Structure, function, and regulation

Functions of CV system

maintain homeostasis and favorable cellular environment, provide continuous and controlled flow of blood through capillaries to every cell, deliver oxygen in nutrients to cells, exchange carbon dioxide and waste for elimination

Components of the CV system

heart, blood vessels, blood cells (erythrocytes, leukocytes, platelets)

Function of heart

pumps deoxygenated blood to the lungs; pumps oxygenated blood out to body; coordinates its own contraction by a conducting system; affects pace-making, electrical signals, and force of contraction

Arteries

thick tunica media (smooth muscle) provides support and changes vessel diameter to regulate blood flow and pressure

Veins

less smooth muscle and connective tissue than arteries; thinner walls bc there is less pressure than arteries; has valves to prevent backflow and keep blood flowing towards heart

Endothelial cells in vasculature

lines both veins and arteries; releases vasoactive substances that affect diameter and flow

Erythrocytes

red blood cells; anuclear, contain Hb, transport oxygen to the lungs

Leukocytes

defense cells of the blood

platelets

component of blood that forms ‘plugs’ to stop leaks in blood vessels

functions of blood vessels

detects presence of blockages, affects muscular tone and structural integrity, pressure drop needed to move blood to and through capillary beds

functions of blood

affects water, electrolyte, and ion balances; affects lipid and protein compositions

Types of cardiovascular diseases

coronary artery disease, peripheral artery disease, heart diseases (angina, heart failure, myocardial infarction)

Cardiovascular disease

an overarching term for all types of diseases affecting heart or blood vessels

Four main systems that drugs target in CVD

hemodynamic system, vascular tone system, RAAS system, adrenergic system

What adrenergic system controls

exocrine excretion, metabolic processes, smooth muscle cells activity, rate and force of heart

other names for adrenergic system

autonomic nervous system, sympathetic nervous system

catecholamines

adrenaline and noradrenaline; released by sympathetic nervous system (fight or flight); released to increase heart rate

Acetylcholine

released by parasympathetic nervous system, which restores equilibrium after sympathetic action; released to decrease heart rate

a1 adrenergic receptors

activation contracts vascular smooth muscle cells; responsible for vasoconstriction

a2 adrenergic receptors

activates neurons to inhibit catecholamine releases; contracts OTHER tissues smooth muscles cells (not vasculature); decrease in insulin and renin release

B1 adrenergic receptor

activation contracts cardiomyocytes; increases heart rate and contractility; increases renin release from kidney

B2 adrenergic receptors

activation relaxes vascular smooth muscle cells and other tissues smooth muscle cells; enhances emotional events in brain, increases insulin release, causes vasodilation of smooth muscle cells, causes bronchodilation of lungs

Causes of anaphylaxis

peripheral vasodilation, smooth muscle constriction, bronchoconstriction

symptoms of anaphylaxis

flushing, increased capillary permeability, hypotension, reduced consciousness, abdominal cramps, uticaria, bradychardia

time to cardiac or respiratory arrest during anaphylaxis

30 min for food allergens, 15 min for insect venom, 5 min for medication

adrenaline use in anaphylaxis

increases peripheral vascular resistance, improvement in blood pressure, reduction in angio-oedema

B-blocker uses

angina to reduce cardiac work, hypertension to reduce cardiac output and renin release, post myocardial infarction to inhibit increase in SNS activity

cardioselective B-blockers

selectively targets B1 adrenoreceptors that are primarily found on cardiomyocytes; does not have central affect, so there is LESS risk of bronchoconstriction

non-selective B-blockers

targets both B1 and B2 adrenoreceptors; have central effects so side effects include nightmares, depression, and insomnia, bronchoconstiction, and hyperglycemia

arterial blood pressure

cardiac output x peripheral vascular resistance

cardiac output

amount of blood a heart pumps in one minutes

heart rate x stroke volume

heart rate

number of contractions of the heart per minute

stroke volume

volume of blood pumped by ventricle with each heart beat

Peripheral vascular resistance

resistance of the blood flow through arteries

venous return (preload)

determines volume of blood in ventricle at each beat

peripheral resistance (afterload)

determines arterial pressure that must be overcome by pumping system

affect of calcium ions

influx causes smooth muscle contraction; the calcium activates myosin kinase which phosphorylates myosin allowing binding to actin giving contraction of the muscle

affect of nitric oxide

influx causes relaxation of smooth muscle cells; activates myosin phosphate which de-phosphorylates myosin, blocking myosin from binding; very short half-life

Renin-Angiotensin-Aldosterone System (RAAS)

regulates blood volume and peripheral vascular resistance through action of a function angiotensin II; acts as our natural hypertensive system; longterm increase in RAAS activity contributes to cardiac and vascular remodeling which are hallmarks of cardiac failure

Drugs targeting RAAS system

angiotensin converting enzyme inhibitors (ACEi); angiotensin II receptor antagonists/blockers (ARA/ARB); aldosterone antagonists (K+ sparing diuretics); renin inhibitors