block 4- the cardiovascular system Flashcards

Question

what is atherosclerosis

Answer 1

= Build-up of calcified plaques in arteries, narrowing lumen and reducing elasticity. - increased resistance to blood flow - decreased circulation - inflammatory disease where cholestrol enters the vessel wall causes -> smoking, salt, diet, no exercise

Answer 2

Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR). - is the volume of blood ejected by one ventricle in one minute Blood Volume: ~5L in the body, with 2/3 in veins at rest.

Answer 3

= dynamics of blood flow Pressure Gradients: Blood pressure decreases from arteries to veins. Heart as Pump: The heart creates pressure to move blood through systemic and pulmonary circuits.

Answer 4

= event that occurs during one heart beat stages: 1. Ventricular Filling: - AV valves open, SL closed - ventricles fill (atria contract first pushing blood into ventricles) - when ventricle pressure exceeds atrial pressure, AV valves shut 2. Isovolumetric Contraction: - AV and semilunar valves closed - pressure builds, blood volume not changing 3. Ejection: Semilunar valves open, blood is ejected. (left and right ventricle eject same volume of blood even at differing pressures) 4. Isovolumetric Relaxation: Pressure drops in ventricles, AV and SL valves close, ventricles begin to refill - each beat takes 0.85 seconds

Answer 5

Sympathetic Nervous System: Increases heart rate (tachycardia), increases contractility. Parasympathetic Nervous System: Decreases heart rate (bradycardia), slows AV conduction.

Answer 6

SA Node: Pacemaker of the heart, intrinsic rate ~100bpm, modulated by ANS. - is a collection of myocytes that depolarize at regular intervals, the rate at which they do this is determined by extrinsic nerves(ANS) Parasympathetic (Vagal): Releases acetylcholine, slows heart rate by hyperpolarizing the SA node. Sympathetic: Releases noradrenaline, increases heart rate, contractility, and AV conduction, decrease myocyte AP length, fibres exit spinal cord at T1-T5

Answer 7

The greater the stretch (preload) of the heart muscle, the greater the force of contraction (stroke volume).

Answer 8

Systemic Circulation (High Pressure) Delivers oxygenated blood to the body. Aorta: ~120/80 mmHg → Arterioles: Major drop (~80-35 mmHg) → Capillaries: ~35-10 mmHg → Veins: ~10-5 mmHg → Right Atrium: ~0-2 mmHg. High pressure needed for long-distance flow & resistance control. Pulmonary Circulation (Low Pressure) Sends deoxygenated blood to lungs for gas exchange. Pulmonary Artery: ~25/10 mmHg → Capillaries: ~10 mmHg → Pulmonary Veins: ~5-10 mmHg → Left Atrium: ~5 mmHg. Low pressure protects delicate lung capillaries.

Answer 9

- electrical impulses spread from sinus node throughout left and right atria - electrical impulses spread from bundle branches throught left and right ventricles

Answer 10

1. Atrial depolarize, initiated by the SA node, causing the P wave 2. impulse is delayed at the AV node 3. ventricular depolarization begins at the apex, causing the QRS complex. Atrali repolarzation occurs 4. ventricular depolarisation is complete 5. ventricular repolarisation begins at the apex, causing the T wave, and is complete.

Answer 11

Diastole: Blood flows into ventricles. Systole: Ventricles contract and pump blood into pulmonary trunk or aortic arch.

Answer 12

Systolic Pressure: 120 mmHg Diastolic Pressure: 80 mmHg Mean Arterial Pressure (MAP) = 2/3 diastolic + 1/3 systolic Time Distribution: 2/3 of the heartbeat is spent in diastole; 1/3 in systole.

Answer 13

End Diastolic Volume: Blood volume in ventricles just before contraction.(120ml) End Systolic Volume: Blood left in ventricles after contraction.(50ml) Stroke Volume (SV): The volume of blood pumped out per heartbeat. (70ml)

Answer 14

= Increased muscle fiber stretch (diastolic distension) enhances contractile force - Higher CVP (Central Venous Pressure) leads to increased venous return to right side of heart, causing more stretch as it fills up quicker and increasing contractile energy.

Answer 15

Fainting occurs when low CVP leads to reduced stroke volume and blood flow.

Answer 16

Vascular Tone: Blood vessel diameter changes affect pressure and flow. Autonomic & Metabolic Control: Blood flow is regulated by these mechanisms via autonomic nervous system and local metabolic needs. Autoregulation: Baroreceptor reflex maintains blood pressure. Resistance: Arterioles are primary resistance vessels, with small radius changes having significant effects on resistance. Poiseuille’s Law: Resistance increases as the radius of blood vessels decreases.

Answer 17

1. baroreceptors are initiated by the stretch receptors in the walls of major arteries 2. the brainstem communicates with nerves which controls the heart and blood vessels -> heart rate, SV, blood vessel diamter 3. changes occur in cardiac output, peripheral resistance and venous capcity 4. blood pressure is restored to normal levels

Answer 18

- hypotension (low BP) - hypertension (high BP) - high systolic pressure - Vascular remodelling occurs to compensate = thicker arterial walls to accommodate increased pressure -> reduces lumen size

Answer 19

Blood flow: Q = (P1-P2)/R, where R (resistance) can be modified by changing the diameter of arterioles. Local Adjustments: Blood flow is redistributed based on local tissue demands (e.g., more oxygen for active muscles). - long narrow tubes have higher resistence than short, wider tubes.

Answer 20

* Large arteries – 2% * Arterioles - 60% * Capillaries - 20% * Venous system - 15%

Answer 21

skeletal muscle 20% oxygen consumption - Therefore receives 20% cardiac output - Exceptions = kidneys, cardiac muscle, brain (ratio is not equal, these take more oxygen) - Continual adjustments depending on factors like: - Standing - Stress - Exercise - Done by changes in ‘vascular tone’ – both ‘intrinsic’ and ‘extrinsic’ mechanisms

Answer 22

4 basal levels of vascular tone that are always going on and affecting flow of blood to specific sites: 1. myogenic response 2. endothelial secretions 3. vasoactive metabolites 4. temperature

Answer 23

- myocytes depolarize when stretched increase in arterial pressure = increase vascular tone = constriction decrease in arterial pressure = decrease in vascular tone = dilation

Answer 24

vasoconstrictor = Endothelin-1 vasodilator = nitric oxide

Answer 25

the sympathetic vasoconstrictor fibres dilate and constrict the vessels: - Dilate with heat = physically contain more blood = skin ‘reddens’ - Constrict with cold = physically less blood = pale / bluish colour - To protect and conserve core temperature - skin is the organ of temperature regulation

Answer 26

- spasm of small arteries supplying the extremeties in response to: cold, stress - an overactivation of temperature response | -

Answer 27

- vasomotor nerves - vasoactive hormones - has a higher level of control- overrides intrinsic controls to meet needs of the whole body

Answer 28

- Sympathetic vasodilators (NT = NA or ACh)- Increases vasoconstriction, raising blood pressure - Parasympathetic vasodilators (NT = ACh)- increase vasodilation

Answer 29

Adrenaline: Causes both vasoconstriction and vasodilation depending on receptor types (α for constriction, β for dilation). Vasopressin: Constricts vessels. Angiotensin II: Constricts vessels. Atrial Natriuretic Peptide (ANP): Causes vasodilation. Insulin: Promotes vasodilation.

Answer 30

Adrenaline vs Noradrenaline: Adrenaline (hormone, from adrenal glands) binds to both α- and β-receptors, causing vasodilation in skeletal muscles, myocardium, and liver. Noradrenaline (neurotransmitter) is primarily a vasoconstrictor.

Answer 31

total peripheral resistance x cardiac output CO = HR X SV

Answer 32

hypertension = Smoking, obesity, poor diet (salt), lack of exercise, genetics. Angina & Heart Failure: Obesity, smoking, high cholesterol, poor diet, stress, lack of physical activity, atherosclerosis.

Answer 33

Primary: Multifactorial (genetic, lifestyle). - 90% Secondary: Caused by other diseases (e.g., renal hypertension). - 10%

Answer 34

Cardiovascular diseases (heart failure, stroke, myocardial infarction, renal failure, retinopathy). Chronic strain on the heart, leading to atherosclerosis, stroke, and heart failure.

Answer 35

40% reduction in stroke risk 25% in myocardial infarction 50%+ in heart failure.

Answer 36

e.g., Propranolol (blocks b1 and b2 receptors) Atenolol (blocks b1) - protects the heart from adrenaline release Block β1 receptors → decrease heart rate, stroke volume, and BP. blocking b2 can restrict airflow in lungs in people with previous issues Side effects: Asthma, exercise intolerance, hypoglycemia, vivid dreams

Answer 37

e.g., Phentolamine (blocks a1 and a2 receptors) Doxazosin (blocks a1) Block α1 receptors → vasodilation, decrease BP via decrease in sympathetic tone in arterioles Side effects: Postural hypotension(dizzy when standing up), reflex tachycardia via baroreceptors, BPH( prostate gland enlarges, trouble peeing in old men)

Answer 38

e.g., Captopril, Enalapril) Blocks angiotensin II formation from angiotensin I → vasodilation, lower blood volume, blocks production of aldosterone reducing the circulating fluid volume angiotensin II -> narrows blood vessels, which can usually cause high BP and forces heart to work harder Side effects: Dry cough, drop in BP on first dose

Answer 39

e.g., Losartan + candesartan (AT1 blockers) - two receptor subtypes (AT1 + AT2) Block AT1 receptor → vasodilation without dry cough. - AT1 receptor brings about vasoconstrictor and aldosterone-releasing actions of angiotensin II - Effective alternative to ACE inhibitors. - no bad side effects

Answer 40

e.g., Bendroflumethiazide Decrease blood volume by blocking sodium/water reabsorption. -> lowering BP Side effects: Low potassium levels.

Answer 41

e.g., Verapamil, Nifedipine Block calcium entry → vasodilation and reduced cardiac output. -Reduce Ca2+ entry into vascular smooth muscle and cardiac muscle by blocking L-type voltage-operated calcium channels - Less calcium going in -> less constriction -> blood vessels will dilate Side effects: Headache, constipation, gum hyperplasia.

Answer 42

1. open channel block so calcium cannot get into cell (verapamil and diltiaze) or 2. allosteric modulation -> binding at allosteric site to reduce channel opening (changes the conformation so calcium cannot get through (nifedipine)

Answer 43

1. reducing peripheral resistance-(block of Ca2+ entry into vascular smooth muscle) 2. reduce cardiac output - (block of Ca2+ entry into cardiac muscle) 1 is preferred over 2

Answer 44

- is chest pain caused by a reduction in oxygen supply to heart by coronary artery types: 1. Stable: Predictable, common 2. Unstable: Unpredictable, due to plaque rupture. 3. Variant: Due to coronary artery spasm. drug treatments: 1. Nitrovasodilators (e.g., GTN, Amyl Nitrite): Dilate veins, reduce preload, rapid release of angina attack, taken before exercise in stable type, both are short lived but have rapid onset, GTN take as a spray, amyl nitrate inhaled, side effect of headaches) 2. Ivabradine: slows the heart rate by blocking the "If" channels in the SA node delaying the electrical signals that trigger the heart to beat, reducing the heart's oxygen demand without affecting its force of contraction. 3. dilate arteries to decrease afterload and 02 demand 4. venous dilation - the main aim is to reduce myocardial 02 demand

Answer 45

afterload = the resistance the heart faces when trying to pump blood out preload = the amount of stretch in the hearts muscle fibres, just before it contracts

Answer 46

= a sympathetic reflex initiated by increased blood in the atria - causes stimulation of the SA node - stimulates baroreceptors in the atria, causing increased SNS stimulation - more blood coming back to heart -> increases force

Answer 47

lipophilic - they readily enter smooth muscle cells and are reduced to nitric oxide (NO)

Answer 48

= when the heart cannot meet the circulatory needs of the body, despite an adequate venous filling pressure

Answer 49

- heart rate - filling - outflow resistance - contractile state of heart

Answer 50

1. haemodynamic overload - excess pressure and volume 2. neurohumoral overload 3. tissue damage - eg from heart attack 4. genetically determined excessive hypertrophic response to pressure

Answer 51

1. left ventricular failure - fatigue - pulmonary oedema 2. right ventricular failure - cyanosis - oedema - venous distension

Answer 52

- goal is to reduce preload/afterload, or improve heart contractility. Diuretics, ACE inhibitors, Vasodilators, Positive Inotropes (e.g., Dobutamine, Dopamine).

Answer 53

= increase contraction force, improving circulation. e.g., Digoxin, Levosimendan

Answer 54

Dopamine = acts via dopamine receptors (D1 and D2) but also via release of noradrenaline Dobutamine = acts mainly via β1 and β2 adrenoceptors -> both are short term inotropic support in advanced heart failure in patients who have not responded to standard treatment.

Answer 55

Digoxin increases the force of the heart's contractions (positive inotropic effect) and slows the heart rate by inhibiting the sodium-potassium pump, which helps treat heart failure and certain arrhythmias. - can have severe adverse effects - early signs of toxicity - nausea, vomiting, altered colour vision

Answer 56

Calcium sensitisers are drugs that enhance the heart's response to calcium, increasing the force of contraction without directly increasing calcium levels. They work by making the heart muscle more sensitive to calcium, improving heart function, especially in conditions like heart failure.

Answer 57

= Fatty streaks form from LDL oxidation, leading to plaque formation. Can cause artery occlusion, leading to myocardial infarction. role of cholestrol: - Essential for cell membranes, steroid production. - Lipoproteins (LDL, HDL) transport cholesterol; HDL helps reverse cholesterol transport to liver - liver monitors levels

Answer 58

- Chylomicrons - Carry TGs from intestines to liver, muscle & adipose tissue - VLDL - Carry newly synthesised TGs from liver to adipose tissue - IDL - An intermediate between VLDL and LDL - LDL - Major reservoir of cholesterol - Taken up via LDL receptors by endocytosis - HDL - Adsorb cholesterol released by dying cells - Also act as “reverse transport” to take cholesterol to liver

Answer 59

= high circulating levels of free and bound cholestrol and TG's - inability to break down lipids or fats in your body, specifically cholesterol and triglycerides secondary causes: diabetes, alcohol, drugs, diet

Answer 60

e.g Simvastatin, Pravastatin, Rosuvastatin -Inhibit cholesterol synthesis, reduce LDL levels in blood by stimulating LDL receptor up-regulation -they act as a competitive inhibitor of the rate-limiting step in cholestrol biosynthesis - Most effective at night when cholestrol synthesis levels are highest

Answer 61

= refers to a group of disorders of the heart and circulatory system including: - coronary heart disease of blood vessels supplying the heart - cerebrovascular disease of blood vessels supplying the brain - peripheral arterial disease of blood vessels supplying the arms and legs - rheumatic heart disease - heart muscle and valve damage due to rheumatic fever - congenital heart disease - malfunction of heart structure from birth - pulmonary embolism - bloot clots in veins which can move to heart and lungs - high global death rate

Answer 62

Ischaemic Heart Disease (IHD) Rates: Over the 15 years between 2001 and 2016, there has been a significant decrease in ischaemic heart disease rates, particularly in men. In 2001, ischemic heart disease was the most common cause of death. A steep decrease was seen in cerebrovascular disease, though dementia and Alzheimer’s disease increased, particularly in women due to their longer life expectancy.

Answer 63

- higher rates in males compared to females across all time points from graph

Answer 64

= narrowing of large arteries by cholesterol plaque and thrombus - in the heart: - partial occlusion of coronary arteries = angina pectoris - total occlusion = heart attack in the brain: - partial occlusion of arteries = transient ischemic attack - total occlusion = cerebrovascular accident in the legs: occlusion of illiac arteries = peripheral vascular disease occlusion = blockage

Answer 65

- genetics - family history - obesity - lack of exercise - type 2 diabetes - diet - stress - hypertension - inflammation - age - race] - gender

Answer 66

Physical Activity: any bodily movement produced by the skeletal muscles that requires an increase in energy expenditure Exercise: shares the above definition, and very +vely correlated with physical fitness, planned/structured & repetitive bodily movement, objective to improve or maintain physical fitness Inactivity: Those performing insufficient amounts of MVPA for health (i.e. not meeting the WHO recommended minimum required MVPA). Sedentary behaviour: Sedentary behaviour is defined as any waking behaviour characterized by an energy expenditure ≤1.5 METs while in a sitting, reclining or lying posture

Answer 67

- Only ‘vigorous’ activity (defined as peaks of activity > 7.5 Kcal/min) appeared to protect against CHD. - older adults unable to do vigorious exercise but walking still helps - lower screen time and more physical activity contribute to better vascular health and reduced CVD risk.

Answer 68

The Physical Activity Guidelines (PAGs) recommend at least 150 minutes of moderate-intensity aerobic activity per week, or 75 minutes of vigorous-intensity activity 180mins of movement per day recommended for 1-5 year olds 5-18 years at least on ehour a day across the week

Answer 69

CVD makes up a third of all deaths, with ischemic heart disease and cerebrovascular disease contributing the largest proportions. These conditions remain the leading cause of death worldwide.

Answer 70

Directly: PA improves endothelial function, which enhances vasodilatation and vasomotor function in the blood vessels. Indirectly: PA contributes to weight loss, glycemic control, improved blood pressure, lipid profile and insulin sensitivity.

block 4- the cardiovascular system Flashcards

(95 cards)