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Body Systems > When the cardiovascular system goes wrong > Flashcards

When the cardiovascular system goes wrong Flashcards

1
Q

What mechanisms is hypertension associated with?

A
  • Venous return
  • Filling time
  • Hormones
  • Vasoconstriction/ dilation
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2
Q

What mechanisms is Atherosclerosis/ thrombosis/CAD associated with?

A
  • Venous return
  • Vasodilation/constriction
  • Contractility
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3
Q

What processes are valve defects associated with?

A
  • end diastolic volume

- end systolic volume

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4
Q

What processes are arrhythmias associated with?

A
  • EDV
  • ESV
  • Heart rate
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5
Q

What mechanisms is heart failure associated with?

A
  • Contractility

- Stroke volume

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6
Q

What is hypertension?

A

associated with high blood pressure

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7
Q

What are the two types of hypertension?

A

Primary and Secondary hypertension

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8
Q

Give features of primary hypertension

A
  • Unknown medical cause
  • Essential/idiopathic
  • Linked to: genetic predisposition, alcohol intake, obesity, lack of exercise, diabetes, intrauterine environment, etc
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9
Q

Give features of secondary hypertension

A
  • Of known medical cause
  • Kidney disease – increased angiotensin II leading to vasoconstriction and expansion of extracellular fluid
  • General endocrine disorders e.g. diabetes
  • Adrenal medulla diseases (phaeochromocytoma) – excessive adrenaline secretion
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10
Q

How can you treat hypertension?

A
  • Angiotensin converting enzyme inhibiter or angiotensin II receptor blockers inhibit the actions of angiotensin II of aldosterone production thereby preventing renal Na+/H2O absorption and blood volume increase, and prevents vasoconstrictor actions of angiotensin II
  • Calcium channel blockers inhibits Ca-channels in cardiac muscle and vascular smooth muscle cells preventing depolarization. Thereby decreasing CO and causing vasodilation, respectively
  • Thiazide diuretics increase Na+ and water loss, thereby decreasing fluid volume which decreases venous return and cardiac output
  • A-Adrenoceptor antagonists (a-blockers) reduce TPR by inhibiting the action of noradrenaline
  • B-Adrenoceptor Antagonists (B-blockers) decreases Cardiac output and SNS activity centrally, decreases renin release leading to favourable secondary actions
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11
Q

What is hypertension a risk factor for?

A
  • Atherosclerosis
  • Stroke
  • Heart failure
  • Renal failure
  • Aneurysms (weakened arterial walls due to elevated pressures over a number of years – eventually ruptures – results in immediate death in major blood vessel such as aorta)
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12
Q

What is atherosclerosis and how does it form?

A
  • Associated with the occlusion of blood flow through blood vessels
  • Fibrous cap of a dense extracellular matrix narrows lumen of vessel and restricts blood flow
  • Cap formed from Lipid accumulation, macrophages, proinflammatory mediators, white cells, endothelial cells, smooth muscle cells etc
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13
Q

What can atherosclerosis lead to and how?

A
  • can lead to a thrombosis

- fragments of plaques can detach and lodge in small vessels

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14
Q

What is a thrombosis?

A

When a blood clot forms in a vein

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15
Q

where is a thrombosis most commonly found?

A

• Most commonly found in a leg vein: deep vein thrombosis (DVT)

  • Most of the problems will start and progress around veins
  • Stasis of blood in venous return
  • Can lead to pulmonary embolisms as clots may travel around the circulatory system
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16
Q

What is a blood clot in the lungs called?

A

A pulmonary Embolism

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17
Q

What are other names for coronary artery disease (CAD)

A
  • ischaemic heart disease

- heart attack

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18
Q

When does CAD occur?

A

When blood flow to the myocardium is insufficient for its needs

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19
Q

What is angina pectoris?

A

ischemia-induced pain mediated by endogenous vasodilators (coronary vasodilators)

  • If tissue becomes compromised (dies) then molecules (endogenous vasodilators) become released and attach to pain receptors
  • Angina pectoris is an early warning sign of a CAD
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20
Q

Where is CAD most frequent?

A
  • in the left ventricle
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21
Q

What is the most common cause of CAD?

A

atherosclerosis of a coronary artery

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22
Q

How quickly does the heart muscle start to die with insufficient supply of blood?

A

within 20 minutes

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23
Q

What are valve defects?

A
  • problems with the movement of blood through the heart

- defects in opening and closing times of the valves

24
Q

What is regurgitation?

A

inadequate closure of valve leading to backflow and turbulence; followed by a decrease in cardiac output

25
Q

What is Stenosis?

A

inadequate opening of valve obstructing blood flow

26
Q

What are the causes of stenosis?

A

thickening of the valve, papillary muscle or cordae tendinae following disease. Rheumatic fever can cause mitral valve stenosis up to 20 years after infection

27
Q

Hypertrophy happens after severe occlusion due to stenosis. What does this do?

A
  • greater contractility to maintain the cardiac output
  • leads to increased blood pressure
  • leads to oedema and dilation of heart chambers (due to disharmony in electrical signals)
  • leads to heart failure
28
Q

What are arrhythmias?

A

Deviation of the heart’s normal sinus (SAN) rhythm

29
Q

What is Bradycardia?

A

A slow rhythm <60 bpm

30
Q

What are the causes of Bradycardia and what is the treatment?

A
  • Causes:
     Slowed signal from the SAN – sinus bradycardia
     ‘Pause’ in the normal activity of the SAN – sinus arrest
     Block of the electrical impulse due to SAN, AV or conducting tissue damage
  • Treatment:
     Artificial pacemaker ad resetting of natural rhythm of heart
31
Q

What is Tachycardia?

A

A fast rhythm > 100bpm

32
Q

What is Sinus tachycardia?

A

Inappropriate Sinus Tachycardia (IST) (where pacemaker cells are generating too fast a signal) can involve caffeine, amphetamines, or overactive thyroid gland which would have an effect on the SNS

33
Q

What is non-sinus tachycardia?

A

 Independent of the SAN

 Results from the addition of abnormal impulses to the normal cycle (outside the SAN). Detected by an ECG

34
Q

What is non-sinus tachycardia caused by?

A

 Automaticity – enhanced pacemaker
 Triggered beats – early or delayed depolarization
 Re-entry activity/ circus activity – smooth conduction profile defect

35
Q

What is ventricular fibrillation?

A
  • type of tachycardia
  • Uncontrolled twitching or quivering of muscle fibres (fibrils)
  • During ventricular fibrillation blood is not removed from heart because ventricles are twitching so much
  • Results in sudden cardiac death
36
Q

What may lead to non-sinus tachycardia?

A

Congenital heart disease; electrocution accidents or injury to the heart; cardiomyopathies; heart surgery; ischaemia – can all lead to tachycardia
- If part of the heart becomes damaged (e.g. after ischaemia) then muscle cells may generate rogue electrical impulses

37
Q

What is triggered beat pathology (LQT syndrome)?

A

 Causes spontaneous multiple depolarizations leading to ventricular arrythmias
 Produce a sustained abnormal rhythm
 Extended action potential profile generating disharmony between mechanical and electrical pathways

38
Q

What do many cases of LQT syndrome arise from and who is LQT syndrome most prevalent in?

A
  • many cases arise from defects in the ion channels that regulate ventricular action potentials
  • most prevalent in under 25s
39
Q

What is chronic heart failure?

A
  • Cardiac output is inadequate despite venous return

* Due to decline in contractility and an inability to develop forceful contracture

40
Q

What happens in systolic and diastolic heart failure?

A
  • Diastolic – heart can’t fill properly because of stiff and thick chambers
  • Systolic – heart can’t pump because of stretched and thin chambers (isn’t ejected from heart properly)
41
Q

What is chronic heart failure caused by?

A
  • CAD
  • Additional work of the heart
  • Hypertension
  • Valve defects
42
Q

What are the symptoms of chronic heart failure and why?

A
  • Breathlessness and fatigue
  • May affect the left, right or both sides of the heart
  • Left ventricular failure: fluid will build up in the lungs due to congestion of the veins of the lungs
  • Right ventricular failure, systemic capillary pressure increases and fluid will accumulate in the body, especially in the tissues of the legs and abdominal organs
43
Q

in angina pectoris when may someone feel pain and what does this pain feel like?

A
  • they may feel pain during exertion or emotional stress
  • may produce a sensation of pressure, chest constriction and pain that may radiate from the sternal area to the arms, back and neck
44
Q

What is a myocardial infraction?

A

A heart attack, linked with CAD

45
Q

What is an infract?

A

Death of an affected heart tissue

46
Q

How may coronary thrombosis occur?

A

: a vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wall

47
Q

How can a myocardial infraction usually be diagnosed and why?

A

with an ECG and blood studies – damaged myocardial cells release enzymes into the circulation and these elevated enzymes can be measured in diagnostic blood tests

48
Q

Give features of premature atrial contractions (PACs)

A

often occur in healthy individuals. The normal atrial rhythm is momentarily interrupted by a surprise atrial contraction. Stress, caffeine and various drugs may increase the incidence of PACs by increasing the permeabilities of the SA pacemakers.

49
Q

What happens in paroxysmal atrial tachycardia (PAT)?

A

a premature atrial contraction triggers a flurry of electrical activity. The ventricles are still able to keep pace and the heart rate jumps to about 180 bpm

50
Q

What happens during atrial fibrillation?

A

the impulses move over the atrial surface at rates of about 500 bpm. The atrial walls quiver instead of producing an organized contraction. The ventricular rate cannot follow and may remain within normal limits. The atria are now non-functional but they have such a small contribution to the EDV that the condition may go unnoticed in older adults

51
Q

When do premature ventricular contractions occur and why?

A

occur when a purkingie cell depolarizes to threshold and triggers a premature contraction. Single PCVs are common and not dangerous. The ectopic pacemaker is the cell responsible. Epinephrine or other stimulatory drugs or ionic changes that depolarize cardiac muscle plasma membranes may increase the frequency of PSCs

52
Q

What is ventricular tachycardua (VT)?

A

is four or more PVCs without intervening normal beats. Multiple PVCs and VT may indicate that serious cardiac problems exist

53
Q

What is ventricular fibrillation responsible for?

A

cardiac arrest. The ventricles quiver and stop pumping blood

54
Q

What is focal calcification?

A

is the deposition of calcium salts following the gradual degeneration of smooth muscle in the tunica media. Some focal calcification is part of the aging process. It may also develop in association with atherosclerosis

55
Q

Why are young women less susceptible to atherosclerosis?

A

Because oestrogen slows plaque formation

Body Systems (20 decks)

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