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Mind and Body > Cardiovascular Diseases > Flashcards

Cardiovascular Diseases Flashcards

1
Q

List some modifiable risk factors in coronary heart disease.

A
  • smoking
  • hypertension
  • diabetes
  • obesity
  • diet
  • physical activity
  • alcohol
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2
Q

List some non-modifiable risk factors in coronary heart disease.

(Brooker et al, 2013)

A
  • age
  • sex
  • ethnicity
  • genetics
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3
Q

What is hypertension and how is it determined?

(Brooker et al, 2013)

A
  • raised arterial blood pressure
  • determined by cardiac output and total peripheral resistance of the circulatory system
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4
Q

What are the consequences of high BP?

(Brooker et al, 2013)

A
  • high BP associated with higher risk
  • can cause stroke, myocardian infarction, kidney issues
  • lowering BP lowers relative risk of developing ischemic heart disease by 22% and stroke by 41%
  • risk of cardivascular diseases increases with increasing blood pressure
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5
Q

What BP would stage 1-3 hypertensive patients have?

(Brooker et al, 2013)

A
  1. 140-159/90-99
  2. 160-179/ 100-109
  3. > 180/>110

Normal BP is between 90-110/ 60-90

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6
Q

What is mean arterial pressure?

(Brooker et al, 2013)

A
  • cardaic output x peripheral resistance

altering either of these will affect blood pressure

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7
Q

How is cardaic output measured?

(Brooker et al, 2013)

A

CO = heart rate x stroke volume

  • expressed as the voluime of blood pumped by the heart in one minute
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8
Q

What is the end systolic and end diastolic volume?

(Brooker et al, 2013)

A

end systolic- how much the heart empties

end diastolic- how much the heart fills

These can increase cardiac output and stroke volume, increasing heart rate

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9
Q

What is systolic and diastolic pressure?

(Brooker et al, 2013)

A

Systolic pressure is the maximum blood pressure during contraction of the ventricles

Diastolic pressure is the minimum pressure recorded just prior to the next contraction

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10
Q

How isthe filling of blood into the heart determined?

(Brooker et al, 2013)

A
  • by the return of blood from the venous system
  • emptying of the heart by the contractibility of the heart muscle
  • increase in blood volume
  • this results in an increase of cardiac output.
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11
Q

What is total peripheral resistance (TPR)?

(Brooker et al, 2013)

A
  • sum of resistance offered by the small arteries and arterials to the flow of blood
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12
Q

What is Pouseuille’s law?

(Brooker et al, 2013)

A

resistance to flow in any blood vessel will be related to the viscoisty of blood, length of vessels and the radius of the vessel

  • small changes in radius will lead to large changes in peripheral resistance and potentially BP
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13
Q

How is blood pressure regulation achieved?

(Brooker et al, 2013)

A
  • through the autonomic system and homronal mechanisms
  • immediate control is managed by baroreceptor reflexes
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14
Q

How is BP controlled short term?

(Brooker et al, 2013)

A
  • sensory endings in cartoid sinuses and aortic arch detected increased BP and decrease the sympathetic stimualtion of the heart, reducing HR and BP short term
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15
Q

How is BP controlled long term?

(Brooker et al, 2013)

A
  • dependent on blood volume and controlled through renin-angiotensin-aldosterone system
  • when blood volume is increased so is stroke colume leading to increased cardiac output, causing BP to rise
  • this normally leads to a decrease in total peripheral reisstance and cardaic outout, restroting BP to normal values
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16
Q

What are the complications of high BP on the heart?

(Brooker et al, 2013)

A
  • left ventirvular hypertrophy
  • may lead to heart failure, cardiac arrythmias, myocardial infarct, sudden death
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17
Q

What are the complications of high BP on the brain?

(Brooker et al, 2013)

A
  • ischaemic or haemorrhagic stroke
  • also associated with imapired cognition in the elderly
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18
Q

What are the complications of high BP on the kidneys?

(Brooker et al, 2013)

A
  • associated with the development of renal disease as both a cause and acceleration of existing renal disease
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19
Q

What are the complications of high BP on the preipheral arteries?

(Brooker et al, 2013)

A
  • atherosclerosis, leading to narrowing of the artery and pain where there is insufficient perfusion of tissues
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20
Q

What lifestyle modifications can help combat hypertension?

(Brooker et al, 2013)

A
  • more exercise
  • balanced diet
  • no smoking
  • limited alcohol intake
  • reduce sodium intake
  • maintain calcium, magnesium, sodium intake
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21
Q

What medications can be taken for hypertension?

(Brooker et al, 2013)

A
  • diuretics
  • calcium channel blockers
  • angiotensin-converting enzyme (ACE) inhibitors
  • beta-blockers
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22
Q

What is ischaemic heart disease?

(Brooker et al, 2013)

A
  • reduced blood supply to the heart, most commonly caused by atherosclerosis, causing a blockage or narrowing of arteries
  • means the arteries are unable to supply sufficet oxygen to the heart muscle for it to function
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23
Q

What does ischaemia present as?

(Brooker et al, 2013)

A
  • angina pectoris, causing pain and discomfort on exertion (chest pain) in minor cases
  • in major irreversible causes it can result in cell death of the heart (myocardian infarction) causing possible death
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24
Q

How are coronary arteries arranged?

(Brooker et al, 2013)

A
  • branch off the aorta to get good supply of oxygenated blood
  • the right runs down and over the right ventricle, with its brances supplying the right ventricle and atrium
  • the left runs over the left ventricle, branching off as ir goes. major branch is called the circumflex branch which runs posteriously around the heart
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25
Q

Why is the left coronary artery very important?

(Brooker et al, 2013)

A
  • supplies larger part of the heart (the left ventricle)
  • area of heart muscle is usually onlu supplied by one branch of artery
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26
Q

What happens when an artery is blocked?

(Brooker et al, 2013)

A
  • the area of muscle it supplies is starved of oxygen and without a rapid intervention will die
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27
Q

What is the normal response of the artery to cardaic ischaemia?

(Brooker et al, 2013)

A
  • vasodialate by reducing its vascular tone
  • usually this is sufficeint enough to restore adequate blood supply is narrowing of vessel is not too severe
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28
Q

What happens if a heart vessel is reduced to less than 70% of its normal diameter?

(Brooker et al, 2013)

A
  • coronary blood flow will be barely sufficient to supply the oxygen demand of the heart muscle at rest
  • if stenosis reduces vessel to less than 90% diameter ischemia will develop
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29
Q

What are the main causes of ischaemia?

(Brooker et al, 2013)

A
  • unstabel angina
  • atherosclerotic plaque becoming exposed plus thrombis formation plus thrombus formation will lead to worsenes ischaemia
  • vascular tone or spasm
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30
Q

What would happen is someone has myocardial ischameia?

(Brooker et al, 2013)

A
  • outcome can depend on:
  • serverity- degree of blood flow reduction
  • duration of ischaemia
  • location of ischaemia
  • compensation from other blood vessels

all can lesd to reversible or irreversible myocardfial damage

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31
Q

What does stable angina look like in a patient?

(Brooker et al, 2013)

A
  • usually mild ischaemia brought on by physical or emotional stress
  • patients usually feel discomfort in chest that will be releived in a minute following rest
32
Q

What does unstable angina look like in a patient?

(Brooker et al, 2013)

A
  • involves rupture of atherosclerotic plaque aggregation and thrombus formation
  • discomfort persists for longer than 10 minutes and is more severe
33
Q

What is myocardial infarction?

(Brooker et al, 2013)

A
  • involves severe ischaemia leading to ATP depletion and loss of contraction within minutes but does not mean full cell death and damage is reversible
  • complete absense of blood flow for 20-30 minutes leads to irrevesible injury with necrosis complete in 6 hours
34
Q

Where do most myocardial infarctions occur?

(Brooker et al, 2013)

A

within the distribution of one cornoary artey

35
Q

What are the treatment options for MI and severe angina?

(Brooker et al, 2013)

A
  • Reduce O2 demand and restore O2 supply!!
  • reduce the work of the heart so it reduces its demand for oxygen can do this by
  • reducing stress both physical and emotional
  • supply oxygen via a mask or nasal cannula to improve the oxygen supply
  • use drugs to vasolite coronary arteries
36
Q

What do you do once a clear diagnosis of a patient who has MI has been made?

(Brooker et al, 2013)

A
  • restore blood supply as much as possible to area of damage
  • pharmacological: antithrombotic meds, fibrinolytic therapy (within 2 hours of onset symptoms) to breakdown thrombus
  • cardiac catheter to introduce assent or even directly remove a clot
    surgical intervention can be possible, would be coronary artery bypass graft
37
Q

How is a normal heartbeat generated?

(Brooker et al, 2013)

A
  • from sinoatrial node or sinus node (natural pacemaker of heart)
  • normal heart rate usually between 60-100 beats
38
Q

What is sinus bradycardia and what causes it?

(Brooker et al, 2013)

A
  • slowness, heart rate is less than 60 bpm
  • can be normal for some people
  • if asymptomatic doesnt require treatment
  • can also be caused by degeneration or damage to cells of sinus node or disease of atrioventricular node conduction
39
Q

How is bradycardia seen physiologically?

(Brooker et al, 2013)

A
  • increased interval between R waves on ECG
  • as it responds to passess of the respiratory cycle as you breathe out, the heart rate will speed up reducing R-R intervals
40
Q

What happens when there is a first degree AV block in the AV conduction system?

(Brooker et al, 2013)

A
  • prolonged interval between P waves and R wave
  • 1 to 1 relationship between P and R waves so P wave is always followed by R wave even if it is somewhat delayed
41
Q

What happens when there is a second degree AV block in the AV conduction system?

(Brooker et al, 2013)

A
  • where P and R relationship begins to be lost
    either gradually extending interval between the P and R waves until an R wave is missed
  • or where there is a constant interval between P and R waves but from time to time the conduction at the AV node fails and an R wave is missed
42
Q

What happens when there is a third degree AV block in the AV conduction system?

(Brooker et al, 2013)

A
  • complete lack of conduction across AV node, so P wave all follow its rhythm and the QRS complex will follow its own slower rhythm leading to a complete lack of relationship between the two
  • leads to lack of blood supply to the brain
43
Q

How may a patient with third degree AV block present?

(Brooker et al, 2013)

A
  • light headedness
  • fatigue
  • shortness of breath
  • fainting
44
Q

What are tachyarrythmias?

(Brooker et al, 2013)

A
  • increased rates of contraction of the atria or ventricles or lack of coordiantres activity contraction
45
Q

What is atrial tachycardia caused by?

(Brooker et al, 2013)

A
  • one or more areas of atria firing off resulting in a continuous or self-exciting activity in the atria.
  • some may resolve spontaneously, require pharmacological treatment, or need cardioversion
46
Q

What is an atrial flutter?

(Brooker et al, 2013)

A
  • continuous cycle of impulse is generated in the atria and so P waves are generated at the maximum rate possible for the atria (around 300 bpm)
  • not uncommon, can be pharmacologically controlled
47
Q

What is atrial fibrillation?

(Brooker et al, 2013)

A
  • chaotic and uncoordinates excitation of cells all over the atria
  • pateints can be symptomatic if ventricles continue to beat in a coordianted, slowed manner paced by AV nose
48
Q

What is ventricular tachycardia?

(Brooker et al, 2013)

A
  • three or more premature ventrivular beats on ECG
  • usually occur when there is structural damage to the heart and may be life threatening
  • can also occur in a normal heart rate
49
Q

What are the symptoms of ventricular tachycardia?

(Brooker et al, 2013)

A
  • dizziness
  • fainting
  • sweating
  • sudden cardiac death
50
Q

What is ventrivular fibrilation?

(Brooker et al, 2013)

A
  • compleley disorganised activity in ventricles
  • very life threatening
  • most common cause of cardiac death
  • treatment is to reboot the hearet asap
51
Q

Why does the heart need valves?

(Brooker et al, 2013)

A
  • prevents back flow through the chambers amd provide unimpeded oward flow of blood to the lungs or body
52
Q

What are the three valve disorders and what is their impact?

(Brooker et al, 2013)

A
  1. stenosis - flaps of valve thicken or fuse together which leads to them not opening fully and resisting the normal flow of blood through the body
  2. regurgitation - valve doesn’t completely close and back flow occurs
  3. atresia - heart flow has no opening at all

valve disorders are usually either congenital heart disorders or acquired valve disorders

53
Q

What valves are associated with the left side of the heart?

(Brooker et al, 2013)

A

aortic valve- semilunar valve normally with 3 cusps positioned between the left ventricle and aorta

  • the Mitral valve or left atrioventricular valve
54
Q

What probalms can affect the aortic valve?

(Brooker et al, 2013)

A
  • aortic stenosis
  • aortic regurgiation
55
Q

What is aortic stenosis?

(Brooker et al, 2013)

A
  • blood flow obstruction through valve which results in a pressure gradient between left ventricle and aorta
  • increases the work of heart in each systole
  • overtime left ventricle compensates by growing larger with thicker walls
56
Q

What happens if LV hypertrophy occurs?

(Brooker et al, 2013)

A
  • initally alright but over time the thickening of the ventricular wall reduces it compliance and makes filling the ventricle more difficult during the diastole making the heart work harder
  • can lead to fibrosis of mycardium, ischaemia, heart failure
57
Q

What is the most common form of aortic stenosis?

(Brooker et al, 2013)

A
  • age related calcification or degeneration of the valve usually presenting in the 60s-80s age range
58
Q

What is the main treatment for aortic stenosis?

(Brooker et al, 2013)

A

Aortic valve replacement

59
Q

What is aortic regurgitation?

(Brooker et al, 2013)

A
  • backflow of blood scross the ortic valve during diastole
60
Q

What are the main causews of aortic regurgitation?

(Brooker et al, 2013)

A
  • rheumatic heart disease
  • endocarditis, hypertenison, and congential bicuspid valve
61
Q

What happens to the heart when these is aortic regurgitation?

(Brooker et al, 2013)

A
  • Because of the backflow, the LV has an increase in blood volume. - immediate response is an increase in HR and contractility to maintain CO, long term there will be a dilation of the LV with hypertrophy.
  • As these adaptations begin to fail there will be a decrease in CO and an increasing back pressure into the pulmonary circulation as well as a reduction in the coronary circulation leading to myocardial ischaemia
62
Q

What problems can affect to mitral valve?

(Brooker et al, 2013)

A
  • mitral stenosis
  • mitral regurgitation
63
Q

What is mitral valve stenosis (MVS)?

(Brooker et al, 2013)

A
  • narrowing of the mitral valve leading to an obstructed blood flow from the left atrium to the left ventricle creating a pressure gradient back into the LA.
  • this damage is either congenital, acquired or rheumatic.
64
Q

How would you treat MVS?

(Brooker et al, 2013)

A
  • reducing the symptoms of pulmonary congestion and heart failure, slowing the progression of pulmonary hypertension and
    control ventricular rate.
  • surgical treatment may involve valve replacement or stretching open the valve with a percutaneous balloon, once the valve has been stretched its function should improve,
    but for patients with severe pulmonary hypertension the average survival time is 3
    years.
65
Q

What is mitral regurgitation?

(Brooker et al, 2013)

A
  • back flow from LV to LA caused by damage to the mitral valve
  • can be a degenerative change with age as well as rheumatic heart disease
66
Q

What valves are on the right side of the heart?

(Brooker et al, 2013)

A
  • pulmonary
  • tricuspid
67
Q

What problems can affect the pulmonary and tricuspid valves?

(Brooker et al, 2013)

A

pulmonary = pulmonary stenosis and pulmonary regurgitation

tricuspid = tricuspid stenosis and tricuspid regurgitation

68
Q

Why is the left side of the heart at more risk of problems than the right side?

(Brooker et al, 2013)

A
  • The right side of the
    heart is a relatively low pressure system avoiding high hydrostatic pressures in the respiratory portions of the lungs, if these pressures increase then fluid would tend to exude into the alveoli and gaseous exchange would be impeded
    or fail.
  • The left side of the heart is a much higher pressure system to drive the blood around the body
69
Q

What is heart failure?

(Brooker et al, 2013)

A
  • occurs when heart can no longer effectively pump blood to the rest of the body to meet its demands during normal activity
  • has high morbidity and mortality
  • end point of majority of heart diseases such as MI, hypertension, valvular heart diseases
70
Q

What is stage A of heart failure?

(Brooker et al, 2013)

A

people with underlying risk factors but no structural abnormality of the heart

71
Q

What is stage B of heart failure?

(Brooker et al, 2013)

A

structural abnormalities of the heart, but no symptoms of HF

72
Q

What is stage C of heart failure?

(Brooker et al, 2013)

A

have signs and symptoms of HF or asymptomatic when treated optimally

73
Q

What is stage D of heart failure?

(Brooker et al, 2013)

A

have signs and symptoms of HF despite being treated optimally

74
Q

Where in the heart can heart failure take place?

(Brooker et al, 2013)

A

can happen in left or right side but is typically both

left side
- due to left ventricular dysfunction, this results in a reduction of cardiac output with increasing back pressure into the pulmonary veins and
congestion.

right side
- dysfunction of the right ventricles limiting venous return from the systemic circulation and signs of fluid retention
in the body

75
Q

What are factors that affect cardiac function?

(Brooker et al, 2013)

A
  • cardiac contractility
  • myocardial relaxation
  • heart rate and rhythm
  • ventricular preload
  • ventricular after load
  • compensatory mechanisms
76
Q

What should nurses consider when caring for patients with heart problems?

(Lindberg, 2023)

A
  • should closely monitor their patients
  • should be able to reach by the patient if they have any concerns or questions regarding their problem
  • emotional support if its needed
  • actively listening to patients
  • encouraging healthy habits such as eating better, more exercise, no smoking, no fatty, high in salt foods, lower alcohol consumption
77
Q

List some references for cardiovascular diseases.

A
  • (Brooker et al, 2013)
  • (Lindberg, 2023)

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