General chest pain Flashcards

1
Q

State the function of blood vessels.

A
  • Circulate nutrient/waste

- Regulate Blood Pressure

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2
Q

State the significance of the parallel arrangement of vessels in the cardiovascular system.

A
  • Allow independent regulation of blood flow to different organs
  • Adapts to metabolic demands of tissues accordingly. (For example, during exercise the skeletal muscles will receive more blood than usual)
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3
Q

What is the average blood flow at rest in the CVS?

A

5 L/min

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4
Q

State the way by which parallel arrangement of vessels in the CVS allows independent regulation of blood flow to different organs.

A
  • Nervous system mediated ways in which we distribute blood (e.g fight or flight)
  • Sphincters control blood flow through capillaries
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5
Q

Which of the following is the correct order of blood vessels:
A) Aorta → arterioles → capillaries → arteries → veins
B) Aorta → venules → capillaries → arterioles → arteries
C) Aorta → arteries → arterioles → capillaries → venules

A

Answer: C

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6
Q
Which of the following figures represents the percentage of blood flow in veins, venules, and venous sinuses at any one time:
A) 9%
B) 45%
C) 64%
D) 84%
A

Answer: C

(84% represents the blood in systemic circulation which involves the arteries too minus pulmonary circulation and the blood in the heart at any one time)

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7
Q

Describe the features of the capillaries that make them the ultimate deliverer of nutrient supply to tissues around the body.

A
  • Smallest diameter blood vessel
  • Simple tube, one thick cell of flattened endothelial cells
  • Allows for diffusion of nutrients, waste etc.
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8
Q

We cannot perfuse all the capillaries in the body at the same time, therefore control of blood flow into certain capillaries is essential. However, the capillaries are non-muscular structures.

A) Name the structure that controls the blood flow into the capillaries.
B) Describe how the metabolic of tissue may control this structure and therefore the capillary responsible for the tissue.**

A

A) Precarpillary sphincters (these are rings of smooth muscles which control the entry of blood from the arterioles into each capillary)
B) Lack of blood supply → ischemia → release of local factors → build up of factors → opening of the local precapillary sphincter (remember, this is because not all capillaries can be perfused at once, hence while one is open other will be closed)

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9
Q

A) What is a compliant vessel?

B) Give an example.

A

A) One that accommodates an increase in volume without generating a huge amount of pressure
B) Veins (more compliant than arteries as they have thinner walls)

non-compliant: capillaries and arterioles.

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10
Q

What are the three ways in which you can control the heart? And which parts of the CNS can control each way.

A
  • Increase rate (Sympathetic)
  • Decrease rate (Parasympathetic)
  • Increase/regulate the force of contraction (Sympathetic)
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11
Q

State the equation for the calculation of mean arterial blood pressure.

A

MABP = diastolic pressure + 1/3 pulse pressure

Pulse Pressure= systolic pressure – diastolic pressure

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12
Q

Due to the effects of gravity, when standing completely, blood pressure gets higher as you go down the body reaching its peak in the legs. Which means we would experience cerebral hypoperfusion and faint if we did not have the compensatory mechanisms.

A) Name two mechanisms by which we compensate for the effects of gravity.

The effects of gravity also mean that when moving immediately from a supine position to an upright position, we experience postural hypotension, which can lead to losing balance due to a feeling of lightheadedness.

B) Describe why this occurs.

A

A)
• Vein valves
• Muscle pumps (aids in pumping blood back up the veins through contraction and movement)
B)
Around 500ml from the upper body to legs → decreased venous return → decreased cardiac output → decreased blood pressure → reduced blood supply to the brain

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13
Q

A) Using La Place’s law, explain how the diameter of a blood vessel influences its ability to contract against the pressure within it.

B) Explain how this applies to capillaries.

A
  • La Place’s Law: T (Tension) = P (pressure against vessel wall) x R (radius)
  • The larger the diameter → the greater the tension required to push against the pressure generated by the blood within the vessel → the thicker the wall of the vessel that is required to generate the tension

B) Capillary’s are under high pressure but have such a tiny radius that the tension is low and they remain only one cell thick

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14
Q

A) What is the Reynolds number?
B) What are factors that may increase the likelihood of turbulent flow based on the equation used to calculate the Reynolds number?
C) Why is turbulent flow problematic.

A

A) It is a measure of the likelihood that flow is turbulent or laminar. Above the calculated value the flow is likely to have turbulence
B) High velocity, larger diameter, low blood viscosity, abnormal vessel wall ( Re = (velocity of flow) x (radius of vessel) / viscosity))
C) Increased turbulence = increased work by heart = heart failure due to higher metabolic demand

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15
Q

State the equation for arterial pressure.

A

Cardiac output x total peripheral resistance

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16
Q

What is the relationship between radius and flow?

A

Positive relationship (bigger the radius the lower the resistance and the higher the flow)

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17
Q

List the structures that form the conduction pathway in the heart in the correct order.

A

SA Node → atrial muscle → AV Node → His Bundle → Bundle branches → Purkinje Fibers → ventricular muscle

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18
Q

Which cells initiate the Action potential, which spreads over the heart?

A

Autorhythmic cells (pacemaker cells)

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19
Q

Which structure of the conduction pathways sets the heart rate?

A

(depolarisation of) SA Node

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20
Q

Name the 4 locations in the heart where you can find the specialized autorhythmic cells (pacemaker cells).

A
  • Sinoatrial Node
  • Atrioventricular Node
  • Bundle of Hiss
  • Purkinje Fibers
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21
Q

As the action potential spreads over the atria, there is only one point where it can move through onto the ventricles.

A) Name this point.
As the action potential reaches the point in (A), there is a delay before it spreads over the ventricles.

B) What is the reason behind this delay?
C) Which segment on an ECG represents this delay.

A

A) Atrioventricular Node
B) Allows time for atrial contraction and blood to move from the atria into the ventricles before systole/ventricular contraction
C) P-R Segment

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22
Q

Cardiac muscles consist of muscle cells interconnected by _________, which contain junctions named _______ junctions which allow action potential to spread and a contraction to take place.

A

Intercalated discs, gap

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23
Q

Describe the generation of an action potential in pacemaker cells.

A

Funny sodium channels open (Na+ slowly enters) → T-type calcium channels also open and help in this slow depolarization → Ca+ and Na+ cause the Membrane potential to rise until pacemaker potential is reached → L-type calcium channel open and calcium slowly flows in → depolarization of cell → once a set threshold is reached Ca+ channels close and K+ channels open → repolarization → -ve RMP → K+ channels close and Funny Na+ channels open.

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24
Q

State the difference between the action potential in a contractile cardiac muscle cell, and an autorhythmic (pacemaker) cell.

A
  1. In pacemaker cells, the depolarization (upstroke on the graph) is due to the inflow of Calcium ions through slow L-type channels
  2. No plateau phase
  3. F-type Na+ channels are responsible for initiating the action potential (they are funny type as they open during hyperpolarization (at –ve rmp)
25
Q

During an action potential in contractile cardiac cells, rapid depolarisation by fast-activating sodium channel occurs (phase 0) then they deactivate, and potassium channels open allowing k+ to move out (phase 1), however, instead of repolarization there is a plateau phase (phase 3). What drives this plateau phase?

A

Slow L-type calcium channels open allowing calcium to flow in which counteracts the effects of the K+ channels which are allowing K+ out

26
Q

Define Hypoxia.

A

deficiency in the amount of oxygen reaching the tissue/organ

27
Q

Define Ischaemia.

A

Inadequate blood supply to an organ/part of the body which leads to hypoxia

28
Q

Complete blockage of the coronary arteries is the most common cause of infarction. Name other causes of infarction in the heart.

A
  • Partial blockage of the arteries (NSTEMI)
  • Hypoxia in anaemic patients
  • Illicit drug misuse (cocaine)
29
Q

State the three conditions which form ACS, and describe them briefly.

A
  • Unstable angina- partial occlusion - no infarction but ischaemia of the muscle wall (troponin negative)
  • NSTEMI - partial occlusion - infarction of the myocardium distally at the location but ischaemia proximally (troponin positive)
  • STEMI - infarction of the muscle wall (across the whole myocardium) (troponin positive)
30
Q

A) State the name of the biomarker that is mainly used for investigation of Myocardial Infarction.
B) Describe what makes this biomarker particularly useful.

A

A) Troponin (others are Creatine Kinase MB and myoglobin)

B) Specific to cardiac muscle necrosis, released early, and has a prolonged effect

31
Q

Define angina.

A

chest pain due to inadequate blood supply to the heart.

32
Q

How does unstable angina differ from stable angina?

A

Unstable may occur at minimal exertion or at rest, it is worsening and lasts longer. Will not respond to GTN or rest. (Supply issue)

Stable angina - chest pain (DULL/heavy/constricting) on exertion or emotional stress due to poor flow of blood through the vessels (demand issue), and relieved by rest (and GTN)

33
Q

What is variant angina (prinzmetal angina)?

A
  • Chest pain at rest

- due to vasospasms of coronary arteries leading to temporary reduced blood flow

34
Q

A) State mechanism of action of beta blockers
B) Give an example used for angina
C) state three side effects of beta blockers

A

A) Depress myocardial contractility + reduce heart rate (B1 Adrenergic receptor antagonist) –> reduce metabolic demand
B) Bisoprolol or Atenolol
C) cold hands and feet, fatigue, bradycardia

35
Q

A) State mechanism of action of nitrates
B) Give an example used for angina
C) state three side effects of nitrates

A

A) Acts on smooth muscle releasing NO –> Peripheral vasodilation, particularly the venous system –> pooling of blood in the venous system –> reduced end-diastolic ventricular volume –> less work done –> reduced metabolic demand
B) Glyceryl Trinitrate
C) Headache, hypotension, fainting/collapse

36
Q

A) State mechanism of action of aspirin

B) State some side effects

A

A) Inhibits the activity of cyclooxygenase –> inhibits the production of thromboxane A2 –> reduced platelet adhesion and aggregation –> reduce mortality from MI
B) Increased bleeding time, gastrointestinal haemorrhage, and bronchospasm

37
Q
A) State mechanism of action of calcium channel blockers. 
B) Give examples of a class of CCB that work on vessels only, and examples that work on heart and vessels
C) State side effects
A

A) block calcium entry into muscle cells upon depolarisation affecting heart and vessels (effects on the heart is by reducing conduction at AV node which also makes it a good anti-arrhythmic drug)
B) Vessels only: amlodipine (dihydropyridine), vessels and heart: verapamil, diltiazem
C) constipation, headaches, ankle oedema

38
Q

List the clinical presentations of ACS.

A
  • Crushing/heavy/restricting central chest pain>20 minutes
  • Radiates to the neck and left arm
  • No relieving factors
  • Sweating
  • Nausea
  • Dyspnea
  • Palpitations
  • Signs of distress, anxiety, pallor, tachycardia (feeling of impending death)
39
Q

Describe the investigations of suspected ACS.

A

Triad: clinical presentation, Blood troponin, ECG

Coronary angiogram shows if narrowing or blockage has occurred and in which artery

40
Q

A) Describe the primary care management of an ACS.

B) Describe secondary care management of an ACS.

A

A) Reassuring the patient

  • 999
  • Clinical assessment (BP, SATS) and check for signs of heart failure (breathlessness, ankle oedema, fatigue, wheeze/cough, confusion)
  • MOAN (Morphine, oxygen if under 92%, Aspirin 300 mg, clopidogrel 600mg, iv heparin 5000 units, nitrates)

B)
First line if available: Immediate primary angioplasty or PCI (Percutaneous Coronary Intervention) (within 90 minutes)
Second line: thrombolysis with fibrinolytic agents (if within 90 minutes to 6 hours)

41
Q

Describe pharmacological treatment post-MI.

A
Aspirin 75 mg - once daily
Ticagrelor 90 mg - twice daily (for 12 months then stop)
Atorvastatin 40 mg - once daily
Ramipril 2.5 mg - once daily
Bisoprolol 2.5 mg - once daily
42
Q

What is the significance of an ST-elevated MI?

A

Require immediate medical care

43
Q

Other than a STEMI, state three causes of ST elevation on an ECG.

A
  • Coronary artery spasm (variant angina)
  • Acute pericarditis
  • Left ventricular hypertrophy
44
Q

Explain the mechanism by which percutaneous coronary intervention (PCI) works in the treatment of coronary artery disease

A

1) MI is due to narrowing or blockage of coronary artery
2) PCI works by X-ray guided injection of contrast material into coronary arteries to find the blockage or narrowing
3) once found, a stent is inserted to re-open the occluded artery and re-establish blood flow into the distal myocardium

(Important to note: PCI is the process of finding a blockage or narrowing, if not found this process is only called PCI but cannot be called an angioplasty, but if its found and a balloon is inserted and stent etc then this process can be called angioplasty)

45
Q

Why might MI cause valve disease?

A

MI will affect the chordae tendinae which usually prevents valve prolapse of mitral and tricuspid during ventricular systole

46
Q

State the difference between primary prevention and secondary intervention.

A

Primary: Concerned with preventing the onset of the disease. Interventions before signs of disease.

Secondary: Concerned with detecting the disease in its early stages before the development of symptoms

47
Q

State the difference between primary prevention and secondary intervention.

A

Primary: Concerned with preventing the onset of the disease. Interventions before signs of disease.

Secondary: Concerned with detecting the disease in its early stages before the development of symptoms.

48
Q

What family history of the cardiovascluar disease is considered to be a relevant risk factor of CVD?

A
  • Father or brother <55

- mother or sister <65

49
Q

State 4 modifiable risk factors of cardiovascular disease.

A
  • Diabetes
  • Smoking
  • Obesity
  • High blood pressure
50
Q

State 3 non-modifiable risk factors of cardiovascular disease.

A
  • Family history
  • Male
  • Increasing age (40+)
51
Q

Describe 3 social determents of ischemic heart disease.

A
  • Poverty - low socio-economic status
  • Depression and anxiety
  • Stress at work and family
52
Q

6 Ps of peripheral vascular disease?

A
  • Pain
  • Pallor
  • paresthesia
  • pulselessness
  • paralysis
  • poikilothermia
53
Q

Why does smoking contribute to ischaemic heart disease?

A
  • The formation of carboxyhaemoglobin
  • Nicotine produces tachycardia
  • Tobacco smoke is atherogenic and thrombotic
54
Q

Describe the red flag clinical features of the following conditions that present with acute chest pain.

  • Aortic dissection
  • Pneumothorax
  • Pulmonary Embolism
  • ACS
  • Boerhaave’s perforation
A

AS: tearing pain, radiates to back
Pneumothorax: expanded and hyper-resonant chest and dyspnea
PE: sudden onset, stabbing pain, dyspnea, haemoptysis, hypoxia in patients with malignancy (d-dimer marker)
ACS: sudden onset, radiating to the jaw and left arm, sweating etc
Boerhaave’s perforation: vomiting immediately before the onset of pain (hole in the oesophagus due to a sudden increase in intrathoracic pressure)

55
Q

Name one skin cause, one psychological cause, and one GI causes of chest pain.

A

Skin: Herpes Zoster (shingles)
Psy: anxiety
GI: GORD

56
Q

Describe the advice you would give a patient regarding a cardioprotective diet.

A
  • Adopt a Mediterranean style diet (rich in nuts, fruits, vegetables, whole grain cereals and olive oil - moderate fish and poultry, and low in red meat, processed meat, dairy products and sweets)
  • Use the Eatwell guide to support this diet in order to restrict saturated fats (reduced LDL cholesterol), sugars and salt intake
57
Q

A) Give an example of a short-acting cholesterol-lowering drug.
B) State when this drug would be prescribed.

A

A) Simvastatin (or pravastatin)

B) Prescribed to be taken at night to prevent peak cholesterol levels in the morning

58
Q

Give an example of a long acting statin.

A

Atorostatin or rosuvastatin

59
Q

Name one organ that may be adversely affected by taking statins.

A

Liver - may cause hepatotoxicity due to the 1st bypass