Summary CVM
disease, hypokalemia, hypoxia
Week 13 Arrythmias
 ECG recordings
o P wave-rounded;(Tall)0.5-2.5mm
(Time) less than 0.11
o QRS : less than 25 mm high,
0.06-0.12 seconds
o T wave- Rounded, less than 5
mm(L) less than 10mm(Chest)
0.10-0.25 seconds
o PR interval 0.12-0.21 seconds
o QT interval 0.35-0.45 seconds
o ST segment 0.08 seconds
 Tachycardia
o Sinus tachycardia
>100bpm. All waves clear visible
Exercise, stimulants, fvsf caffeine
Fever, hypovolemia, PE
Sinus rhythm
Shortened T-P interval
o Atrial Flutter
Rapid regular atrial
180-350bpm
Sawtooth p wave
Pre-existing heart disease
Re-entry
Not all waves are conducted to the
ventricles, slower vent rate
Treat-cardioversion,pharmacologic,
catheter
o Atrial Fibrillation
350-600bpm
Disorganised atrial depolarisatins-no
effective atrial contraction
P wave not discernible
Partial transmission to ventricles
L/R atrial enlargement due to
increase size, pressure (HF,
Hypert,CarteryD, Pulmonary)
Risk- hypotension,pulm congestion,
thrombus formation
Treat-ventricular rate control
Restire sinus rhythm
Anti coagulation
o Premature Ventricular Complexes
Additional beats of vent, severity
depends on f, often occur
sporadically.
Normal in adol,young adults; heart
No treatment/sup K
Widened QRS complex
Not related to preceding P wave
o Ventricular Tachycardias
A series 3/more PVC’s
Sustained VT more than 30s
Non sustained self terminating
Re-entry
SA node independent QRS.
QRS overwhelm P wave
T wave not discernible
Bigeminy- every 2nd beat is VPBeats
o Ventricular fibrillation
Life threatening
Disordered rapid stim ventricles, no
coordinated contraction
Initiated episode VT/ PVC
Elec defribillatio,. Antiarry drugs
Chaotic irregular appearance
No QRS
Non productive contractions
NO CO
o Torsades de pointes
VT with QRS changing amplitude
appear to twist around
200-250bpm
Therapeutic drugs(K channel
blocker(, Long QT syndrome,
inherited ion channel
mutation),electrolyte disturbances
o SVT
Atria tachycardia
>130 bpm
No P wave
Diagnosis Adenosine to distinguish
 Bradyarrythymias
o Sinus Bradycardia
HR <60bpm
 At rest/ sleep, highly trained,
medications that depresses SA
node activity
Ischemic heart/cardiomyopathy
depresses intrinsic automaticity
Sinus rhythm
Prolonged T-P interval
o Escape Rhythm
Emerge from more distal latent
pacemakers
True escape=SA node failure
Pace set by next available nodal
tissues
AV-His-branches-Purkinje
 Conduction blocks
Impaired conduction atria-vent
3 degrees AV conduction block
Ischemic damage to nodal tissue
Often involves escape rhythm
o First Degree
Prolonged delay atria-vent
depolarisation
High PR interval
More 0.21seconds
1:1 relations P:QRS
o Second Degree Mobitz Type 1
Intermittent failure AV conduction
Some p not followed by qrs
Degrees AV delay gradually
increases with each beat until an
impulse completely blocked
o Second degree type 2
Loss AV conduction
No gradual PR lengthen
Block persist 2 or more beats
o Third Degree
Complete heart block
Complete failure conduction atria-
vent
No rship P:QRS
Pacemaker!
o R/L bundle branch Block
Either one bloecked-
Ant conduct impuls
Vent depolaris consecutively not
simultaneously
Wide QRS
QRS confg depends which branch
is blocked
 Mechanisms of tachyarrythmias
o Re-entry
Constitutes an ectopic focus
Create a single additional/ full
rhythm
-normal conduction conductile to
contractile cells
-signals spread, movement ions
gap junctions, coordinated
-transient block one side. Cells
another side unaware
-conduction rapid non blocked
and normally signals stop at the
bottom (meeting signals,)
-but none
-transient block one-start receive
signals while other cells ready to
contract
Transimission of signals amongst
previously blocked very slow.
Don’t contract with other cells
Other cels contract
After signal pass through the
blocked cells, others finished AP.
Now ready to receive ne signal
Each signal ion drive, other cellas
cant distinguig signal is myocyte
derive
Myocytes rapid pass new
message (as if came from SA
node)
Extra beat of hearts.previously
blocked have small contractions
but not noticed by heart
o Early after-deplarisation
During repolarisation phase
Late 2/3 phase
When AP duration is increased
Ionic current depends on
membrane voltage at which the
triggered event occurs
 o Larger size with up LV & Atrial
P(to increase filling)
o Structural changes in LV (fibrous),
residual filament Ca activation for
preceding systole->prolonged
isovolumic relaxation
 After heavy exercise
o Dilation
o Preload Up(30%), Up EDV and
filling pressure
o Delayed after-depolarisation o Afterload Up (30%) esp ESV up
Shortly after repolarisation is o contractility down(60%)
complete o SV no change (as young)
High Ca intracellular conc o Ejection Fraction Down 15%
Digoxin digitalis toxicity o HR 25% down
Lead series rapid deplarisation o CO lower 25 %
o Digoxin o Total VO2max down 50%, (lower
Block Na/K pump. Na accumulate skeletal mass, strength)
in. Block Na/Ca exchanger as o Plasma Catecholamines Up
well. Increased Na stops o B-adr sensitivity decrease
exchanger form working. Ca cant
(cardiac and vascular)
leave the cell, RMP increases
Cost of Dilation: P in ventricles & atria is
toward threshold.
higher than young. High P in L heart difficult
blood to flow form lung. Blood back up- signal
sent to brain shortness of breath in elderly (as if
HF) but is not HF per se but the effect of age
Overtime, adaptations finally- further loss of
pump capacity(failure) and lung function
oedema.
 Young during Increase Afterload
o Up load on fibers from
o Up vent radius at end of diastole
and throu ejection period
o Up peripheral VR
o Increase BP
o BP= COxPVR
Week 12 Age exercise and CV disease  Young at exercise
o Heart stays same size,
 Heart at rest
o Pump harder and faster
o CO no change
 Old increase BP
o HR down 10% SV Up 10%
o Stiffening of arteries
o Preload EDV Up– up in late filling
o With exercise, BP higher in given
o Afterload down stiffer walls
workload
o Contractility no change  Aerobic Exercise and CV aging
o Ejection Fraction No change o O2 consumption Max
o L ventricular mass Up heart size o Ejection Fraction Up
wit age o Contractility Up
 During limited exercise o Preload down (less EDV less
o SV doesn’t change much
LAP, greater P gradient lung to
o CO increase a few fold 5-10L/min heart. Heart doesn’t need to dilate
o VO2max half than 20 yo much
o Because 25% lower COmax and o Arterial stiffness Down
o Same SV as young by  Pharmacotherapy
 o Drugs reduce arterial stiffness, o Bulbus cordis, primitive ventricle,
cardiac fibrosis, vent hypertrophy, primitive atrium, sinus venosus
increase efficiency o AV canal betweem Primitives
o Antoxidants o Fold and twist
 Disease related to Ageing o Septation weeks 4-6
o Atheroscelorosis  Foetal circulation
o Hyertens o PlacentaUmbilical vein ductus
o HF. DIAbetes venosus Inferior Vena cava
o Inflammarion o Umbilical veinportal
Sedentary lifestyle-contribute largely age veinRAforamen
related changes in heart, vascular system ovaleLALVAorta
 Issues higher CVD o RA RV PAductus arteriosus
o Diet aorta
o Lifestyle  Transition after birth
o Gender o Lung replace placenta
o Social status o Shunts close
o Demographics DV-
DA-rising O2 tension and reduction
Myocyte loss, enlarge, loss arterial compliance, in PGE1
calcification ofo conduction vessels and valves. Foramen Ovale-
Mitral valves closes more slowly, lV fills more, o Pulmonary vascular resistance falls
cavities LA and LV increase Mechanical lung inflation.
Desenteisied B receptor- reduced response/ Vasodilation of pulm vasculature
greater no occupied due to higher level  Cyanosis
catacholamines o Bluish discolouration skin and
Less stimulation less able to increase Ca mucous membrane
sarcolemmal channels, decrease intracellular o Excess dHb in blood 5mg/100ml
Ca decrease contractility  Septal Defects (LR)
Hole in septum either A/V cause mixing of
1. Lower HR
blood. Initially L-R due to high P later
Older people have lower heart rates because diastolic filling
takes longer in aged untreated R-L due to increase BV in
People pulmonary circuit
Treat direct suture closure with pericardial/
2. Oxygen consumption IS NOT the same and synthetic patch
contraction/relaxation properties of o Atrial Septal (intraatrial septum)
the heart CHANGE with age
Perisistent openings
3. Aged person’s “exercised-induced” increase in HR Defect size determine flow
and strength ofcontraction NOT achieved o Ventricular septal (commoner)
4. More female 2x
Other factors that may relate to reduced heart rate
Pronounced decrease in number of pacemaker cells in SA node 50% smaller shunts close
by age 60 spontaneously by 2 yo
Modulation of sympathetic and parasympathetic tone Pulm hypertension
Both sympathetic and parasympathetic blockade are  PVR increase, shunt reverses
diminished with age marked cyanosis
 Patent Ductus Arteriosus
Week 11 Congenital Heart Defects
o PAdescending aorta
o Fails to close afer birth, admixing O2
 Heart Development
o Week 3: Formation CV system blood
 Valvular Stenosis (90%)
o Placenta primary organs of gas,
o Aortic Stenosis
nutr,waste exchange
Narrowing, obs aortic valve
o Superior-truncus arteriosus->aortic
Bicuspid leaflet-3 leaflet config
arches
Male 4 times
Affects Cardiac Cyle
 o Pulmonic stenosis
At Pulmonic valve of RV OR in PA
10% of valve stenosis
Severity determined by systolic
transvalvular pressure
 Coarctation of the Aorta
o Narrowing aortic lumen
o Impede full CO to lower body
o Preductal- fully O2 low V
o Postductal- mix blood due to
presence of PDA
o LV increased P load  LV
hypertrophy, dilatation of collateral
blooad vessels form intercostal
arteris bypass coarctation
o Less oxygenated blood to the lower
body means that the potential for
growth/development is limited
compared to the upper body.
 Tetralogy of Fallot
o VSD
o Subvalvular pulmonic stenosis
o Overriding aorta(receive blood
form both ventricle)
o Right Ventricular hypertrophy
o MOST COMMON CAUSE OF
CYANOSIS AFTER INFANCY
Dyspnea on exertion, when crying
Irritability, cyanosis, hyperventilate, syncope,
convulsion. Clubbing fingers toes, Alleviate,
squat increase systemic vasc resistance
 Transposition of great arteries
o MOSt common Cyanosis in neonatal
o Aorta originates form RV.
o PA from LV
o Parallel systemic and pulmonary
circuits not series(blood movement)
o Extremely hypoxic, cyanotic neonate
o Lethal without treatment
o DA/FA remain patent. Comm between
circuits maintained allow sufficient
amount of O blood to reach brain, vital
organs
 Operations
o Atrial switch(Mustard Senning
Procedure)
Systemic venous blood diverted
through mitral valve
Pulmonary venous return rerouted
through tricuspid valveas the patient
ages, primarily because of the strain placed
on the right ventricle trying to generate
sufficient force to push blood into the
systemic circulation.
o Arterial switch (Jatene)
Arterial trunks transected,
reanastomosed to contralateral root
Coronary arteries relocated to new
aorta
Marfan Syndrome
CT disorder, CVD alteration
Down Sydnrome
AV canal defect. Incomplete formation
AV valves, blood travel without interruption.
VSD also common
Additional Symptoms with congenital
Digeorge syndrome’turner syndrome, Williams,
Holt-oram etc
Week 9 Heart Failure
Heart has low CO from previous myocardial
infarction,coronary artery disease, problems
with the heart valves, or a problem with the
heart muscle that may be due to previous
viral infection of the heart.
Many people are not aware that their heart is
not pumping normally until they notice
shortness of breath or tiredness
when exercising.
Congestive Heart failure
Heart failure that causes swelling of the ankles
and lung congestion
Low CO fires up the neurohormonal systems.
Kidneys release renin and angiotensin II.
Angiotensin II is a very strong vasoconstrictor. It
causes the body to retain salt and water,
which causes the body to produce aldosterone.
The extra aldosterone makes the body retain
salt and water even more, which leads to
edema.
Retaining salt and water increases preload and
pressure in the heart, allowing it to beat more
strongly. Epinephrine (adrenaline) speed up
the heart AND increase contractility.
At first these reactions by the body are a GOOD
thing in trying to increase CO via Frank Starling
Neurohormonal Activation = VISCIOUS CYCLE
Increased preload and pressures put extra strain on
the heart. Body has high water and salt load instead
of removing load.
Heart responds by remodeling- larger and rounder
and makes it weaker
Treatment
(1) diuretic drugs, excretion of salt and water in
the urine (decrease afterload, preload and oedema)
(2) ACE inhibitors = block formation of angiotensin
(block Angio I to Angio II, increase vasodilation and
increase salt and water
excretion and decrease afterload, preload and
oedema)
(3) ß-blocker drugs. block the effects of raised levels
of Noradrenaline (Copernicus trial). Not patients
with low HR
The heart normally receives blood flow at low filling
pressures during diastole and pumps it against higher
pressures in systole. Failure begins to develop when
the heart muscle is
damaged and/or asked to perform greater work
(operating against hiBP, at EDV or EDP or
preloads)
•Heart failure may be defined as inability of the
heart to pump blood at sufficient rate to meet
metabolic needs
•Heart failure may be the principal manifestation of
many forms of cardiac disease including
atherosclerosis, myocardial infarction, valvular
diseases, arrhythmias, and cardiomyopathies
(chronic diseases affecting heart muscle)
Many patients with chronic heart failure are
asymptomatic for long periods because imbalance is
mild or because dysfunction
being compensated for by Frank Starling
mechanism, hypertrophy and/or neurohumoral
mechanisms.
Symptoms may include shortness of breath, fatigue,
fluid retention, pulmonary congestion, feeling
unwell
Chronic heart failure is increasing in part because of
the aging population,and because interventions are
significantly prolonging survival after acute cardiac
insults.
Muscle mass increases by synthesis
of sarcomeres in parallel with the old:
termed concentric hypertrophy
Muscle mass increases by
synthesis of sarcomeres in
series with the old: termed
eccentric hypertrophy
Directional heart failure:
Backwards heart failure:
o Inadequate emptying of the venous
reservoirs.
o The ventricle is not pumping out all the
blood that comes into it.
o increases the ventricular filling pressure
and systemic or pulmonary edema.
o In fact, the heart can only meet the
needs of the body if the ventricular filling
pressure is high.
Forward heart failure:
 The heart is not pumping out enough
blood to meet the needs of the body.
 Reduced ejection of blood under
pressure into the aorta and pulmonary
artery.
 Because less blood reaches the kidneys,
they conserve salt and water, which
contributes to excess fluid retention and
edema.
 also decreases the blood flow to
various organs, causing weakness and fatigue.
Forward failure and backward failure often
coexist due to the circular direction of
blood flow.
Left-sided heart failure:
 LV can't pump out enough blood,
 gets backed-up in the lungs (behind the
left ventricle), causing pulmonary
edema, a build-up of fluid in the lungs.
 This brings about shortness of breath.
Left-sided heart failure often leads to
right-sided heart failure
.
Right-sided heart failure:
 RV cannot pump out enough blood,
causing fluid to back up in the veins and
then in capillaries of the body (behind
the right ventricle)
 Fluid leaks out of the capillaries and
builds up in the tissues, a condition
called systemic edema.
 Edema is especially noticeable in the
legs because the lower half of the body
drains into the right side of the heart
Low arterial pressure and tachycardia
  are manifestations of low CO
 Low CoLow arterial pressure (mean
arterial pressure = CO x TPR)
 Tachycardia is a baroreceptor reflex
mediated attempt to increase CO.
 Tachycardia may also result from atrial
stretch causing a Bainbridge reflex.
What are the compensatory processes?
• Increased secretion of catecholamines from
sympathetic nerve endings in the heart, the
periphery, and adrenal glands
• Recruitment of the Frank-Starling mechanism
• Myocardial hypertrophy
 The Frank-Starling relationship describes
the relationshipthe greater the end-
diastolic volume (i.e., the volume present
in the ventricle just before it contracts),
the greater the stroke volume and
cardiac output.
 Just as we have a length-tension
relationship in skeletal muscle based on overlap
of thick and thin filaments, there is a
similar relationship in ventricular muscle. The
degree of overlap of thick and thin
filaments determines the number of cross-
bridges that can cycle (which requires
Ca2+) and the magnitude of tension developed.
Note that in skeletal muscle, the length-tension
curve has an ascending limb (as muscle length
increases, overlap increases and tension
increases), a plateau where there is maximal
overlap and maximal tension, and a descending
limb (as length increases, there is less overlap
and less tension).
In ventricular muscle, there is an ascending
limb of the curve in the Frank-Starling
relationship: as muscle length increases, there
is greater overlap and greater tension
produced.
Define cardiomyopathy. List the diseases that
must be excluded before the
diagnosis of cardiomyopathy can be considered
(Robbins 6th Ed., p. 578-
579).
 Literally means heart disease;
conventionally used to describe heart
disease resulting from a primary
abnormality in the myocardium.
 dilated cardiomyopathy,
 hypertrophic cardiomyocpathy,
 restrictive cardiomyopathy.
NOT Ischemic heart disease, valvular heart
disease, hypertensive heart disease, congenital
heart disease, hypertensive heart disease,
aortic stenosis, pericardial contstriction
WEEK 8 Myocardial ischemia
1. Myocardial Ischemia
a. Severe reduction of coronoray
blood flow to myocardium
b. Inadequate O demands of tissues
c. Due to atherosclerotic disease of
coronary arteries
2. Myocardial Infarction
a. Region myocardial necrosis
b. Prolonged cessation blood sup
c. History angina pectoris
3. Angina Pectoris
a. Caused by myocardial ischemia
b. Ischemic myocardium accumulate
lactic acid/abnormal stretching
c. Irritates myocardial nerves
d. Afferent SNS C3-T4 variety
locations, radiation of pain
e. Often confused with digestion
f. Women don’t exhibit claasic
symptoms of pain associated with
men
4. Stable angina
a. Caused- gradual narrowing/
hardening CA
b. During Myocardial O2 demand
increases(exercise,emotion)
c. Pain relieve by rest, vasodilators
d. No permanent cell damage.
e. Lack pain relief with
interventonsdevelop infract
5. Prinzmetal angina
a. Transient myocardial ischemia
b. Often at rest
c. Vasopasm of major CA with(out)
atheroscelorosis
d. Hyperactive SNS, increase Ca
influx in arterial SM/abnormal PG
production/relief
6. Silent ischemia
a. No angina,asymptomatic
b. Interspersed with periods of
angina
c. Abnormal afferent innervation of
left ventricle/release of fewer
inflammatory mediators
7. Unstable angina
a. Signals infarct may soon follow
b. At rest and exercise
 c. Atheroscelotic plaqure ulcerates
causing
d. transient thrombotic occlusion,
vasoconstriction CA
e. if no more than 20 mins- no significant
Minfarct doesn’t occur
8. Risk Coronary artery disease
a. Age Men>45 women >55(or premature
menopause, no E2 replacement)
b. Family History MI/sudden death prior to
55 father/1st degree relatives. 65 for
mother
c. Smoking curren/quit past 6 mths
d. Hyperte 140/90 current medicated
e. HCholester
f. Diabetes fasting glucose >110mg/dL
confirmed 2 separate occasions
g. P,Inactivity
h. Obesity
9. Causes for Impaired O supply to heart
a. O2 supply coronary BF, O
saturation blood, Hb conc
b. Demand wall tension(after,pre)
HR, hi inotropic state hi velocity
10. Parameters heart workload
a. HR
b. Wall stress transmural P(EDV)
c. Inotropic
11. Troponin
a. Diagnosis ischemic chest pain
b. High sensitivity specificity fo m
cell damage
c. Elevated 3-12 hrs
d. Peak 12-24hrs
e. Remain elevated several days
f. Majority elevated within 6 hours
after onset
12. CKMB Troponin I
a. Second attack CKMB
b. Elevated CKMB maybe due to
skeletal imuscle inury
c. Elevate Trop I essential to confirm
myocardial damage
d. Trop repeat at least 6 hours adter
onset pain(8-12)
e. Normal Trop I = no MInfarct
f. Trop always specific for
myocardium. Never exposed to
sekelatl muscle at any time
13. Reperfusion Injury
a. Damage to tissues caused when
blood supply returns after period
of ischemia.
b. Restoration of circulation resulst
in inflammation, oxidative
edamage throu oxidative stress
rather restiration nrmal fx
Week 7 Atherosclerosis
Primary initiating event is linked to LDL
accumulation in sub-endothelial matrix
• Accumulation is greater when blood LDL rises
• Plaque rupture occurs in >90% MI cases and
common in patients with unstable angina
Inflammation!
Diagnosis
Invasive – catheter via femoral, fed into coronary
artery for X ray-angigraphy
Non invasive - CT angiogram
Unstable plaque
Every cell is activated- similar to chronic
inflammatory conditions Rheumatoid arthritis
Week 5
as lateral as the midaxillary line (will depend on
the patient, their size and their thoracic
anatomy) *Talley and O’Connor states the 4th
intercostal space.
Tricuspid: 5th intercostal space at one of right
sternal margin, lower left sternal border, or even
over the sternum
Aortic: 2nd intercostal space at right border of
sternum
Pulmonic: 2nd intercostal space at left border of
sternum
Week 4 Intro to circulation
1. Elastic arteries
a. Amount of elastin in vessel walls
b. Major distribution vesels
c. Numerous. Concentric sheets of
elastin (protective in case of
glancing punctures)
d. Stretch of tehse vessels sotred E
e. Thin vessel wall
f. Kinitec move blood along
g. SM spiral, longitudinal, transverse
h. Constriction limited effect on
lumen size
i. Aneursyms, overstretchpouch
formationrupture
 j. Lose elasticity, easily compressed
without springing back
k. Nicotine release elastase loss
elasticity chew up elastin
2. Muscular arteries
a. Single sheet of elastin
b. Likely to have tear
c. Aneurysm (blood build up
between layers of wall, clots,
presses vessel closed.disecting
aneurysms)
d. SM concentric rings (greater
control vessel diameter)regulation
e. Microtears for athero plaques
prove anchor site, loss BF
f. Physical blockage rather than
collapse
g. Thicknes might be protective but
minimally
3. Movement of blood
a. Recoil of blood stretching in
vessels wall that mobilises
b. Use sheets of elastin
c. Movement in muscular v.
mediated primarily due to P
differential n F behind blood
generatedin elastic vessels
d. Musc prevent rapid movement of
blood (vconstriction)
e. To control v diameter, influence
BP
4. Nervous system input SM in arteries
a. Alpha adrenergic. SNS release
NA vconstriction
b. Resting small degree activateion
vascular tone prevent fully dialting
c. Vasomotor center(medulla/pons)
generalised vconstrict, modified
for blood rerouting
d. B adr in coronary arteries vdilation
(cardiac tissue is not
compromised in increased work)
e. B adr vascular beds skeletal
muscle fight fight
f. SNS-skeletal Ach
g. S surge dilate vascular in skeletal
improve perfusion of tissue
maintain performance
h. Ach recperor in skeletal is
muscarinic-require changes in
level of intracellular signalling
mocleculs to cause cellular
changes
5. Transition to arterioles
a. BP regulation
b. Primary Resistance vessels
c. Sheer no of capillaries,
Resistance less than arterioles
d. Limited elastin(little capacity to
stretch, augmenting R
e. Hebaily innervated with SNS
neurons (increase capacity to
restrict)
f. Activation, markedly narrow,
increase friction of blood against
wall, and the P against blood
6. Arterioles
7. Capillaries
a. Intercellular cleft between endo
cells facilitate movement small
molecules, water, skeletal, SM,
CT and lungs receive
b. Kidney, cili sSI, relyon
fenestrations. Some larger
molecules than intercellular clefts
can ccomodate
c. Sinusoidal capillaries- larger inter
clef, fenesrtatios of endo cells,
create larger gap, larger
molecules, even blood
cells(monocytes-macrophages) to
transevrse memebrane of
capillaires in bone marrow, liver,
spleean, apituri, parathyroid
glands
d. Capillary P= B hydors P
e. P behind blod generate dby blood
f. No real impact o movement of
fluid, as it sgen cloase to 0. And
lymphatic systems ensure, little
fluid is allowed to persist in
ISpace.
g. alter the hydrostatic pressure in the
venous end of the capillary bed, to
prevent re-absorption of water.
8. Venules
a. Lower than capillary bed
b. Near 0 in RA
c. Valvualr incompetency, blood not
working way back to heart,
pooling in veniles, impede BF
d. Atrophy skeetalmsucles prapaleg,
quadrp blood not move as it
should if P in RA eleveated. Ig RA
P high enough collapse incoming
veins
9. Veins
a. Lower P than arteris
b. Sturdy walls low pressure
 c. Easily compromised when P o Venous edn 17mmHg NHP, NCP
changes in disease state 25
d. Venous return relies on skeletal
muscle to assits in mobilising 12. Ca channel blocker
blood, valves to trap blod that has a. Nodal cells
susccessfuly moved along b. Change depolarisation
e. Cpaeble of marked relaxation, c. HR
f. Capcity hold substantial volume of d. Decreased HR
blood e. Myocyts less Ca,
g. 4L can be founf Shorter AP durationincoming calcium and the
h. Angina, HF, hyepertension, ability outgoing potassium that is the hallmark of the
to relax venous ystsem decreass plateau
preload P in righ side, reduce phase of the myocyte action potential is going
work load heart to be tipped slightly in favour of the outgoing
i. A slight reduction allow to potassium
optimise heart(compromisd heart) and therefore the slope will be a slightly steeper
j. Up SV up CO(reduce ESV) decline (see below), allowing the balance of the
k. Overtsretch venules/veis destroy potassium channels to be activated sooner and
ability to regulate vessel dameter. the calcium channels closed sooner (as they
Cant adequate mobilze blood are voltage
when need. gated and won’t stay open in the lower
l. Overtstretch/overtax vein/v job membrane potential
long period standing, protracted ST segment shorter.
period time busdriver Need enormous Ca to cause this
m. Lose structural integriy of veins,
aloow blood bacwrad pooiling
n. Up RA P collapse veins, block
filling RA impede CO. loss of
skeletal muscle impede venous
retrun limit CO
10. Neurovascular bundle
11. Oedema
a. Atypical accumulation of fluid in
the interstitial space= tissue
swelling
b. Caused by any event that
increases the flow of fluid out of
the blood vessel or hinders its
return
c. ↑ CHP can result from: •
Incompetent valves, Localised
blood vessel blockage,
Congestive heart failure, High
blood volume
d. Fluid Loss accelerated by:
i. Increase BP (CHP)
ii. Increase Cpermbiality
(ongoing inflammateory
response)
 Starling Force Capillary bed P
K+ channel blocker
o NFP= NHP-NCP
Delay repolarisation both nodal, myocyte AP
o IHP usualy 0mmHg
Delay repolarisation will change the rate at
o Arteriole end 35mmHg NHP, NCP which the heart beats,
25 Decrease HR,
T wave longer(repolarisation of myocytes)
Prolonged AP
Amplitude T same

radial pulse is actually a

representation of the reverberation wave through the
blood vessel walls that corresponds with the impact
of the ejected blood slamming into the aortic wall. So,
the HR as calculated from the ECG trace is based
on the electrical wave going through the heart but
says nothing about whether any blood was ejected in
association with that electrical wave