Topic 11 Flashcards
2 major parts of the cardiac physiology
- heart
- conduction system
Heart
dual pump with valves
Muscle cells of the heart connected by..
gap junctions
Conduction system produces
aps spontaneously (no stimulus) but at different rates
Conductions system is composed of…
non contractile cardiac muscle cells
Non contractile cardiac muscle cells are ..
modified to initiate and distribute impulses throughout the heart
4 parts of the conduction system
- sinoatrial (SA) node
- atrioventricular (AV) node
- bundle of His (AV bundle) and bundle branches
- purkinje fibres
Sinoatrial (SA) node
in right atrium. produces APs faster than other areas (pacemaker)
Sinoatrial node rate =
100 APs/min (modified by PSNS to be 75 aps/min at rest)
Atrioventricular (AV) node location and rate =
in right atrium . 50 aps/min
Bundle of His (AV bundle)
originates AV node. only route for electrical activity to go from atria to ventricles
Bundle branches
right and left. 30 APs/min
Purkinje fibres
terminal fibres stimulate contract of the ventricular myocardium
Purkinje rate
30 APs/min
Artificial pacemakers
stimulate if SA or AV node damaged
If conduction system damaged ..
next faster part becomes pacemaker (if SA damaged then AV node takes over)
Cells of the APs of SA and AV nodes
non contractile autorhythmic cardiac muscle cells (self excitable) and -40mV is threshold
Pacemaker potenital
- low K permeability (K voltage gates closed).
- slow inward leak of Na (Na voltage gates open)
- causes slow depolarization toward threshold (-40mV)
AP depolarization for pacemaker potential
- at threshold –> AP
- Ca voltage gates open so Ca moves in and depol. (Na voltage gates close at threshold so not involved in AP)
- Ca voltage gates close at peak
AP repolarization for pacemaker potential
- K voltage gates open at peak so K out leads to repol.
- K gates close below thereshold
Na channels open at -50 mV for pacemaker potential then it..
starts pacemaker potential again. once K gates close so a continuous cycle.
Note for pacemaker activity
NO RMP!!
APs in ventricule myocardium
- cells = contractile.
- purkinje fibre AP –> ventricular (contractile) myocardial AP (spread cell to cell by gap junctions)
- Resting MP= -90 mV
Depolarization of ventricular myocardial APs
- Na voltage gates open fast = same gates as neuron, skel. muscle.
- MP to +30 mV
Plateau of ventricular myocardial APs
- Na channels close and inactivate (slight drop in MP)
- Ca slow voltage gates are open
Repolarization of ventricular myocardial APs
- Ca channels close.
- K voltage gates open therefor K outflux and MP decreases to resting
Absolute refractory period of ventricular myocardial APs
LONG Na channels inactivated until MP to close to -70 mV
1st step in excitation contraction coupling in myocardial cells
open voltage gates Ca channels of AP = small increase cytosolic Ca (from ECF) so not enough trigger contraction
2nd step in excitation contraction coupling in myocardial cells
opens chemically gated Ca channels on SR so cytosolic Ca increases so it binds to troponin and leads to contraction
3rd step in excitation contraction coupling in myocardial cells
contraction. sliding filament mechanisms. begins a few msec after AP begins. duration of AP of 250 msec and duration of twitch is 300 msec therefor contraction almost over when AP ends. so NO summation and NO tetanus
Electrical activity (ECG)
small currents due to deploy/repol of heart move through salty body fluids. recording seen as waves which = sum of electrical activity of ALL myocardial cells (not AP)
Potential difference measured on body surface using..
electrode pairs: 1 pair = a lead
3 ECG waves
- p wave
- QRS wave
- T wave
P wave of ECG
atrial depol. which is followed by contraction
QRS wave of ECG
ventricular depol. which is the contraction but is also atrial repol which causes relaxation. (masked by larger ventricular electrical event/ larger muscle mass)
T wave of ECG
ventricular repol. followed by relaxation
3 ECG intervals
- P-Q
- S-T
- T-P
P-Q interval for ECG
atria contracted, signals passing through AV node
S-T interval for ECG
ventricles contacted, ratio relaxed
T-P interval for ECG
heart at rest
3 abnormalities of heart beat
- tachycardia
- bradycardia
- heart block
Tachycardia
resting HR more than 100 bpm
Bradycardia
resting HR less than 60 bpm
Heart block
when conduction through the AV node slowed. get increased P-Q interval and ventricular may not contract after each atrial contraction
3rd degree heart block
no conduction through AV node, atria fire at SA node rate (75 APs/min), ventricles at bundle/purkinje rate (30 APs/min)
2 main events of the mechanical activity of the cardiac cycle
- systole= contraction/emptying
- diastole= relaxation/filling
1 complete heartbeat =
diastole and systole of atria AND diastole and systole of ventricles
Timing of mechanical events
average resting HR = 75 beats/min therefore 0.8 sec/beat
Blood flow through heart due to..
- pressure changes
- valves
- myocardial contraction (raises P)
In diast. ventricules have..
lowest P and blood flows into them
In syst. ventricules have ..
highest P and blood flows out of them
2 steps during ventricular systole
- higher P in ventricles than atria forces AV valves shut therefore turbulence of blood gives first heart sound (LUB) shortly after QRS wave starts
- P rises so higher P in ventricle than aorta/pull trunk pushes semilunar valves open and blood enters vessels
2 steps during ventricular diastole
- P drops, higher P in aorta/pulm trunk than ventricles forces semilunar valves to shut therefore turbulence into 2nd heart sound (=DUB). mid T wave
- AV valves open when P in ventricle drops below P in atria
2 heart sounds
- turbulent flow= noisy due to blood turbulence when valves shut
- laminar flow= no sound
Sounds of Kototkoff
turbulence heard in brachial artery during blood pressure measurements.
Begin and stop of Kototkoff sounds
- begin = systolic pressure
- stop = diastolic pressure
Cardiac Output (CO)
volume of blood ejected by EACH ventricle in 1 min (ml/min)
Equation for CO
CO= heart rate x stroke volume
Stroke volume (SV)
volume ejected by each ventricle per beat
Stroke volume is equal
to the difference between EDV and ESV
End diastolic volume (EDV)
volume of blood in each ventricle at end of ventricular diastole (preload). approx 120 mL
End systolic volume (ESV)
volume of blood in each ventricle at the end of the ventricular systole (whats left after ejection) approx. 50 mL
therefore SV =
120 mL- 50 mL = 70 mL
How often does the total blood volume (5L) pass through both ventricles
every minute
CO may increase ___ during exercise
5 times
Control of heart rate
basic rate set by SA node (intrinsic control so built in) modifiers of HR (extrinsic control) so a change (not AP)
3 types of extrinsic heart rate control
- neural
- hormonal
- other
SNS (thoracic nerves) neural extrinsic controls
Na channels open wider therefore increase Na permeability at SA node and increases slop of pacemaker potential therefore each threshold faster and increases HR
PSNS (vagus nerve) neural extrinsic controls
- keeps resting HR lower than pace set by SA node alone. (sends continuous impulses)
- increase K permeability at SA node therefore more -‘ve on repol. and decrease HR so further to go to threshold and takes longer
Hormonal extrinsic controls of heart rate
- epinephrine, NE increase HR (some as SNS)
- thyroid hormone direct effect to increase HR (slow and takes days)
- increase number of epi receptors so more sensitive to epi
Ions as a extrinsic factor of heart rate
- high K in ISF: MP more +’ve than normal so pacemaker Na channels may not open and can’t reach threshold. slows repol. which decrease in HR can lead to cardiac arrest
- low K in ISF: evidence that K channels in some cells change specificity and allow Na through instead of K so it depol. membrane and increase HR (feeble beat abnormal)
Fever as an extrinsic factor of heart rate
increase temp so increase HR
Age as an extrinsic factor of heart rate
newborn = high
Fitness as an extrinsic factor of heart rate
increase fitness = decrease HR
Intrinsic control of stroke volume is..
hearts built in ability to vary SV and adjust to demands.
Intrinsic control of stroke happens by..
increase venous return so EDV increases so increase heart muscle stretch and force of contraction and increase SV within physiological limits
Relationship between EDV and SV (frank starlings low of the heart)
force of ejection is directly proportional to length of ventricular contractile fibres
In intrinsic control of stroke volume you get increase venous return due to..
- exercise: venous return speeded up
- lower HR so had longer to fill and less of an effect than exercise
Extrinsic controls of stroke volume
- ANS - SNS
- hormones
- other factors
ANS SNS extrinsic controls
-increase force of contraction (for given EDV) and increase SV. (SNS stimulation ⇑ opening of Ca channels ⇒ ⇑ Ca into cytosol ∴ more cross bridges ∴ ⇑ force)..
BUT SNS also ⇑ HR = less time to fill ∴ have ⇓ EDV at higher HR. However, ⇑ force ⇓ ESV - compensates for ⇓ in EDV
-by increase both force and HR allows at least maintenance of SV even at high HR
Overall for extrinsic controls of stroke volume
SNS increase CO and PSNS decreases CO
Hormones as an extrinsic control of stroke volume
- Epi, NE - same mechanism as SNS - ⇑ force - thyroid hormone - ⇑ force (+ ⇑ epi receptor #)
Force increase of stroke volume by..
- ⇑ external Ca++ (more Ca++ moves in on AP) - digitalis (drug) - ⇑ Ca++ inside
Force decrease of stroke volume by..
- acidosis - ⇑ external K+ - Ca++ channel blockers (drugs) e.g. verapamil
Blood flow
volume of blood flowing through any tissue/min (i.e. mL/min)
Blood flow in a vessel determines by..
pressure and resistance
Relationship for blood flow
F = ΔP
R
Relationship for blood flow where F =
flow
Relationship for blood flow where ΔP =
blood pressure gradient (difference) between 2 points
- ⇓ blood pressure from: aorta ⇒ arterioles (resistance vessels) ⇒ large veins (capacitance vessels)
Relationship for blood flow where R =
resistance. it opposes flow - friction of blood rubbing against vessel walls
Resistance for blood flow depends on…
a) vessel length †
b) viscosity of blood: these normally do not change
c) radius of arterioles most important: - major resistance vessels
- controlled by smooth muscle innervated by SNS
Vasodilation
increase radius therefore decrease R and increase F. P in arty is low and P in organs is high so more blood to capillaries
Vasoconstriction
decrease radios therefor increase distance and decrease flow. P in artery is high so blood backs up. P in organ is low so less blood flow into organ capillaries
Blood flow to organs controls by..
- vasodilatation
- vasoconstriction
- If vasoconstriction/
dilation is local (i.e. to 1 organ)
no observable change in systemic (arterial) BP
If vasoconstriction/dilation is systemic then ..
systemic BP will change
Vasoconstriction/dilation (arteriolar radius) controlled by
- intrinsic regulation
- extrinsic regulation
Intrinsic regulation of vasoconstriction dilation allows..
organ to control its own blood flow
Myogenic regulation
(intrinsic) when smooth muscle is stretched, it contracts ∴ if ⇑ systemic blood P ⇒ arterioles constrict.
Example of myogenic regulation
- on standing ⇒ high arterial bp in feet (gravity) ∴ arterioles constrict ⇒ ⇓ flow into capillaries
- on standing ⇒ low arterial bp in brain (gravity) ∴ arterioles dilate ⇒ ⇑ flow to brain capillaries
Metabolic regulation
(intrinsic) if blood levels of e.g. O2 ⇓, CO2⇑, pH ⇓ (⇑ metabolism in organ) - endothelial cells + hemoglobin release nitric oxide ⇒ vasodilation ⇒ ⇑ blood flow to organ
Both myogenic regulation and metabolic regulation maintain..
blood gases, pH levels and very important in heart, skel. muscle and brian
Extrinsic regulation of vasoconstriction and dilation
external control by nervous system and endocrine system
Neural (SNS) regulation of vasoconstriction and dilation
- arteriolar vasocon. (except in brain - intrinsic regulation only) - vasodilation due to ⇓ SNS signals (only important PSNS effect = dilation of arterioles of penis/clitoris) - also venoconstriction (vein constriction)
Hormonal regulation of vasoconstriction and dilation (epinephrine)
- vasocon: skin, viscera - reinforces SNS - vasodil: heart, skel muscle, liver - opposes SNS
SNS causes release of epi - what is arteriolar response?
- in skin, viscera: both ⇒ vascon (blood shifted away to where it’s needed) - in heart, skel. muscle, liver: opposite effects ⇒ response mainly determined by metabolic regulation
What does angiotensin 11 and ADH do to arteriolar response
vasoconstriction
What does histamine do to arteriolar response
vasodilation
Blood pressure
hydrostatic P exerted by blood on wall of vessel (clinically on the walls of the arteries)
Systolic pressure
arterial bp produced by ventricular contraction
Diastolic pressure
arterial bp due to recoil of elastic arteries (when ventricles are relaxed)
What we measure in an artery…
120/80 = syst./diast
Pulse pressure
systolic - diastolic
Mean arterial pressure (MAP)
regulated by the body i.e. what the body measures
= average blood P through cardiac cycle BUT diastole is longer than systole, so MAP = diast. P + 1/3 pulse P
MAP regulation
- F = ΔP/R ∴ ΔP = FxR
- ΔP = MAP - venous P (P in veins ~ 0 ∴ ΔP = MAP)
MAP regulated by controlling ..
- cardiac output
- TPR (arteriolar radius)
- blood volume (affects venous return ∴ SV; also MAP directly)
Neural control of MAP contain
- baroreceptors
- chemoreceptors
Baroreceptors reflexes
short term changes (standing) stretch receptors that monitor MAP in carotid sinus (brain bp) and aortic arch (systemic bp)
Chemoreceptors reflexes
peripheral chemoreceptors respond to pH, CO2 (and O2) and found in aortic arch and carotid sinus (called “bodies”)
-involved in regulation of respiration, but affect bp
Epinephrine in MAP
⇑ HR, force of contraction ∴⇑ CO ⇒ ⇑ MAP
Renin-Angiotensin system in MAP
plasma angiotensinogen to angiotensin 11.
Angiotensin ll causes..
- ⇑ vasocon, ⇑ venocon ∴ ⇑ MAP - ⇑ aldosterone, ADH ∴ ⇑ renal Na+, H2O abs; ⇑ thirst ∴ ⇑ blood vol ⇒ ⇑ MAP
Atrial natriuretic peptide (ANP) in MAP causes..
⇓ renin (∴ angio II), ⇓ aldosterone, ⇓ ADH = ⇑ urine production ∴⇓ blood vol. and ⇓ vasoconstriction
SO overall = ⇓ MAP
Capillary exchange is between…
blood and ISF
Capillary exchange is when solutes enter and leave capillaries by
- diffusion
- vesicular transport
- mediated transport
Diffusion of solute from capillary
major route (except brain). includes CO2, O2, ions, aa, glucose, hormones etc -usually between endothelial cells
Vesicular tranport of solute from capillary
includes large proteins (e.g. antibodies)
- occurs via transcytosis
- endocytosis from blood into endothelial cell, then exocytosis from endothelial cell into ISF
Mediated transport of solute from capillary
requires membrane carrier protein and important in the brain
Fluid (h2o) enters (absorption) or leaves (filtration) capillaries by..
- osmosis
- bulk flow (pressure differences)
4 pressures involved with bulk flow in capillaries
- blood hydrostatic P (BHP) = blood pressure
- blood osmotic P (BOP) – due to plasma proteins
- ISF hydrostatic P (IFHP) = 0 mmHg
- ISF osmotic P (IFOP) - due to ISF proteins
Net filtration pressure (NFP)
sum of hydrostatic and osmotic pressures acting on the capillary
Bulk flow in capillaries in the body
- 90% of filtered fluid reabsorbed to blood
- 10 % enters lymph ∴ ISF vol. remains relatively constant
Edema
accumulation of fluid in the tissue (ISF) causing swelling
Edema due to..
1) high blood pressure (⇑ BHP) 2) leakage of plasma proteins into ISF ⇒ inflammation (⇑ IFOP) 3) ⇓ plasma proteins (malnutrition, burns) (⇓BOP) 4) obstruction of lymph vessels - elephantiasis, surgery
Circulatory shock is..
inadequate blood flow (⇓ O2, nutrients to cells)
3 types of circulatory shock
- Hypovolemic
- Vascular
- Cardiogenic
Hypovolemic shock
decrease blood volume. due to blood loss, severe burns, diarrhea, vomiting
Vascular shock
blood volume normal but vessels expanded. due to systemic vasodilation of blood vessels (decrease bp)
2 example of vascular shock
- anaphylactic shock (allergic reaction/ histamine)
- septic shock (bacterial toxins)
Cardiogenic shock
pump failure so decrease CO and heart cannot sustain blood flow
1st stage of shock: Compensatory
mechanisms can restore homeostasis by themselves. trigger SNS
- ⇑ HR, generalized vasocon. (except to heart, brain) = ⇑ bp
- ⇓ blood flow to kidneys triggers renin release - get angio II + aldosterone, ADH release ∴ vasocon., ⇑ Na+, H2O retention (maintain blood vol.), ⇑ thirst
Compensatory stage includes..
- baroreceptors
- chemoreceptors
- ischemia (lack of O2) of medulla
2nd stage of shock: Progressive
- mechanisms inadequate to restore homeostasis - requires intervention
- CO ⇓ ∴ ⇓ bp in cardiac circ ∴ ⇓ cardiac activity
- ⇓ blood to brain ⇒ ⇓ cardiovascular control
- damage to viscera due to ⇓ blood flow, especially kidneys (can lead to renal failure)
3rd stage of shock: Irreversible
⇓ CO ⇒ too little blood to heart ⇒ ⇓ CO. self-perpetuating cycle and leads to death
Blood contains what 2 things
plasma and formed elements
Plasma contains..
- H2O
- proteins
- electrolytes
- other solutes (nutrients, wastes, gases, hormones)
H2O in plasma
transport medium and carries heat. (90.5%) of plasma is water
Proteins in plasma
- albumins (58%)
- globulins (38%)
- fibrinogen (4%)
Protein functions in plasma
- produce osmotic pressure (albumins
- buffer pH (7.35-7.45)
- α, β globulins: transport lipids, metal ions, hormones
- γ (gamma) globulins = antibodies
- clot formation
Electrolytes (ions) in plasma
functions are membrane excitability and buffers HCO3
Formed elements of blood include
- RBC
- WBC
- platelets
RBC functions
- transport - O2 on iron (Fe) of heme; CO2 on globin
- buffer - globin binds to H+ reversibly
- carbonic anhydrase (CA) important for CO2 transport in blood
Hemoglobin
Hb = 4 hemes + 4 globins (protein)
1 iron (Fe)/heme =
4 Fe/Hb
Hemeglobin brown down by macrophages into..
- heme
- globin
Heme
- Fe removed + stored (liver, muscle, spleen)
- from stores (or diet) ⇒ bone marrow cells make heme ⇒ RBCs
- non-iron portion ⇒ bilirubin ⇒ excreted in bile from liver
Jaundice
excess bilirubin in blood
Jaundice is due to..
- excess RBC breakdown; or
- liver dysfunction (neonates ⇒ liver immature); or
- blockage of bile excretion
Globin
converted to amino acids (recycled)
RBC have no..
nuclei/mitochondria so only anaerobic respiration
WBC are either..
granulocytes or agranulucytes
3 types of granulocytes
- neutrophils
- eosinophils
- basophils
Neutrophils
phagocytosis/ 1st to enter infected area
Eosinophils
attack parasites. break down chemical released in allergic reactions
Basophils
secrete histamine (inflammation) and secrete heparin (inhibits clotting)
2 types of agranulocytes
- monocytes
- lymphocytes
Monocytes
enters tissues, enlarge to become phagocytic macrophages
3 types of lymphocytes
- T lymphocytes
- B lymphocytes
- Natrual killer cells
T lymphocytes
helper T (Th) + cytotoxic T (CTLs) lymphocytes
B lymphocytes
when activated give rise to plasma cells and secrete antibodies
Natural killer cells (NKs)
attack foregone cells, normal cells
Platelets
cell fragments from megakaryocytes in red marrow
Functions of platelets
- form platelet plug which prevent excess blood loss.
- contains granules (coagulation factors/ clotting)
Hemostasis
process of stopping bleeding.
Hemostasis involves
- vascular spasm
- platelet plug formation
- clot formation
- clot retraction and repair
- fibrinolysis
Vascular spasm
vasoconstriction of damaged arteries, arterioles. ⇓ blood flow (min. to hrs.)
Platelet plug formation
- platelets stick to damaged blood vessel, release chemicals (factors)
- neighbouring healthy endothelial cells release a chemical, preventing spread of plug
- plug formation requires a prostaglandin – PG formation inhibited by aspirin
Factors of platelet plug formation do..
a) cause more platelets to stick (+ve feedback)
b) promote clotting
c) begin healing
1st stage of clot formation: production of prothrombin activator by..
– extrinsic pathway - uses factors released by damaged tissues
– intrinsic pathway - uses factors contained in blood
→ usually both occur together - require Ca++, tissue, platelet and /or plasma factors
2nd stage of clot formation ..
Prothrombin converted to thrombin
3rd stage of clot formation
Fibrinogen converted to fibrin
Thrombin
+ve feedback to ⇑ its own formation ⇒ thrombin trapped in clot, inactivated by plasma factors, washed away ∴ limits clot spread
Clot retraction and repair
retraction: blood vessel edges pulled together
repair: fibrinoblasts from new CT, new endothelial cells repair lining
Fibrinolysis
clot dissolution. fibrin digesting enzyme (plasmin). phagocytes then remove clot clumps
Thrombus
stationary clot in an undamaged vessel
Embolus
free floating clot
Hemophilia
clotting abnormal/absent about 83% = type A and lack clotting factor Vlll
