Heart and Circulation Flashcards
Describe the phases of the cardiac AP in muscle cells
0 - upshoot;rapid Na influx
1 - early repolarisation; cesation of Na influx
2 - plateau - Ca influx
3 - repolarisation - K+ efflux
4 - back to RMP, Balance of ongoing K+ efflux vs Na influx - close to Em for K of -90mV
The rate of rise of the AP in SA and AV node is slower than in myocytes because….
It is due to Ca current only
Speed of conduction in SA and AV nodes
0.05m/s
Normal axis is between
+110 and -30
The chest ECG leads are located…
V1 R 4th ICS, sternal boarder V2 L 4th ICS, sternal boarder V3 L 4th ICS, mid clav line V4 apex - 5th ICS V5 5th rib lateral V6 ?ant ax line
How does vagal stimulation slow the heart rate
Opens K+ channels (M2, Ach, G protein, cAMP) - antagonises the funny current - slows rate of rise of pacemaker potential
How does sympathetic stimulation increase the heart rate
NA - B1 receptors, - cAMP - opening of L type calcium channels increases the rate of rise of the pacemaker potential
PR interval duration
0.12 - 0.2
Does the PR interval change with heart rate?
yes - at rest 0.18 - at 130/min - 0.14
QRS duration
< 0.1s
QT interval
<0.43s
Long PR interval is called
first degree heart block
LAFB ecg findings?
Left axis deviation, widened qrs
LPFB ecg findings?
Right axis deviation, widened qrs
dropped QRS complexes, PR interval constant
Second Degree Heart Block Type 2. Dangerous - block almost always occuring in the distal his-perkionje system and may progress to 3rd degree block - if it does, it is likely no escape rhythm will generate
dropped QRS complexes, PR lengthens until dropped beat
Second Degree Heart Block Type 1 (WenckeBack), usually medically benign - unlikely to progress to complete HB. Almost always a disease of the AV node
Bundle of Kent
An extra abnormal bundle of conducting fibres between the atria and ventricles
HR in atrial tachycardia
up to 220/min
HR in Atrial Flutter
200-350/min - due to large counter-clockwise movement in the R atrium - produces the saw tooth pattern on ECG
What is the max conduction rate of the AV node?
230/min
Atrial rate in AF?
300-500 beats/min. The AV node discharges at irregular intervals producing a ventricular rate usually 80-160/min
why do fast heart rates cause 1) heart failure and 2) angina
1) HF due to insufficient time for ventricular filling - cardiac output decreases
2) The coronary arteries are perfused only during diastole - with fast rates, diastole is shortened more than systole.
Vagal stimulation has what effects on the AV node?
Increases the degree of AV block - lowers the ventricular rate in tachyarrythmias
Why is the t wave a dangerous time to give a shock
Some of the ventricular muscle is depolarised, some repolarised, some is incompletely repolarised - perfect conditions for setting up a circus movement - VF
peak pressure in L andSV R ventricles
120mmHg and 25mmHg
SV at rest is _____
EDV at rest is ______
SV 70-90mL, EDV is about 130ml
a wave
due to atrial systole - some backflow of blood from atria into VC
c wave
due to bulging of the tricuspid valve during ventricular systole
v wave
mirrors atrial filling pressure
phase 1 of cardiac cycle
atrial systole, 0.1s, p wave
Phase 2 of cardiac cycle
isovolumetric ventricular contraction, 0.05s, RS segment on ecg
Phase 3 of cardiac cycle
Ventricular ejection, 0.3s, until end of t wave on ecq
Phase 4 of cardiac cycle
Isovolumetric ventricular relaxation,
Phase 5 of cardiac cycle
Ventricular filling
When the heart rate increases which shortens more out of systole and diastole
Systole; 0.27 -> 0.16
Diastole; 0.62 -> 0.14
at HR 65:200
why is cardiac muslce unable to undergo tetany
Becuase of the prolonged Action Potential. It cannot respond to a second stimulus until near the end of the initial contraction.
1st heart sound
closure of the AV valves
2nd heart sound
closure of the semilunar valves
C.O. at rest
about 70 mL x 72 beats/min = 5.0L/min
anxiety and excitement on CO
50-100% increase
Eating on CO
30% increase
Exercise on CO
up to 700%
Pregnancy
increase
hot temperature
increase
Sitting or standing from lying
DECREASE by about 20-30%
catecholamines exert they action on the heart through….
Beta1 receptors, Gs, cAMP
How do xanthenes such as cafiene and theophylline exert their effects on the heart
They inhibit the breakdown of cAMP
How does digitalis affect the heart
Inhibits NaKATPase in the myocardium which in turn causes a decrease in calcium removal from the cytosol by Na/Ca exchange
Depressants of myocardial contractility
Hypercapnia hypoxia acidosis quinidine procainamide barbiturates Heart Failure
oxygen consumption by myocardial tissue (not beating)
2ml/100g/min
O2 consumption by beating heart at rest
9ml/100g/min
Compare arterial pressure and stroke work for the right and left side of the heart
7x higher pressure in the aorta than pulmonary artery = 7x stroke work
Does an increase in afterload or preload cause a greater increase in oxygen consumption
Afterload - pressure work requires more oxygen than volume work for unknown reasons. This is why angina is more common in aortic stenosis than regurg
Endothelial Vasoconstrictors
Endothelin-1
Local platelet serotonin
Thromboxane A2
Endothelial Vasodilators
Nitric Oxide
Kinins
Prostacyclin
Circulating neurohormonal vasoconstrictors
Epinephrine (except in skeletal muscle and liver) Norepinephrine Arginine vasopressin Angiotensin II Endogenous-digitalis-like substance Neuropeptide Y
Circulating neurohormonal vasodilators
Epinephrine in skeletal muscle and liver Calcitonin G related protein Substance P Histamine ANP Vasoactive Intestinal peptide
Stimulation of atrial stretch receptors
Hypotension, tachycardia
Raised ICP causes
Hypertension and bradycardia
Baroreceptors are found…
aortic arch, carotid sinus,right and left atria, superior and inferior vena caval entrances, pulmonary veins and circullation. They are located in the ADVENTITIA of the vessels.
The vasomotor area is located…
Rostral Ventrolateral Medulla (RVLM)
The carotid sinus is connected to the RVLM by the…..
carotis sinus n which is a branch of the glossophrangeal n.
The aortic arch baroreceptors are connecte to the RVLM by the….
aortic depressor n, a branch of the vagus n
BEFORE affecting the RVLM the fibres from the aortic depressor n and the carotid sinus n
terminate in the Nucleus of the tractus solitarius
excitatory projections from the NTS also extend to….
Nucleus ambiguus and dorsal motor nucleus - activate vagal outflow in response to baroreceptor activation
NTS action on the RVLM is _____
inhibitory - inhibits sympathetic outflow
Direct stimulation of the RVLM is by
CO2 and hypoxia
Excitatory inputs to the RVLM….
Cortex via hypothalamus mesencephalic periaqueductal gray Brain stem reticular formation pain pathways somatic afferents carotid and aortic chemoreceptors
Inhibitors inputs to the RVLM…..
Cortex via hypothalamus Caudal ventrolateral medulla Caudal medullary raphe nuclei Lung inflation afferents Carotid, aortic and cardiopulmonary baroreceptors.
why does raised ICP cause bradycardia and hypertension
Raised ICP threatens the blood supply to the RVLM - the neurons respond by increasing the BP to preserve their blood supply. The raise in BP causes decreased carotid baroceptor firing which acts to decrease the heart rate.
Hypercapnia does what to the peripheral circulation
Locally acts as a vasodilator. It actually stimulates the RVLM to vasoconstrict but its peripheral local action is stronger.
myogenic theory of autoregulation
stretch due to increased BP causes smooth muscle in the vessel wall to contract, reducing the radius to offset the effect of increased pressure…. in order to maintain flow
metabolic theory of autoregulation
vasodilatory substances accumulate in active tissues, Accumulation is increased in states on low flow… these metabolites then act locally to dilate vessels, increase flow, and instigate their own removal.
how do injured vessels cause constriction?
Local liberation of serotonin from platelets.
Thromboxine A2 vs Prostacyclin
Thromboxine A2
- produced by platelets
- causes platelet aggregation and vasoconstriction
Prostacyclin
- produced by endothelial cells
- causes vasodilation and prevents platelet aggregation
How does Aspirin alter the thromboxine A2 / Prostacyclin balance
Aspirin produces irreversible inhibition of cyclooxygenase - reduces production of BOTH… but endothelial cells produce new cyclooxygenase in a few hours, platelets can not. half-life of a platelet is about 4 days
NO causes ______ by activation of ______
Vascular SM dilation through activation of guanylyl cyclase and elevated cyclic GMP
NO release is stimulated by
ACh Bradykinin Histamine on H1 receptors VIP Substance P
It is produced in the endothelium and diffuses into vascular SM cells
Endothelin 1
Most potent vascoconstrictor
Produced by upregulation of gene transcription
Is released locally and into blood
Not stored in secretory granules
Stimulators of endothelin 1 transcription
Angiotensin II Catecholamines Growth Factors Hypoxia Insulin Oxidised LDL HDL Shear Stresss Thrombin
Inhibitors of endothelin 1 transcription
NO
ANP
PGE2
Prostacyclin
Cerebral circulation flow and o2 consumption
750ml/min and 3.3ml/100g/min
Volume and rate of turnover of the CSF
150ml, produced at 550ml/day so turned over about 3.7x/day
Route of flow of the CSF
Choroid plexus -> ventricles -> through foramens of magendie and Luschka -> subarachnoid space -> arachnoid villli -> veins/sinuses
Lumbar CSF pressure is
70-180mmHg
What substances are passive rapidly transported across BBB
CO2, H20, O2
What substances are transcellular regulated across BBB
H+, HCO3-
What substances are actively atransported across BBB
Glucose, AAs, Choline
The four regions of the brain OUTSIDE the BBB are:
1) Posterior Pituitary
2) Area Posterna
3) Organm vasculosum of lamina termialis (OVLT)
4) Subfornical organ (SFO)
Area Posterna does….
chemoreceptor trigger zone -> vomitting in respose to chemical changes in plasma
OVLT does….
Angiotensin II action to increase thirst.
Osoreceptor for vasopressin secretion.
Interleukin -1 acts here to produce fever.
SFO does…
Angiotensin II also acts here to cause thirst
Brain energy metabolism; % of O2 consumption is ____, RQ is_______. % reliant on glucose for enery is _____
20% of body O2 consumption
90% reliant on glucose for energy
brain RQ is 0.95 - 0.99
Coronary circulation flow is ____
250ml/min, 5% of C.O.
Branches of RCA
Marginal branch
Posterior descending branch
Branches of LCA
Anterior Descending
Circumflex
Marginal branch
3 types of anastomotic vessels in the coronary circulation
Arteriosinusoidal cessels
Thesbian vessels
arterioluminal vessels
Cutaneous circulation flow
1-150ml/100g/min
Describe tripple response
1) red reaction - capillary dilation
2) wheal - capillary permeability
3) Flare - spreading redness due to arteriolar dilation
How does blood flow relate to pressure and resistance
Flow = Pressure / Resistance
How does velocity relate to flow and area
Velocity = Flow / Area
Compare CSA of capillaries to aorta
capillaries have 1000x CSA than aorta
How is Flow and Resistance related to radius of a vessel
Flow is directly proportion to r^4
Resistance is inversely proportional to r^4
How is Flow and Resistance related to Length of vessel
Flow is inversely proportional to L
Resistance is directly proportional to L
Explain the Law of Laplace
Relates wall tension to radius of a vessel of sphere and pressure. E.g. dilated heart has to produce much more tension to cause the same increase in pressure. E.g. small vessels like capillaries have much lower wall tension than large diameter arteries
HbA is made up of…
2 alpha and 2 beta subunits
HbA2 is made up of
2 alpha and 2 delta subunits
HbF is made up of
2 alpha and 2y subunits
What is required for the platelet plug to for a definite clot
Fibrin.
Activation of Fibrin
Fibrinogen is activated to Fibrin by Thrombin
Extrinisc Pathway
7 -> 7a
activates X
X catalyses prothrombin to thrombin
Intrinsic Pathway
12 -> 11 -> 9
activates X
X catalyses prothrombin to thrombin
Antithrombin III and heparin complex to inhibit which factors
9,10,11,12
Protein C and Protein S inhibit which factors
5,8
Warfarin depletes which factors
2,7,9,10, Protein C and Protein S
Which part of the cascade prevents clot formation
tPA converts plasminogen to plasmin, this acts to inhibit fibrinogen and fibrin
What is the pressure drop from the aorta to the end arterioles
120/70, PP 50 -> 30-38mmHg, PP5
What is the pressure drop from the arterial to venous end of the capillary
32mmHg -> 15mmHg, PP 5 -> PP 0
MAP at heart level, at head level and at foot level
heart 100 mmHg
Head 62 mmHg
Foot 180 mmHg
How does the BP change with age?
Systolic increases. Diastolic tends not to increase much. As such the PP increases
What percent of blood volume is in the capillaries
ONLY 5%
Transit time and velocity in capillaries
transit time 1-2s
velocity is SLOW - 0.07cm/s
Describe Starling forces in the capillary
The diference between the hydrostatic pressure gradient and the oncotic pressure gradient. This is positive at the arterial end of the capillary favouring fluid movement out and negative at the venous end favour fluid movement in. The oncotic pressure does not change but the hydrostatic pressure decreases along the capillary as a result of the decreasing blood pressure towards the venous system.
Absolute refractory period of the heart in seconds…
0.20s
Relative refractory period in seconds
0.05s
duration of the cardiac action potential
0.25s
duration of cardiac cycle at hr75
0.8s
glucagon’s effect on contractility
positive ionotrope - increases the formation of cAMP
Fuel for the heart at basal conditions
60% fat, 35% carbohydrate, 5% by ketones and AAs
C.O. can increase by ____ % during exercise
700%
O2 extraction by the heart can increase by ___% during exercise
100%
