cardiovascular system Flashcards
define cardiac output
volume of blood ejected from the left ventricle into the aorta each minute
what is the equation for cardiac output
cardiac output = stroke volume x heart rate
what is stroke volume
the volume of blood ejected by the ventricle after each contraction
what are the 3 factors that regulate stroke volume
preload - degree of stretch before contraction
contactility - forcfullness of contractions
afterload - the pressure that must be exceeded for the ventricles to eject blood
what is preload
filling pressure detected by stretch receptors in myocytes
roughly equates to end diastolic pressure/volume
what is afterload
peripheral resistance
what are the two main forces in fluid balance across a capillary
hydrostatic pressure
colloid osmotic pressure
in oedma, what are the changes to the capillary
decreased colloid osmotic pressure (low albumin)
damage to alveolar membrane
lymphatic blockage (cancer)
increasedhyfrostatic pressure
what causes pulmonary oedema in heart failuer
increased filling pressure due to higher preload causes hydrostatic pressure in pulmonary capillaries to go so high that fluid leaks out faster than lymphatics can take it away
what are some compensatory mechanisms that are devloped to cope with mitral stenosis
thickened alveolar capillary membrane
increased drainage
two main effects of heart failure
not enough blood is getting to the body which can cause fatigue
ongestion/fluid accumulation
heart failure can be classified into two groups
acute and chronic
what are the three main courses of heart failure
patient remains stable on meds
gradually deterioates
patient sufferes repeated insults in stepwise fashion slowly losing LV function
describe acute heart failure
Acute heart failure is the sudden worsening of the signs and symptoms of heart failure,
typically includes difficulty breathing (dyspnea), raised JVP, leg or feet swelling, and fatigue.
what is anasarca
gross fluid retention and oedema everywhere
what is cardiogenic shock
an extreme version of heart failure, where somebody has e.g. had a
very large MI and killed so much of their heart that they can’t survive
what is the bodies response to acute heart failure
similar to acute blood loss-
Sympathetic outflow
-Raises BP, heart rate
-Preserve flow to vital organs at expense of limbs
Salt and water conservation
-Thirst, ADH
-Shut down kidneys
symptoms of pulmonary oedema
Breathlessness
Difficulty talking
Orthopnoeia - Lying down may kill them (flood
all the alveoli)
Frightening - Experience ‘angor animi’ (fear of
certain impending death)
Use of accessory breathing muscles
Pink, frothy sputum - Alveolar fluid with blood
Sweating
Cold, clammy
what are the models of progression for chronic heart failure
haemodynamic
neurohormonal
peripheral
metabolic
what is law of laplace equation
Tension within wall of the LV (T) = [Pressure inside ventricles (P) x Radius of the ventricle (R)]
/Ventricle wall thickness (h
what is the effect on RAAS in heart failure and why
activation of RAAS
as kidney perfusion/blood pressure is low
causes vasoconstriction and water /salt retention
what is ergoreflex
Reflex generated by exercising muscles - With exercise, muscle being exercised sends signals
to the brain to breath more.
The ergoreflex increases as exercise capacity falls and increases as ventilatory response to
exercise increases.
which reflexes are inhanced and which are poor in those with heart failure
enhanced chemo /ergo - increase ventilation
poor baro/cardio reflexes
what are the two types of left sided heart failure
systolic - left chamber lacks the force to push blood into circulation
diastolic - left chamber fails to relax normally as muscles have become stiffer
what are the symptoms of left sided heart failure
Increased rate of breathing
Increased work of breathing
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Fatigue
Rales or crackles heard in the lung bases (in severe cases, if heard throughout the
lung this indicated pulmonary oedema)
Cyanosis
Laterally displaced apex beat (occurs if the heart is enlarged)
Gallop rhythm
Heart murmurs may indicate the presence of valvular heart disease as either a cause
(e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure
what are the causes of right sided heart failure
muscle injury, such as a heart attack localised to the right ventricle,
damage to the valves in the right side of the heart or elevated pressure in the lungs.
what are some causes of heart failure
Past heart attacks
CHD
High blood pressure
Heart valve disease
Heart muscle disease or inflammation of the heart
Congenital heart defects
Lung conditions
Alcohol/drug abuse
what medications are used to treat pulmonary oedema
oxygen!
diuretic (furosemide)
vasodilator (nitrate/GTN)
IONOTROPIC SUPPORT if blood pressure is low - dobutamine
how is anasarca treated
induce diuresis
bed rest
fluid restriction
catheter
diuretics
heparin - to prevent DVT
example of loop diuretics
bumetanide
furosemide
what is the mechanism for loop diuretics
block na/k 2cl transporter in loop of henle
what is the mechanism for EDCT diuretics
block na/cl/co transporter
what is an example of EDCT diuretics
thiazide
what may a larger P wave indicate
enlargment of atrium
what may a larger Q wave indicate
myocardial infarction
what may a large R wave indicate
enlarged ventricles
what may a flat T wave indicate
heart muscle recieving insuffecient oxygen
what is atrial fibrillation
muscle fibres are a synchrinous - atrial pumping may cease all together
describe a fib in ECG
typically no clearly defined P wave + irregularly spaced qrs complexes
what is atrial extrasystole
Atrial extrasystole is where the stimulus is thought to arise in the atrium elsewhere than at the SA node
what is ventricular extrasystole
Atrial extrasystole is where the stimulus is thought to arise in the atrium elsewhere than at the SA node
what are the cardiac effects of digoxin
- Cardiac slowing and reduced rate of conduction through AV node, due to increased vagal activity
- Increased force of contraction
- Disturbances of rhythm, especially block of AV conduction and increased ectopic pacemaker activity
what are the mechanisms of digoxin
Digoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. The sodium calcium exchanger tries to extrude the sodium and in so doing pumps in more calcium. Increased intracellular concentrations of calcium may promote activation of contractile proteins (actin and myosin). This strengthens ventricular contractions so that the heart is able to pump more blood with each beat. It also helps to slow the heart rate by blocking the number of electrical impulses that pass through the AVN into the ventricles.
what family of medication is digoxin
glycosides
what are some draw backs of digoxin
Adverse effects are common and can be severe. One of the main drawbacks of glycosides, such as digoxin, in clinical use is the narrow margin between effectiveness and toxicity.
what are the cardiac effects of adrenaline
- Increases heart rate
- Direct stimulation of cardiac muscle which increases the strength of ventricular contraction
what is the mechanism of adrenaline
nonselective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, β3, to produce a ‘fight or flight’ response. Its mechanism of action is via membrane receptors, which trigger a second messenger response. Action on the β1 receptors increases the heart rate and contractility of the heart.
What are the 4 main components of vascular walls
a. Endothelial cells
b. Elastic fibres
c. Collagen fibres
d. Smooth muscle cells
- What are the three layers of blood vessel walls
a. Intima
b. Media
c. Adventitia
What blood vessel has the most collagen fibres
a. Vena cava
which blood vessel has the most smooth muscle
a. Medium arteries /vena cava
Why are arteries elastic
a. High compliance to allow for peak ejection flows
b. Recoil forces blood to move on
What causes varicose veins
a. Leaky valves allowing black flow
What is the function for the precapillary sphincter
a. Redirects blood to deficit region
Where are precapillary sphincters found
a. Mesenteric and cerebral circulations
What is a met arteriole
a. Short microvessel that links arterioles to capillaries
What are the three groups of capillaries and where are they found
a. Continuous capillary – skin, muscle (intercellular clefts)
b. Fenestrated capillaries – glands, villi, kidney glomeruli
c. Sinusoidal (discontinuous) capillaries – liver bone marrow
What type of junctions do capillaries in the blood brain barrier have
a. Tight junctions
What maintains the shape of erythrocytes
a. Glycophorin
b. Band 3 cl HCO3 exchanger
Examples of granulocytes
a. Neutrophils
b. Eosinophils
c. Basophils
Examples of non granular
a. Lymphocytes
b. Monocytes
What cells do platelets bud off from
megakaryocytes
What structures are found in platelets
a. Mitochondria
b. Lysosomes
c. Peroxisomes
d. Alpha granules
i. Van willebrans factor
ii. Clotting factor
iii. Fibrinogen
What is the function of platelets having serotonin
a. Cause recruitment of other platelets
What is blood viscosity dependent on
a. Haematocrit
b. Fibrinogen
c. Vessel radius
d. Linear velocity
e. Temperature
When does blood vessel turbulence occur
a. When the radius is large
b. When the velocity is high
c. Local stenosis
What is transmural pressure
c. Difference between intravascular pressure and tissue pressure
What factors cause van Willebrand release
a. Shear high forces
b. Cytokines
c. Hypoxia
What structures make up a blood clot
a. Erythrocytes
b. Leukocytes
c. Serum
d. Mesh of fibrin
When is the intrinsic pathway activated
a. Through surface contact activation
b. Membrane of activated platelets
When is the extrinsic pathway activated
a. In response to an outside trauma and blood leaving the vascular system
Describe the intrinsic pathway
a. Initiated due to blood exposure to negative surface
b. This activates factor 12 into factor 12a
c. Factor 11a cleaves prekallikrien to form kallikrein
d. Factor 11a converts 9 to 9 a
e. Factor 8to 8a
f. 10 to 10a
g. 10a with co factor 5a converts prothrombin to thrombin
Describe the extrinsic pathway
a. Platelet plug formed due to tissue injury
b. This causes expression of tissue factor
c. Tissue factor and factor 7a activate factor10
d. 10a and factor 5a convert prothrombin into thrombin
What is the importance of thrombin
a. Cleaves fibrinogen into fibrin
What 2 layers make up the pericardium
a. The parietal pericardia
b. The visceral pericardia
What is the name for the right atrioventricular valve
a. the tricuspid
what is the name for the left atrioventricular valve
a. the mitral valve
what heart wall layer produces pericardium fluid
epicardium
what type of cells make up the heart
a. contractile cells
b. conducting cells
what 2 types of cell junctions link cardiac cells
a. desmosomes anchor fibres together
b. intercalated disc gap junctions form channels
What is the P wave represent
a. The depolarisation of the atrium
What does the PQ region represent
a. The time the impulse travels from the SA node to the AV node
What does the QRS complex represent
a. The firing of the AV node and ventricular depolarization
What does the Q wave represent
a. Depolarization of interventricular septum
What does the R wave represent
a. Depolarization of the main mass of the ventricles
What does the S wave represent
a. The last phase of the ventricles depolarizing
What signal is obscured by the QRS wave
a. Repolarization of the atrium
What does the ST segment represent
a. The myocardial contraction
What does the T wave represent
a. Ventricular repolarization
When does atrial contraction occur on the ECG
a. About 0.1 milliseconds after the P wave
What is the dicrotic notch
a. A blip when aortic valve closes
How is pulse pressure calculated
a. Systolic pressure – diastolic pressure
In the short term how is blood pressure regulated
a. Baroreceptors in carotid and aortic sinuses
b. Nucleus tractus solitarius in the brain stem
How is arterial pressure regulated long term
a. Renin angiotensin aldosterone system
Where is decreased pressure detected in the renin/angiotensin system
a. Decrease in renal perfusion
b. Mechanoreceptors in afferent kidney arterioles
What does the reduced renal perfusion stimulate
a. Prorenin to be converted to renin
b. Renin converts angiotensinogen to angiotensin
c. ACE catalyses its conversion to angiotensin 2
What are the affects of angiotensin 2
a. Adrenal cortex synthesize and secrete aldosterone
b. Increase NA absorption
c. Increase thirst
d. Vasoconstriction
What is chronic hypertension
a. Baroreceptors do not perceive the elevated BP as abnormal
b. Hypertension not corrected
Examples of diseases high BP can increase risk
a. Heart related
b. Aneurysms
c. Vascular dementia
d. Kidney disease
e. Stroke
What are the treatments for CHBP
a. ACE inhibitors
b. Angiotensin 2 receptor blockers
c. Diuretics – thiazide
d. Calcium channel blockers – prevents calcium from entering cells of heart and arteries
e. Alpha blockers – relax blood vessels
f. Alpha agonists
g. Renin inhibitors
Under which structures of the ribcage is the right side of the heart found
a. Between the 3rd and 6th
Under which structures of the ribcage is the left side of the heart found
a. 2nd costal cartilage and 5th intercostal space
What three vessels enter the right atrium
a. Superior and inferior venae cavae which together deliver blood to the heart from rest of the body
b. Coronary sinus which returns blood from the walls of the heart
What is the name of the outflow tract that leads to the pulmonary trunk
a. The conus arteriosus
What is the septomarginal trabecula
a. Bridge between lower portion of interventricular septum to base of the anterior papillary muscle
How do the trabeculae carneae differ in each ventricle
a. Finer and more delicate in the left than in the right
Which coronary artery provides both ventricles and left atrium with blood
a. Left coronary artery
Which cardiac vein drains the areas supplied by the LEFT CA
a. Great cardiac vein
Which cardiac vein drains areas supplied by the posterior interventricular branch of the right coronary artery (left and right ventricles
a. Middle cardiac vein
What vein drains the right atrium and right ventricle
a. Small cardiac vein
What vein drains the right atrium and directly empties into the right atrium
a. Anterior cardicac veins
Name of the tissue that lines the inner heart wall
a. Endocardium – squamos epithelium
What are the layers of the pericardium
a. Fibrous pericardium – tough
b. Serous pericardium
i. Parietal pericardium
ii. Visceral pericardium
Pericardial cavity is between which two layers
a. Parietal and visceral
What is STEMI
a. Elevated ST segment myocardial infarction – the artery Is completely blocked off
b. Hump shape
What is NSTEMI
a. Non-ST elevation myocardial infarction
b. Partial blockage of coronary artery – raised troponin levels
What are the cardinal symptoms of acute coronary syndromes
a. Chest pain
b. Arm pain
c. Breathlessness
d. Palpitations
e. Syncope
What are the differences of symptoms between angina and MI
a. Angina is often exercise
b. Angina is worsened by cold
c. MI is 30 minutes +
What are the symptoms of pericarditis
a. Sharp stabbing pain
b. Worse with inspiration
c. Worse lying flat
d. Eased y sitting up + NSAIDS
e. Hours to days
What are the causes of pericarditis
a. Infection
b. Pericardial infusion – infection, malignancy, lymphoma
What are the changes on the ECG for pericarditis
a. Concave scooped ST elevation – U SHAPE
What are the symptoms of aortic dissection
a. Sudden, tearing, knife-like pain
b. Excruciating
c. Radiated to back
d. Often seen in elderly population with hypertension
e. Seen in people with stressful jobs with hypertension at a young age
What are the symptoms of pulmonary embolus
a. Over infarcted area
b. Pleuritic pain
c. Associated with SOB
d. Tachycardia/AF
e. Tachypnoea
What is an aortic dissection
a. a serious condition in which a tear occurs in the inner layer of the body’s main artery
what is a pulmonary embolus
a. blockage in the lungs
what is dyspnoea
a. abnormal uncomfortable awareness of breathing
what is tachypnoea
a. fast breathing
what is paroxysmal nocturnal dyspnoea
a. Paroxysmal nocturnal dyspnea (PND) causes sudden shortness of breath during sleep. As a result, you wake up gasping for air.
b. PND is caused by the failure of the left ventricle. When this happens, it is unable to pump as much blood as the right ventricle, which is functioning normally. As a result, you experience pulmonary congestion, a condition in which fluid fills the lungs
What are the symptoms of paroxysmal nocturnal dyspnoea
Wake from sleep (2 to 4 hours)
b. Cough, wheeze
c. Have to sit up while sleeping - Ask how many pillows they sleep with at night
d. Frightening
e. Lasts 15-30 minutes
What is syncope
a. Transient loss of consciousness (fainting) and postural control (collapse) due to cerebral hypoperfusion
What can cause a S3 heart sound
a. Occurs with cardiac problems such as a failing left ventricle as in dilated congestive
b. heart failure
c. * Caused by the oscillation of blood back and forth between the walls of the ventricles
d. after the rush of blood from the atria
what can cause S4 heart sounds
a. Just after atrial contraction/end of diastole before S1 * Produced by the sound of blood being forced into a stiff or hypertrophic ventricle (caused by aortic stenosis, hypertension, hypertrophic cardiomyopathy)
What blood pressure would be hypertension
a. Systolic blood pressure of 140
What do you see in chronic hypertension
a. Increased vascular tone
b. Enhanced sympathetic activity
c. Increased levels of angiotensin
What is Renal artery stenosis
a. he narrowing of one or more arteries that carry blood to your kidneys
what causes renal artery stenosis
a. caused by atherosclerosis
what is atherosclerosis
a. build up of plaque in the inner lining of an artery
what is Primary hyperaldosteronism (Conn’s syndrome)
a. Adrenal tumours (or more commonly hyperplasia) that produces aldosterone.
What is pheochromocytoma
a. Rare adrenal medullary tumours secreting catecholamines.
b. * α-mediated vasoconstriction
c. * β-mediated cardiac stimulation
What is coarction of the aorta
a. Rare congenital disease - If the isthmus of the aorta (just after the left subclavian artery) doesn’t develop properly it is stenosed. Narrower than usual
What are the affects of hypertension on the aorta
a. Atheroma
b. Aneurysm
c. Aortic dissection
What are the affects of hypertension on the brain
a. Thrombotic
b. Increased carotid atheroma
c. Haemorrhagic
What are the affects of hypertension on the kidneys
a. Glomerular damage
b. Renal artery stenosis/atheroma
What are the affects of hypertension on the eye
a. Hypertensive retinopathy
b. Pailloedema
what are the 5 types of medications used to treat CHF
diuretics
ace inhibitor
angiotensin receptor blocker
beta blockers
mineralocorticoid receptor blockers
what is the mechanism for ace inhibitors
ACE inhibitors block angiotensin converting enzyme in the lungs, to lower blood pressure
what type of medication is ramipril
ace inhibitor
what is the mechanism of ARBs
angiotensin receptor blockers, prevents ang II being converted to aldesterone
what type of medication is losartan
angiotensin receptor blocker
what is coughing a common side of effect of which medication
ACE inhibitors
what is the mechanism for MRAs
Mineralocorticoid receptor agonists are potassium sparing diuretics which block the effects of aldosterone
what type of medication is eplerenone
MRA
what type of medication is spironolactone
MRA
which beta blockers are used in heart failure
carvedilol, metaprolol, bisoprolol
what is the mechanism of ivabridine
IF current is responsible for spontaneous depolarisation in pacemaker cells which
results in heart beating, ivabridine blocks IF so slows down the rate of spontaneous depolarisation which slows the heart rate - This is the only effect it has so very specific (no change in BP
etc)- voltage gated sodium channels
what class of drug is ivabradine
hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blockers
what is the mechanism of sacubitril/valsartan
- The heart produces natriuretic peptides - Vasodilators that
make you excrete salt and water in urine - Natriuretic peptides (ANP and BNP) are broken down by neutral endo-peptidase
(NEP) - sacubitril inhibits NEPs
- valsartan
why are drugs such as digoxin and amlodopine avoided in heart failure
amlodipine - negative inotrope
digoxin - possible toxicity?
antihypertensives
a - ACE inhibitors
b - beta blockers
c - calcium channel blockers
d - diuretics
what is the mechanism of calcium channel antagonists
Block calcium entry into smooth muscle cells
Causes smooth muscle cells to relax (vasodilation)
Slows heart rate and useful for angina
what are the two classes of calcium channel antagonists
dihydropiridines/non - dihydropirines
what type of medication is amlodipine
dihydropiridine calcium channel antogonist
what type of medication is nifedipine
dihydropiridine calcium channel antagonist
what type of medication is verapamil
non-dihydropiridine calcium channel antogonist
what type of medication is diltiazem
non-dihydropiridine calscium channel antagonist
what is the mechanism for alpha blockers
Mediate sympathetic vasoconstriction
what class of drug is doxazosin
alpha blocker
what is the mechanism for central agents
Stimulate central alpha receptors to decrease sympathetic outflow. Side effects include
sedation and dry mouth.
what type of medication is clonidine
central agent
what process forms cardiac cells
myogenesis
describe pace maker cells
autorythmic, contract in the absence of neuronal innervation
what are intercolated discs
contain gap junctions, provide communication channels between cells, allow waves of depolarization to sweep across cells
what actin makes up cardiomyocytes
2 strands of alpha globular protein
how is the cardiac action potentiol different from normal muscle cells
repolarization takes longer to occur and there for cannot be stimulated at high frequency, prevented from going into tetanus - prolonged contraction
what is atrial systole
lasts 0.1 seconds, atria are contracting, ventricles are relaxed
what is ventricular systole
0.3 seconds, ventricules are contracted, atria are relaxed
which valves are the AV valves
tricusbid and mitral
what is the first heart sound
blood turbulence associated with the turbulence of closure of AV valves
what is the second heart sound
blood turbulence associated with the closure of SL valves
what is cardiac reserve
the difference between a person’s maximum cardiac output and their cardiac output at rest
where is the cardiovascular system in the brain
medulla oblongatat
what division of the nervous system is directly responsible for heart rate
autonomic division of the peripheral nervous system
role of parasympathetic nerous system in heart
- Decreases heart rate
- Reduces force of contraction
- Constricts the coronary arteries
from the right and left vagus nerve
role of the sympathetic nervous system
- Increases heart rate
- Increases the force of contraction
- Vasoconstriction
from the sympahtic trunk
the effects of adrenaline and noreadrenaline
enhance the heart’s pumping effectiveness, they increase both heart rate and contractility.
the role of thyroid hormones on heart rate
enhance cardiac contractility and increase heart rate.
the effect of elevated K or Na
decreases heart rate and contractility, na blocks ca inflow decreasing forces of contraction, excess k blocks generation of action potentials
excess intistitial ca
speeds up heart rate and strnegthens heart beat
