Cvs 2 Flashcards
(179 cards)
1
Q
How do you calculate cardiac output?
A
HR x SV
2
Q
What allows a valve to remain open?
A
When the flow of blood is going in the direction that the valve allows. The direction of blood flow is determined by the pressure gradient.
3
Q
Describe the change in pressure in the ventricle
A
Ventricular pressure steadily increases in diastole due to the flow of blood from the atria this decreases as the ventriclar pressure equals the atrial pressure. In systole the pressure in the atria increases upon contraction forcing a slight of more blood into the ventricle. The ventricle then contracts iso-volumetrically but as soon as the pressure in the ventricle exceeds that in the aorta then volume of the ventricle goes down.
4
Q
What can cause sound abnormalities in the heart?
A
Murmurs arise due to stenosis or valve incompetence. Stenosis is where a valve cannot allow the normal amount of blood through due to narrowing incompetence is where blood travels back through the valve, this is known as regurgitation. Additionally extra heart sounds can be generated by other atypical blood flows.
5
Q
Describe how the action potential spreads across the heart
A
It starts at the SAN and spreads out across the atria finishing at the AVN. This causes atrial contraction. Then the impulse is held in the AVN for 120ms after which it travels down the bundles of his in the IV septum. It then travels out across the endocardium trough the myocardium and then finally up towards the AV valves. The heart relaxes in the reverse of contraction (from the outside in).
6
Q
Describe the venous drainage of the heart
A
On right small cardiac draining into the posterior coronary sinus. On the left is the great cardiac vein which merges with the marginal and becomes the coronary sinus which communicates with the posterior vein.
7
Q
Describe the formation of the primitive heart tube
A
Cephalocaudal folding brings the cardiac centre central in the embryo and lateral folding causes the 2 cardial tubes to fuse together forming the primative heart tube.
8
Q
What are the parts of the primitive heart tube?
A
Sinus venosus, atria, ventricle, bulbus cordis, truncus arteriosis, Aortic roots.
9
Q
Describe the developement of the sinus venosus and the atria.
A
To start with the L and R sinus venosus are of equal size however the L receeds and R enlarges resulting in the coronary sinus and the Vena cava forming respectively. The RA forms from the best part of the atria, the LA has a small contribution from the atria however the majority of its tissue is due to the pulmonary arteries which is envelops as it grows.
10
Q
How does the transverse coronary sinus develop?
A
Due to the folding of the primitive tube. This occurs due to the pericardium being of finite space and so as the tube grows it bends in the middle allowing it to fill the space better. The upper half folds ventral, caudal and to the right. and the sinus venosus moves dorsal, cranial and to the left.
11
Q
What is the significance of the ligamentum arteriosa?
A
Remnant of the ductus arteriosus.
Allows blood to flow from the pulmonary artery to the aorta in the embryo circulation. Most blood passes into the left atria via the foramen ovale however a small amount passes into the RV and so this must be removed hence the presence of the ductus arteriosus.
12
Q
Describe how path of the recurrent larygeal nerve and explain the reason for the asymmetry in its paths.
A
Left loops around the sup clavian and the right around the ductus arteriosis (from anterior to posterior). This is due to the manner that the great vessels develop. in the embryo there is a remodelling of the major vessels so that the series of arches is disrupted. on the right 3 becomes the corotid 4 becomes the sub clavian on the left 3 is also the corotid however 7 forms the sub clav. the ductus arteriosus forms the 6th arch on the left however on the right this diconnects so it doesnt impede the recurrent laryngeal nerve.
13
Q
What dictates the degree of contraction that the smooth muscle undergo in the aterioles?
A
sympathetic stimulation to a degree however the biggest affect on vasoconstriction/vasodilation is the presence of cellular products of metabolism (H+, K+ adenosine, CO2).
14
Q
What dictates venous pressure?
A
proportional to volume. and volume is proportional to (volume in/volume out). Volume in is controlled by degree of muscle pumping, the affects of gravity and the volume of return from the capillaires. The degree of volume out is based on cardiac output.
15
Q
Why is there always a degree of vasomotor tone in resistance vessels?
A
allows the vessel to change the degree of resistance that the blood experiences based on varying demand. If there is no vasomotor tone then there cant be a decrease in PR.
16
Q
What is reactive hyperaemia?
A
Occulusion of blood to tissue for a period of time. Then when the blood returns it increases the degree of flow. This is due to the build up of metabolites that have built up in the vessles resulting in vasodilation.
17
Q
How can average BP be measured?
A
diastolic + Pulse pressure/3
18
Q
What is pulse pressure?
A
The difference between the systolic and diastolic blood pressures
19
Q
Why is it essential that arteries are stretchy?
A
This allows blood to flow during diastole. It also decreases resistance for increased blood flow. This is due to there being an increase in radius of vessel. They have elastic recoil that moves the blood during the diastolic period.
20
Q
What is mitral stenosis? and what does it result in? what are the common causes of?
A
Mitral stenosis is where the mitral valve is unable to open as fully as in normal. This results in it being harder for blood to flow from the LA to the LV. Consequences of mitral valve stenosis include atrial stretching and resultant arythmias, less blood flowing through the valve leading to pulmonary oedema and also pulmonary hypertension. The resultant hypertension means that a greater amount of pressure is required to overcome the increased resistance and so leads to RV hypertrophy.
21
Q
How does the regulation of flow through the pulmonary circulation differ to the systemic?
A
Supply driven instead of demand led.
22
Q
What are the 2 blood supplies to the lung?
A
Pulmonary for gaseous exchange and bronchial circulation for supplying the lung tissue with oxygen and metabolites.
23
Q
Why is the resistance of the pulmonary circulation low?
A
Due to the cappilaires being arranged in parallel, large lumens and spare smooth muscle of arterioles.
24
Q
What is the typical time for blood to flow through the pulmonary circulation? what is the minimum for 100% saturation of HB? Why is there this apparent redundancy?
A
1 second, 0.3 seconds, allows an increase in flow thorough the lungs without reducing the oxygen saturation preventing cyanosis.
25
what are the pressures in the heart chambers?
RA: 0-8mmHG
RV: 15-30/4-12mmHG
LA: 1-10mmHg
LV: 100-140/1-10mmHg
26
How is gaseous exchange optomised in the lungs?
Decreasing diffusion distances, increasing surface area and increasing cappillary density.
27
What is the VQ ratio?
A ratio between air supplied and blood supplied to the alveoli. This tends to be maintained at 0.8 although it tends to be higher at the apex and lowest at the base.
28
How can the VQ change in disease?
Higher means more air then blood ratio. This can occur in pulmonary embolism for example. it will decrease when there is less air able to get to the tissue. This could be because of increased lung fluid such as in pulomonary oedema or in infections.
29
Describe septation of the heart. (atria, ventricle and outflow tract)
First Dorsal ventral divide forms in the AV canal.
Endochondral cushions from neural crest cells form causing the divide.
Then atrial septation. First septum primum which gives rise to the ostium primum which gets progressively smaller and vanishes. As it goes the ostium secundum forms in the septum primum. Septum secundum begins to grow in a horse shoe shape downwards. This forms the foramen ovale.
This is a R-->L shunt in the embryo.
Then the Ventricle undergoes septation. Upgrowth of muscle and a membranous section forms the septum.
Spetation of the outflow tract spirals as the endochondral cushions are staggered.
30
What is the role of the ductus venousus?
Allows placenta blood supply to bypass liver.
31
Describe the coronary arteries
--A.I.V
--D
L --C
--M
--S.A.N
R --Marginal
--A.V.N
-- P.I.V
32
Describe the venous return from the heart
Great cardiac vein travels up the AIV groove and then follows the path of the circumflex artery. Middle cardiac vein joins and it becomes the coronay sinus. From the R side the small cardiac vein joins the coronary sinus.
33
What factors influence the flow of fluid through tubes?
```
Flow= velocity x area.
Flow=pressure/resistance.
Area=Pi x r^2
Friction
Pouisellus law
Reynold number of fluid i.e laminar vs chaotic
viscosity of fluid.
```
34
Define flow
The volume of fluid that passes through a particular area in a given period of time (litres x area/ time)= flow
35
Define velocity
Change in displacement per unit time. (ms^-1)
36
What is laminar flow? How does it compare to chaotic fluid flow?
When a fluid flow is unidirectional and in "tidy" concentric layers without any loss of uniformity in all layers of the fluid.
Chaotic is where the fluid is tumbling in a non-uniform manner that gives rise to the breakdown of the concentric layers of fluid. Chaos is a predictable behavior that has a specific starting value that any deviation in this value will lead to a deviation in the end result i.e the two slightly different initial values will give rise to progressively divergent functions.
37
Describe the consequences of pousielles law
```
flow is equal to the radius to the power 4 multiplied by Pi, and the pressure divided by 8 times the dynamic viscosity of the fluid and length.
Flow can be increased by decreasing...
-length of tube
-decrease viscosity
and increasing...
-radius
-pressure
```
38
Define resistance
A measurement of how hard it is to push a flow through a section of a circuit.
How many joules are required to overcome the resistance per unit time ( JS^-1)
39
What affect flow resistance in blood vessels?
Smooth muscle and pericytes contracting. This is regulated by the SNS and also the presence of metabolites in the blood. like ATP, NO, adenosine, H+ and K+.
40
How do resistors get summated?
in parallel using a 1/Rsum=1/Ra + 1/Rb
| in series through simple addition.
41
How does pressure change across the circulation?
Pressure will drop across the system due to the expenditure of energy to overcome resistance.
42
How does flow change across the circulation?
Flow depends on CO. But it should be constant if CO is so. This is due to a decrease in blood velocity when the number of vessels increases just like the arterioles and capillaries.
43
How does vessel stretchy-ness feature in flow and pressure?
Resistance will decrease as radius increases.
so a stretching of arteries in systole allows an increase in blood flow.
The stretching allows blood to flow in diastole as the pressure remains high due to the deforming of the elastic on the large elastic arteries.
44
How do vessels show capacitance?
When they can act as momentary blood stores.
Arteries store blood during the influx during systole
Veins store blood allowing for a variable CO.
45
What is the significance of the concentric layers of fluid in laminar flow?
There is a change in volume from Vmax in the center to zero at the edge. The higher flow rate in the center results in the cells in the blood travelling there so RBCs travel faster then the plasma at the peripheral.
46
What are the observable markers of chaotic blood flow?
Noise
Decrease in velocity
Higher resistance
Thrombosis.
47
What is the effect of a drop in blood pressure on resistance vessels?
The will close completely as a degree of basal pressure is required to oppose the resistance.
48
Describe reactive hypernemia
Occlusion of tissue of blood that leads to an increase in metabolites used and more waste products excreted into the blood vessels.
When the blood is allowed to return there is a transient increase in flow. This is due to the decrease in resistance due to the products of metabolism resulting in vasodilation of the smooth muscle in the vessels.
49
How does the heart exhibit demand led supply?
An increase in HR--> higher flow, all products of metabolism washed away.
This leads to an increase in TPR
Leads to a drop in venous return
Leads to a drop in Vp
stroke volume is dependent on Vp so CO will return to how it was before.
This demonstrates that blood flow is only going to tissues as demand dictates.
50
What determines venous pressure?
Venous pressure is due to venous volume. Blood in:
- Low TPR
- High tissue demand for metabolites
- Muscle pumping
51
How is cardiac output calculated?
stroke volume x HR
52
Describe the various mechanisms that can give rise to arrythmias
Extra conduction pathways (wolff parkinson white), damage to various parts of the heart due to hypoxia/trauma/infection/congenital defects. leading to a disruption in the normal conducting pathways.
These could be uni-directional and none conducting regions of heart tissue that can give rise to re-entry loops, early depolarisations can arise due to action potentials taking a long period of time. This is commonly due to Long QT which can arise from being very healthy in athletic heart syndrome.
Stretch and required growth of tissue in stress results in pathways being deranged from normal.
53
What are the plausible causes of congenital heart disease?
toxins (alcohol and cocaine)
infection (rubella, toxoplasmosis)
genetics (trisomy 21 and marfans)
54
Describe aortic coarction
Narrowing of the aorta typically below the subclavian, if not then disruption to rate and rythym. Individual will develop LV hypertrophy as a result and premature congestive heart failure without treatment.
55
Describe dextro-transposition of the great vessels
The Aorta goes to the body from the RV so bypasses the lungs: this is not compatible with life after the ductus arteriosus has been closed. Treatment is surgical correction and prostoglandin to keep the ductus arteriosus open.
56
Describe hypoplastic left heart syndrome
LV underdeveloped. Baby kept alive only until the ductus ateriosus is closed.
57
Describe pulmonary atresia
Poor pulmonary flow resulting in no oxygen getting to tissue around the systemic circulation. Treatment will be surgical and the giving of prostaglandin.
58
Describe tetraology of fallot
- overriding aorta
- ventricular septal defect
- pulmonary stenosis
- RV hypertrophy
59
describe tricuspid atresia
Absence of the RAV connection so oft hypoplastic RV and an inibility to pump blood through the pulmonary circulation.
60
Describe univentricular heart
Only one ventricle develops.
Can be due to lack of septum developement.
RA can be isomerised resulting in 2 SAN.
61
Describe total anomolous pulomonary venous drainage
The 4 pulmonary veins fail to join the LA like in normal physiology.
Results in no blood going through the left side of the heart.
Not compatible with life.
62
What is cyanosis? what must be present for this to occur?
cyanosis is the presence of deoxy blood in the systemic circulation
Due to a R-->L shunt at any level.
63
What can cause a L--> R shunt?
Atrial septal defect
Ventricular septal defect
patent foramen ovale and pulmonary stenosis.
64
What nerves are PSNS?
s2-->4 and cranial 10, 9, 7 and 3
65
What nerves are SNS?
T1-->L2
66
Describe the action of the vagus nerve on the heart
Provides the parasympathetic control. Innervates the SAN and increases the time taken for each depolarisation.
Also due to activated Kach channels there is a greater degree of hyperpolarisation so threshold takes longer to be achieved.
Role in the vasovagal response, sinus arrythmia/bainbridge reflex and in the dive response.
67
How is the rate of SAN action potential up or down regulated?
Based on the levels of cAMP in the SAN cells.
| . If upregualted by cAMP directly.
68
What is the sympathetic effect on heart contraction?
PKA phophorylates delayed rectifier. and also phospholabam.
If this is high then more PKA activated causing more L type Vocc action through phophorylation
-increased force of contraction, increased conducting velocity and increased heart rate.
69
How is blood pressure regulated?
Through baroreceptors in the blood vessels.
These are found in the corotid sinus and arch of the aorta. They provide feedback to the brain's cardiac centre as to whether there needs to be an increase of decrease in CO. Also there is the bainbridge/ sinus arrythmia which is due to the pressures in the right atria and lungs respectively.
70
What is the role of the ANS?
homeostasis of the subconscious basal requirements of the body.
71
What is the action of the PSNS on cardiac contraction?
Decreases the rate of contraction but has no effect on the force of contraction as no innervation to the ventricle.
72
How does the SNS affect blood vessels systemically?
Depends on the location of the vessels.
In the liver, skeletal and small coronary vessels there are beta 2 adrenoceptors which undergo vasodilation.
In the skin, and GI tract there is alpha 1 which vasoconstrict.
73
What neurotransmitters function at the tissue/post ganglionic neurone junction?
In Muscarinic; ACH
| in Adrenoceptors: NA
74
Describe the nerves in the PSNS and SNS
```
PSNS
Long pre short post, Ach only Pre=myelinated and originates from s2-->4 and cranial nerves 10,9 7 and 3.
SNS
Shot pre, long post, Ach and then NA
Pre=myelinated, originates from T1-->L2.
```
75
Describe the role of the sympathetic nervous system
Fight or flight response.
76
What is the role of ivabradine?
It blacks the funny current of the SAN and decreases the rate of cardiac contraction.
77
How is the funny current activated?
By hyperpolarisation. This opens the funny channels that allow an efflux of K+ and influx of Na+.
78
Describe the pacemaker potential.
Spontaneously depolarises to threshold due to funny current. Upstroke due to ca2+ (T and then L) influx and hyperpolarisation due to K+ influx.
goes from -70 to +10mv
79
Describe the cardiac myocytes action potential.
-80 to plus 50 (due to fast VONaC being opened due to depolarisation). Dips due to rapid delayed K+ channels and NCX. Plateaus due to Ca2+ influx which are open for 250ms. Drop due to VOCC close and more K+ open.
80
How does the voltage pass from cell to cell in the cardiac myocytes?
Each cell is connected by low resistance gap junctions known as intercalating disks.
This allow the excitation to pass from region to region. From one part of a cell to another the influx of Na+ causes more Na+ channels to open due to depolarisation and the flow moves away.
81
What happens to intracellular calcium levels in a cardiac myocyte?
Depolarisation of the membrane opens VOCC inducing an influx of Ca2+
This acts upon the ryanodine receptor in the sarcoplasmic reticulum.
This causes CICR.
This leads to a massive increase in local calcium concentrations. Also the increase in calcium leads to a positive charge being inside the cell. This involves the reversal of the NCX leading to further increase.
Calcium is sequestered by the SERCA or the mitochondrial uniporter where it can then be used for the next contraction.
Calcium is buffered in the cell by calsequestrian and calbindin. Calmodulin binds calcium which upregulates the activity of the PMCA.
If SER is empty then orai and stim coordinate a response to increase the calcium influx independent of a contraction.
82
How can adrenaline increase force of contraction in a ventricular myocyte?
Adrenaline binds to beta 1 in the heart.
G- alpha-S activated.
Leads to an increase in PKA.
More PKA phosporylates phospholamban and VOCC so more sequestring and more calcium influx.
83
What is proportional to intracellular calcium concentration?
the force of contraction.
84
how can arrhythmias arise?
Any abnormality in the flow of current across the heart.
- Stretching
- ischimia
- fibrosis
- enlargement pathologically
- extra conducting pathways
- channelopathies
- Necrosis of tissue leading to ectopic beats
- Drugs that can cause any of the above
- excess sympathetic/PSNS stimulation
85
How do organonitrates relieve the symptoms of angina?
```
NO--> activates guanylate cyclase
more cGMP
more PKG
lowers calcium concentrations
relax smooth muscle.
results in collateral arteries vasodilatation, and also venous dilatation. This drops venous pressure and increases blood flow in angina.
```
86
What cardiac conditions can lead to A fib?
- atrial dilatation
- extra conduncting pathways
- dual chamber pacemakers
- re-entrant pathways
- pulmonary hypertension
- mitral stenosis
- mitral regurgiatation
87
How is a fib managed?
Antithrombotics: heparin and warfarin.
antiarrhythmics: prolong the effective refractory period by blocking Na channels with lidocaine (class 1) or K+ (class 3)
surgery: Cox maze
88
How are drugs used in heart failure?
Low CO: beta antagonists (class 2)
Oedema: Ace inhibitors and diuretics
Tissue perfusion:.
low contractile force: glycosides block Na/K atpasa, increasing calcium(i) concentration.
89
When would ionotrophic drugs be used?
| name some drugs and their mechanisms
Increase in force of contraction. This is beneficial to remove the symptoms of heart failure.
Digoxin is the current drug of choice when A fib is also involved however in the long term has no improvement on associated morbidity.
90
Describe the therapeutic uses of beta antagonists
Sympathetic overdrive can give rise to arrythmias in moderate/compensated heart failure. This is because of several channelopathies.
Increased leaky ryanodine, less SERCA pumping.
Adrenaline leads to the increase in SER stores but due to the leaky ryanidine can cause DADs--> arrhythmia.
In short beta blockers stop arrythmia (good) from this mechanism but decrease contractility (bad)
91
describe the classes of anti-arrhythmic drugs and their various therapeutic aspects
I- sodum channel blockers
II- beta antagonists- slow HR and reduce O2 demand of heart, also reduce risk of arrythmias. (propanolol, atenolol and metoprolol)
III- K+ channel blockers- cause long GT in most cases.
IV- VOCC blockers (Verapamil and DHP)- reduce the force of contraction and also reduce upstroke in AVN and SAN.
Amiodarone- doesnt belong to any particular group- used to treat wolff parkinson white.
92
Define heart failure
A state at which the heart fails to maintain the required blood flow for the needs of the body despite an adequate filling pressure.
93
What are the common causes of Left ventricular failure?
```
hypertension
Cardiomyopathy
Coronary stenosis and ischimia
Myocardial infarction (2/3 of patients have this)
Aortic stenosis
```
94
What is the most common cause of right ventricular failure?
Pulmonary hypertension.
95
How can Left heart failure result in right heart failure?
The decrease in pumping efficacy of the left heart results in a backlog of blood into the pulmonary circulation. This results in pulmonary hypertension; the most common cause of right ventricular failure.
96
What are common causes of cardiomyopathy?
```
Infection
alcohol/drugs
pregnancy
idiopathic
hypertrophy
Old age.
```
97
What are the key cellular changes in heart failure? what are the consequences of these?
-Reduced calcium pumping into sarcoplasmic reticulum- less force of contraction possible due to contraction requiring calcium.
-leaky SR calcium channels- impairs diastolic relaxation increasing stiffness of the ventricles and also causes inappropriate Ca2+ release.
-upregualtion of NCX and downregulation of K+ channels: this results in more K+ in and more Na+ in so only a small leak of Ca2+ is needed to trigger a DAD.
The downregulation of the K+ channels results in increased QT interval increasing risk of re-entry circults.
98
What are the classes of heart failure? What are the symptoms of each class?
1- no symptomatic limitation of activity
2- slight limitation upon exertion, no symptoms at rest.
3- severe limitation upon exertion but no symptoms at rest
4- symptoms at rest worsened by any exertion.
99
What are the symptoms of Left ventricular failure?
Dsypnoea
orthosnoea
pulmonary congestion and oedema
exercise intollerance
100
What are the symptoms of right ventricular failure?
Peripheral oedema
hepatomegaly and ascites
raised JVP
exercise intollerence
101
How does heart failure affect contractility?
decreases it.
102
Describe the mortality of heart failure in relation to the various classes
1-10% @6 years
2+3-40% @6 years
4- 80% @ 3 years
103
What is the normal cardiac output?
5 litres/min
104
What is normal stroke volume at rest and in exercise?
75ml/beat
| 115ml/beat
105
what is normal mass of a heart?
330grams
106
What is a typical p wave duration?
0.08 seconds
107
What is the typical PR interval?
<0.2 seconds
108
What is normal QRS wave length?
<0.1s
109
What is normal heart rate at
- rest
- maximum
60
| 190
110
What is the intrinsic pacemaker rate?
100 beats per minute
111
What is normal central venous pressure?
0-10mmHg
112
What is normal LV pressures?
4-->125
113
what is normal RV pressures?
0--> 25mmHg
114
what is a normal ejection fraction?
66%
115
what is normal end diastolic volume?
120ml
116
what is the cardiac resting potential?
-80mv
117
What is the peak of the cardiac action potential?
20-->30mv
118
What is the resting potential of a pacemaker cell?
-60mv
119
What is the duration of a cardiac action potential?
0.2-->0.4 seconds
120
by what factor does intracellular concentration of Ca2+ increase during cardiac systole?
20
121
What is aortic impedence?
Afterload
122
what factors affect cardiac output?
HR, Preload, Afterload, contractility
123
Describe systolic dysfunction morphological changes)
increased LV capacity, reduced contractility, thinning of the myocardial wall (fibrosis and necrosis and matrix proteases), mitral valve incompetence.
Loss of muscle mass and loss of elastin, myocyte hypertrophy.
124
Describe how ventricular dilatation can occur?
MI--> scar tissue. Heart protects scar by increasing the ventricular volume.
In response to increased after load. first hypertrophy then dilatation.
125
Describe natriuretic hormones in heart failure
```
Oppose RAAS.
Good marker
B- ventricular
A- atrial
C- localised in endothelium
```
126
Describe ADH in heart failure
Release increased in HF worsening the HF.
127
Describe prostaglandins/NO in heart failure
Vasodilators, NSAIDS block PG synthesis, NO production can be deranged in coronary artery stenosis.
128
Describe the role of RAAS in heart failure
Renin secretion induced by adrenaline and low blood supply to the kidney.
Renin cleaves angiotensinogen to angiotensin 1.
ACE converts this to angiotensin 2.
ACE breaks down bradykinin.
The result of A2 is vasoconstriction, increased sympathetic activity. , increased NO release,
NB: NEP convert A1-->A3. which is a vasodilator.
129
What is the effect of the SNS on heart failure?
Operated through the baroreceptors in the corotid sinus and arch of the aorta and stimulation increased as BP falls.
Short term: increased CO as both HR and contractility increased also veno and vasoconstriction.
Long term: RAAS induced, cardiac hypertrophy, inotropic effects removed due to down regulation of adrenoceptors.
Venoconstriction/high filling pressures result in RV dilatation and systemic hypertension results in dilatation.
130
What is the role of endothelin 1?
Secreted by vascular endothelium
| aggressive vasoconstrictor
131
Describe some of the important changes systemically in HF
Skeletal muscle: poor blood flow results in atrophy and can result in fatigue and exercise.
Renal effects: decline in function due to drops in kidney blood flow.
anaemia: ACEi can cause bone marrow suppression and asprin can cause GI bleeding. Also renal failure can result in low EPO.
132
describe diastolic dysfunction in the heart
Stiffening of the heart due to lack of elastin thickened myocardium and increased levels of Ca in the cytoplasm during diastole resulting in a decreased ability to relax. This requires a higher Vp to fill resulting in venous oedema.
133
What is the current treatment for heart failure?
```
Treatment of the underlying cause.
Reduce blood pressure, stenosis etc
Antiarrythmics
Delay progression of disease.
Lifestyle changes to reduce risk of progression. (diet exercise alcohol and smoking)
```
134
Describe the common causes of chest pain
Heart and great vessels: MI angina, pericarditis, aortic dissection
Lungs and pleura: pleuritis, PE, pneumothorax and pneumonia.
GI system: acid reflux, peptic ulceration, biliary cholic and cholic cystitus
Chest wall: rib fractures or malignancies, costochondral joint inflammation, muscle aches and skin (herpes zoster).
135
Describe the perfusion of coronary blood flow
Mostly during diastole. This is because of the compressing forces of the heart on the vessels during systole. The flow is from the superficial epicardium through the myocardium to the endocardium.
136
How does an increase in Heart rate affect coronary vessel perfusion?
decreased length of time in diastole so less time for blood flow to occur at the maximum.
However increased metabolite production.
this results in vasodilation
resulting in an increase in flow.
137
How can collaterals develop in the heart?
Through angiogenesis triggered by ischaemia.
138
What factors affect the myocardial oxygen supply?
Levels of Hb in blood
Resistance of vessels
diastolic pressure
Length of diastole
139
What factors affect rate of O2 demand in the heart?
heart rate, preload and afterload, contractility and wall tension
140
What is the most common cause of coronary artery disease.
IHD
141
What are the major risk factors for IHD?
Age, gender, familial traits (Apolipoprotein E phenotypes)
Diet, smoking and exercise, diabetes
Hypertension.
142
Describe the signs and symptoms of acute pericarditis
Caused by infections, AI and cardiac surgery
presents with central/leftsided chest pain which gets more severe with inspiration. inproved by leaning forwards.
Pericardial rub and effusion can be detected.
On ECG all leads elevated with ST concavity.
treatment would be to manage symptoms and treat underlying cause.
143
Describe surgical techniques in coronary artery disease treatment/management
Percutaneous coronary intervention using a balloon. Oft guided by angiography.
CABG: use of great saphoneous vein after it has had the valves placed in the correct direction.
144
Describe the key biomarkers in a MI
Tropnin I (up to 5 days) and cardiac creatine kinase (up to 3 days)
145
How can cardiac markers be used to differentiate between NSTEMI and unstable angina in a patient with acute coronary syndrome
unstable releases no cardiac markers into the blood. This is due to no tissue being necrosed.
146
How does an MI appear on an ECG?
STEMI= elevation of ST seqment.
Inverted T waves that persist for weeks
and pathological Q waves that persist for years
NSTEMI present with either no ECG changes or ST depression and T inversion.
147
Differentiate stable with unstable angina
stable: atheroma has a strong fibrous plug.
Symptoms are reproducible upon exertion, blood flow sufficient at rest, can be triggered by stress, cold and exertion.
unstable: atheromateous plague is unstable and can rupture producing a thrombosis. This results in a transient full occlusion or a partial occlusion of the coronary vessel. No tissue death occurs as no cardiac biomarkers present. Oft it can occur at rest with no apparent trigger.
Both appear on ECG with a depressed ST interval.
148
Differentiate unstable angina with an NSTEMI
in unstable there is no necrosis so there is no biomarkers in the blood
149
Differentiate NSTEMI with a STEMI
stemi is trans mural and shows ST elevation on an ECG.
150
Why would an exercise stress test be used?
Patient who has ST depression only on exertion. Allows clinician to replicate these settings to determine if angina is the cause. Exertion up to target heart rate UNLESS chest pain or arrhythmia develops.
151
What are the symptoms of angina?
central transient chest pain, can radiate to left arm and even up neck. brought on by exertion/cold/stress but in unstable can occur at rest.
152
What is the management for angina?
Reduce heart demand: beta blockers, nitrates for preload, ACE I for afterload, Ca2+ c blockers.
Increase oxygen supply: asprin, nitrates, reduce LDL via diet and statins. Also stent.
153
Describe stemi management
Pain control, anti ischaemic therapy, antihypertensives, antithrombotics and antifibrinolytics like warfarin. if within 2 hours then surgical intervention.
154
Describe management for nstemi
asprin and antithrombotics possibly surgical intervention.
155
What can cause decrease venous flow?
Superfical varicose veins: torturous due to valve damage,
| DVT: deep veins of the leg usually, tender warm swollen and red tissue, can cause PE.
156
What is shock?
a complete circulatory failure that is due to a fall in arterial blood pressure. This results in essential tissues receiving insufficient oxygen and metabolites resulting in ischaemic necrosis.
157
What 2 factors can change to result in shock? What can cause a change in them?
Cardiac output (mechanical and TPR
158
how can sepsis cause shock?
Distributive
endotoxins released from bacteria
TNF alpha IL1 and histimine and leukotriene released in response to injury.
cause vasodilatation
cause a drop in TPR
fall in arterial pressure (detected by baroreceptors)
poor organ perfusion
capillaires become leaky so blood volume reduces.
High venous return due to low TPR and high heart rate so CO up
treat underlying infection. manage symptoms.
159
How can anaphylaxis cause shock?
distributive
Release of histimine in response to allergen from mast cells.
Vasodilation and drop in TPR so drop in Ap.
CO goes up but not enough to increase blood pressure.
Also get bronchoconstriction and laryngeal oedema.
Treat with adrenaline.
160
Describe hypovolaemic shock
| What happens if not halted and treated before decompensation?
Loss of circulating volume i.e from hemorrhage/dehydration/burns.
classes are 15, 15-->30, 30-->40, >40.
Severity of shock is based on volume and rate of loss.
Vp falls, so cardiac output falls.
increase in sympathetic activity in response to low arterial blood pressure. results in veno/vasoconstriction and increased contractility. Also autotransfusion from ECF-->cappilaires.
symptoms: high HR, weak pulse, pale and clammy skin.
Eventually occluded vessels vasodilate due to the build up of metabolites resulting in a drop in TPR and a subsequent fatal drop in arterial blood pressure.
161
Describe cardiogenic shock
Pump failure by Myocardial infarction, heart failure and arrhythmias.
CVP will be high, heart fills but wont pump effectively
drop in BP
Heart is poorly perfused so problem gets worse
Kidneys get poor blood supply so RAAS activated and reduced urine production.
Solution is to solve the underlying pathology. Defib/antiarrhythmics, if acute decompensated heart failure then treat cause to reverse effect. thrombolysis for acute MI and treat coronary artery disease.
162
Describe mechanical heart failure
Physical obstruction to the normal flow of blood around the heart.
causes:
cardiac tamponade|: affects both sides of heart, build up of fluid in the pericardial space, restricts bilateral filling of heart. High Vp and low Ap. Electrical activity occurs until hypoxia disrupts this. treat with cardiocentesis and also underlying cause.
,pulmonary embolism: Blocking of the pulomonary circulation. So no flow from RV to LA. High pulmonary pressure, high venous pressure due to backlog of blood. Low filling of LV so arterial blood pressure is low. Also has chest pain. Treat with fibrinolytics to break up thromboemboli such as heparin and in the long term warfarin.
neoplasia and any other SOL?
163
Describe neurogenic/spinal shock
damage to spinal nerves or CNS that results in a decrease in heart function that results in a drop in arterial blood pressure.
164
Define hypertension
140/90mmHg.
165
What causes the triple JVP beat?
1-tricuspid valve opens at the start of diastole.
2-atrial contraction in the latter stage of diastole.
3- regurgiation that causes the valve to close.
166
What are the major differences between the systemic and pulmonary circulation?
Pulmonary is a low resistance and low pressure system.
There is signinficantly less muscle around the arterioles and also the lumens are much larger in the lung. Role of pulmonary is to collect oxygen instead of deliver it. So the gradients are opposite between the 2 circulations.
167
What are the normal pressures in the pulomonary
- artery
- cappilaries
- veins
1) 15-->12
2) 12-->9
3) 5
168
What is ventilation perfusion matching?
The optimum for Gas exchange is o.8
This is 5 litres of air in to 4 litres of blood supplied to the lungs.
When there is an occlusion of blood (PE) this will go up and when there is an air obstruction it will go down (LV failure, mitral stenosis or regurgitation or infection).
169
What does a low VQ in a particular portion of lung result in?
In low oxygen supply the vessels undergo hypoxic pulomary vasoconstriction.
This is a response to get the V/Q back to 0.8 so a reduction in O2 needs a reduction in blood. This blood is diverted to other areas of the lung which has better oxygen supplies.
170
Describe the flow of blood through the pulmonary circulation
Varies from 5--> 25 litres per minute.
period of time the blood is in the lungs varies from 1--> 0.3 seconds. This is the minimum time frame that allows Hb saturation with oxygen.
171
Describe how the myocardiums work load relates to its blood supply
directly proportional.
The greater the work the greater the demand.
Drop in resistance by vasodilation. This is mediated by metabolic hyperaemia. Also No produced in the heart vessels walls induces vasodilation in the collateral supplies.
172
What is significant about the coronary arteries being end arteries?
If occluded results in NO BLOOD AT ALL getting to the tissue that the occluded vessel supplies. This leads to angina in atheroma formation due to the inability of other arteries to take some of the strain in metabolic demand.
173
How does venous pressure affect the reforming of blood plasma in the pulomonary circulation?
The higher this is the greater the driving force for ECF to be formed. This results in increased fluid being formed resulting in P. Oedema.
Venous pressure has the greatest effect on tissue fluid formation as the high arterial pressure is kept back from forming too much tissue fluid by the arterioles.
174
Describe skeletal muscle blood circulation
Basal= 1/20 of max flow, at basal vasoconstriction and 50% vessels occluded.
In exercise massive dilation and this is due to a combination of metabolites and sympathetic stimulation. Also recruitment occurs increasing blood flow to tissue.
Degree of perfusion varies from muscle to muscle and person to person.
175
Describe acral/apical skin circulation
High SA to volume ratio so good for heat loss.
Release of bradykinin in sweat glands which results in vasodilation. This acts on arteriovenous anastomoses. Thus heat loss can still occur even in stress situations with high sympathetic stimulation.
176
Describe the regulation of the cerebral circulation (myogenic autoregulation, metabolites, cushings reflex and hyperventilation)
Vasodilators: K+, H+, adeonsine, high CO2.
Cushings reflex- pressure on brain reduces flow to cardiac center in medulla oblongatta results in increased sympathetic flow to increase blood perfusion.
Cerebral autoregulation: this is the process of in low arterial pressure cerebral vessels vasodilate to maintain perfusion and vice versa in high blood pressure. This only works between approx 50--> 160 mmHg.
Hyperventilation: results in hypocapnaia. thus vasocontriction and syncope.
177
What is the action of NO? Synthesis and release?
Lowers vascualar tone in veins and in large musclular arteries. This is due to cGMP activation that lowers Ca2+ conc, leads to activation of MLC-phosphotase and hyperpolarisaion through more K+ channels. inhibits platelat aggregation and vascular smooth muscle proliferation having a net anti-atheroma effect.
Released in response to sheer stress causing flow induced dilatation, inflammatory mediators such as bradykinin cause a release of NO as well.
Synthesised from L-arginine by nitric oxide synthase.
178
What is the role of VWF?
Von Willebrand factor
Usually kept in isolation by endothelium.
Carrier for factor VIII, and release is triggered by thrombin.
Binds to subendothelial collagen and promotes platelat adhesion.
179
How does NO respond to superoxide production?
Healthy arteries respond to Ach by producing NO. However in atheroma the levels of NO are depleted. This is due to the superoxides in the atheromas reacting with forming ONOO- Which can then form OH radicals. It is a positive feedback loop then that formation of atheroma leads to a drop of NO which causes further atheromateous developement.
