricles contracting)

1) Isovolumetric contraction - SLV: closed. AVV: closed S1 lub sound
2) Rapid ejection - SLV: open AVV: closed
3) Reduced ejection - SLV: open AVV: closed

DIASTOLE: (ventricles filling)

1) Isovolumetric relaxation - SLV: closed S2 dub sound. AVV: closed
2) Rapid filling - SLV: closed AVV: open
3) Reduced filling - SLV: closed AVV: open

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6
Q

What causes mitral valve stenosis?

A

Rheumatic fever causes commissural fusion

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7
Q

Name 3 factors that lead to RV hypertrophy in mitral valve stenosis, as a result of LA dilation

A

Dyspnoea
Pulmonary oedema
Pulmonary hypertension

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8
Q

What causes dysphagia in mitral valve stenosis?

A

Oesophagus is compressed as a result of LA dilation

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9
Q

Why do patients with mitral valve stenosis have a higher chance of getting a stroke?

A

LA dilation leads to atrial fibrillation, stasis of blood in atria leads to thrombus formation, this can emboli and travel to the brain

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10
Q

What sound would be heard in mitral valve stenosis?

When would this sound be heard:
A) Diastole or systole
B) closure or opening of atrioventricular valves?

A

Diastolic rumble/mid diastolic murmur

Be heard in diastole, when the AVV open

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11
Q

Describe the pathophysiology of mitral valve regurgitation

A

Chordae tendineae and papillary muscle weakness leads to the prolapse of the mitral valve during systole (when they are meant to be closed)

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12
Q

What chamber undergoes hypertrophy in mitral valve regurgitation?

And how?

A

LV as during systole more blood flows back into the LA so the preload, for the next cycle is greater.

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13
Q

What sound would be heard in mitral valve regurgitation?

Specifically, when would the sound be beard?

A

Holosystolic/pan-systolic murmur heard in systole all the way from S1 (AVV closure) to S2 (SLV closure)

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14
Q

Name 3 causes of aortic valve stenosis

A

Calcification

Fibrosis

Chronic rheumatic fever - commissural fusion

Congenital - bicuspid instead of tricuspid valve formation

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15
Q

What abnormal valve function can lead to left sided heart failure?

How?

A

Aortic valve stenosis as there is more blood in the LV, leading to increased LV kpa so get LV hypertrophy but as time goes on tissue undergoes necrosis and cannot pump as much blood to the body (so get syncope) through the aorta.

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16
Q

Why do you get angina in aortic valve stenosis?

A

Not enough O2 blood entering the coronary arteries (via the aorta) to supply the heart muscle

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17
Q

What sound do you hear in aortic valve stenosis?

When is it heard?

A

Crescendo-decrescendo/ejection systolic murmur

Heard shortly after the 1st heart sound in systole

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18
Q

What type of anaemia does aortic valve stenosis cause?

A

Microangiopathic haemolytic anaemia

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19
Q

In aortic valve regurgitation, when does blood flow back into the LV (systole/diastole)?

What heart murmur is heard

Name 4 clinical signs seen in this condition

A

Diastole

Early (decrescendo) diastolic murmur

  1. Increase in systolic kpa (>120 mmHg)
  2. Decrease in diastolic kpa (<80 mmHg)
  3. Quinke’s sign
  4. Head bobbing (with each beat of the heart)
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20
Q

What is Quinke’s sign?

A

Nail bed goes pink then pale with each beat of the heart

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21
Q

What does the ductus arteriosus connect?

What does it by pass?

A

Pulmonary trunk to aorta

Lungs

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22
Q

What does the foramen ovale connect?

What does it by pass?

A

RA to LA

By pass right ventricle and lungs

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23
Q

What does the ductus venosus connect?

What does it by pass?

A

Placenta to IVC

By pass liver

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24
Q

How do the shunts close?

A

Respiration begins:

  • increasing the kpa in the LA so foramen ovale closes
  • DA contracts

Removal of placenta:
- DV close

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25
Q

What is the pathophysiology of an acyanotic heart defect?

Give 5 examples

A

Blood flowing from the left side of the heart to the right:

  • Ventricular septal defect
  • Atrial septal defect
  • Patent ductus arteriosus

Not enough blood leaving the heart

  • Aortic valve stenosis
  • Coarctation of the aorta
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26
Q

The formation of the 4th and 6th arch arteries will eventually become the great vessels.

List all the arteries that supply pharyngeal arches 1-6.

A

PA 1 + PA 2: Pharyngeal arteries (eventually regress)

PA 3: ICA

PA 4: L - Arch of aorta R - Brachiocephalic artery

PA 6: Pulmonary arch arteries

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27
Q

Name a congenital malformation of the great heart vessels that does not lead to cyanosis.

Discuss why

A

Patent ductus arteriosus (failure of the DA contracting post birth) as blood flows from aorta to pulmonary trunk

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28
Q

In PDA, a continuous murmur will be heard, throughout systole and diastole. What is this murmur called?

A

Machinery murmur

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29
Q

What happens to the LV in PDA?

Discuss.

A

Get LV hypertrophy due to the increased preload into the LV as a result of a greater volume of blood entering the pulmonary trunk and then back to the left ventricle.

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30
Q

What 4 factors make up Tetralogy of Fallot?

A

Pulmonary stenosis
Right ventricular hypertrophy
Overriding aorta
Ventricular septal defect

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31
Q

What is an overriding aorta

A

Instead of the aorta being connected to the left ventricle, it is connected to the ventricular septal defect

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32
Q

Fully discuss 2 congenital malformations of the heart vessels that lead to cyanosis

A

Tetralogy of fallot:
Pulmonary stenosis worsens RV hypertrophy thus the shunting of the ventricular septal defect is right to left and the overriding aorta leads to the distribution of mixed blood.

Transposition of the great vessels:
Aorta is connected to the right ventricle so deoxygenated blood redistributed.

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33
Q

Formation of the inter-atrial septum

A
  1. Ostium primum is an inital opening in the septum primum
  2. Septum primum fuses with the endocardial cushions (from neural crest cells) and an ostium secundum forms
  3. Septum secundum forms and foramen ovale forms
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34
Q

Formation of the inter-ventricular septum

A
  1. Muscular wall of the the ventricular septum grows up towards the endocardial cushions
  2. Small gap is left
  3. Endocardial cushions produces connective tissue to close the small gap - forms membranous portion of the ventricular septum
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35
Q

What are the resting potentials of

A) SkM
B) Cardiac muscle
C) Nerve cells
D) Smooth muscle

A

A) -90 mP
B) -80 mP
C) -70 mP
D) -50 mP

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36
Q

How is the resting potential, -80 mP, of a cardiac myocyte generated?

A

Passive efflux of K+

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37
Q

Describe the processes of excitation - contraction coupling in
ventricular myocardial cells.

A

Depolarisation of the sarcolemma leads to the opening of the L-type VGCC in the T tubule. Leading to an influx of Ca2+ into the cytoplasm. Ca2+ binds onto the RYANODINE receptor on the sarcoplasmic reticulum (contributes to 75% of Ca2+ causing contraction), this leads to the opening of the CICR (calcium induced calcium release receptor) on the sarcoplasmic reticulum. Ca2+ in the cytoplasm now acts on the actin-myosin complex.

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38
Q

What is hypokalaemia’s effect on the heart?

A

Get EADs - early after depolarisations, which lead to oscillations in the cardiac membrane, leading to ventricular fibrillations (cardiac arrest)

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39
Q

Describe the actin-myosin theory in cardiac myocytes

A

Ca2+ binds to Troponin I and T, leading to conformational change of tropomyosin, the myosin binding site is now revealed on the actin filament. Myosin head, along with its ATPase, can now bind on its binding site (ADP + Pi formed, leading to power stroke)

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40
Q

After cardiac myocyte contraction, how are cytoplasmic Ca2+ levels reduced?

A
  1. Sarcolemma Ca2+ ATPase
  2. SERCA (SR/SR Ca2+ ATPase)
  3. Sodium-calcium exchanger (NCX, 3NA+-Ca2+-exchanger)
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41
Q

Describe two ways in which the myosin light chain:

A) cannot be phosphorylated
B) is dephosphorylated

thus leading to the vasodilation of vascular smooth muscle (so arteries and veins)

A

A) B2 adrenoceptor on VSM has (physiological) adrenaline bound to it (released from sympathetic postganglionic cells) leading to the activation adenyl cyclase thus more ATP is converted to cAMP. More cAMP activates PKA. PKA phosphorylates MLCK thus inhibiting Myosin Light Chain Kinase from phosphorylating the myosin light chain

B) Myosin light chain phosphatase dephosphorylates the myosin light chain (this process is always working)

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42
Q

Describe the excitation-contraction process of smooth muscles

focus on the main pathway

A

Noradrenaline binds to a1 adrenoceptor (or adrenaline when its levels are above physiological levels) (on SM cell membrane), activating this receptor and thus the Gq receptor. This then activates Phospholipase C, thus catalysing this reaction PIP2 -> IP3 + DAG. IP3-R on the sarcoplasmic reticulum membrane opens, thus allowing the efflux of Ca2+. Ca2+ binds to and activates calmodulin. This new complex activates and binds to MLCK. This new complex phosphorylates the myosin light chain thus activating myosin so its power strokes with the actin molecule can now happen.

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43
Q

Activation of which receptors in the ANS lead to an

A) increase in heart force of contraction and heart rate
B) decrease in heart force of contraction and heart rate

Are each receptor found in the SNS or PNS?

A

A) B1 in the SNS

B) M2 in the PNS

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44
Q

When the parasympathetic preganglionic vagus nerve synapses in the AVN and SAN, what happens next?

chronotropic - HR

A

ACh is released from the postganglionic cells, and binds to M2 receptors causing a reduction in heart rate (- chronotropic effect) and a decrease inAVN conduction velocity

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45
Q

When the sympathetic preganglionic fibres from the sympathetic trunk synapse in the ventricular myocardium, SAN and AVN, what happens next?

chronotropic - HR
inotropic - force of contraction

A

NA/A is released from the postganglionic cells and binds to B1 adrenocepter. This causes an increase in heart rate (+ chronotropy) and increase in force of contraction (+ inotropy)

46
Q

What effect does hypertension have on afterload?

A

Increases afterload.

This is all just extra info:
So CO decreases so:
1. LV Hypertrophy so get left sided heart failure (so get syncope)
2. Get angina or MI due to reduced coronary artery flow and thus myocardium perfusion

47
Q

What is the sympathetics nervous systems effect on the PCT?

A

Stimulates:

Apical surface - Na/H exchanger
Basolateral surface - Na/K/ATPase

48
Q

What 2 sites in the kidney does ADH act on?

Describe

A

Upregulates Aquaporins on apical membrane of CD

Stimulates Na/K/Cl co-transporter on apical membrane of thick ascending limb

49
Q

What is synthesised and stored in atrial myocytes, leading to the reduction of BP?

How does it decrease BP?

A

Atrial natriuretic peptide

(Increased atrial filling leads to more stretch of the atria so more ANP is released from the atrial myocytes which:)

  1. increases Na+ excretion
  2. vasodilates a.a. so GFR increases so more Na+ is excreted
50
Q

What is a tumour of the adrenal medulla called and how does it cause secondary hypertension?

A

Pheochromocytoma secretes NA and A which activated a1 adrenocepters > B2 adrenoceptors of VSM leading to vasoconstriction of arteries and veins

51
Q

Where do you place leads V1-V6?

Include their colours

A 
Ride your green bike blood pressure
(Anteroseptal:)
V1: red - right 4th ICS, parasternal
V2: yellow - left 4th ICS, parasternal
V3: green - left between V2 and V4
V4: brown - left 5th ICS MCL

(Lateral:)
V5: black - left 5th ICS anterior axillary line
V6: purple - left 5th ICS MAL

52
Q

Where do you place the limb cords?

Do in order of colours

A

Ride your green bike

Red - right wrist
Yellow - left wrist
Green - left ankle
Blue - right ankle

53
Q

Regarding repolarisation and depolarisation, when would you get a positive complex with an upwards deflection?

A
  • Depolarisation wave going towards an electrode

- Repolarisation wave going away from an electrode

54
Q

Regarding repolarisation and depolarisation, when would you get a negative complex with a downwards deflection?

A
  • Depolarisation wave away from an electrode

- Repolarisation wave towards an electrode

55
Q

What causes the irregular and fast ventricular contractions in ventricular fibrillation?

A

Multiple ectopic foci, in the ventricular muscle wall, firing off irregularly

56
Q

Describe what first degree heart block is and what effect will this have on ECGs?

A

Slow AVN conduction leading prolonged PR interval

57
Q

Describe second degree heart block and what effect will this have on ECGs?

A

Intermittent failure of AVN conduction (being sent out) so some P waves are not followed by QRS complexes (so sometimes the ventricles do not depolarise)

58
Q

What are my Golden 4 Information regarding Third degree heart block (Complete heart block)

A
  1. No communication between atria and ventricles
  2. SAN impulses do not reach the ventricles
  3. Bradycardia
  4. Ventricles depolarise at their own slower rate
59
Q

What is the blood pressure in the pulmonary artery, pulmonary capillary and pulmonary vein

A

Pulmonary artery - 12-15 mmHg
Pulmonary capillaries - 9-12 mmHg
Pulmonary vein - 5 mmHg

60
Q

How is the left atrium and pulmonary oedema linked?

A

If the pressure in the left atrium increases to about 20-25 mmHg (from its normal of 1-10 mmHg), then you get pulmonary oedema as the high pulmonary vein pressure now leads to a high pulmonary capillary pressure, which leads to HP>OP

61
Q

How does the body ensure that the coronary artery has a high basal flow?

A

Coronary artery capillaries release NO - which is a vasodilator

62
Q

Describe pericarditis symptoms

A

Sharp, central, localised pain worse on inspiration and coughing

63
Q

Describe the pathophysiology of an MI

A

1) Atherosclerotic plaque forms
2) Atherosclerotic plaque ruptures
3) Platelets aggregate and a thrombus forms
4) Thrombus (completely) occludes the coronary artery

64
Q

What are 7 signs and symptoms found in left ventricular heart failure?

Describe each

A
  1. Fatigue
  2. Breathless on exertion
  3. Orthopnoea
  4. Pulmonary oedema so hear basal pulmonary crackles
  5. Paroxysmal nocturnal dyspnoea
  6. Sputum cough (late stage)
  7. Cardiomegaly so the LV hypertrophy leads to a displaced apex beat
65
Q

What are 5 signs and symptoms found in right ventricular heart failure?

A
  1. Lethargy
  2. Breathless
  3. Raised JVP
  4. Pitting - peripheral oedema
  5. Liver congestion - tender, smooth, enlarged liver
66
Q

How do you calculate the ejection fraction?

A

stroke volume/end diastolic volume

67
Q

Describe Frank Starlings law of the heart

A

As preload initially increases, stretch and contraction of cardiac myocytes increases until a point - thus SV/CO increases up to a point

68
Q

Discuss 3 factors that lead to a reduction in SV in heart failure

A
  1. Increased afterload
  2. Decrease in preload (ventricular filling worsens as heart failure develops)
  3. Reduction in inotropy (force of contraction - due to weakness of cardiac muscle)
69
Q

What % value would you class as a reduced ejection fraction?

Describe what causes reduced ejection fraction (3).

A

Less than 40%

(Systolic dysfunction), ventricular contraction issue which can be caused by:

  • overstretched sarcomeres so LV enlarges
  • thin LV wall
  • fibrosed LV wall
70
Q

What % value would you class as a preserved ejection fraction?

Describe what causes preserved ejection fraction (1).

A

More than or equal to 50%

(Diastolic dysfunction), where LV wall hypertrophy leads to poor ventricular filling

71
Q

What 2 factors can lead to haemodynamic shock?

Are these factors reduced or increased?

A

Reduction in CO

Reduction in TPR

72
Q

What can lead to a reduction in TPR?

A

Excessive arteriole vasodilation

73
Q

What 3 types of shock can lead to a reduction in CO?

Briefly discuss each shock

A
  1. Mechanical shock - pump cannot fill
  2. Cardiogenic shock - pump failure
  3. Hypovolemic shock - loss of blood volume
74
Q

Biologically, what is distributive shock?

Discuss it fully.

A

The body is normovolaemic but due to high concentrations of vasodilators, there is excessive arteriole vasodilation so TPR reduces, thus MAP/BP reduces so get poor tissue perfusion (which could lead to multi-organ failure)

75
Q

Name 2 causes of distributive shock

A

Anaphylaxis (leads to anaphylactic shock - a type of distributive shock)

Sepsis (leads to septic shock - a type of distributive shock)

76
Q

In anaphylactic shock, why do you give adrenaline?

A

Binds to a1 adrenoceptors of VSM (of arteries and veins) - leading to vasoconstriction to counteract the extreme vasodilation caused by the excess release of mast cell granules containing vasodilators

(Vasoconstriction increases BP -> tissue perfusion.

77
Q

Name 2 causes of hypovolemic shock

A

Haemorrhage

Severe burns

78
Q

Name 2 causes of cardiogenic shock

A

MI

Heart failure

79
Q

Name 2 causes of mechanical shock

A

Pulmonary embolism

Cardiac tamponade

80
Q

How does a loss of volume lead to hypovolemic shock?

A

Reduced venous return leads to reduced cardiac output

-> reduced BP -> tissue perfusion -> organ failure

81
Q

What causes cardiac tamponade?

What is cardiac tamponade?

A

Pericardial effusion leading to the fibrous capsule around the heart being unable to expand so cardiac output and arterial BP reduces due to heart compression

82
Q

What is central venous pressure also called?

Just give 1

A

Preload, left ventricular end diastolic pressure, end diastolic pressure

83
Q

How does a pulmonary embolism lead to a high central venous pressure?

A

Due to RV dilation the inter-ventricular septum bows into the LV, thus leading to mechanical shock as the LV cannot fill properly

84
Q

What are two components of basic life support?

A
  1. External ventilation

2. Chest compressions

85
Q

Describe advanced life support

A

Defibrillation, where an electrical current is given to the heart to depolarise all the cells and put them into a refractory period

86
Q

Why do you give a defibrillator to a patient that is in cardiac arrest?

A

The ventricular fibrillation leads to chaotic, irregular impulses. Defibrillator puts the heart back into rhythm.

87
Q

What does a doppler ultrasound measure?

A

Velocity and direction of blood flow in arteries and veins

88
Q

What are 4 causes of acute limb ischaemia?

A
  1. Trauma (rare)
  2. Embolus/thrombus
  3. AF
  4. AAA
89
Q

What are 6 signs and symptoms of acute limb ischaemia?

A 
Pain
Pallor
Paraesthesia
Perishing with cold
Pulseless
Paralysis
90
Q

How do the calf muscles ensure venous return?

A

Contraction of the calf muscles lead to the deep vein valves opening and flowing upwards against gravity

91
Q

Describe the pathophysiology behind varicose veins (a type of peripheral venous insufficiency)

A

Varicose veins typically occurs in the (short/long) saphenous veins due to calf muscles not contracting efficiently, thus valves malfunction thus get retrograde blood flow so the veins dilate and due to the increased pressure the vein walls thin out. Veins also twist on themselves.

92
Q

Why might a varicose vein be painful?

A
  • Haemorrhage

- Thrombophlebitis (a vein clot)

93
Q

Name some symptoms of peripheral venous disease

A 
Heavy
Aching
Throbbing
Thin, itchy, bulging skin
Muscle cramps
94
Q

Name some symptoms of varicose veins

A 
Heavy
Aching
Throbbing
Thin, itchy, bulging skin
Muscle cramps
95
Q

What factors make up Virchow’s triad?

A

Stasis, blood vessel wall damage and hypercoagulability

96
Q

What is end systolic volume?

A

Volume of blood left in the heart after systole

97
Q

GTN is administered sublingually. Why?

What is the MOA of Glyceryltrinitrate GTN?

4

A

Very rapidly absorbed into the bloodstream

Releases nitric oxide so:
1. Causes venodilation so preload decreases MOST IMPO MOA thus workload of the heart decreases as the hearts O2 demand has decreased

  1. Dilates arteries (not arterioles)
  2. Dilates collateral coronary arteries so heart blood supply improves
  3. Relaxes VSM
98
Q

What is the pathophysiology behind paroxysmal nocturnal dyspnoea?

A

When lying flat the hydrostatic pressure in the gravity dependent capillary beds reduce. Thus more fluid is returned to the circulation. So blood volume increases and this worsens pulmonary oedema and congestion

99
Q

Where is the apex beat best heard?

A

Left 5th ICS MCL

100
Q

Where is the aortic valve best heard?

A

Right 2nd ICS parasternal

101
Q

A patient has aortic valve stenosis.

In order to treat it, a transcatheter aortic valve implantation, a TAVI, is going to occur, where the aortic valve is replaced.

How do they make their way to the aortic valve from a vessel in the femoral triangle?

A

Femoral artery -> external iliac artery -> common iliac artery -> ascending aorta (abdominal aorta -> thoracic aorta -> arch of aorta)

102
Q

Stroke volume definition

Cardiac output definition

A

SV: Volume of blood leaving the left ventricle per heart beat

CO: Volume of blood leaving both ventricles per unit time

103
Q

If you hear a third heart sound, what does this indicate?

A

Congestive heart failure

104
Q

Name 2 examples of Acute Coronary Syndrome, ACS

A

NSTEMI

STEMI

105
Q

Subendocardial infarction has ischaemia of the myocardium (proximal to the artery found in the epicardium) and infarction of the myocardium (proximal to the endocardium/distal to the artery in the epicardium).

What MI is associated with a subendocardial infarction?

A

NSTEMI

106
Q

Describe the progression of a transmural infarction caused by a complete occlusion of the LAD (for example).

What type of MI is a transmural infarction seen in?

A

First get infarction of the myocardium distal to the epicardium. Then this infarction slowly travels more proximally (towards the portion of the myocardium that is closer to the LAD found in the epicardium)

STEMI

107
Q

Describe the pathophysiology of an aortic dissection

A
  1. Tunica intima tears

2. Blood escapes and pools in the layer between the tunica intima and the tunica media

108
Q

What is trifascicular block?

A
  1. Right bundle branch block + First degree AV block + left anterior (common) or left posterior (rare) fascicular block
109
Q

Why do you see tall QRS complexes in V1 of an ECG in Right bundle branch block?

QRS complex is also wide

A

V1 electrode is near to and faces the RV.

Due to the right bundle branch receiving it’s signals at a delayed time, the RV has delayed depolarisation as the impulses that are sent to the RV comes from the left bundle branch depolarising the LV then coming back up to the RV - to cause RV depolarisation

110
Q

Right bundle branch block:

Why do you have a wide S wave in the 4 lateral leads of the heart?

What are the 4 lateral leads of the heart?

A

You have slurred S waves in leads I, aVL, V5 and V6 because you have late signals travelling towards the right ventricles away from the left side

Cardiology (5 decks)

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