MedicoPlexus

Physiology

Raghib Siddiqui, Arjun Ajithan

Cardiovascular Physiology

Circulation – consists of:

-The Heart (Pumps the Blood) – surrounded by the pericardium; double walled sac ( Fibrous and Serous layer)

Heart Wall:

1.Endocardium

2.Myocardium

3.Epicardium

Heart Valves ( Bicuspid, Tricuspid, Aortic and Pulmonary) open and close as a result of Pressure difference between the atria and ventricles (atrioventricular valves), or the ventricles and blood vessels(Semi-lunar valves).

When Pa>Pv = AV valve opens resulting in ventricular diastole

When Pv>Pa = AV valve closes

When Pv>P.AorticV/PulmonaryV= SL valves open

When P.Aortic/PulmonaryV>Pv= SL valves close

Cardiac Muscle Cells – Cardiomyocytes:

Contractile, Autorhythmic cells, usually with 1 nucleus. They are striated with Intercalated disks (with gap junctions and desmosomes) and numerous mitochondria. 

Intercalated disks– structural formations that play vital roles in bonding cardiac muscle cells and transmitting signals between them.

•occur at the Z lines. 

• contain two types of contacts: 

– desmosomes (hold the cells tightly together) => the pull of one contractile unit can be transmitted to the next. 

– gap junctions (permit APs to spread from one muscle cell to adjacent cells with low electrical resistance).

Extracellular Calcium initiates cardiomyocyte contraction. 

Cardiac Conducting System – 

1. Nodes (pacemakers) 

– Sinoatrial (SA) node- The Hearts Pacemaker, generates the hearts rhythm. Located in the RA, near superior vena cava.  ~100 per/min

– Atrioventricular (AV) node- Located in the posterior portion of the interatrial septum. Responsible for slowing the impulse to allow optimum filling. ~40-60 per/min

2. Conduction fibers 

– Atrial internodal tracts – anterior, middle, posterior 

– Bundle of His (AV bundle) – ~40-60 per/min

 – left and right bundle branches. ~30-40 per/min 

– Purkinje fibers – rapid conduction ~30-40 per/min

Action Potential in Cardiomyocytes:

By Action_potential2.svg: *Action_potential.png: User:Quasar derivative work: Mnokel (talk) derivative work: Silvia3 (Action_potential2.svg) [CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons

Absolute Refractive Period – regardless of the strength of a stimulus, the cell cannot be depolarized (excited).

Relative Refractory Period – stronger than normal stimulus can induce depolarization.

Excitation-Contraction Coupling in Cardiac Muscle: Link provided by Calcium Ions

Cardiac muscle contraction is similar to skeletal muscle, with some key differences-

-Cardiac muscle contracts as a unit. 

• AP is initiated in pacemaker cells (SA node) 
• AP opens Ca2+ channels in cell membrane => Ca2+ induces Ca2+ release from SR stores. This is called Ca2+ induced Ca2+ release mechanism
  • Sarcolemma: DHPR (dihydropyridine receptor) = VG Ca2+ channel => It activates Ca2+ release from the SR via protein-protein interactions with the ryanodine receptor (RyR) = Ca2+ release channel on the SR membrane
• Can be influenced by nerves, hormones, etc.

Autonomic Nervous Supply to the  Heart-

(Sympathetic + Parasympathetic Nervous system)- They exert opposite effects on the heart.

Bradycardia = HR < 60 

Tachycardia = HR >100

Ps fibers are restricted to the atria; end near to the SA and AV nodes. 

• Increased activity of vagus decreases heart rate (HR) and the rate of conduction of the impulse at the AV node.
• Ps nerves are dominant on HR at rest.
• Sympathetic fibers innervate all parts of the heart 
• An increase in S activity increases HR, force of contraction and shortens the delay at the AV node.
• S nerves are dominant with exercise

The stimulation of beta1 receptors by catecholamines induces positive cardiac effects: 

• +ve chronotropic effect – increased HR 
• +ve dromotropic effect – increased rate of conduction through AV node 
• +ve inotropic effect – increased contractility 
• +ve bathmotropic effect- increased excitability of membrane. 
• +ve lusitropic effect – increased rate of relaxation 

=> increase of cardiac output and oxygen requirement

Hyperkalemia and Hypokalemia:

The Cardiac Cycle: Basically, one complete heartbeat

2 phases: Systole (contraction), Diastole (relaxation)  -approx. 0.8seconds

By OpenStax College [CC BY 3.0], via wikimedia Commons

Phonocardiogram – a graphic record of heart sounds & murmurs

The cardiac cycle can be divided into 4 phases:

1. Isovolumetric contraction
2. Ventricular ejection 
3. Isovolumetric Relaxation
4. Ventricular Filling 

1 and 2 – Systole (0.3s), 3 and 4- Diastole (0.5s)

Ventricular Volumes: 

Stroke Volume= EDV (End Diastolic Volume) – ESV (End Systolic  Volume) = ~70ml

EDV=~130ml

ESV=~60ml

Pressure Volume Curves and Volume Pressure Diagram-

https://www.researchgate.net/figure/Pressure-Volume-diagram-of-the-left-ventricle-showing-the-different-phases-in-a-complete_fig3_281729252

Work Output of the Heart

Work is defined as the product of the force applied and the displacement of the object by the applied force (FxS)

In the case of a pressure moving a fluid, the work done is the product of the pressure applied & the volume of the fluid displaced (volume-pressure work).

Heart Sounds and Murmurs – 

-Normal heart sounds – caused by acceleration & deceleration of blood. 

-Abnormal sounds (heart murmurs) – caused by turbulent flow (produces vibrations in the tissues).

Functional (flow) murmurs Due to increased flow across normal orifice. Caused by: 

– ▼ blood viscosity – anemia (moderate, severe) 

– ▲blood flow (CO) – hyperthyroidism, pregnancy.

Valvular Defects ( resulting in murmurs)

– Stenosis (narrowing) – valve is less than fully open 

– Insufficiency (regurgitation, incompetence) – valve is less than fully closed

https://www.heartfoundation.org.nz/your-heart/heart-conditions/heart-valve-disease

–Blood Vessels (Conduits)

• Arteries, Arterioles, Capillaries, Veins and Venules

Classification- 

Elastic arteries (aorta, pulmonary .a, carotid a.) 

– wide lumen, elastic wall 

– damp pressure variations 

Muscular arteries (other arteries)

 – wide lumen, strong non-elastic wall 

– low resistance conduit 

 Resistance vessels (arterioles) 

– narrow lumen, thick contractile wall 

– control resistance & flow => regional redirection of blood 

 Exchange vessels (capillaries) 

– narrow lumen, thin wall 

 Capacitance vessels (venules & veins) 

– wide lumen, distensible wall 

– low resistance conduit & reservoir of blood 

– allows fractional distribution of blood

Factors that govern blood flow include:

Pressure, Velocity, Flow (laminar/turbulent), Area, Volume, Resistance, Viscosity 

Hemodynamics and Ohm’s Law-

pressure = the force (F) per unit area (A)

Pressure gradient (Δ P) moves fluid => 

Fluid moves from an area of higher pressure to an area of lower pressure.

 Δ P = P1 – P2 

Blood flow = Actual volume of blood flowing through a vessel, organ or the entire circulation in a given period. It is : 

• Measured in ml /min 
• Equivalent to cardiac output (~ 5 L/min). 
• Relatively constant at rest. 
• Varies widely through individual organs, according to needs.

Flow ~ Δ P (P1 – P2 )

Resistance is inversely related to flow:    Flow ~ 1/R

Factors that determine Resistance:

• Viscosity (η) – the friction developed between the molecules of a fluid as they slide over each other during flow of the fluid. 
• R ~ η 
• Blood vessel length (L) R ~ L 
• Blood vessel radius (r) R ~ 1/ r4

Total Peripheral Resistance (TPR) – 

the sum of the resistances to flow offered by all systemic blood vessels

Small arteries & arterioles are the major site of the resistance to blood flow

Components of Arterial Blood Pressure:

• Systolic pressure (SP) – the highest arterial pressure during systole ~ 120mmHg.

• Diastolic pressure (DP) – – the lowest arterial pressure that is achieved between beats ~ 80mmHg.

• Pulse pressure (PP)  = Systolic BP – Diastolic BP ~ 40mmHg

• Mean arterial pressure (MAP) – the pressure driving blood into the tissues averaged over the entire cardiac cycle (= NOT the average of systolic & diastolic pressure)

MAP = DP +1/3 PP, ~ 93 mmHg

Arterial blood pressure values 

• Optimal BP < 130 / < 85 
• High normal 130–139 / 85–89 

Hypertension 

• Stage 1(mild) 140 – 159 / 90–99 
• Stage 2(moderate) 160–179 /100–109 
• Stage 3 (severe) ≥ 180 / ≥ 110

Cardiac Output –

Depends on Contractility, HR, Preload and Afterload

-Cardiac Output = The amount of blood the heart pumps through the circulatory system in a minute (~ 5L/min) 

Stroke volume = the volume of blood pumped out by a ventricle with each beat.

Factors affecting Stroke volume –

• Preload – the muscle length prior to contraction, it is dependent of ventricular filling (EDV) 
• Afterload – the tension (arterial pressure) against which the ventricle must contract 
• Contractility – the intrinsic ability of cardiac muscle to develop force for a given muscle length. It is also referred to as inotropy. 
• HR

Cardiac reserve = the maximum percentage that the CO can increase above normal 

• CO may be 2-5 x the resting value (10 – 25 L/min) => Cardiac reserve ~ 100 – 400%  

Cardiac index = CO per 1m2 body surface area (BSA) ~ 3 L/min/m2 BSA. (average BSA 1.7m2 ) 

• directly dependent on an individual’s size. • varies with age (4-2.5L)

Ejection Fraction – 

EF= SV/EDV x100

Normal Ejection Fraction > 50% (55-70%)

Factors affecting Heart Rate- 

Increased HR can be caused by: 

• Increased activity of SNS; Increased E, NE (adrenal medulla) 
• Decreased vagus n. activity. 
• Increased Thyroid hormones (Hyperthyroidism ) 
• Increased Nicotine, Caffeine. 
• Increased Temperature. 
• Drugs: beta agonists, Atropine 

Decreased HR can be caused by: 

• Increased vagus n. activity. 
• Decreased temperature; – Drugs: Beta blockers, Ca2+ channel blockers,
• Control of Stroke Volume

1.Intrinsic Control – 

A. Heterometric Autoregulation, Frank – Starling Law of the Heart

Increase in strength of contraction due to an increase in EDV (venous return) 

• Increased end-diastolic volume (▲ stretch of cardiac muscle fibers) => ▲ strength of cardiac contraction => ▲ stroke volume. 

▲EDV => ▲SV

B. Homeometric Autoregulation of the Heart

-Anrep Effect 

The ventricle responds to a rapid increase in arterial pressure by augmenting contractility and stroke volume. 

• Bowditch effect (The staircase effect, Treppe, Effect of Heart rate) 

▲HR => ▲strength of contraction of cardiomyocytes

Venous Return (VR) – = the volume of blood flowing from veins into the right atrium each minute.

• ~ 60% of blood – in systemic veins 
• • CO = VR: the volume of blood entering the heart equals the volume leaving it. 
• • Frank- Starling law of the heart: the greater the stretching of the heart, the greater the CO. As stretch depends on VR 

=> the greater the VR the greater the CO.

Venous Pressure – 

Central venous pressure (CVP) = the pressure measured in the cava veins at the level of the heart or in the right atrium

Pressure gradient – most important force in venous return ~ 7 mmHg

Pressure gradient= (MCP- RAP)

Factors that can increase venous return: 

1) Increased blood volume 

2) Venoconstriction 

3) Decreased peripheral resistance (dilation of arterioles).

Contractility – 

Increased activity of the sympathetic nerves and epinephrine (adrenal medulla) increase contractility

A positive inotropic effect produces greater ventricular contraction => increased stroke volume and cardiac output.

Positive inotropic effect (▲ contractility) 

– Catecholamines (NE, E), 

– ▲[Ca2+], 

– Drugs: cardiac glycosides, phosphodiesterase inhibitors, etc. 

Negative inotropic effect (▼ contractility) 

– Increased activity of vagus nerves 

– hypoxia of myocardium 

– acidosis 

– Decreased [Ca2+] / Increased [K+]; 

– Drugs : Ca2+ channel blockers; beta-blockers.

Microcirculation

Microcirculation refers to the circulation in the capillaries. Capillaries contain about 5% of blood in the human body. This system helps to exchange oxygen, carbon dioxide, metabolic wastes and nutrients between blood and interstitium.

A microcirculatory unit contains:

• Terminal arteriole
• Metarteriole (vascular shunt)
• True capillaries 
• Venules

Capillaries are the smallest blood vessels with the diameter of 5 to 10 micrometer and allows only a single RBC to pass. Capillaries consist of 2 layers- inner endothelial cell layer and the outer pericyte layer. There are three types of capillaries based on their structures:

Continuous capillaries– like in the brain where few substances need to be explained. They also make up the blood- brain barrier which functions to protect brain from toxins, pathogens and maintain homeostasis.

Fenestrated capillaries– in places of tissues where a large amount of molecular exchange occurs -Remember: absorption-small intestine, secretion-endocrine organs  and filtration-kidneys.). 

Sinusoidal capillaries– are of large diameter to facilitate permeability and is seen in liver, bone marrow and spleen. 

Capillary exchange

Can be:

• Paracellular diffusion- between cell junctions
• Transendothelial transport- through the cell (endocytosis, exocytosis)
• Bulk flow- as a result of Starlings forces

Bulk flow occurs when small particles pass through the gap between nearby endothelial cells. Filtration, i.e the flow out of capillaries occurs at the arterial end while the flow into capillaries (reabsorption) occurs at the venous end. Bulk flow is an important factor in regulating distribution normal BP by maintaining constant fluid balance in plasma and interstitial fluid. 

Starlings forces

To understand plasma filtration, we need to understand starlings forces- hydrostatic and oncotic pressures.

Hydrostatic pressures at the capillaries are produced by blood pressure which forces fluid out. It decreases along length of capillaries from 35mmHg at the arterial end and 17 mmHg at the venous end. Usually represented as HPc.

Hydrostatic pressure of the interstitial fluid is considered zero. Represented as HPif

Plasma colloid osmotic pressure is a force trying to pull fluid into the capillary. It is created by plasma proteins like albumin. Value is around 25mmHg. OPc

Interstitial colloid osmotic pressure is pressure of interstitial fluid which draws fluid out and is 1mmHg. OPif.

Generally, net filtration> net absorption and can be understood by using Net Filtration Pressure (NFP) 

NFP = (HPc – HPif) – (OPc – OPif) 

OPif can be calculated as zero sometimes.

At the arterial end HPc = 35mmHg, so the equation becomes: 

NFP = 35 25 = 10 mmHg thus stating that there is net filtration.

At the middle of the capillary, HPc 25mmHg so  

NFP 2525 0mmHg. There is NO filtration or absorption.

At the venous end HPc 18mmHg 

NFP 1825 = 7mmHg which indicates net reabsorption. 

Image rights belong to rkmd.com

Lymphatic system

Is a circulatory network which functions as to transport lymph. The excess filtrate from the capillaries go into the lymphatic system and return it into the blood through the subclavian veins by- the right lymphatic duct and the thoracic duct.

Lymph is a clear fluid from blood plasma forms as a result of the capillary bed filtrate. It is similar to plasma but contains very low proteins. Normal lymph volume is 3 to 4L/24h. Lymph also serves to transport lipids absorbed by the intestines back to the blood. 

Lymph vessels contract rhythmically as a result of muscle contraction to pump the lymph up. The walls of lymph vessels are attached to surrounding tissues.

The main functions of the lymphatic system are: returning excess interstitial fluid to blood, assist immune functions and help in lipid absorption.

Lymph nodes are structures which filter lymph. They have an outer medulla and an inner cortex. The medulla contains macrophages which phagocytose and destroy foreign material while the cortex has lymphocytes.

The spleen is the largest lymphoid organ which removes RBCs as well as acts as a RBC storage structure. The thymus is the site of T cell maturation and disappears in adulthood.

An edema can be defined as excess fluid in interstitial space. Caused by:

high hydrostatic pressure in capillaries (eg. heart failure) hypoproteinemia (eg. renal diseases) capillary injury (eg. inflammation) lymphatic obstruction (eg. cancer, surgery)

Control of blood flow

Blood vessels have a vascular tone determined by the contraction or relaxation of the smooth muscle cells in the vessel wall.

The control of blood flow is maintained by vasoconstriction and vasodilation which are influenced by:

• Local control by tissues
• Nervous control
• Hormonal control

1. Local control 

“Blood flow of tissues is proportional to the metabolic need.” Organs with higher metabolism and specific functions have higher blood supply, for example the kidneys receive around 20 percent of the cardiac output. This local control can be acute- changing diameter in seconds or long term where tissues control blood supply by increasing or decreasing the overall number and size of blood vessels. An increase in blood flow is usually a result of 

Increase in tissue metabolism

Reduced O2 availability

Factors of local control	examples
Vasodilator metabolites	K, H, lactate, CO2, adenosine, decreased O2
Endothelium derived factors	NO, endothelins, prostaglandins
Local hormones	Histamine, kinin, prostaglandin
Physical influences	Stretch, stress, temperature

Oxygen demand theory

When O2 availability decreases, blood flow increases as a result of vasodilation. 

Decreased O2 in muscles → decreased contraction (relaxation) → vasodilation → increased blood supply.

Vasodilator theory

Increased rate of metabolism increases vasodilator substances. These are:

CO2-end metabolic product

H+, lactate- from anaerobic respiration 

Adenosine- from ATP breakdown

ADP, K+, histamine, temperature. 

Reduced O2

Autoregulation- an adaptive system by which blood vessels maintain a near constant flow to an organ even with changes in perfusion pressure. It is much developed in cerebral, renal and coronary circulation as they are highly sensitive.

Image is used from https://www.neurovascularmedicine.com/. MedicoPlexus does not own this image.

Autoregulation is controlled locally by metabolic and myogenic mechanisms. They may act together or by themselves.

Metabolic metabolism: increased blood pressure → increases blood flow → wash out of vasodilators and more O2 supply → contraction of SMC in vessel wall → leads to decreased blood flow. The endothelial cells of the vascular wall can also react to certain hormones, neurotransmitters and vasoactive factors which can affect the vascular tone.

Myogenic mechanism: constant stretch of SMC acts as negative feedback and contracts the vessel (also vice versa). This response occurs as a result of change in transmural pressure (relative pressure inside vs outside).

Endothelium

Is a single layer of endothelial cells which forms interface between the lumen and the wall. It functions as:

Selective barrier- to transport materials according to demand

Control of vascular tone by producing vasoactive substances

Maintain fluidity of the blood by secreting antithrombic substances like Anti-thrombin III

Producing growth factor for angiogenesis

The endothelium also produces a variety of substances:

Substance	Function
NO	Vasodilator, maintain normal BP, anti-thrombotic, anti-inflammatory, anti-proliferative, NO is responsible for erections
Endothelins	Vasoconstrictor
Prostaglandins-Prostacyclin PGI2	Vasodilator. platelet aggression inhibitor
Prostaglandin-PGH2	Vasoconstrictor
AnticoagulantsTFPI	Prevent coagulation
Plasminogen activator	Stimulate fibrinolysis
vWF	Help platelet aggression
VEGF	Angiogenesis

Humoral control

Is a type of local control mediated be autacoids. These hormones have a short half life and acts close to the site of synthesis (paracrine). Examples include amines- histamine, serotonin; lipids- eicosanoids; peptides- kinins; adenosines, etc.

Bradykinin and lysylbradykinin (kallidin) are two vasodilator peptides. They are released in sweat and salivary glands, pancreas, prostate, intestine, etc. It causes arteriolar dilation, increased vascular permeability and pain.

Histamine is released by basophils and mast cells in allergic reactions. They are short lived, dilate arteries and increase capillary permeability to cause edema.

Eicosanoids- prostaglandins, leukotrienes, thromboxane. 

PGI2, PGD2, PGE2 are vasodilators

PGH2, PGF2alpha are vasoconstrictors

Thromboxane A2 causes vasoconstriction, platelet aggression and is released from platelets.

It is very important for the body to have a balance between TXA2 and PGI2.

Nervous control

Most of the blood vessels receive nerve fibers from the sympathetic nervous system. Capillaries and precapillary sphincters are not innervated. Large arteries and veins are poorly innervated while arterioles are highly innervated. The sympathetic fibers are vasoconstrictors. Parasympathetic fibers are only in blood vessels of GI glands, pancreas and salivary glands and external genitals. Remember P.S = rest and digest). 

NE acts on alpha 1 adrenergic receptors responsible for constriction

E acts on alpha 1 (constrictors) as well as beta 2 (dilators)

The dilating receptors are present in blood vessels of skeletal muscles Fight or flight). There are also a few sympathetic cholinergic receptors in skeletal muscles. Most vessels are under the influence of sympathetic NE system so they vasoconstrict. Even though vasodilation is a result of decreased sympathetic activity, genital erectile tissue, salivary glands, pancreatic exocrine glands, gastric and colonic glands have PS fibers. Sympathetic activity is most strong in skin, kidney and splanchnic organs.

Vascular control and MAP

An increased SNS leads to vasoconstriction → 

-reduction in radius of arterioles → increased BP or

-reduced radius in veins → increased venous return → increased Cardiac Output →  increases BP

Hormonal control

Vasoconstrictors – Epinephrine, Angiotensin II, ADH, vasopressin 

Vasodilator – Atrial natriuretic peptide 

One of the most important systems to regulate BP is the Renin- Angiotensin System. 

The kidneys release Renin as a result of decreased BP. This renin converts 

Angiotensinogen from the liver to AT1. AT1 is acted on by the Angiotensin Converting Enzyme ACE made by the liver to become AT II. ATII acts on blood vessels to induce vasoconstriction; organs like the kidney to retain water; increase aldosterone secretion from adrenal glands, etc.

Image taken from First Aid for Step 1. All credits go to USMLE Rx and First Aid.

Another mechanism by which hormones control the BP is by the antidiuretic hormone mechanism- ADH

ADH is a peptide released from the posterior pituitary and cause water reabsorption of water as well as vasoconstriction of BV. 

ANP is a vasodilator released by the atria of the heart in response to increased stretch due to increased blood volume. It acts by dilating renal arteries and veins, decreasing ADH and renin secretion and by decreasing Na+ reabsorption. 

Coronary circulation

Circulation to the heart itself. Done by left and right coronary arteries. Takes up about 4 percent of the cardiac output since its tissue needs constant supply of oxygen.  If the O2 supply is low, adenosine is released into the coronary arterioles for dilation.

CADs- coronary artery diseases are the most common type of heart disease. They cause occlusion of the arteries to cause a myocardial infarction.

Regulation of arterial blood pressure

Blood flow equation is: Q=ΔP/R   (change in pressure by resistance)

In the vascular system:  CO= MAP/TPR 

Thus MAP= CO x TPR 

Short term control is regulated by making changes in CO and peripheral resistance while long term control is made by changes in blood volume.

Short term control of BP

The autonomic NS controls the cardiovascular system- modulates the CO, blood flow distribution via altering the diameter. It is accomplished by the help of receptors in the body- chemical, baro (stretch) receptors.

Baroreceptors are two types: Peripheral which senses the pressure and cardiopulmonary which senses filling of the heart. These then send information to the cc in the brain. 

 The cardiovascular center is affected:

Directly by hypoxia

Excitatory by stress, pain, chemoreceptors, etc

Inhibitory by cardiopulmonary receptors, stretch receptors, lung receptors

Peripheral baroreceptors like carotid sinus and aortic arch mechanoreceptors are stretch receptors. When an increase in stretch is encountered, they send signals to the brainstem which will: increase vagal activity to heart, depresses sympathetic flow. and vice versa.

https://thoracickey.com/arterial-blood-pressure/. Not property of medicoplexus

Baroreceptor reflux

Rapid control of BP. During high BP, the cardiovascular system is stimulated, which inhibits sympathetic activity of heart to vasodilate and decrease BP. Low BP, decreased baroreceptor activity stimulates sympathetic activity of heart, vasoconstriction of peripheral vessels, increase venous return, and inhibits cardioinhibitory area. It serves as a compensatory mechanism not a restoring one. 

Cardiopulmonary receptors

Stretch receptors in atria, big veins and pulm. artery. They monitor the filling of heart and regulate blood volume. It decreases BP by: decreasing sympathetic activity and inhibiting ADH release.

Arterial chemoreceptors

Peripheral chemoreceptors which synapse with CN X and CN IX, found within aortic and carotid bodies. They regulate ventilation to prevent hypoxia. Decreased blood flow through these arteries cause a “pressor effect” which increases HR and vasoconstriction. 

At extremely low BP, MAP below 60mmHg) the vasomotor centers are stimulated as brain doesn’t get enough oxygen. It causes powerful activation of the sympathetic NS and constricts blood vessels. 

Cushing reaction

Response to an increase in intracranial pressure which compresses cerebral arteries and initiates a BP increasing response. It presents with high BP with decreased HR.

Intermediate control of BP

Stress relaxation mechanism Capillary fluid shift mechanism

Hormonal control of BP

Regulated by:

Hormone	Function
AT II	Vasoconstriction, increases BP
Hormone	Function
E, NE	Increases BP
ADH	Vasoconstriction, increases BP
ANP	Decreases blood volume and BP
Aldosterone	Increase blood volume and BP

Renin Angiotensin Aldosterone System (RAAS)

Body’s mechanism to increase blood pressure and blood volume by increasing water and Na+ reabsorption as well as stimulating thirst. RAAS is discussed in the previous pages.

ACE inhibitors- prevent formation of AT II, to decrease BP in hypertension, for preventing kidney failure. ARBs- Block AT II receptors from acting on blood vessels.

Adrenal medulla hormones

E, NE cause increased cardiac function, vasoconstriction of most splanchnic organs (vasodilation in skeletal muscles)- the fight or flight response. 

ADH (vasopressin)

Produced in hypothalamus and released via posterior pituitary in response to high plasma osmolarity or low BP. Increases blood volume by stimulating H2O reabsorption.

Long term control

Maintained by kidneys. Alters blood volume, CO and MAP. Hormonal effectors RAAS, ADH, ANP.

https://www.cvphysiology.com/. Not owned by medicoplexus.

-Blood (Transport Medium)

• Blood Cells and Plasma

Functions of the Circulatory System : 

Transportation of nutrients, metabolites, gases, hormones, Temperature Regulation, pH Regulation, Immune functions 

The Circulation has 2 subdivisions-

1.The Cardiovascular system, which further has 2 circuits:

-Systemic circulation –  carries oxygenated blood from LV to the capillaries in the tissues of the body. High Pressure with Vascular Beds arranged in Parallel. 

-Pulmonary circulation – carries deoxygenated blood from RV to the lungs. Low pressure with vascular beds arranged in series.

2. The Lymphatic System