Cardiovascular system Flashcards

(31 cards)

1
Q

What makes up the circulatory system?

A

The heart (pump), the blood vessels (pipes) and the blood (the fluid to be moved). Its function is impacted by the endocrine system, nervous system, and kidneys.

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2
Q

What are the 2 loops of the cardiovascular system?

A

Systemic:
Carries blood from the heart to the major parts of the body and back to the heart. Blood leaves the left ventricle via the aorta. It branches to form systemic arteries. It branches to form the microcirculation- arterioles, venules, capillaries. Venules form the veins which form the inferior (collects blood from below heart) and superior (collects blood from above heart) vena cava.

Pulmonary:
Carries oxygen-poor blood to the lungs and back to the heart. Blood leaves right ventricle through the pulmonary trunk which divides into pulmonary arteries- takes blood to both lungs. Arterioles, capillaries, venules, and veins are in the lungs. Blood returns to the left atrium via 4 pulmonary veins.

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3
Q

What is the difference between artery and pulmonary artery, and vein and pulmonary vein?

A

Blood vessels: arteries, arterioles, capillaries, venules, veins

Arteries carry oxygenated blood away from the heart; the pulmonary arteries carry deoxygenated blood to the lungs, where oxygenated blood is collected. High pressure.

Veins carry deoxygenated blood to the heart; the pulmonary vein carries oxygenated blood to the heart from the lungs. Very low pressure.

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4
Q

What is pressure, flow and resistance and what are the contributions to resistance?

A

Pressure- the force exerted, measured in mmHg.
Flow- the volume moved in the time, measured in mL/min.
Resistance- how difficult it is for blood to flow between 2 points at any given pressure difference- the measure of the friction that impedes flow. Increase resistance=decrease flow. As vessel diameter decreases, resistance increases; flow decreases.

Contributions to resistance:
Blood viscosity (thickness)- affected by volume and number of erythrocytes.
Total blood vessel length- how much ‘tubing’ is needed.
Blood vessel diameter- vasodilated vessels decrease resistance, vasoconstricted vessels increase resistance (biggest contributor).

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5
Q

What are elastic/conduit arteries and muscular arteries?

A

Elastic/conduit arteries:
Near the heart and carry blood for circulation (e.g. the aorta).
Large lumen (low resistance), contains more elastin than the muscular arteries.
Act as ‘pressure reservoirs’- expand and contract as blood is ejected by the heart, allows flow to be continuous.

Muscular arteries:
Deliver blood to specific organs (e.g. mesenteric artery, renal artery).
Have proportionally the most smooth muscle and are very active in vasoconstriction.
Play a large role in the regulation of blood pressure.

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6
Q

How does compliance relate to pressure?

A

If the walls stretch, lots of volume can be added, without a rise in pressure. A small amount of volume in less stretchy walls causes high pressure.

Compliance- how easily a structure stretches.

Pressure wouldn’t change if an equal volume of blood flowed into and out of an artery. About 1/3 of stroke volume leaves arteries during systole; the rest stays during systole- arteries distend them and raise the arterial pressure. After ventricular contraction, the artery recoils passively, and blood drives into arterioles.

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7
Q

What is systolic and diastolic blood pressure and pulse pressure?

A

Systolic blood pressure- maximal arterial pressure reached during peak ventricular ejection.

Diastolic blood pressure- minimal arterial pressure reached just before ventricular ejection.

Pulse pressure- difference between systolic and diastolic pressure.

Plaque build-up in arteries increase blood pressure, this may cause a cardiovascular issue (e.g. heart attack).

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8
Q

What are arterioles?

A

The smallest arteries, their function is controlled by neural, hormonal, and local chemicals.
Control minute-to-minute blood flow into capillary beds, they impact blood pressure.
If they contract, blood is diverted away from their tissues.
If they dilate, blood flow to the tissue increases.
The smallest are just a single layer of smooth muscle which spirals around the endothelium.
Arterioles have basal level of contraction (intrinsic tone).
Smooth muscle is regulated autonomically by local or extrinsic control.

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9
Q

How do arterioles control blood pressure?

A

Increase resistance by vasoconstriction and keep pressure the same, then flow to tissue decreases.
Increase flow to tissue, then increase pressure or vasodilate to decrease resistance.
Total arteriolar pressure that influences systemic arterial blood pressure, governed by total peripheral resistance.
If one tube opens too widely, then cardiac output must be increased to maintain arterial blood pressure- happens during exercise.

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10
Q

What are the 2 ways arterioles control resistance?

A

Local control:
Response to local metabolic or local blood flow changes. Blood flow increases to an organ due to an increase in metabolism. Local inflammation is characterised by increased blood flow. Leads to a decrease in oxygen, but an increase in CO2, potassium ions, nitric oxide, hydrogen ions and adenosine.

Extrinsic control of resistance:
Hormones- epinephrine (vasodilates or constricts depending on tissue), angiotensin II (constricts most arterioles), vasopressin (constricts most arterioles).
Sympathetic nerves- always some sympathetic tone, can be reduced resulting in vasodilation, by withdrawing sympathetic activity.

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11
Q

What are the 3 types of capillaries?

A

Capillaries are the smallest blood vessels, where gas and nutrient exchange take place

Continuous capillary- found in skin, muscle, most common kind have tight junctions.
Fenestrated capillary- more permeable- found in intestines, hormone-producing tissues, kidneys.
Sinusoidal capillary- only one with an incomplete basement membrane, found in liver, bone marrow and lymphoid tissues.

They develop and grow through angiogenesis (muscle adaptation, tumours), vascular endothelial cells release angiogenic factors (e.g. vascular endothelial growth factor)

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12
Q

How does blood flow through capillaries?

A

Blood flow through capillaries depends on other vessels in the microcirculation.

In some tissues and organs, blood enters capillaries through metarterioles. Capillaries can be damaged by high blood pressure.

The site at which a capillary exits from a metarteriole is surrounded by a ring of smooth muscle, the precapillary sphincter., which relaxes and contracts in response to local stimuli.

Slow movement of blood through capillaries maximises the time for substance exchange across the capillary wall- diffusion is a key process for gas, nutrient and waste product exchange. Blood velocity is dependent on the cross-sectional area of the vessel type.

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13
Q

What are veins?

A

Blood flows from capillaries into venules, then into veins.
Acts as low pressure conduits returning blood to the heart, they have thin and very compliant walls for low pressure (61% of blood is in the veins).
Maintain peripheral venous pressure.
Amount of blood in veins and compliance of walls are factors determining venous pressure.
Veins have valves which stop blood going backwards and allows the flow to continue to the heart, the valves will shut if blood tries to move backwards.

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14
Q

What is the pericardium, epicardium, myocardium and atrioventricular septum?

A

Pericardium- muscular sack enclosing heart.
Epicardium- fixes inner layer of pericardium to heart.
Myocardium- muscular wall of the heart formed from cardiac muscle cells.
Atrioventricular septum- muscular wall separating the ventricles.

The inner surface of chambers are lined with endothelial cells- endothelium.

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15
Q

What is the Atrioventricular (AV) valves, semi-lunar valves, chordae tendinae and papillary muscles?

A

AV valves- permit flow from atrium to ventricle but not backward.
Left AV valve has 2 fibrous flaps- the bicuspid/mitral valve.
Right AV has 3 fibrous flaps- tricuspid valve.
Pulmonary semi-lunar valve- blood from right ventricle to pulmonary trunk.
Aortic semi-lunar valve- blood from left ventricle into aorta.
Chordae tendinae- fasten AV valves to the papillary muscles.
Papillary muscles- limit movement to prevent backward flow of blood (don’t interact with AV valves).

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16
Q

How does blood flow through the heart?

A

Superior/inferior vena cava->Right atrium->Right AV valve->Right ventricle->Pulmonary valve->Pulmonary trunk->Pulmonary arteries->Capillaries of lungs->Pulmonary veins->Left atrium->Left AV valve->Left ventricle->Aortic valve->Aorta->Body

17
Q

What are cardiac muscles?

A

Cardiac muscle cells have 1 to 2 nuclei that are centrally located. They’re striated and use the sliding filament mechanism to contract. They’re branching cells with gap junctions that are for the heart to be electrically stimulated. They have large mitochondria to prevent heart from failing. Node cells stimulate their own action potentials- automaticity or auto-rhythmicity.

18
Q

How do cardiac muscle cells work?

A

When walls of a chamber contract, they come together and exert pressure on the blood they enclose. Every heart cell contract with every heartbeat- only 1% of heart muscle cells are replaced per year.

1% of cardiac cells don’t function in contraction but have specialised features needed for normal heart excitation. These cells are the conducting system of the heart (initiates the heartbeat); they’re in electrical contact with the cardiac muscle cells via gap junctions.

19
Q

How do the sympathetic and parasympathetic nervous systems innervate the heart?

A

Sympathetic nervous system innervates the entire heart muscle and node cells and release norepinephrine to increase heart rate. The receptors for norepinephrine are beta-adrenergic.

Parasympathetic nervous system innervates the node cells and release acetylcholine to slow down heart rate. The receptors for acetylcholine are of the muscarinic type.

20
Q

How does depolarisation occur in the heart?

A

The right and left sides of the heart pump separately but simultaneously- atria then ventricles. Contraction is triggered by depolarisation of the plasma membrane. Gap junctions between myocardial cells allow transmission of the action potential.

Initial depolarisation:
Sinoatrial node->Atrial muscle cells->Atrioventricular node->Bundle of His (collection of heart muscle cells for electrical conduction)->Left and right bundle branches->Left and right Purkinje fibres->Ventricular muscle cells

21
Q

What are the sinoatrial node, atrioventricular node and purkinje fibres?

A

Signal starts in the sinoatrial node (75 signals per minute). The wave of depolarisation travels through the internodal pathway to the atrioventricular node. The signal has a 0.1s delay allowing atria to contract and fill the ventricles before they contract. Purkinje fibres supply the papillary muscles which tell them to contract before the rest of the atria to help prevent backflow through the valves.

22
Q

What is an electrocardiogram (ECG)?

A

A graphic record of the heart’s electrical activity, not a single action potential.

The P wave results from the depolarisation wave from the SA node to the AV node. Atria contract 0.1s after P wave starts. The QRS complex results from the ventricular depolarisation and precedes ventricular contraction. The T wave is caused by ventricular repolarisation.

The atrial repolarisation is obscured by the QRS complex. Atrial fibrillation=electrical impulses in the atria fires chaotically.

23
Q

What is cardiac output, stroke volume and heart rate?

A

Cardiac output- the amount of blood pumped out of each ventricle in one minute, HR x SV, can reach 35 L/min during exercise.

Stroke volume- the difference between end diastolic volume and the end systolic volume. Volume of blood pumped from the left ventricle per beat.

Heart rate- if blood volume drops, SV declines and CO is maintained by increasing HR.
Positive chronotropic factors and the sympathetic nervous system increase HR. Negative chronotropic factors and the parasympathetic nervous system decrease HR.

24
Q

What is Frank Starling mechanism and Contractility?

A

Frank Starling mechanism- the ventricle contracts more forcefully during systole when it’s been filled to a greater degree during diastole. The greater the end diastolic volume, the more the muscles are stretched, the greater the contraction.

Contractility- norepinephrine acts on beta-adrenergic receptors to increase ventricular contractility- the strength of contraction at any given end-diastolic volume. Increased contractility results in greater stroke volume due to more complete ejection of the end-diastolic volume.

25
What is mean arterial pressure and what are mean cardiac output and stroke volume dependent on?
Mean arterial pressure- the major cardiovascular variable being regulated. Mean arterial pressure=Diastolic pressure+1/3 (systolic pressure-diastolic pressure) Mean arterial pressure is dependent on: Mean arterial pressure=Cardiac output x Total peripheral resistance Mean cardiac output is dependent on: Cardiac output=Heart rate x Stroke volume Mean stroke volume is dependent on: Stroke volume=End diastolic volume-End systolic volume
26
What are arterial baroreceptors?
They respond to changes in arterial pressure. Nerve endings are highly sensitive to stretch or distortion, the degree of stretching is directly proportional to blood pressure. Steady rate of neuronal discharge at normal mean arterial pressure. Over time, baroreceptors adapt and the only way to adjust blood pressure is by changing blood volume.
27
Where is the primary integrating centre for the baroreceptor reflexes?
A network of connected neurons called the medullary cardiovascular centre, in the medulla oblongata. Neurons receive input from the various baroreceptors; input determines action potential frequency from the CV centre. Increased firing of baroreceptors, decreased sympathetic outflow to heart, arterioles, veins and an increase in parasympathetic outflow to the heart. Decreased arterial pressure, increased plasma concentrations of angiotensin II and vasopressin, which increase arterial pressure by constricting arterioles.
28
How can high blood pressure (hypertension) be treated?
Diuretics- increase excretion of sodium and water, decreasing cardiac output with no change in peripheral resistance Beta-adrenergic receptor blockers- reduce cardiac output Calcium channel blockers- reduce entry of calcium in vascular smooth muscle cells=weaker contractions=lowers peripheral resistance Angiotensin-converting enzyme inhibitors- final step in formation of Angiotensin II is mediated by an ACE. Blocking this enzyme causes vasodilation lowering peripheral resistance.
29
What is the Renin-angiotensin system?
The kidneys regulate blood pressure- intra-renal baroreceptors detect changes in stretching due to lower blood volume which stimulates an increase in the production of renin. Angiotensin-converting enzymes are found on endothelial cells. Aldosterone- slow-acting steroid hormone that stimulates sodium reabsorption by kidney tubules. Vasopressin (anti-diuretic hormone)- rapid-acting peptide produced by the pituitary gland which stimulates water reabsorption. Interaction with the heart- cardiac cells produce atrial natriuretic peptide which: Inhibits sodium reabsorption by kidney tubular cells. Acts on renal blood vessels to increase filtration rate causing sodium excretion. Inhibits the action of aldosterone.
30
What happens hours and days after blood loss?
Within hours of blood loss: Compensatory movement of interstitial fluid into the capillaries to increase plasma volume. This is a redistribution of fluid, not a replacement of fluid. Slower effects- an increase in thirst, decrease in salt and water excretion. Mediated by hormones and kidney function: renin, angiotensin and aldosterone. Within days of blood loss: Replacement of cells- erythropoiesis, haematopoiesis.
31
What's the immediate response to blood loss (hemorrhage)?
Decreased arterial pressure and firing by arterial baroreceptors. Decreased parasympathetic and increased sympathetic discharge to the heart, increasing HR. Increased sympathetic discharge to veins and arterioles, increasing constriction in veins and arterioles. Increased venous pressure, venous return and end-diastolic volume. Increased stroke volume, cardiac output and total peripheral resistance increases arterial pressure towards normal.