block 4- the cardiovascular system Flashcards
describe the position, surfaces and borders of the heart
position = sits diagonally, left side more posterior and right side mainly visible
apex of heart= the point at the bottom of ventricles, between the 5th and 6th rib( 5th intercostal space)
base = back of the heart, mostly left atrium
surfaces:
anterior = mainly right side, behind sternum and ribs
borders of the heart:
superior = top, great vessels enter and leave
inferior = bottom, lies on diaphragm
right = faces right lung
left = faces left lung
what is the mediastinum?
= central compartment of thoracic cavity containing heart, great vessels, thymus, trachea and oesophagus
what are the anterior landmarks of the heart
- Coronary Sulcus:
- seperates the atria and ventricles
- contains the right coronary artery - Anterior interventricular sulcus
- separates the ventricles
- contains left descending artery - Auricles
- increases atria volume/capacity by acting as an extension chamber for when more blood needs to be pumped back to the heart
what are the posterior landmarks of the heart
- coronary sulcus
- contains coronary sinus
- divides atria and ventricles - posterior interventricular sulcus
- the back division of the ventricles
- has descending arteries that can arise from the left or right coronary artery
describe the pericardium and layers of the heart
pericardium = fluid filled sac that surrounds and protects heart
- fibrous connective tissue
- tough, inelastic
- attatched to diaphragm
Serous:(next part of pericardium)
Parietal (outer layer).
Visceral layer (Epicardium) (inner, attached to heart).
Pericardial Cavity: Contains fluid for lubrication, is the space between the these two layers
describe the heart wall layers
- Epicardium (outer,visceral serous pericardium ).
- Myocardium (muscle layer, middle).
- Endocardium (inner lining, continuous with vessels).
describe the chambers of the heart
Right Atrium (RA): Receives deoxygenated blood (from vena cavae & coronary sinus).
Right Ventricle (RV): Pumps blood to lungs (via pulmonary trunk).
Left Atrium (LA): Receives oxygenated blood (from pulmonary veins).
Left Ventricle (LV): Pumps blood to aorta (systemic circulation).
Thicker LV wall (pumps to whole body vs RV pumping to lungs).
describe the valves of the heart
Atrioventricular (AV):
Right = Tricuspid (separates RA → RV).
Left = Bicuspid (Mitral) (separates LA → LV).
Semilunar (SL):3 cusps
Pulmonary (RV → Pulmonary trunk).
Aortic (LV → Aorta).
Chordae Tendineae & Papillary Muscles: Prevent backflow by tightening AV valves.
describe the great vessels of the heart
Vena Cavae (RA): Carry deoxygenated blood to right atrium (superior + inferior)
Pulmonary Trunk (RV) → Right & Left Pulmonary Arteries (deoxygenated blood to lungs from RV).
Pulmonary Veins (LA): Oxygenated blood from lungs.
Aorta (LV): Sends oxygenated blood to body.
Branches:
- Brachiocephalic (→ Right Subclavian & -Right Common Carotid).
- Left Common Carotid.
- Left Subclavian.
circulation systems of the heart
- pulmonary = RV -> lungs -> LA
- Systemic = LV -> body -> RA
- coronary (supplies oxygenated blood to heart with venous drainage via the coronary sinus which is a hole between LCA and RCA)
Pulmonary & Systemic circuits must pump equal blood volume!
what are the functions of blood
- Transport (O₂, nutrients, waste).
- Protection (immune system).
- Regulation (hormones, temperature).
describe red blood cells
erythrocytes
- Made in bone marrow (requires Erythropoietin from kidneys).
- No nucleus (more room for oxygen).
- Contains Haemoglobin (binds O₂).
Disorders:
Anaemia (low RBC, iron deficiency).
Polycythaemia (high RBC, thicker blood).
describe white blood cells
leukocytes
Defense (Phagocytosis, immune response, protection).
Types:
1. Granulocytes: Neutrophils, Eosinophils, Basophils.
2. Agranulocytes: Lymphocytes, Monocytes.
Disorders:
Leukopenia (low WBC, infections).
Leukocytosis (high WBC, inflammation).
describe platelets
thrombocytes
- Cell fragments
involved in clotting to control blood loss
Normal Count: 150,000 – 450,000/μl.
Disorders:
Thrombocytopenia (low platelets, excessive bleeding).
Thrombocytosis (high platelets, risk of clots).
describe plasma
- 55% of blood.
- Contains water (92%), proteins (albumin), glucose, electrolytes.
- is the extracellular matrix of the blood
what are the 4 main compoennts of blood
= red cells, white cells, platelts and plasma
define the vasculature
= the network of blood vessels in the body or within an organ
what are the three types of blood vessels
Arteries: Carry oxygenated blood away from the heart.
Veins: Carry deoxygenated blood back to the heart.
Capillaries: Site of exchange between blood and tissues.
describe the basic structure of a blood vessel
Tunica Interna (Intima): Endothelium, contacts blood directly.
Tunica Media: Smooth muscle & elastic tissue (varies by vessel type).
Tunica Externa (Adventitia): Connective tissue.
describe the different types of arteries
- Large Elastic Arteries: High elastic fibres, low smooth muscle, largest diameter in tunica media layer, large lumen, wall thickness of all layers is <10% of total vessel diameter
Example: Aorta. - Medium Muscular Arteries:
- Predominantly smooth muscle in tunica media, less elastic fibres, distributes the blood, wall thickness of 3 layers <25% of total diameter
- Example: Brachial artery. - Arterioles:
- Smallest arteries, most resistance, smooth muscle, less elastic fibres, wall thickness is 50% of total diameter, only one or two layers
what are anastomoses
= the point where two blood vessels join or merge
- e.g Circle of Willis connects anterior and posterior blood supply and sits at the base of the brain
describe the structure and characteristics of capillaries
Smallest Blood Vessels: One layer of endothelial cells and a basement membrane
- highly permeable
- squamous cells for exchange
Types:
Continuous: Most common, in lungs.
Fenestrated: Found in kidneys, extra holes for filtration.
Sinusoid: Found in liver, more gaps for exchange.
venules
= carry deoxygenated blood
two types:
1. post capillary
- no tunica media, thin walled and very porous
- smallest
2. muscular
- 1-2 layers of smooth muscle
- tunica media
- microscopic
- no exchange with interstitial fluid
- both types have sparse tunica externa
describe veins
venules increase in size turning into veins
Structure: Large lumen, poorly developed tunica media, sit closer to surface than arteries
Function: Low-pressure blood return to heart; contains 60-70% of blood.
Varicose Veins:
- Caused by weak vein walls that loose elasticity,
- backflow of blood due to incompetent valves -> blood collecting in veins, dilating and weakening
- risk - obesity, walking too much
- skeletal muscle and valves pump blood by squeezing on veins
what is atherosclerosis
= 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
cardiac output and stroke volume
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.
define hemodynamics
= 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.
describe the key features of the cardiac cycle
= 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
- Isovolumetric Contraction:
- AV and semilunar valves closed
- pressure builds, blood volume not changing - Ejection:
Semilunar valves open, blood is ejected. (left and right ventricle eject same volume of blood even at differing pressures) - Isovolumetric Relaxation:
Pressure drops in ventricles, AV and SL valves close, ventricles begin to refill
- each beat takes 0.85 seconds
describe the nervous control of the cardiac cycle
Sympathetic Nervous System: Increases heart rate (tachycardia), increases contractility.
Parasympathetic Nervous System: Decreases heart rate (bradycardia), slows AV conduction.
Sinoatrial (SA) Node & Autonomic Nervous System (ANS)
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
what is starlings law
The greater the stretch (preload) of the heart muscle, the greater the force of contraction (stroke volume).
difference in pressure circuits between systemic and pulmonary circulation
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.
where do electrical impulses spread from in atria and ventricles
- electrical impulses spread from sinus node throughout left and right atria
- electrical impulses spread from bundle branches throught left and right ventricles
describe the heartbeat process from the ECG
- Atrial depolarize, initiated by the SA node, causing the P wave
- impulse is delayed at the AV node
- ventricular depolarization begins at the apex, causing the QRS complex. Atrali repolarzation occurs
- ventricular depolarisation is complete
- ventricular repolarisation begins at the apex, causing the T wave, and is complete.
differenc between diastole and systole
Diastole: Blood flows into ventricles.
Systole: Ventricles contract and pump blood into pulmonary trunk or aortic arch.
outline the pressures of interest
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.
outline the blood volumes of interest
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)
desribe the frank starling mechanism
= 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.
why does fainting happen?
Fainting occurs when low CVP leads to reduced stroke volume and blood flow.
describe the peripheral control of haemodynamic function
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.
describe the baroreceptor reflex
- baroreceptors are initiated by the stretch receptors in the walls of major arteries
- the brainstem communicates with nerves which controls the heart and blood vessels -> heart rate, SV, blood vessel diamter
- changes occur in cardiac output, peripheral resistance and venous capcity
- blood pressure is restored to normal levels
what happens when the baroreceptors are not working?
- hypotension (low BP)
- hypertension (high BP) - high systolic pressure
- Vascular remodelling occurs to compensate = thicker arterial walls to accommodate increased pressure -> reduces lumen size
the control of blood flow
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.
distribute the amount of total peripheral resistance in the circulation to the different blood vessels
- Large arteries – 2%
- Arterioles - 60%
- Capillaries - 20%
- Venous system - 15%
explain the flow distribution at rest
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
intrinsic control
4 basal levels of vascular tone
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
what is the myogenic response
- myocytes depolarize when stretched
increase in arterial pressure = increase vascular tone = constriction
decrease in arterial pressure = decrease in vascular tone = dilation
outline the vasocontrictor and the vasodilator of endothelial secretion
vasoconstrictor = Endothelin-1
vasodilator = nitric oxide
temperature as an intrinsic control
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
what is Raynaud’s syndrome?
- spasm of small arteries supplying the extremeties in response to: cold, stress
- an overactivation of temperature response
-
extrinsic control of flow
- vasomotor nerves
- vasoactive hormones
- has a higher level of control- overrides intrinsic controls to meet needs of the whole body
the vasomotor nerves and autonomic control
- Sympathetic vasodilators (NT = NA or ACh)- Increases vasoconstriction, raising blood pressure
- Parasympathetic vasodilators (NT = ACh)- increase vasodilation
the vasomotor hormones
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.
Fight or Flight Response (Extrinsic Mechanism)
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.
how to calculate blood pressure and cardiac output
total peripheral resistance x cardiac output
CO = HR X SV
risk factors for hypertension, angina and heart failure
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.
what is the differenc ebetween primary and secondary hypertension
Primary: Multifactorial (genetic, lifestyle). - 90%
Secondary: Caused by other diseases (e.g., renal hypertension). - 10%
consequences of chronic hypertension
Cardiovascular diseases (heart failure, stroke, myocardial infarction, renal failure, retinopathy).
Chronic strain on the heart, leading to atherosclerosis, stroke, and heart failure.
what are the clinical benefits of reducing blood pressure
40% reduction in stroke risk
25% in myocardial infarction
50%+ in heart failure.
the use of beta-blockers
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
the use of alpha-adrenoceptor blockers
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)
the use of ACE inhibitors
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
the use of angiotensin II receptor blockers
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
the use of diuretics
e.g., Bendroflumethiazide
Decrease blood volume by blocking sodium/water reabsorption. -> lowering BP
Side effects: Low potassium levels.
the use of calcium channel blockers
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.
what is the mechanism of the L-type channel blockers
- open channel block so calcium cannot get into cell (verapamil and diltiaze)
or
- allosteric modulation -> binding at allosteric site to reduce channel opening (changes the conformation so calcium cannot get through (nifedipine)
how do calcium channel blockers lower blood pressure
- reducing peripheral resistance-(block of Ca2+ entry into vascular smooth muscle)
- reduce cardiac output - (block of Ca2+ entry into cardiac muscle)
1 is preferred over 2
what is Angina pectoris, the three types and the drug treatments
- 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:
- 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)
- 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.
- dilate arteries to decrease afterload and 02 demand
- venous dilation
- the main aim is to reduce myocardial 02 demand
what is afterload and preload
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
what is the bainbridge reflex
= 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
why are all nitro-vasodilators classed as pro-drugs
lipophilic - they readily enter smooth muscle cells and are reduced to nitric oxide (NO)
what is heart failure?
= when the heart cannot meet the circulatory needs of the body, despite an adequate venous filling pressure
factors contributing to cardiac output
- heart rate
- filling
- outflow resistance
- contractile state of heart
causes of chronic heart failure
- haemodynamic overload
- excess pressure and volume - neurohumoral overload
- tissue damage
- eg from heart attack - genetically determined excessive hypertrophic response to pressure
symptoms of heart failure
- left ventricular failure
- fatigue
- pulmonary oedema - right ventricular failure
- cyanosis
- oedema
- venous distension
treatments for heart failure
- goal is to reduce preload/afterload, or improve heart contractility.
Diuretics, ACE inhibitors, Vasodilators, Positive Inotropes (e.g., Dobutamine, Dopamine).
what are positive inotropic agents?
= increase contraction force, improving circulation.
e.g., Digoxin, Levosimendan
role of dopamine and dobutamine
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.
role of digoxin
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
what are calcium sensitisers?
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.
atherosclerosis and lipid management
= 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
the different lipoproteins and their role in carrying cholestrol
- 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
what is hyperlipoproteinemia
= 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
role of statins
also known as HMGCoAR Inhibitors
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
definition of cardiovascular disease
= 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
Epidemiological Evidence of cardiovascular disease
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.
coronary heart disease and sex
- higher rates in males compared to females across all time points from graph
atherosclerosis
= 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
risk factors for cardiovascular disease
- genetics
- family history
- obesity
- lack of exercise
- type 2 diabetes
- diet
- stress
- hypertension
- inflammation
- age
- race]
- gender
definitions of physical activity, exercise, inactivity and sedentary behaviour
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
association between physical activity and cardiovascular disease
- 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.
Recommended Physical Activity for Health (PAGs)
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
Major Causes of Death (Including CVD)
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.
direct and indirect effects of physical activity
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.
