CARDIOVASCULAR SYSTEM

CARDIOVASCULAR SYSTEM

The organs and tissues involved in circulating blood and lymph through the body.

CARDIOVASCULAR SYSTEM PRIMARY PURPOSES

• delivery of O2 and substrates for metabolism, growth and repair

• removal of by products of cellular metabolism (CO2)

CARDIOVASCULAR SYSTEM SECONDARY PURPOSES

• fast cell communication (hormones)

• heat transfer

• inflammatory and defence responses to foreign organisms

CARDIOVASCULAR SYSTEM COMPONENTS

1. heart

2. blood and lymph

3. vessels

SYSTEMIC CIRCULATION

• high pressure

• perfuses most of the tissues and organs with blood

PULMONARY CIRCUIT

• low pressure

• takes blood to and from the lungs

CARDIAC OUTPUT RULE

The cardiac output of the right side of the heart = cardiac output of the left side of the heart.

BLOOD DISTRIBUTION

Pulmonary circulation = 9%

Heart = 7%

Systemic circulation = 84%

• Veins = 64%

• Capillaries = 13%

• Arteries = 7%

• systemic veins are essentially blood volume reservoirs

• the ‘reserve’ can be utilised when needed

BLOOD FLOW

The pressure gradient drives blood flow.

PRESSURE = FORCE / AREA

FLOW = PRESSURE (1) - PRESSURE (2) / RESISTANCE

Highest velocity of blood flow is in the middle.

RESISTANCE FACTORS

• geometry of blood vessels and type of flow

• blood viscosity

• vessel length

• vessel width

LAMINAR FLOW

Laminar flow: R = 8(viscosity)(vessel length) / π(radius)^4

THEREFORE…

FLOW = Change in pressure / Resistance

THEREFORE…

FLOW = π(pressure difference)(radius)^4 / 8(viscosity)(length)

IMPLICATIONS OF POISEUILLE’S LAW:

• fluid must be compressible

• tube must be simple geometry - straight, rigid, cylindrical and unbranched (NOT ALL VESSELS ARE RIGID)

• Velocity of fluid at wall must be zero

• flow must be laminar not turbulent

• blood flow must be steady (IT IS ACTUALLY PULSATILE)

• Blood viscosity must be constant

CARDIAC OUTPUT

The amount of blood that the heart pumps through the circulatory system in a minute. Approx. 5L.

CO = STROKE VOLUME X HEART RATE

HAEMODYNAMICS

BLOOD FLOW SYSTEMIC

• Mean Arterial Pressure (MAP) = 97mmHg

• Central Venous Pressure (CVP) = 2mmHg

• Difference in pressure drives blood flow

CO (of whole systemic circuit) = △P (MAP-CVP) / TPR (total peripheral resistance)

TOTAL PERIPHERAL RESISTANCE

TPR = Rarteries + Rarterioles + Rcapillaries + Rvenuoles + Rveins

MEAN ARTERIAL PRESSURE

MAP = average pressure through one cardiac cycle.

CO = (MAP - CVP) / TPR

But CVP is close to zero so disregard…

CO = MAP / TPR

Rearrange…

MAP = CO x TPR

BLOOD VESSEL STRUCTURE

• Inner lumen - passageway for blood flow

• Surrounded by endothelium (TUNICA INTIMA)

• Smooth muscle layer of varying thickness (TUNICA MEDIA)

• Outer fibrous layer (TUNICA EXTERNA)

• Variable amount of elastic connective tissue

ARTERY + ARTERIOLES

• transport blood FROM heart to capillaries

• thicker walls than veins

• more connective tissue and muscle than veins

• little resistance due to large radius

• pressure fluctuates in relation to systole and diastole

• arterial pressure doesn’t drop to 0mmHg during diastole

• arterioles are main resistance vessels

VASCULAR TONE

Vasoconstiction = smaller lumen (pathway)

Vasodilation = larger lumen (pathway)

EXTRINSIC CONTROL OF TONE:

• autonomic nervous system

• endocrine system

INTRINSIC CONTROL OF TONE:

• metabolic factors

• local signals

• local temperature

• stretch

• can override extrinsic

CAPILLARIES

• Microscopic lumen

• supply blood to tissue via perfusion

• one endothelial cell thick

• site of nutrient, waste and fluid exchange

CAPILLARY COMPONENTS

Pre-capillary sphincters

• smooth muscle that controls the flow into the capillary beds

• regulated by local factors

Interstitial fluid:

• between plasma and cells

Lymph vessels:

• important for fluid uptake

CAPILLARY FLUID MOVEMENT

Driven by opposing pressure gradients:

• Capillary Hydrostatic Pressure = blood pressure of capillaries

• Blood Colloid Osmotic Pressure = due to presence of proteins in blood

CHP > BCOP = fluid out of capillaries

CHP = BCOP = no net fluid movement

CHP < BCOP = fluid moves into capillaries

LYMPHATICS

Lymph = fluid that flows through the lymphatic system

• part of ECF

• similar composition to interstitial fluid

• branched network of ducts which terminate in small blind-ended (open) capillaries in the tissue

LYMPH FUNCTIONS

• return excess fluid into circulation

• immune defence

• transport of lipids from GI tract

LYMPH FLOW

• Interstitial fluid enters the lymphatic system via pores in the lymph capillaries

• lymph is propelled by smooth muscle contractions and external pressure from skeletal muscle squeezing lymph vessels

• they have valves to prevent back flow

OEDEMA

Swelling in soft tissue as a result of fluid accumulation - shift in the balance in the capillaries.

Excess interstitial fluid → increased distance between blood and cells → decreased rate of diffusion → inadequate nutrient supply.

VEINS AND VENUOLES

• bring blood BACK to the heart

• large lumen, thin walls

• valves to prevent backflow

• low resistance, low pressure

• less smooth muscle and elastin than arteries

• stretchy but no recoil

• expand when filled with blood

VENOUS RETURN REASONS

1. Valves to prevent backflow

2. Skeletal muscles contractions squeeze veins

3. Lung pressure acts like a pump

4. Cardiac suction due to atrial enlargement

+VE EFFECTS ON HEART RATE

Sympathetic Nervous System

• Adrenaline

• Noradrenaline

Hormones

• Adrenaline

• Thyroid T3 and T4

Body temperature

• fever

Ions

• hypercalcemia

-VE EFFECTS ON HEART RATE

Parasympathetic Nervous System

• acetylcholine

Ions

• Hypocalcemia

CARDIAC OUTPUT - HEART RATE

• Controlled by SA node

• at rest parasympathetic NS is more dominant

CHRONOTOPIC AGENTS = drugs that affect heart rate

CARDIAC OUTPUT - STROKE VOLUME

Stroke volume is the volume of blood ejected in each ventricular contraction.

• usually 70ml/beat @ rest

SV = EDV (end diastolic vol.) - ESV (end systolic vol.)

CARDIAC LENGTH TENSION RELATIONSHIP

• similar to skeletal muscle in that it has a length-tension relationship

• sarcomere length determines tension developed = stroke volume

• normal cardiac operating zone lower than skeletal

• no negative relationship (no descending limb)

heart failure does not equal too much stretch (unlike skeletal)

FACTORS AFFECTING STROKE VOLUME

1. Preload

2. Afterload

3. Contractility

PRELOAD

The myocardial sarcomere length just prior to contraction.

A function of:

• ventricular filling

• ventricular & pericardial compliance

• ventricular wall thickness

Frank-Starling Law.

AFTERLOAD

The force against which the ventricles must act in order to eject blood.

• sum of elastic and kinetic forces

• ‘resistance’ to flow

Main opposing forces:

• arterial blood pressure

• vascular tone

CONTRACTILITY

Inherent vigour of contraction of the heart muscle during systole OR pumping strength.

• independent of pre and after load

• shift in Frank Starling curve

• All impact Ca2+

Shift to left

• Positive inotropic agents

Shift to right

• Negative inotropic agents

BARORECEPTOR REFLEX

• Receptors in aortic arch and carotid sinus = arteriol baroreceptors

• measure high pressure (MAP)

• impulses relayed to CVS control centres in medulla

BARORECEPTOR PATHWAYS

CHEMORECEPTOR REFLEX

• mainly regulates ventilation but also has CVS effects

• arterial not venous detection

CENTRAL CHEMORECEPTORS

• within medulla oblongata

• detect changes in cerebral spinal fluid

• respond to high PCO2 - low pH

PERIPHERAL CHEMORECEPTORS

• carotid and aortic bodies

• respond to low pH in blood

CVS RESPONSES

• Hypocapnia / hypexia (increase CO2 and peripheral resistance)

• Hypercapnia (decrease CO2, bradycardia)

CARDIOVASCULAR CONTROL

SENSOR (AFFERENT NEURONS)

• baroreceptors, chemoreceptors, proprioreceptors

INTEGRATION CENTRE

• CVS centres in medulla oblongata

EFFECTOR (EFFERENT NEURONS)

• Autonomic nervous system and hormones (adrenaline)

MAP REGULATION

OTHER BARORECEPTORS

CARDIOPULMONARY BARORECEPTORS

• in atria @ junction between large veins and pulmonary artery

• impulses sent via vagus nerve to CVS centers in medulla

• low pressure ‘stretch’ baroreceptors

• measures venous return and blood volume

• efferent effects include vasopressin

OTHER BARORECEPTORS PATHWAY

VASOPRESSIN

• Neurohormone released from posterior pituitary

• decrease water excretion from kidneys

• vasocontriction

Secretion regulators:

• osmoreceptors in ECF

• cardiopulmonary baroreceptors in blood

Increase solute concentration:

• Osmoreceptors in brain → increase vasopressin

Decrease solute concentration:

• Active low pressure baroreceptors → decrease vasopressin

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

Targets longer-term blood volume regulation

BLOOD PRESSURE REGULATION OVERVIEW

SENSORS

• baroreceptors and chemoreceptors at different locations

INTEGRATION

• medulla oblongata

EFFECTORS

• autonomic nervous system and hormones

  • adrenaline, vasopressin, angiotensin, aldosterone

*baroreceptor reflex = short-term control

*blood volume regulation = long-term control

BLOOD LOSS

During mild/medium blood loss a reduction in capillary hydrostatic pressure causes the movement of interstitial fluid into the blood vessel to partially restore plasma volume.

CENTRAL ISCHEMIC REFLEX

Emergency back-up reflex activated when cerebral blood flow is critically compromised.

SENSED:

• increased CO2 and metabolite that cause direct stimulation of medullary vasomotor centres

RESPONSE:

• massive SNS outflow to increase cardiac output and vasocontriction

REALITY:

• drives extreme tachycardia (heart rate increase) to prevent BP decline

• kicks in at <60mmHg systolic BP

PULMONARY CIRCULATION

• purpose = respiratory gas exchange

• blood passes through lungs

• low pressure circuit

• relatively short circuit

• branches immediately = increase exchange area = decrease resistance

• less muscle = increase compliance

• vascular response to hypoxia = vasoconstriction

HYPO AND HYPERTENSION

HYPOTENSION

• too low MAP = inadequate blood flow

• not enough blood for normal function

• organ failure → shock → death

HYPERTENSION

• too high MAP

• extra work for heart and tissue damage

• cardiac, vascular, renal failure → shock → death

PRIMARY VS SECONDARY HYPERTENSION

PRIMARY

• multi-factorial pathogenesis

• not one distinct cause

SECONDARY

• has an identifiable cause

HYPERTENSION

BLOOD PRESSURE:

• Systolic BP > 140mmHg

• Diastolic BP > 90mmHg

RISK FACTORS:

• diet

• obesity

• excessive alcohol consumption

• inadequate exercise

CONSEQUENCES:

• stroke

• heart failure

• heart disease

• chronic kidney disease

ADAPTATION TO HYPERTENSION

• Baroreceptors adapt/reset operate/maintain a higher MAP

• they dont bring BP down but buffers acute BP fluctuations

HYPERTENSION PATHOPHYSIOLOGY

Hypertension = increase pressure = increase flow x resistance

• causes too much volume → increase pressure → potential damage

HYPERTENSION CONSEQUENCES ON VASCULAR ARCHITECTURE

• increased shear stress

• endothelial cell damage

• fibrotic scar tissue

• atherosclerotic plaque

HYPERTENSION CONSEQUENCES ON BLOOD VESSELS

1. Stenosis = narrowing vessels → myocardial infarct

2. Thrombosis = clot from plaque formation & rupture → stroke

3. Aneurysm = bulge due to weakened wall → stroke

HYPERTENSION CONSEQUENCES ON HEART

Muscle hypertrophy → change in shape → more muscle → less space → less efficient

• less compliant

• less prelaod

• lower EDV

• lower SV