EXAM FC

Role of the cardiovascular system:

primary transport system the body, pumping blood daily

Right Side of the Heart

Right Side:

• Right Atrium

• Right Ventricle

• contains deoxy blood

• low pressure

• sends blood to the lungs to get O2

Left Side:

• Left Atrium

• Left Ventricle

• Contains Oxy Blood

• High Pressure due to greater Blood volume

• Pushes blood to whole body

Heart Valves

ensure blood is travelling in one direction based on pressure gradients

prevents backflow

Why is Left side of heart more thicker?

• Left ventricle pumps blood around the whole body

• Higher Pressure required and more muscle required cox a large amount of blood

• t only pumps blood to the lungs and is a low pressure system.

Tricuspid Valve?

RA → RV

Pulmonary Valve

RV → pulmonary artery

Mitral (Bicuspid) Valve

LA → LV

Aortic Valve

LV → Aorta → Body

Describe the Cardiac Cycle?

The events happening during one heartbeat

• atria contract → ventricles fill → end diastolic volume reached = atria systole

• Ventricles contract → pressure rises → all valves close → volume no change = isovolumetric ventricular contraction

• Ventricular pressure is more than arterial pressure → semilunar valves aorta + pulmonary open → blood ejected which is stroke volume = Ventricular Systole

• Ventricles Relax → less pressure → less valves closed → volume unchanged = Isometric relaxation

• Ventricular pressure is less than arterial pressure → atrioventricular valves open (mitral and bicsupid) → ventricle fill with blood

• cycle repeats

Stroke Volume?

The amount of blood ejected from the ventricles

SV = diastolic - systolic volume

Cardiac Output

Amount of blood pumped per minute

CO = SV x HR

e.g. HR = 70bpm SV = 70mL

CO- 70 × 70 = 4900 Ml/min

4.9L/min

Factors that affect CO

• Preload

• Frank Stirling Mechanism

• Contractility

• Afterload

What is Venous Return?

flow of blood from body back to the right side of the heart

How does Preload affect CO

Definition: stretch of the heart before contract

Affected by: Venous Return and EDV

• higher preload → more stretch → stronger contractions → higher SV → higher CO

How does the Frank Starling Mechanism effect CO

Def: more filling causes an increased force of contraction

• more stretch → more actin-myosin cross bridges

• stretch increases Ca2+ sensitivity

• more EDV = mote stretch → more force → more SV → more CO

How does Contractility affect CO?

force of contraction due to external factors such as NA

• more force → more SV → more CO

Afterload

resistance the heart must overcome to pump blood into the body

• resistance ventricles must overcome to eject blood

• Hypertension → heart works faster → less blood ejected → less SV → Less CO

What is Automaticity?

Ability of cardiac cells to generate spontaneous a.p.

unique ability to pacemaker cells

Describe the structure of the Heart

Electrical signals from the Heart

generates and converts electricity into contractions

• spread through heart → cardiac muscle depolarise → ca2+ influx → muscle contracts → blood pumped

What does myogenic mean?

The heart generates its own electrical activity w/o nervous system

Cardiac Muscles cells are connected by

• intercalated discs - allow for spread of electrical signals between cardiac myocytes

• gap junctions - allow ions to spread electrical signal rapidly from one cell to another

NS changes how fast or strong Heart beat is

Where does the electrical signal travel?

• SA Node - hearts natural pacemaker in the RA

• Atrial Muscles

• AV Node - delays the conduction = alllow ventricles to fill up before contracting

• Bundles of His

• Bundle Branches - fast conduction network delivering electrical impulse and allow both ventricles to contract at same time

• Punkenje Fibres

• Ventricular Muscles

Factors that affect the Heart Rate

• Intrinsic rate of SAN

• Extrinsic factors - autonomic nervous system

Why is the AV Nodal delay important?

allows for the ventricle to be filled up before it contracts

Sino Atrial A.P. Graph?

There is no stable m.p.

Action Potential happens in 3 parts

• Phase 4 → depolarisation (relationship between depolarising current and K+ efflux)

• Phase 0 → L type Ca2+ influx

• Phase 3 → K+ efflux

SAN A.P. Phase 4

Pacemaker Depolarisation

M.P. from -60mv to -30mv

membrane slowly depolarises it self

caused by 4 currents

• Funny Current

  • occurs through the HCN channels

  • Na+ influx and K+ efflux at the same time

• NCX Current

  • 3 na+ ions for every ca2+ ion it removes

  • net (+) charge = depolarisation

• Potassium Current

  • efflux of K+

  • hyperpolarisation

• Ca2+ channels

  • influx of Ca2+ ions

  • depolarisation

SAN A.P. Phase 0

Upstroke

from -30mv to 20mv

• rapid depolarisation

• caused by influx of ca2+ through L type Ca2+ channels

SAN A.P. Phase 3

Repolarisation

• efflux of K+ ions via channels

• goes back to -60mv

Ventricular A.P. Graph

Phase 0: rapid Na+ influx = fast depolarisation

Phase 1: brief k+ efflux = small initial repolarisation

Phase 2: Plateau Phase

• ca2+ influx and K+ efflux are equal

• m.p. remains constant

• allows for ventricle contraction

Phase 3: K+ efflux = repolarisation

Phase 4: Stable m.p. around -85mv

Compare SA A.P. and Ventricle A.P.

SA

• Automatic A.P.

• 3 phases

• Phase 0 = Ca2+ influx

• No resting M.P.

• pacemaker

Ventricle

• Not automatic

• 5 phases

• Phase 0 = Na+ influx

• Stable M.P.

• Contractile Cell

What is CICR

Calcium Induce Calcium Release

How electrical activity = contraction via Ca2+

• Ventricular A.P. reaches T tubules → L type Ca2+ channel open → small amount of Ca2+ influx → Ca2+ activates Ryanodine Receptor (RyR) on the SR → releases higher conc of Ca2+ → Ca2+ influx → actin myosin cross bridges formation → contractions

How is Calcium Removed to make relaxed

SERCA

• pumps Ca2+ back into SR → less Ca2+ → muslce relaxes

What is the Autonomic Nervous System

Automatic Bodily functions

Split into

• Parasym

• Sympa

What is the role of the parasympathetic NS

Rest and Digest → Conserve energy

• slows HR (negative chronotropic effect)

• lessens contracting force (negative inotropic effect) → less SV

• less automacity → SA a.p. threshold is met slower → less a.p. firing

• More AV delay → Ventricles receive electrical impulse slower → slower contractions

What is the role of the sympathetic NS?

Fight or Flight → preps body for action

• increases HR (positive chronotropic effect)

• Increases contracting force (positive inotropic effect) → higher SV

• higher automacity → SA threshold met faster → more a.p. fired

• Less AV conduction delay → ventricle receive electrical impulse quicker → faster contractions

How does the Sympathetic NS prep the Heart for Fight or Flight?

Sympa Nerve releases NA → binds to Beta 1 receptors → activate Gs → GDP to GTP → adenyl cylase → ATP to cAMP → PKA → phosphorylates Ca2+ channels → more Ca2+ → more MLCK → actin myosin cross bridges form → contractions → positive chronotropic

Sympa Nerve releases NA → binds to Beta 1 receptors → activate Gs → GDP to GTP → adenyl cylase → ATP to cAMP → increase Funny current → increases phase 4 depolarisation → threshold reached sooner → faster HR

How does the Parasym prep the heart to conserve energy?

Parasym nerve → release ACh → bind to muscarinic receptors → activate Gi → inhibit adenyl cylase → less cAMP → less PKA → less ca2+ → less MLCK → less contractions → less HR → negative chronotropic

Parasym nerve → release ACh → bind to muscarinic receptors → activate Gi → inhibit adenyl cylase → less cAMP → less HCN channels open → less funny currents → slower Phase 4 → threshold met later → slower HR

What is Vagal tone?

Slows down the SA node intrinsic firing for resting HR

• mediated by vagus nerve in parasymp

How would Beta 1 Blockers effect HR

drug: Propanalol

• Block Beta 1 receptors → adrenaline cannot bind → no Gs activation → no cAMP → less funny current → less Ca2+ → Less Heart rate

How do muscarinic antagonist effect HR

Drug: atropine

block the M2 receptor → ACh cannot bind → cAMP produced → more Ca2+ → contractions → more funny currents → increased Heart Rt=ate

What do Cardiac Glycosides do for contractions?

DIGOXIN

inhibit Na+/K+ ATPase Pump

• normally pumps put 3 NA+ out and 2K+ in

• Digoxin blocks this pump → NA+ build up in cell

• more NA+ → less sodium gradient so Ca2+ remains in the cell in the SR

• More CA+ releases during each heart beat → stronger contractions (positive inotropic)

What do digoxin do for heart rate

• slow down HR by increasing vagal tone

  • slows down SA node firing

  • slows down AV node conduction