blood pressure

Question 1

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

Answer 1

Wall tension is directly proportional to pressure.

Question 2

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

Answer 2

Wall tension is directly proportional to the radius.

Question 3

How does vessel size affect wall tension?

Answer 3

The larger the vessel, the greater the wall tension.

Question 4

What is vessel compliance?

Answer 4

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

Question 5

What factors can affect vessel compliance?

Answer 5

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

Question 6

What is laminar flow?

Answer 6

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

Question 7

What conditions are more likely to cause turbulent flow?

Answer 7

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

Question 8

What are some causes of turbulence in blood flow?

Answer 8

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”).

Question 9

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

Answer 9

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

Question 10

What are the components of the arterial media layer?

Answer 10

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

Question 11

What is the innermost part of the arterial wall?

Answer 11

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

Question 12

What is atherosclerosis?

Answer 12

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.

Question 13

What are the stages of plaque development in atherosclerosis?

Answer 13

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

Question 14

What can trigger a blood clot in atherosclerosis?

Answer 14

Plaque rupture can trigger the formation of a blood clot.

Question 15

What are the components of intimal plaque in atherosclerosis?

Answer 15

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

Question 16

What is the effect of medial thinning in atherosclerosis?

Answer 16

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

Question 17

What is adventitial erosion in atherosclerosis?

Answer 17

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

Question 18

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

Answer 18

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.

Question 19

What are some endothelium functions in local vessel tone control?

Answer 19

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

Question 20

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

Answer 20

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

Question 21

What are nitric oxide and prostacyclin?

Answer 21

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

Question 22

What does it mean for something to be thrombogenic?

Answer 22

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.

Question 23

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

Answer 23

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.

Question 24

What is plaque in the context of myocardial infarction?

Answer 24

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.

Question 25

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

Answer 25

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

Question 26

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

Answer 26

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.

Question 27

What are the consequences of decreased LV contractility?

Answer 27

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.

Question 28

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

Answer 28

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.

Question 29

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

Answer 29

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.

Question 30

What is remodelling in the context of cardiovascular physiology?

Answer 30

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.

Question 31

What can cause pressure overload in the cardiovascular system?

Answer 31

Pressure overload can be caused by narrow valves or hypertension.

Question 32

What can cause volume overload in the cardiovascular system?

Answer 32

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

Question 33

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

Answer 33

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

Question 34

What are the outcomes of remodelling in the cardiovascular system?

Answer 34

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.

Question 35

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

Answer 35

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.

Question 36

What formula calculates mean blood pressure (BP)?

Answer 36

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

Question 37

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

Answer 37

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

Question 38

What is systemic arterial blood pressure?

Answer 38

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

Question 39

What are some consequences of blood pressure being too low?

Answer 39

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).

Question 40

What are some consequences of blood pressure being too high?

Answer 40

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

Question 41

What are the determinants of blood pressure?

Answer 41

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

Question 42

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

Answer 42

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

Question 43

How does gravity affect blood pressure?

Answer 43

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

Question 44

What is arterial compliance?

Answer 44

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.

Question 45

How does blood viscosity affect blood pressure?

Answer 45

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

Question 46

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

Answer 46

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

Question 47

How is cardiac output calculated?

Answer 47

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

Question 48

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

Answer 48

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

Question 49

What is blood volume composed of?

Answer 49

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

Question 50

What is plasma made up of?

Answer 50

Plasma is composed of water, salt, and proteins.

Question 51

How do the kidneys regulate blood volume?

Answer 51

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.

Question 52

What is the intrinsic heart rate?

Answer 52

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

Question 53

How does the autonomic nervous system control heart rate?

Answer 53

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.

Question 54

What circulating substance can affect heart rate?

Answer 54

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

Question 55

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

Answer 55

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

Question 56

What is the cardiac pressure-volume relationship?

Answer 56

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.

Question 57

What is Starling's Law?

Answer 57

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.

Question 58

What factors contribute to preload (venous return)?

Answer 58

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).

Question 59

How is the force of contraction translated into stroke volume?

Answer 59

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.

Question 60

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

Answer 60

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.

Question 61

Why is the RAAS necessary for blood pressure control?

Answer 61

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.

Question 62

What are the local controls that regulate tissue perfusion?

Answer 62

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.

Question 63

What are the effects of circulating catecholamines on blood pressure?

Answer 63

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.

Question 64

Which receptors do adrenaline and noradrenaline act on?

Answer 64

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

Question 65

What are the sensors involved in blood pressure regulation?

Answer 65

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

Question 66

What are the control centres for blood pressure regulation?

Answer 66

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.

Question 67

What are the effectors involved in blood pressure regulation?

Answer 67

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.

Question 68

What is hypotension?

Answer 68

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

Question 69

What is hypertension?

Answer 69

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).

Question 70

What is shock?

Answer 70

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.

Question 71

What are some effects of chronic hypertension on the body?

Answer 71

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).

Question 72

What are some acute effects of severe hypertension?

Answer 72

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

Question 73

What are faints (vaso-vagal episodes)?

Answer 73

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.

Question 74

What is tLoC?

Answer 74

tLoC stands for transient loss of consciousness during fainting episodes.

Question 75

What is shock?

Answer 75

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.

Question 76

What are the symptoms of shock?

Answer 76

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

Question 77

How is shock diagnosed?

Answer 77

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.

Question 78

How is shock treated?

Answer 78

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.

Question 79

What are some common causes of shock?

Answer 79

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).