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blood pressure Flashcards

1
Q

What is the relationship between wall tension and pressure in a cylinder?

A

Wall tension is directly proportional to pressure.

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2
Q

What is the relationship between wall tension and radius in a cylinder?

A

Wall tension is directly proportional to the radius.

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3
Q

How does vessel size affect wall tension?

A

The larger the vessel, the greater the wall tension.

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4
Q

What is vessel compliance?

A

Vessel compliance is the volume change caused by a change in pressure.

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5
Q

What factors can affect vessel compliance?

A

Age and wall pathologies can affect vessel compliance (e.g., atherosclerosis or calcification).

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6
Q

What is laminar flow?

A

Laminar flow refers to the smooth, streamlined flow of fluid where the velocity is slower at the edges.

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7
Q

What conditions are more likely to cause turbulent flow?

A

Turbulent flow is more likely to occur with increased velocity and low fluid viscosity.

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8
Q

What are some causes of turbulence in blood flow?

A

Turbulence in blood flow may be caused by vessel junctions (e.g., vessel branching), obstacles (e.g., foreign bodies), and mixing (e.g., “holes-in-the-heart”).

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9
Q

What are the layers of the arterial wall from outermost to innermost?

A

The layers of the arterial wall from outermost to innermost are adventitia, media, and intima.

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10
Q

What are the components of the arterial media layer?

A

The arterial media layer consists of the external elastic membrane, smooth muscle, and internal elastic membrane.

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11
Q

What is the innermost part of the arterial wall?

A

The innermost part of the arterial wall is the endothelium, located in the intima layer.

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12
Q

What is atherosclerosis?

A

Atherosclerosis refers to the build-up of fats, cholesterol, and other substances in and on the artery walls, forming plaques that can restrict blood flow and lead to heart attacks, strokes, and peripheral arterial disease.

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13
Q

What are the stages of plaque development in atherosclerosis?

A

The stages of plaque development in atherosclerosis are fatty streak, fibrous plaque, occlusive atherosclerotic plaque, and plaque rupture.

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14
Q

What can trigger a blood clot in atherosclerosis?

A

Plaque rupture can trigger the formation of a blood clot.

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15
Q

What are the components of intimal plaque in atherosclerosis?

A

Intimal plaque in atherosclerosis can progress from fatty streak to fibrous plaque to calcified plaque, eventually leading to plaque rupture.

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16
Q

What is the effect of medial thinning in atherosclerosis?

A

Medial thinning in atherosclerosis leads to increased compliance of the artery.

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17
Q

What is adventitial erosion in atherosclerosis?

A

Adventitial erosion refers to damage or erosion of the adventitia layer of the arterial wall in atherosclerosis.

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18
Q

What are some functions of the endothelium in regulating blood vessels?

A

The endothelium plays a role in the local control of vessel tone, local control of thrombogenicity, capillary filtration, and release of vasodilator substances such as nitric oxide and prostacyclin.

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19
Q

What are some endothelium functions in local vessel tone control?

A

The endothelium regulates local perfusion and can induce vasodilation by releasing substances like nitric oxide and prostacyclin.

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20
Q

What are some functions of the endothelium in the local control of thrombogenicity?

A

The endothelium conceals collagen and plaque constituents, secretes antithrombotic factors such as prostacyclin, and prevents excessive blood clot formation.

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21
Q

What are nitric oxide and prostacyclin?

A

Nitric oxide and prostacyclin are vasodilator substances released by the endothelium.

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22
Q

What does it mean for something to be thrombogenic?

A

Thrombogenic means that it is liable to provoke blood clotting, either through the activation of platelets, the activation of the blood clotting cascade, or both.

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23
Q

What is the process of myocardial infarction caused by coronary thrombosis?

A

The process involves plaque rupture, exposing collagen and lipid in a thin cap, “vulnerable” plaque, leading to platelet adhesion and activation of the clotting system, ultimately resulting in the occlusion of the coronary artery.

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24
Q

What is plaque in the context of myocardial infarction?

A

Plaque refers to the build-up of fats, cholesterol, and other substances in and on the artery walls, with a lipid-rich core covered by a fibrous tissue cap.

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25
Q

How does a thrombus form in the context of myocardial infarction?

A

A thrombus, or blood clot, forms when blood is exposed to collagen and lipids, activating platelets and the blood clotting pathways.

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26
Q

What are the stages in the ischemic cascade as ischemia severity increases over time?

A

The stages in the ischemic cascade are hypoperfusion, metabolic disturbance (including arrhythmia), diastolic dysfunction, systolic dysfunction (leading to acute heart failure), ECG changes, chest pain, and myocyte necrosis.

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27
Q

What are the consequences of decreased LV contractility?

A

Decreased LV contractility leads to increased left atrium/pulmonary vein pressures, which can cause pulmonary oedema, as well as increased pulmonary artery/right ventricle/right atrium pressures, which can cause peripheral oedema. It also results in increased venous return (preload) and can cause an increase in cardiac output.

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28
Q

How does decreased cardiac output affect fluid retention and cardiac production?

A

Decreased cardiac output leads to increased renin/angiotensin/aldosterone levels, which in turn cause renal sodium and water retention. This leads to increased contractility and eventually increased cardiac output.

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29
Q

What is another pathway by which decreased cardiac output leads to increased fluid retention and cardiac output?

A

Another pathway involves increased sympathetic activation, increasing renin/angiotensin/aldosterone levels and subsequent renal sodium and water retention. This, in turn, increases contractility and, eventually, cardiac output.

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30
Q

What is remodelling in the context of cardiovascular physiology?

A

Remodeling refers to chronic changes in tissue shape, size, and function in response to injury. It can occur due to pressure overload, volume overload, or myocardial damage.

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31
Q

What can cause pressure overload in the cardiovascular system?

A

Pressure overload can be caused by narrow valves or hypertension.

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32
Q

What can cause volume overload in the cardiovascular system?

A

Volume overload can occur due to conditions such as leaky valves.

33
Q

What are some causes of myocardial damage that can lead to remodelling?

A

Myocardial damage can be caused by myocardial infarction (MI), alcohol consumption, viral infections, etc.

34
Q

What are the outcomes of remodelling in the cardiovascular system?

A

Remodeling can result in hypertrophy and/or dilation of the affected structures. These changes may be compensatory initially, but they can become pathological over time.

35
Q

What happens during sympathetic activation in response to low cardiac output?

A

Sympathetic activation occurs, leading to increased contractility and cardiac output. However, it also increases afterload and can cause catecholamine cardiotoxicity, leading to structural and functional changes in cardiomyocytes, left ventricular (LV) dilation, adverse remodelling, and increased LV systolic dysfunction.

36
Q

What formula calculates mean blood pressure (BP)?

A

Mean BP = Systolic BP (SBP) + 2 × Diastolic BP (DBP) / 3

37
Q

How does blood flow differ in different parts of the circulatory system?

A

Blood flow is pulsatile in the aorta and large arteries but becomes laminar in the capillaries and veins.

38
Q

What is systemic arterial blood pressure?

A

Systemic arterial blood pressure is the pressure exerted by blood on the arterial walls in systemic circulation.

39
Q

What are some consequences of blood pressure being too low?

A

When blood pressure is too low, it can lead to symptoms such as fainting (vaso-vagal attack) and shock, which can result in tissue acidosis (pH <7.35).

40
Q

What are some consequences of blood pressure being too high?

A

When blood pressure is too high, it can cause tissue damage.

41
Q

What are the determinants of blood pressure?

A

The determinants of blood pressure are cardiac output (the amount of blood pumped by the heart) and vascular resistance (mainly determined by arteriolar constriction).

42
Q

How can blood pressure be represented using Ohm’s law?

A

Blood pressure (BP) can be represented as the product of cardiac output (CO) and systemic vascular resistance (SVR): BP = CO × SVR.

43
Q

How does gravity affect blood pressure?

A

Blood pressure is higher in the feet and lower in the head due to the influence of gravity.

44
Q

What is arterial compliance?

A

Arterial compliance refers to the ability of arteries to stretch and store elastic potential energy during systole, which is released to maintain flow during diastole. Stiff arteries, such as those associated with old age, reduce compliance and increase systolic blood pressure.

45
Q

How does blood viscosity affect blood pressure?

A

Blood viscosity contributes to resistance to flow. Blood with high protein content or hypercellularity has a higher viscosity, requiring higher pressure to maintain flow.

46
Q

What factors affect cardiac output (CO) and systemic vascular resistance (SVR)?

A

The factors affecting CO are stroke volume (SV) and heart rate (HR), while SVR is influenced by vessel diameter, blood viscosity, and arterial compliance.

47
Q

How is cardiac output calculated?

A

Cardiac output is calculated by multiplying stroke volume (SV) by heart rate (HR). CO = SV x HR.

48
Q

What is the human body’s average stroke volume and heart rate?

A

The average stroke volume is approximately 80 mL/beat, and the average heart rate is approximately 60 beats per minute.

49
Q

What is blood volume composed of?

A

Blood volume comprises cells (red and white blood cells) and plasma.

50
Q

What is plasma made up of?

A

Plasma is composed of water, salt, and proteins.

51
Q

How do the kidneys regulate blood volume?

A

The kidneys play a role in regulating blood volume through the action of hormones such as aldosterone and antidiuretic hormone (ADH). Aldosterone promotes salt retention in the distal convoluted tubule, while ADH promotes water retention in the distal convoluted tubule and collecting ducts. These hormones are released in response to increased plasma osmolarity.

52
Q

What is the intrinsic heart rate?

A

The sinus node in the right atrium sets the intrinsic heart rate.

53
Q

How does the autonomic nervous system control heart rate?

A

The sympathetic nervous system, through β1 receptors, increases heart rate, while the parasympathetic system (via the vagus nerve) slows heart rate through M2 muscarinic receptors.

54
Q

What circulating substance can affect heart rate?

A

Adrenaline (epinephrine) can increase heart rate by acting on β1 receptors.

55
Q

What is the relationship between heart rate and sympathetic/parasympathetic stimulation and circulating adrenaline?

A

Sympathetic stimulation, adrenaline, and β1 receptor activation increase heart rate, while parasympathetic (vagal) stimulation and M2 muscarinic receptor activation slow the heart rate.

56
Q

What is the cardiac pressure-volume relationship?

A

The cardiac pressure-volume relationship shows the changes in pressure and volume within the heart during a cardiac cycle. It involves the opening and closing of the mitral valve (MV), aortic valve (AoV), and tricuspid valve (AV) at different stages.

57
Q

What is Starling’s Law?

A

Starling’s Law states that the mechanical energy released during the transition from the resting to the active state of cardiac muscle fibres is proportional to the length of the fibre. The length of the fibre is determined by the end-diastolic volume, which is influenced by venous return. The force of contraction is translated into stroke volume.

58
Q

What factors contribute to preload (venous return)?

A

Preload, or venous return, is determined by factors such as circulating blood volume (e.g., dehydration, major bleeding, kidney failure, over-transfusion) and venous tone, which is regulated by the autonomic nervous system, circulating vasoconstrictors (e.g., adrenaline), and local vasoactive substances (e.g., nitric oxide, prostacyclin, endothelin).

59
Q

How is the force of contraction translated into stroke volume?

A

The force of contraction, influenced by Starling’s Law, is proportional to the length of the cardiac muscle fibre (determined by end-diastolic volume). This force generates stroke volume, the amount of blood ejected from the heart with each contraction.

60
Q

What is the Renin-Angiotensin-Aldosterone System (RAAS)?

A

The RAAS is a hormonal system that regulates blood pressure and fluid balance. It involves the conversion of angiotensinogen to angiotensin I by renin, followed by angiotensin I to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II stimulates vasoconstriction and the release of aldosterone, which promotes sodium and water reabsorption, leading to increased blood volume and blood pressure.

61
Q

Why is the RAAS necessary for blood pressure control?

A

The RAAS is crucial in maintaining blood pressure within a normal range. Promoting vasoconstriction and increasing blood volume through sodium and water reabsorption helps elevate blood pressure when it is too low.

62
Q

What are the local controls that regulate tissue perfusion?

A

Tissue perfusion is autoregulated at the level of the arterioles. Local controls include vasodilation in response to low oxygen or high carbon dioxide levels, acidosis, and the release of nitric oxide and prostacyclin. Conversely, endothelin promotes vasoconstriction.

63
Q

What are the effects of circulating catecholamines on blood pressure?

A

Circulating catecholamines, such as adrenaline and noradrenaline, have general and sustained effects in response to acute changes. They act on various receptors, including alpha and beta receptors. Alpha receptors mediate vasoconstriction, beta receptors in systemic arterioles promote vasodilation (specifically beta-2 receptors in muscles), and beta-1 receptors in the heart increase heart rate and force of contraction.

64
Q

Which receptors do adrenaline and noradrenaline act on?

A

Noradrenaline predominantly acts on alpha receptors, while adrenaline can stimulate alpha and beta receptors.

65
Q

What are the sensors involved in blood pressure regulation?

A

Baroreceptors located in the aortic arch and carotid body (at the carotid bifurcation) act as sensors for blood pressure regulation.

66
Q

What are the control centres for blood pressure regulation?

A

The brainstem houses the cardiovascular control centres, including the cardio-accelerator centre, cardio-inhibitory centre, and vasomotor centre. These centres integrate sympathetic and parasympathetic responses.

67
Q

What are the effectors involved in blood pressure regulation?

A

Sympathetic nerves release noradrenaline, induce vasoconstriction (except in muscles where vasodilation occurs), and increase heart rate and force. Parasympathetic nerves release acetylcholine, causing vasodilation, while the vagus nerve decreases heart rate.

68
Q

What is hypotension?

A

Hypotension refers to abnormally low blood pressure. Dehydration, blood loss, medication side effects, or underlying medical conditions can cause it.

69
Q

What is hypertension?

A

Hypertension is abnormally high blood pressure. It can be caused by conditions such as chronic kidney disease, renal artery stenosis, aortic coarctation, hormonal imbalances (e.g., high aldosterone or catecholamine levels), pregnancy/pre-eclampsia, or essential hypertension (multifactorial with genetic, lifestyle, and environmental factors).

70
Q

What is shock?

A

Shock is a life-threatening condition characterised by inadequate blood flow and oxygen delivery to the body’s tissues. It can result from various causes, such as severe blood loss, heart failure, infection, or allergic reactions.

71
Q

What are some effects of chronic hypertension on the body?

A

Chronic hypertension can lead to heart muscle damage (heart failure), large vessel damage (e.g., aortic aneurysm, cerebrovascular disease, coronary artery disease, peripheral vascular disease), and microvascular damage (e.g., kidney dysfunction, brain dysfunction, exacerbation of vascular effects in diabetes).

72
Q

What are some acute effects of severe hypertension?

A

Acute effects of severe hypertension can include aortic dissection, acute heart failure due to high afterload, confusion (encephalopathy), cerebral haemorrhage, and retinal haemorrhage.

73
Q

What are faints (vaso-vagal episodes)?

A

Faints, also known as vaso-vagal episodes or neurally-mediated syncope, typically occur as a reaction to a stressful episode. Disproportionate parasympathetic activation causes arteriolar dilation, slowing of heart rate, and a fall in blood pressure, resulting in reduced cerebral perfusion and transient loss of consciousness.

74
Q

What is tLoC?

A

tLoC stands for transient loss of consciousness during fainting episodes.

75
Q

What is shock?

A

Shock is a state of organ hypoperfusion characterised by persistently low blood pressure (<90mmHg systolic). It is a condition with reduced perfusion of vital tissues, resulting in cellular dysfunction and potential death.

76
Q

What are the symptoms of shock?

A

Symptoms of shock include altered mental status, tachycardia (rapid heart rate), hypotension (low blood pressure), and oliguria (reduced urine output).

77
Q

How is shock diagnosed?

A

Diagnosis of shock is primarily clinical, involving blood pressure measurement and sometimes measuring markers of tissue hypoperfusion such as blood lactate levels or base deficit.

78
Q

How is shock treated?

A

Shock treatment involves fluid resuscitation, including blood products if necessary. The underlying disorder causing shock should be addressed, and in some cases, vasopressors may be required to increase blood pressure.

79
Q

What are some common causes of shock?

A

Causes of shock include cardiogenic causes (e.g., large myocardial infarction leading to low cardiac output), sepsis (resulting in low systemic vascular resistance), anaphylaxis (causing low systemic vascular resistance), and low blood volume due to conditions such as bleeding, burns, or severe diarrhoea, which lead to low cardiac output. Other factors contributing to shock include sympathetic activation, redistribution of blood flow to vital organs, poor tissue perfusion, organ malfunction (especially the kidneys), and acidosis (elevated lactate levels).

HLB (40 decks)

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