Cardiovascular system Flashcards

(52 cards)

1
Q

What are the functions of the cardiovascular system?

A

1) Circulation (to deliver them to the tissues) of oxygen and nutrients

2) Circulation (to remove them from tissues) of carbon dioxide and other waste

3) Circulation of hormones for communication

4) immune defense

5) temperature regulation

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2
Q

What are the 2 divisions of circulation and differences between them?

A

Pulmonary circulation:
1) right atrium recieves deoxyggenated blood from vena cava (from tissues)

2) deoxygenated blood comes from right atrium to right ventricle

3) deoxygenated blood comes to lungs from the right ventricle through pulmonary artery

Systemic circulation:
4) left atrium recieves oxygenated blood from pulmonary vein

5) right atrium recieves oxygenated blood from right atrium

6) tissues recives oxygenated blood from the right ventricle through aorta.

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3
Q

What is the first branch of aorta?

A

Coronary arteries, which feed heart itself.

They empty into inferior vena cava.

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4
Q

What are the 2 types of vena cava?

A

Superior vena cava: collects deoxygenated blood from head (including brain) and arms.

Inferior vena cava: collects deoxygenated blood from the trunk, hepatic vein, renal vein, pelvis and legs.

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5
Q

What are portal systems?

A

Blood traveling through two sets of capillaries before entering veins of systemic circulation.

There
1 in the body:
- hepatic portal system: capillaries from digestive tract –> hepatic portal vein –> liver capillaries –> hepatic vein.

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6
Q

What is septum?

A

Central wall of the heart which divides the left and the right side.

Prevents deoxygenated and oxygenated blood from mixing.

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7
Q

Do the left and the right side of the heart contact on different time intervals?

A

No, the left and the right atria contact simultaneously, after that, the right and the left ventricle contract simultaneously.

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8
Q

Does heart contract continously?

A

Yes, it only rests for millisecons between beats.

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9
Q

What is the difference between ventricles and atria?

A

Atria recieve blood from the vessels. They contract to send blood to ventricles.

Ventricles transfer blood to the vessels (away from the heart) by contracting.

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10
Q

What is pericardium?

A

A tough sac surrounding the heart filled with fluid to protect the heart and decrease friction as heart beats.

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11
Q

What are atroventricular valves?

A
  • prevent blood backflow from ventricles to atria
  • their parts are connected to the ventricle bottom with chordae tendinae (thin collagen tendons)
  • chordae tendinae is connected to papillary muscles but they do not control opening of the valve
  • blood flow alone opens the valves
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12
Q

What are semilunar valves?

A
  • prevent blood backflow from arteries to ventricles
  • there is aortic and pulmonary semilunar valves
  • consist of 3 parts
  • are not connected to anything
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13
Q

Are atrioventricular valves and semilunar vales opened and closed at the same time?

A

No.

During ventricular contraction, atrioventricular valves are closed and semilunar valves are open.

It is other way round during ventricular relaxation.

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14
Q

What are the 2 types of atrioventricular valves?

A

Mitral (bicupsid) valve at the left side.

Tricupsid valve at the right side.

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15
Q

What are the features of contractile heart myocytes?

A
  • 99% of heart myocytes
  • like skeletal muscle fibres are straited and have sarcomeres
  • smaller than skeletal muscle fibres
  • only one nucleus per cell
  • mitochondria take 1/3 of cell
  • connected to each other with intercalated discs with desmosomes
  • gap junctions allow rapid depolarisation of cells and simultaneous contraction
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16
Q

What are the features of authorythmic cells (pacemakers)?

A
  • 1% of all cardiac myocytes
  • no sarcomeres
  • generate signals for heart contraction with no nervous system involvement (myogenic contraction)
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17
Q

What is action potential for contractile cardiac myocyte?

A

Lasts for >200 msec; have STABLE resting potential of -90 mV.

1) Na+ channels rapidly open at value just above -90 mV, almost “vertical” depolarisation.

2) Na+ channels close at +20 mV, slow repolarisation.

3) At +10 mV, Ca2+ channels open and K+ fast channels close; forms plateau phase.

4) At -10 mV, Ca2+ channels close and K+ slow channels open; repolarisation, untill resting potential is reached.

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18
Q

What is muscle twitch?

A

Muscle contracts and that relaxes.

One action potential corresponds to one muscle twitch in the heart in time.

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19
Q

What is refractory period?

A

Period during which another action potential cannot be triggered.

Crucial for heart muscle: gives ventricles enough time to become fully filled before next contraction.

Plateau phase makes action potential long, it prevents different action potentials from overlaping (summation) and hence prevents tetanus (too frequent heart contraction)

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20
Q

What is action potential for pacemakers?

A

Have unstable resting potential (-60 mV is the lowest value) - this allows spontaneous generation of action potentials.

Have IF-channels which are permeable to both Na+ and K+.

1) At -60 mV, IF channels open, more Na+ comes inside than K+ comes out. Leads to slow depolarisation.

2) At -40 mV (threshold), IF channels close, few Ca2+ channels open, Ca2+ comes inside.

3) Positive feedback: opening of few Ca2+ channels trigger opening of more and more Ca2+ channels. Leads to rapid depolarisation.

4) At +20 mV, Ca2+ channels close and slow K+ channels open. Results in rapid repolarisation.

5) At -60 mV slow K+ channels close and IF channels open again.

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21
Q

What is the order of electrical conducting system of the heart?

A

1) Sinoatrial node depolarises (a group of authorythmic/pacemaker cells)

2) Internodal pathways

3) Antrioventricular node

4) Antrioventricular bundle (Bundle of His) in septum.

5) Bundle branches, left and right (traveling to heart apex)

6) Purkinje fibers traveling from heart apex (bottom) to its top on both left and right sides.

22
Q

What is the main heart pacemaker?

A

Sinoatrial node, sets the rythms as a leader.

If sinoatrial node is damaged, atrioventricular node sets the rhythm, but it leads to much slower heart rate.

23
Q

What is the difference in depolarisation speed in atria and ventricles?

A

Atria depolarise quickly from top to bottom.

Ventricles depolarise slowly from bottom to top. Antrioventricular node slows down conduction.

24
Q

What is electrocardiogram?

A

The recoding of how heard depolarises during time. Corresponds to heart contraction patterns (not individual action potentials!!).

Einthhoven triangle:
- negative electrode on right arm

  • positive electrode on the left arm
  • positive electrode on the left leg.
25
What is a typical ECG?
1) P wave (part of PR interval): atria depolarisation 2) QRS compex (part of QT interval): atria recovery and ventricle depolarisation 3) T wave (another part of QT interval): ventricle recovery Diagnostic interpretation: - look if waves, intervals and segments are consistent in length - look if cycles are too frequent or too infrequent. - look if rhythm is irregular.
26
Is blood pressure in systemic circulation always the same?
No, there are pulses of blood pressure due to heart and hence arterial contractions. Systolic pressure: highest; in aorta; when ventricles contract; 120 mm Hg. Diastolic pressure: lower (not the lowest); in aorta; when ventricles relax; 80 mm Hg. Pulse pressure = systolic pressure - diastolic pressure
27
How to calculate mean arterial pressure?
Diastolic + 1/3(pulse) Depends on: - cardiac output (heart rate × stroke volume) - peripheral resistance (how much blood flows in arteries and arterioles)
28
What is the formula of just arterial pressure?
Cardiac output × peripheral resistance
29
How blood pressure is measured and what is Korotkoff sound?
Measured with sphygmomanometer. Cuff inflates - compression of artery - gives systolic pressure. Cuff deflates - artery is decompressed - blood squeezes with turbulent flow - Korotkoff sound. Cuff completely deflates - artery is completely decompressed - Korotkoff sounds disappears - diastolic pressure.
30
What is normal blood pressure?
120/80 mm Hg Hypertension: 140/90
31
In what part of the brain the blood pressure is controlled?
In cardiovascular control centre in medulla obolongata.
32
Where blood pressure is monitored and how it is corrected?
1) Baroreceprors in carotid artery and aorta sence blood pressure and send it to medulla obolongata through sensory neurons. 2a) decreased sympathetic output: less noreadrenaline to alpha receptors = vasodilation 2b) increased parasympathetic output: more acetyl choline to muscarinic receptors on sinoatrial node = decreased heart rate.
33
What are the differences between gallops, clicks and murmurs?
Those are sounds you can hear when listening to someone's chest using stethoscope. Gallops: sounds of turbulent blood flow into heart chambers after lup-dub (normal). Clicking: abnormal movement of valves (abnormal). Murmurs: too much blood leaking away from badly closed or too narrow valves (abnormal).
34
What is lub-dup?
Lub: sound of closing atrioventricular valves. Dup: sound of closing semilunar valves.
35
What are the main cardiovascular diseases?
- atherosclerosis - coronary (ischaemic) heart disease. Subtypes: - angina (stenocardia) - heart attack (myocardial infarction) - stroke (cerebrovascular accident) - hypertension - congestive heart failure - congenital heart disease such as: - mitral valve stenosis - septal defects - ductus arteriosus
36
What is the difference between HDL-cholesterol and LDL-cholesterol?
Both HDL and LDL are apolipoprotein carriers for cholesterol. High density lipoprotein: - "good cholesterol" - high levels - less chance for heart attacks - no receptors for them on endothelium - does not damage arteries Low density lipoprotein: - "bad cholesterol" - most of it is taken and processed by liver - when levels are too high, are also taken by endothelium, leading to atherosclerosis
37
What is ateroma?
Damaging fatty deposits on arteries caused by accumulation of LDL-cholesterol in endothelium.
38
How does atherosclerosis develop?
FATTY STREAK: 1) Endothelial cells transport elevated LDL-cholesterol into extracellular space. 2) LDL-cholesterol accumulates between endothelium and elastic connective tissue and becomes oxidized. 3) Macrophage ingest LDL-cholesterol and become foam cells. 4) Activated by macrophage cytokines, smoth muscle cells divide and also absorb LDL-cholesterol. STABLE FIBROUS PLAQUE: 5) accumulation of foam cells and smooth muscle cell and further addtion of LDL-cholesterol makes bigger and bigger lipid core. 6) Fibrous scar tissue develops to surround lipid core. 7) Dividing smooth muscle cells make the arterial walls thicker. 8) Calcified depositions in the plaque. VUNERABLE PLAQUE: 9) Macrophage release enzymes which degrade collagen in Fibrous scar tissue. 10) Platelets, exposed to collagen, form blood clots.
39
What are the complications of atherosclerosis?
1) Clot formation around vulnerable plaque or clot stuck in the narrower lumen due to stable fibrous plaque leads to blood supply blockage. This is especially dangerous in coronary arteries. 2) oxygen starvation in miocadium leads to accumulation of lactate and there are less ATP. 3) Less ATP - less Ca2+ is pumped out of cells. 4) Too much Ca2+ in cytosol - gap junctions are closed. 5) Routes for action potentials are limited, leads to arrhythmia or heart failure.
40
What are treatments for coronary heart disease?
- replace saturated fats with oily fish in the diet - no smoking - more exercising - antioxidant drugs - statins to decrease cholesterol synthesis in the liver (by competitively inhibiting HMG Coenzyme A reductase) and increase cholesterol uptake by other cells
41
What is the most common cause of coronary heart disease?
Coronary ateroma, which obstructs blood flow into myocardium.
42
What is the main cause of angina?
Lactic acid building up in the myocardium. Leads to intense pain not just in the chest, but left shoulder, arm, neck, jaw, back.
43
How is angina treated?
- vasodilators - thrombolitic agents (to dissolve clots) - angioplasty (using ballon to stretch artery) - coronary artery bypass (insering another vessel around blocked one to renew blood supply)
44
What is myocardial infarction and how it is treated?
This is the death of myocardium parts due to oxygen deprivation and damage due to irregular heart beat. Treatment: - thrombolitic agents (aspirin) - beta-blockers to reduce heart rate - face mask to give oxygen - coronary artery bypass.
45
What is stroke?
Disruption of blood supply to brain, leads to death of many neurons. Most common cause of disabling neurological damage. Leads to loss of speech and motor function on one side of the body. But many may recover from this.
46
What is hemorrhagic stroke?
High blood pressure leads to vessel rupture in the brain, blood leaks out. Surgery is needed to remove this blood and repair vessel.
47
What are the symptoms and causes of congestive heart failure?
- shortness of breath - pinkish liquid from caught - pulmonary edema Causes - heart muscle damage due to: - infections - diabetes - overactive thyroid - ateroma - hypertension
48
What are the features of hypertension?
- Baroreceprors lose their sensitivity and medulla obolongata does not try to reduce heart rate anymore - hypertrophy of myocardium to deal with more pressure - may lead to stroke, heart failure or atherosclerosis
49
What are the causes of hypertension?
Primary causes (95% of cases): - lack of vasodilators like nitric oxide - too much vasocontrictors like endothelins - chronic stress that overstumulates sympathetic nervous system - too stiff arterial walls - abnormalities in renin-angiotensin-aldosterone system Secondary causes (5% of cases): - water/salt retention - hormonal imbalance - damage of vasomotor centre in brain - atherosclerosis of aorta
50
How is hypertension treated?
- less salt and less fat - no alcohol, smoking - diuretics to decrease blood volume - beta-blockers to decrease heart rate - calcium channel blockers for vasodilation - inhibitors of angiotensin II
51
What are the causes of congenital heart disease?
- mutations (Marfan syndrome) - chromosome abnormalities (Down syndrome, Williams syndrome) - autoimmune - terarogens (alcohol, retinoic acid) - premature birth - infections
52
What are the consequences of mitral stenosis and septal defects?
Mitral stenosis: - mitral valve becomes too thick and rigid - it increases resistance - right ventricle hypertrophy to compensate Septum defects: - a hole between ventricles - blood flows from the left to right side, giving extra pressure - pulmonary hypertension and edema