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CMS1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Describe the circulatory system. How many circuits is there?

A

Made of 2 circuits → Systemic and pulmonary circulation
Pulmonary circulation supplies the lungs with deoxygenated blood via the pulmonary arteries. Carbon dioxide is released.
Oxygen enters which will then return to the left side of the heart via the pulmonary vein.
Oxygenated blood is then pumped through the aorta around the body via parallel circuits
Deoxygenated blood is returned to the right side of the heart via the vena cava and the blood returns to the lungs

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2
Q

Can you name all the different types of vessels?

A

Arteries, arterioles, capillaries, venules, veins

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3
Q

What are arteries and arterioles?

A

Arteries → carry blood from the heart with thick walls and elastic. Relaxation of the arteries between each beat causes stored blood to continue to flow between heartbeats.

Arterioles → Lie between the arteries and capillaries. Can constrict or dilate to control blood flow to a specific tissue.

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4
Q

What are capillaries?

A

highly branched, thin walled vessels with large SA to allow for gas exchange

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5
Q

What are veins and venules?

A

Venules → Lie between the veins and capillaries.
Veins → contain valves that prevent backflow. Blood is entering the heart.

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6
Q

Can you name all the valves in the heart and where they are situated?

A

Atrioventricular valves
Tricuspid valve → between the right atrium and right ventricle
Mitral valve → between the left atrium and left ventricle

Pulmonary valve → between the pulmonary artery and right ventricle

Aortic valves → between the aorta and left ventricle

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7
Q

What is the purpose of valves?

A

STOP backflow to the heart

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8
Q

What happens during diastole?

A

RELAXATION
AV valves open, aortic/pulmonary valves closed.
Blood flows from atria to ventricles.

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9
Q

What happens during systole?

A

CONTRACTION
Atria contract.
Higher pressure in ventricles than in atria so AV valves close.
Atria refill.
Ventricles contract.
Aortic and pulmonary valves open.
Blood flows out of ventricles.

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10
Q

What is the Frank Starling Mechanism?

A

The greater the heart is stretched, the stronger it contracts due to intrinsic properties of the cardiac muscle cells

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11
Q

What are the steps for the conducting system?

A

1) SA node (pacemaker) generates electrical signal that causes artia contraction
2) AV node picks up electrical
signal, there’s a delay to allow complete atria
contraction
3) The action potential (AP) then travels down the bundle of His into the purkinji fibres
4) Ventricles contract - blood ejected out of
the heart

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12
Q

What does the AV node have to ensure the signal can’t pass through the ventricle?

A

non - conductive fibrous tissue called annulus fibrosis.

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13
Q

What are the different waves on an ECG?

A

P wave = depolarisation/contraction of atria.

QRS complex = ventricular depolarisation/contraction (and repolarisation/relaxation of atria).

T wave = repolarisation/relaxation of ventricles.

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14
Q

What is Tachycardia and Bradycardia?

A

Tachycardia >100bpm.
Bradycardia <60bpm.

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15
Q

Cardiac output =

A

Cardiac output = Heart Rate X Stroke Volume

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16
Q

Blood pressure =

A

Blood Pressure = Cardiac Output X Total Peripheral Resistance

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17
Q

What causes an increase in HR?

A

Reduced parasympathetic inhibition of the heart rate. Increase in sympathetic stimulation.

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18
Q

What can we do to increase cardiac output?

A

Increase the venous return by constricting blood vessels that are in the splanchnic circulation (found in spleen and GI tract) into the circulation so that it can be redistributed elsewhere where it’s needed and it increases that circulating volume.
OR
Use respiratory and skeletal pumps. Changes in thoracic pressure by breathing and the compressive action of the diaphragm on abdominal vessels can increase respiratory rate = increase venous return = increase cardiac output

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19
Q

What is the mechanism for LOW BP?

A

Triggered by baroreceptors
Sympathetic nervous system
Increased heart rate
Increased stroke volume
Constrict arterioles and veins

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20
Q

What is the mechanism for HIGH BP?

A

Triggered by baroreceptors
Parasympathetic nervous system
Reduced heart rate
Dilation of arterioles and veins

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21
Q

How is Heart Rate controlled?

A

Through the SA node primarily, but also through the parasympathetic and sympathetic nervous system.

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22
Q

Describe the long term mechanisms for controlling blood pressure.

A

Renin-Angiotensin System (long term BP control):
Involves blood flow to the kidneys and hormone regulation
Low BP → Low blood flow to kidneys → less Na and water excretion → kidney then produces renin.
Renin converts angiotensin to angiotensin I which travels around the blood
Angiotensin I → Angiotensin II via the angiotensin converting enzyme (ACE). This happens in the lungs.
Angiotensin II trigger the adrenal glands to release aldosterone which cause vasoconstriction and Na and water reabsorption.
THEREFORE we increase circulating volume and increase BP

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23
Q

What is CPR?

A

Cardiopulmonary Resuscitation:
Compressions: 1/3 the depth of the chest.
Ventilations: roughly half the bag.
Ratio 30:2.
AED delivers shock – if shockable.

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24
Q

Issue with CPR?

A

increasing pressure within the thorax which will increase pressure in the head, causing a rise in intracranial pressure. This compresses on the vessels and reduces brain perfusion.

SOOOO,,,, THAT WHY RECOIL IS GOOD BECAUSE IT ALLOWS CEREBRAL PERFUSION!

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25
Q

When you take a pulse, What do you need to assess?

A

you should assess its rate, rhythm & character

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26
Q

In a normal regular pulse, Where is the rythm from? and what is the difference in case of arrythmia?

A

sinus rhythm, however arrhythmia can be due to rhythm starting elsewhere or a problem with circuitry of heart

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27
Q

Name the different types of arrythmia:

A
  1. Tachyarrhythmias
  2. Bradyarrhythmia
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28
Q

Is Tachyarrythmias fast or slow irregular heart rate?

A

Fast

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29
Q

Is Bradyarrhythmias fast or slow irregular heart rate?

A

Slow

30
Q

Give example of conditions which are considered as Tachyarrhythmia

A
  • Sinus tachycardia
  • Supraventricular tachycardia (fast heart rate, originates above the ventricles but not from sinus node)
  • Atrial flutter
  • Atrial fibrillation
  • Ventricular tachycardia (originates in ventricles)
31
Q

How does tachyarrhythmia cause low BP?

A

tachyarrhythmia causes heart to beat in less coordinate way. because it is fast, there is less time for the heart to recoil and fill with blood in which it lowers its stroke volume. Therefore, leads to lower blood pressure

32
Q

how can we reverse control tachyarrhythmia?

A
  • with “cardioversion” Which is delivering carful timed shock to reset heart”
  • with rate controlling medication to maximize the time heart has to fill between beats.
33
Q

what are the consequences of not treating arrhythmia?

A

it can convert from acute to chronic arrhythmia which leads to heart failure

34
Q

Give example of conditions which are considered as Bradyarrhythmia

A
  • Sinus bradycardia
  • Sick sinus syndrome
  • Heart block
  • Ventricular escape
35
Q

What is the effect of Bradyarrhythmia on Cardiac output and why? and how is it different from tachyarrhythmia?

A

They both reduce the cardiac output
- In Brady, Cardiac output is low (Bad). due to lower heart rates
- In Tachy, Cardiac output is low due to low stroke volume
- CO: HR x Stroke volume

36
Q

Describe the mechanism by which Bradyarrhythmia reduces heart rate

A
  • It’s due to conduction issue either at atrioventricular node or bundle of His
  • This causes excessive delays between atrial and ventricular conduction and so heart contraction.
  • Therefore, causing slow irregular heartbeat .
37
Q

If there is no electricity in the heart, is there another source of electricity or will the heart go to cardiac arrest?

A

If there is no electricity conducted , the ventricles have their own very slow regular rhythm called
“ventricular escape”

38
Q

What is ventricular escape?

A

If there is no electricity conducted in the heart (from SA to AV, same as in bradyarrhythmia) the ventricles have their own very slow regular rhythm called
“ventricular escape”

39
Q

What happen in the heart in the Atrial fibrillation?

A

Rhythm of heart originating somewhere in atria but not SA node , result in dis coordinated fibrillation of atria with some of the electricity being conducted down the ventricles but not all. Result in :
1. Irregular pulse
2. Risk of stroke,

40
Q

What is the result of Atrial fibrillation

A
  • irregular pulse
  • risk of Stroke
41
Q

How can Atrial Fibrillation put the heart at risk of Stroke?

A
  • Atrial fibrilation happens when the heart rhythm start from somewhere other than the SA node, resulting in dis-coordinated fibrillation in which not all the electricity from atria is passed to ventricle.
  • This causes irregular pulse
  • Very chaotic fibrillation, the flow of blood in atria becomes ideal for clot formation
  • If clot forms in left atrium it will pass into systemic circulation to the brain leads to stroke
42
Q
  • Why during the Atrial fibrillation, not all the electricity is passed from the atria to the ventricles?
A
  • Atrial fibrillation is an example of Tachyarrhythmia in which heart rate is high.
  • Time needed for cells to repolarize before being able to conduct another impulse.
  • That’s why not all electricity is
    Is conducted down to ventricles
43
Q

How to manage Atrial Fibrilation?

A

patient with chronic AF will be put on Anticoagulant ( warfarin old, DOAC new stable and better than warfarin

44
Q

Describe the mechanism of action of different classes of Anti-Dysrhythmic medication and give some examples of each class:

A

Class 1: act to stabilise the membrane such as (procainamide,quinidine,lidocaine,flecainide)
2. Class 2: Beta blockers such as (Bisoprolol)
3. Class 3 : act on potassium channels such as (Amiodarone)
4. Class 4: calcium channel blockers
5. Glycosides : digoxin

45
Q

What is Syncope?

A
  • temporary reduction of blood perfusion to the brain (type of loss of consciousness)
  • it is as a result of arrythmia
  • it can be a simple vasovagal or red flag!
46
Q

Describe the Posture, Provoking Factors and the Prodromal symptoms of Vasovagal Faint and how will they recover

A
  • Posture: up right
  • Provoking Factors: e.g. dental procedure
  • Prodromal Factors: hot, dizziness, faint
  • Recover: by laying down
47
Q

What are the symptoms of red flag faint?

A
  1. Prolonged slow recovery
  2. Absence of warning signs (symptoms)
  3. Blood pressure is not enough to keep patient in upright position
  4. Have significant cardiac history or family history of sudden death, or heart problems
  5. Chest pain
48
Q

What is the two different consequences to the valve in Heart valve disease? And briefly explain what they mean

A

Stenosis: heart valve becomes stiffer
Regurgitation: heart valve becomes very floppy

49
Q

How would valve stenosis affect the action of the heart

A
  • When the valves become stiff, the amount of blood pass through the valve is limited
  • This means the heart has to pump harder to generate more pressure to push the blood out
50
Q

How would valve Regurgitation affect the action of the heart

A
  • Because the valves are floppy and open, blood goes backwards the wrong way through the valves,
  • Means there is larger blood to push on with each beat
  • Forcing heart to complete larger contraction to push blood onwards
51
Q

what are the different causes of valve disease?

A
  1. calcification can cause stenosis in older patients
  2. damage of the little papillary muscles that stops the valve from opening the wrong way by cardiac ischemia
  3. Infection which damage valve such streptococcus infection can cause rheumatic fever, where immune response
    damages mitral valve causing stenosis or regurgitation or both!
  4. Endocarditis, where bacteria grow on infection and damage heart valve .
52
Q

Whci patient are at risk of Endocarditis?

A
  • Those with already damaged heart valves, or artificial heart valves as bacteria like to grow on these.
53
Q

What are the signs and symptoms of Endocarditis?

A
  • Fever,
  • Weight loss,
  • Septic emboli (infective materials that flow in blood stream then ends up blocking blood vessel somewhere)
54
Q

What is the treatment of Infective Endocarditis?

A

Infections endocarditis is serious condition and need several weeks of intravenous antibiotics to treat it or surgery to replace damage valves.

55
Q

What is the treatment of valve diseases?

A

valve replacement (just throw the old valve :) )

56
Q

Define Heart failure

A

When heart beats insufficiently as result of it being too stiff and can’t refill or too weak that can’t contracts,,, reducing its cardiac output

57
Q

How can Hypertension cause Heart Failure?

A

The heart has to push against the higher pressure in aorta ,
- It will become hypertrophied “thickened “ where left ventricle
become big and thick
- This reduce the amount of room in LV, lead to reduce stroke volume , thus the CO = heart failure

58
Q

How can Myocardial infarction cause Heart Failure?

A

The heart muscle is damaged, so it can’t pump harder which reduce stroke volume, CO = hearts failure

59
Q

How can valve disease cause Heart Failure?

A

In stenosis, the heart become hypertrophied & in regurgitation larger blood volume which stretches the heart which
become dilated “weak contraction “= heart failure

60
Q

How can Arrhythmia cause Heart Failure?

A

Heart can decompensate , if there was chronic arrhythmia such atrial fibrillation due to chronically reduced stroke volume

61
Q

Name some symptoms of Heart failure?

A
  • Fainting
  • Tiredness
  • Kidney disease
  • Breathlessness (pulmonary oedema) - as body receives less oxygen from reduced perfusion to tissues
  • Leg swelling (blockage of systemic veins)
  • Liver and spleen swelling
  • Impaired gastric absorption
62
Q

What is the treatment of Heart Failure?

A
  1. Lifestyle modifications:
    * Diet
    * Limit alcohol consumption
    * Exercise
    * Stop smoking
    * Annual flu vaccines
    * Pneumococcal vaccine
  2. Pharmacological:
    Diuretics: reduce volume overload in Heart failure by increase amount of fluid that pt urinate out
    * ACE-inhibitors/ Nitrates: if hypertension is problem, these are vasodilator that can reduces preload to heart so the heart less overloaded
    * Beta-blockers:if hypertension is problem, these are vasodilator that can reduces preload to heart so the heart lessoverloaded/ it also slow the heart if tachycardia is the problem
    * Digoxin : increase contractility
  3. Ventricular assist device: Device help to mechanically push the blood around the heart, However it requires open heart surgery to put it in as well as power source that patient has to carry everywhere
  4. Transplant
63
Q

What is infectious endocarditis and how is it relevant to dental practice?

A

Infections endocarditis is serious condition and need several weeks of intravenous antibiotics to treat it or surgery to replace damage valves.
- Pt with hypertrophic cardiomyopathy or congenital heart defect are more at risk of Endocarditis
- We need to advice
more on oral health to prevent bleeding gums which ↑ risk of bacteria entering Blood stream

64
Q

Your patient has heart failure. What accommodations might you need to make when they visit your practice?

A
  • Never lay them flat on the dental chair
65
Q

(C2) What causes hypertension?

A

Causes:
* Non-modifiable risk factors:
o Genetics
o Age
o Ethnicity
* Obesity (addressed with diet and exercise)
* Alcohol
* Sodium (normally salt is removed by kidneys the water from blood follows which would normally reduce venous return and cardiac output and BP. High salt diet causes you to retain more water and leads to higher BP)
* Smoking (Chemicals in cig smoke impair vasodilation and cause atherosclerosis (stiffening the blood vessels) -> increasing BP)
* Stress (through fight and flight response)
* Kidney and endocrine disease (kidney disease can cause hypertension. Endocrine disorders that cause increase in catecholamines (hormones and neurotransmitters in the sympathetic nervous system-> can cause hypertension)
* Drugs (some medications may increase BP either deliberately or as an unwanted side effect, or perhaps multiple medications may interact and prevent anti-hypertensive medication from being effective).

66
Q

(C2) Why is hypertension bad?

A

It’s bad because it can cause damage to the blood vessels and causing them to thicken, this can reduce the diameter lumen. It can lead to heart failure as the heart needs to work harder to pump blood around the body, which can then lead to ventricular hypertrophy and ultimately heart failure. It can also lead to chronic kidney disease and hypertensive retinopathy. It can also lead to brain damage such as from strokes. It can also increase the tough collagen and calcium deposits on artery walls making them stiffer, thus increasing the risk of aneurysms, atheroma and peripheral vascular disease.

67
Q

(C2) A patient attends and tells you they have recently been diagnosed with hypertension by doctor. You note that they are obese, smoke cigarettes and drink excessive amounts of alcohol. Their diet mainly consists of takeaway. What advice would you give them?

A

I would give them diet advice addressing their frequent takeaway consumption. I would explain that these takeaways are high in fats and increase risk of hypertension and other health complications such as heart disease. This is because it can lead to fatty plaque deposits inside the blood vessels, thus narrowing them and reducing the blood flow to the heart and other organs as a result.
I would also give smoking cessation advice explaining that the chemicals in cig smoke impair vasodilation (dilation of the blood vessels) and cause thickening of the blood vessels- thus increasing blood pressure.

68
Q

(C2) Describe how a fatty streak may progress to cause acute cardiac ischaemia.

A

A fatty streak in a coronary artery wall would then become a fibrolipid plaque as collagen deposits making the vessel wall stiffer and forming a fibrotic cap over the fatty streak. This cap then gets damaged by the high BP of blood flowing past, forming complicated fibrolipid plaque. This would in turn reduce the diameter of the lumen of the coronary artery, thus reducing blood perfusion to the cardiac muscle. As a result, acute cardiac ischaemia could be caused as the heart muscles would lack blood and thus oxygen, leading to ischaemia.

69
Q

(C2) Your patient has known angina and experiences symptoms on attending your clinic. What questions will you ask to help differentiate Stable Angina from ACS?

A

Use THE DRS (Trigger/History/Episodes/Duration/Resolution/Severity)
-What triggers the chest pain/symptoms?
-Do you have history have angina/chest pain?
-Have you experienced an increase in episodes of chest pain/angina attacks?
-How long do the symptoms last usually?
-How does it resolve usually? Does it resolve quickly?
-How does the pain feel in comparison to typical chest pain?

70
Q

(C2) What are the symptoms of acute cardiac ischaemia? Explain why these symptoms occur.

A
  • Discomfort
    o Pressure builds up behind the heart at the pulmonary side of the circulation (blood in pulmonary vein not efficiently moved out and onwards so pressure builds up) and can cause fluid to be leaking out of the blood vessels in the lungs = causing pulmonary oedema (fluid in the tissue of the lungs). This fluid in turn reduces the efficiency of gas exchange in the lungs. Hypoxia potentially a sign of ACI – may be seen as cyanosis (peripherally: bluish tinge to fingertips. Centrally: often around mouth). More likely to see hypoxia through fast HR and fast respiratory rate.
  • Breathlessness
    o As cardiac cells get damaged or die, they’re unable to contract as efficiently = reduced stroke volume = affected cardiac output and perfusion to other organs = pt breathless as trying to compensate for lack of oxygen to organs
  • Lightheaded
    o Reduced perfusion to brain because of affected cardiac output.
  • Clammy
    o The sympathetic nervous system will kick in to inc HR and SV and maintain the CO and the BP. But this can make pt appear clammy as they sweat as a side effect of the sympathetic nervous system, but cold to touch as peripheral vasoconstriction happening too.
  • Nausea
    o Sympathetic nervous system makes pt feel nauseous
  • Palpitations
    o Cardiac damage in ischaemia can result in abnormal electrical rhythms within heart -> irregular heartbeat (palpitations). Note: pt might describe increase HR as palpitations so need to take a manual pulse to check if the “palpitations” is arrhythmia.
    o If pt has irregular heart rhythm, may affect HR -> due to abnormalities in recovery period between heartbeats.
    o If pt has irregular heart rhythm, may affect SV -> because if heart is beating very fast, it has not got much time to refill between beats.
    o Can also have slow arrythmias eg heart block
    o Certain types of arrhythmias will often precede a cardiac arrest (cardiac arrest is when heart malfunctions and suddenly stops beating unexpectedly. Heart attack is myocardial infarction, when there is a blockage of blood flow to heart).
71
Q

(C2) Your patient has recently been told they have an abdominal aortic aneurysm.
1) How does this occur and what are the risks? 2) What follow up and treatment might they have?

A

1) Weakening of artery walls leading to aneurysms.
Aneurysm may create a fistula (abnormal connection or passageway that connects two organs or vessels that do not usually connect) into nearby vessels or may compress nearby structures.

2) Regular long-term radiological follow-up to monitor how big the aneurysm has got.
Monitored on size and may have it surgically fixed once it reaches certain size to prevent it from rupturing.

72
Q

(C2) What is a thrombosis and what symptoms might it cause?

A

Thrombosis is the coagulation/clotting of blood. It is a mass of platelets, RBCs and fibrin sitting on the vessel wall. Can be formed due to stickiness of the blood constituents, blood flow and damage to vessel wall. Symptoms depend on the location of the thrombus and include pain (in leg for example), swelling, chest pain. This is because there is reduced blood flow leading to stress to tissues causing infarction.

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