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CVS Flashcards

1
Q

When are the 1st and 2nd heart sounds heard?

A

-1st = Closure of AV valves (mitral and tricuspid) -2nd = Closure of outflow valves (aortic and pulmonary)

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2
Q

What causes the 3rd heart sound? What condition is it common in?

A

-Rapid ventricular filling causes oscillation of blood back and forth between the ventricles mid diastole-Heart failure

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3
Q

What causes the 4th heart sound? In what conditions is 4th heart sound NOT possible?

A

-Atrial contraction against a stiff ventricle-AF or atrial flutter (requires atrial contraction)

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4
Q

Name the main branches of the arch of aorta

A

-Brachiocephalic (right subclavian and right common carotid)-Left common carotid-Left subclavian

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5
Q

Describe the coronary arterial supply

A

-Coronary arteries branch off aorta and travel near auricles-Left coronary artery is very short and splits immediately into left circumflex and left anterior descending-Right coronary is longer and gives off right marginal and then travels around the back -Posterior interventricular artery arises from right coronary and LAD joins it and it travels in interventricular groove

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6
Q

What drains into right atrium?

A

-SVC/IVC-Coronary sinus-small tributary veins

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7
Q

State the borders of the heart on xray

A

-Left border =mainly LV-Right border = mainly RA-Diaphragmatic = LV and RV

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8
Q

Briefly describe the pericardium and its function.

A

-Fibrous sac consisting of 2 layers, an outer fibrous and inner serous (parietal and visceral) -Tough and non distensible which protects the heart and prevents over filling-Pericardial fluid between serous layers provided lubrication for friction free movement

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9
Q

What is pericardial effusion/cardiac tamponade and how does it present

A

-Abnormal collection of fluid within the pericardial cavity-Becomes tamponade when the heart becomes compromised by restriction of filling and pumping-Buldging neck veins, muffled heart sounds and low bp

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10
Q

State where the left and right laryngeal nerves loop

A

-Left = arch of aorta-Right = right subclavian

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11
Q

Name the layers of the artery wall. In which layer does atherosclerosis occur. describe the pathogenesis of atherosclerosis

A

-Tunica intima, tunica media and tunica adventitia-Tunica intima-Oxidised LDL infiltrates the tunica intima and is taken up by macrophages which are now known as foam cells and form a fatty streak on the vessel wall. Smooth muscle cells migrate from the media into the intima and fibroblasts deposit collagen and structural proteins. Smooth muscle lines up beneath the endothelium and forms a fibrous cap. this is now a simple plaque. More migration of cells and platelet infiltration and adherence to endothelium causes development of plaque and cholesterol cleft and calcifcation occur in the centre forming a complex plaque

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12
Q

Describe the spread of excitation through the heart

A

-Originates at SAN and spreads over surfaces of atria to AVN-AVN holds for 120ms before it passes down the septum and down L and R bundle of his then through the ventricular myocardium from in to out causing ventricle contraction from the apex upwards

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13
Q

Briefly describe the cardiac cycle from late systole

A

-Ventricles contracted and intraventricular pressure greater then arterial pressure so outflow valves open and blood expelled into arteries-Intraventricular pressure falls and backflow closes the outflow valves= isovolumetric relaxation-Pressure in ventricles falls below atrial pressure which have been filling with blood and are now contracting -> av valves open and ventricles begin to fill-Pressure in ventricles becomes greater then atria and backflow closes AV valves = isovolumetric contraction-Intraventricular pressure rises greater than arterial and cycle starts again

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14
Q

What is the cardiogenic field and how does this form the primitive heart tube?

A

-An undifferentiated area within an embryo from which the heart, vessels and blood cells arise from-Pair of endocardial tubes form and lateral folding results in fusionat the midline, forming the primitive heart tube

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15
Q

What is the effect of cephalocaudal folding on the heart tube?

A

-Relocates the primitive heart tube, within the pericardial cavity, to the correct anatomical location

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16
Q

Describe the primitive heart tube and state the fates of each bit

A
  • sinus venosus= RA
  • primitive atrium= RA and LA
  • primitive ventricle= LV
  • bulbus cordis= RV
  • truncus arteriosus= Aorta and PT
  • aortic roots= arterial branches
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17
Q

Why is looping a key developmental event?

A

-Ensures septation of chambers and outflow tract-Development of transverse sinus-Optimises space for growth

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18
Q

What is looping of the primitive heart tube?

A

-Continued elongation of the primitive heart tube results in the tube bending and folding upon itself-The primitive ventricle pushes ventrally, caudally and right-The primitive atrium pushes dorsally, cranially and left

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19
Q

What is the atrioventricular canal?

A

-A constriction between the primitive atrium and the primitive ventricle which allows communication between the atria and ventricles before septation occurs

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20
Q

When is the oblique sinus formed?

A

-During formation of the left atrium when the LA absorbs the pulmonary veins and expands

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21
Q

What happens to the sinus venosus during atrial development?

A

-As venous return shifts to the right side of the heart, the left horn of sinus venosus recedes and the right atrium absorbs the right sinus horn

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22
Q

What do the right and left atria develop from?

A
  • Right =Most of the primitive atrium and the right sinus horn-Left = LA sprouts pulmonary veinand thenproximal portions of these branches and expands to form complete LA
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23
Q

Name the shunts in the feotal system and state their functions in utero

A

-Ductus arteriosus -> allows blood from the PT into aorta to bbypass the lungs-Ductus venosus -> allows the blood to bypass the livr and pass from umbilical vein to IVC-Foramen ovale -> allows oxygenated blood to streamn across the right atrium into the left atrium

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24
Q

What are the aortic arches?

A

-A bilateral system of arched vessels, connected to the primitive heart, which undergo extensive remodelling to create the major arteries leaving the heart

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25
Q

What are the derivatives of the 4th and 6th aortic arch?

A

-4= Right -> right subclavian artery -Left -> arch of aorta-6= R-> Right pulmonary artery -L->Left pulmonary artery and ductus arteriosus

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26
Q

What is the function of the recurrent laryngeal nerve?

A

-Innervate the intrinsic muscles of the larynx

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27
Q

Briefly describe atrial septation

A

1) endocardial cushions form on dorsal/ventral av canal and fuse in the midline
2) Septum primum grows towards the endocardial cushions -> ostium primum before fusion
3) Ostium secundum appears by apoptosis in septum primum and fusion occurs with endocardial cushions
4) Septum secundum grows in a cresent shape and forms a functional shutter valve over ostium secundum. this is foramen ovale

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28
Q

Briefly describe ventricular septation

A
  • Muscular septum grows upwards from midline of primitive ventricles towards endocardial island
  • Stops before fusion
  • Membranous septum grows down from conotruncal septum and fuses with muscular septum and endocardial island to close
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29
Q

Briefly describe outflow septation

A
  • Pair of staggered endocardial cushions appear in truncus arteriosus
  • Septum grows from staggered cushions and develops caudally to fuse with muscular ventricular septum
  • Splits left and right heart with relevant outflow tracts
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30
Q

How are ventricular myocytes electrically and mechanically coupled?

A

-Intercalated discs and adherens junctions

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31
Q

Explain the jugular venous pressure wave

A
  • a = atrial contraction
  • c = ventricular contraction
  • x = atria relaxation
  • v = atrial filling against closed av valve
  • y= opening of av valve and ventricular filling
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32
Q

Describe the fates of the shunts after birth

A
  • DA -> respiration begins and lung resistance greatly decreases. PaO2 increases causing smooth muscle contraction forming ligamentum arteriosus. Entive RV output now enter lungs.
  • FO -> as pressure in lungs decreases, pressure in RA falls. Pressure in the LA increaes as blood from lungs is increased and pumped through systemic circ. LA>RA causing closure of FO as it it forced closed -> eventual fusion creating fossa ovails
  • DV -> Removal of placental supprt causes closure and becomes ligamentum venosum
  • Umbilical vein regresses and becomes ligamentum teres hepatis
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33
Q

In which direction are the shunts in acyanotic and cyanotic congenital heart defects? Give examples of each

A
  • Acyanotic = L->R (ASD, PFO, PDA, VSD, coarctation of aorta)
  • Cyanotic = R->L (tetralogy of fallot, tricuspid atresia, transposition of great arteries, univentricular heart, hypoplastic left heart)
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34
Q

What is an ASD and describe the haemodynamic consequences of it

A
  • An opening in the atria which persists after birth
  • Increased RH volume causing increased pulmonary bf (rarely pulmonary hypertension)
  • Can lead to RV overload and eventual RVF
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35
Q

How does a pfo differ from an asd? What is a paradoxical embolism?

A
  • Will be functional closure in pfo because pressure in LH>RH
  • A venous embolism which has entered the arterial system due to the presence of a ASD/PFO and a transient increase in RH pressure eg coughing which allows blood to flow transiently in opposite direction
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36
Q

Describe the haemodynamic changes which occur with a VSD. Where is the most common place a vsd occurs?

A
  • Increased LV volume due to increased pulmonary bloodflow -> can lead to LV overload and LVF
  • Pulmonary venous congestion and hypertension
  • Membranous portion of septum
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37
Q

What is Eisenmengers?

A

-Reversal of bloodflow through a PDA causing cyanosis due to remodelling of pulmonary system smooth muscle causing a pressure increase which is greater than that in arterial system

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38
Q

Why do you get radial femoral delay in coarctation of aorta?

A

-Narrowing of aorta, usually at site of ligamentum arteriosus causes decreased blood flow after the narrowing. Branches to head and limbs often come before narrowing so bf not affected there,

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39
Q

Describe the defects in tetralogy of fallot. What determines the severity of disease?

A
  • Overriding aorta
  • Pulmonary stenosis
  • RV hypertrophy
  • VSD
  • Extent of pulmonary stenosis
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40
Q

What must be present in tricuspid atresia for it to be compatible with life?

A

-ASD and VSD

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41
Q

What is transposition of the great arteries?

A

-Conotruncal septum is straight producing RV attached to systemic circ and LV to pulmonary circ. Generates 2 closed off systems in parallel

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42
Q

Describe the AP in the ventricular myocyte

A
  • AP arrives at plasma membrane and VONa channels open causing a rapid influx of Na -> depolarisation of membrane towards ENa
    2) Opening of VOK channels and transient efflux of K+ brings MP back down a little until. Na channels inactivate
    3) VOCC open and Ca influx to the cell causing plateau phase as balances K efflux
    4) VOCC inactivate and delayed VOK channels open causing efflux of K and repolarisation of the membrane potential
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43
Q

Describe the pacemaker potential in the SAN

A
  • These cells have no RMP and instead they are controlled by a gradual influx of Na through hyperpolarisation cyclic nucleotide activated channels which slowly increase the MP until threshold
    2) VOCC to open and Ca influx
    3) VOCC inactivation and VOK channels open causing Efflux of K and hyperpolarisation of the MP which opens HCN channels and the cycle begins again
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44
Q

By what mechanisms is the calcium concentration increased in a cardiac myocyte when the cell is depolarised?

A
  • Localised entry of Ca through VOCC caused by depolarisation
  • This causes Ca to bind to Ryanodine receptors on SR which causes Sarcoplasmic calcium channels to open and Ca to influx into the cell -> CIRC
  • Also reversal of NCX brings in calcium
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45
Q

When the cell is repolarised, what happens to decrease the intracellular calcium?

A
  • SERCA pumps back into SR
  • NCX pumps Ca out in exchange for Na
  • PMCA pumps Ca out into the ECF
  • Mitrochondrial uniporter
46
Q

How does smooth muscle contract on stimulation of A1-adrenoreceptors in SM?

A
  • Activation of Gaq -> activates PLC -> Coverts PIP3 -> IP3 and DAG
  • IP3 activated IP3R to cause CA influx from SR
  • DAG activates PKC which increases Ca concentration via channels on the SR. PKC also inhibits myosin light chain phosphatase
  • Increase Ca binds to calmodulin forming 4ca-CaM -> activates myosin light chain kinase which phosphorylates the myosin head allowing it to bind to actin and enter the latch state
47
Q

How does relaxation of SM occur?

A
  • Decreased AP decreases activation of IP3R and PKC
  • This decreases intracellular calcium and removes the inhibition from MLCP
  • Increase in cAMP inhibits MLCK via PKA
48
Q

Which neurones in the ANS use Ach and what receptors do they synapse onto?

A
  • Both preganglionic onto nicotinic
  • Post ganglionic of parasymp onto muscarinic
  • Sweating and ejaculation of the sympathetic onto muscarinic
49
Q

What neurones use NA in the ANS and onto what receptors?

A

-Postganglionis of SNS -> a and b adrenoreceptors

50
Q

Wy are the adrenal chromaffin cells different?

A

-They are a specialised postganglionic neurone which directly releases adrenaline into the blood stream

51
Q

What GPCRs are attached to a and b adrenoreceptors and m1,2,3 muscarinic receptors?

A
  • a1=q,a2=i b1=s, b2=s

- m1=q, m2=i, m3=q

52
Q

What does the ANS control in relation to the CVS?

A
  • Inotropy
  • Chronotropy
  • Peripheral resistance
53
Q

Via what receptors in the heart does the parasymp and symp work? What effect does this have?

A
  • Symp=b1 in SAN, AVN and myocardium. increasing cAMP in SAN opens HCN channels. ventricular myocytes via Gas activating PKA which opens Ca channels
  • parasymp =M2 in SAN decreases rate via decreasing cAMP and therefore decreasing activation of HCN channels, in AVN decreased conduction velocity
54
Q

What receptors do coronary vessels and skeletal muscle have? What effect do each of these produce?

A
  • a1 and b2 adrenoreceptors
  • a1 causes vasoconstriction via Gaq
  • B2 causes vasodilation via Gas activating PKA which inhibits MLCK
55
Q

What are vasodilator metabolities? How does this autoregulat blood flow?

A
  • Metabolites produced by tissues which cause vasodilation of vessels eg K+, H+ adenosine
  • Increased production of metabolites in high metabolising tissues causes vasodilation which increases bloodflow and delivery of o2 to the tissue
56
Q

Where are the baroreceptors and how do they work?

A
  • In carotid sinus and aortic arch
  • Mechanoreceptors which detect stretch and decrease firing when stretched. Causes decreased activation of sympathetic NS which causes vasodilation and bradycardia to decrease BP
57
Q

What is flow?

A

-The volume of a fluid passing a given point per unit time

58
Q

How do you calculate CO and BP?

A
  • CO=SV x HR

- BP = COxTPR

59
Q

What is capacitance?

A

-Refers to the concept that the distensibility of veins allows more blood to flow in than out and vice versa therefore they act as a store of blood

60
Q

What are the main 3 factors which effect systolic pressure?

A
  • Afterload
  • Total peripheral resistance
  • Compliance of the arteries (stretchiness)
61
Q

Is systolic pressure or diastolic pressure a better measure of TPR and why?

A

-Diastolic as not effected by the stretch of the walla

62
Q

What is pulse pressure? What CVS disease would cause a wide or narrow pulse pressure?

A
  • The difference between systolic and diastolic pressure
  • Wide= Aortic regurg
  • Narrow = Aortic stenosis
63
Q

What is vasomotor tone?

A

-Tonic contraction of the smooth muscles in vessels

64
Q

What is reactive hyperaemia?

A

-The effect of no blood supply causing massive vasodilation of BVs due to accumulation of vasodilator metabolites so that when bloodflow is restored it is at extremely high levels

65
Q

What determines central venous pressure?

A
  • The amount of blood in the veins
  • The CO
  • Gravity and muscle pumping
66
Q

What is starlings law? How is it affected in systolic HF?

A
  • States that the greater the EDV the greater the contractility of the heart the greater the SV
  • Venous congestion fills the heart to an extent that the stretch will be resisted and the contractility will decrease as the heart cannot pump properly -> SV decreases
67
Q

Why does the heart fill inadequately over approx 150bpm?

A

-Diastole is shortened and the heart doesnt fill properly and become inefficient

68
Q

What effect does a rise in central venous pressure have on CO in a healthy individual?

A

-Increases end diastolic volume, increases contractility

69
Q

What effect does a fall in arterial pressure have on CO in a healthy individual?

A
  • Increases SV due to decreased afterload

- Increase HR via baroreceptors

70
Q

What effect does a fall in TPR have on venous and arterial pressure?

A
  • Venous rises

- Arterial falls

71
Q

What effect does a rise in TPR have on venous and arterial pressure?

A
  • Fall in venous pressure

- Rise in arterial pressure

72
Q

What mechanisms occur in haemorrhage to try and increase pressure?

A
  • Autotransfusion

- Veno-constriction

73
Q

What determines the amplitude of a signal on an ecg?

A
  • How much of the muscle is depolarising,

- How directly towards the electrode the excitation is moving

74
Q

Why do the lungs have 2 blood supplies?

A
  • Bronchial circulation attached to systemic

- Pulmonary circulation to provide blood to alveoli for gas exchange

75
Q

How are the pulmonary vessels effected by gravity? How does this change during exercise?

A
  • Greater hydrostatic pressure in the lower part of the lungs causing distention of vessels
  • Vessels at the level of the heart are continually open
  • Vessels in the apex collapse dueing diastole due to lack of pressure
  • During exercise CO is increased causing slight increase in pulmonary arterial pressure due to increased volume -> apical capillaries remain open to and maintain V/Q ratio as O2 uptake increased
76
Q

Why is there minimal lymph produced in the lungs?

A

-Low hydrostatic pressure

77
Q

Give 2 causes of pulmonary oedema

A
  • Mitral valve stenosis

- Left ventricular failure

78
Q

What is myogenic autoregulation in the brain and kidney?

A
  • Increase in BP causes vasoconstriction to limit flow and decrease BP
  • Decreased BP causes vasodilation to increase flow and raise BP
79
Q

How do cerebral vessels react to changes in pCO2?

A
  • Hypercapnia causes vasodilation

- Hypocapnia causes vasoconstriction

80
Q

How is the heart adapted to ensure an adequate blood supplt to itself?

A
  • High capillary density
  • Continuous NO production to maintain high flow
  • High levels of metabolic hyperaemia to ensure flow meets demand
81
Q

How is skeletal muscle specialised to increase bloodflow during exercise?

A
  • At rest not all the capillaries are open meaning there is an allowance to increase bloodflow to the muscles by increasing capillary recruitment
  • Metabolic hyperaemia
82
Q

How to arteriovenous anastomoses help control body temp?

A

-Decreased temp causes vasoconstriction of AVAs diverting blood away from apical skin and vice verse

83
Q

Give some causes of AF

A
  • Alcohol
  • Ischaemic heart disease
  • Thyrotoxicosis
  • Hypertension
  • PE/Pneumonia
  • Rheumatic heart disease
84
Q

What does AF look like on ECG

A
  • Narrow complex tachycardia
  • Loss of P waves
  • Loss of isoelectric baseline
85
Q

What is heart failure? What is the difference between systolic and diastolic failure?

A
  • When the cardiac output is insufficient to maintain the bodys requirement due to defects in systole, diastole or both
  • Systolic failure is when the contraction of the heart is insufficient to eject an efficient ejection fraction
  • Daistolic failure is when the heart fails to relax fully and there is a reduced end diastolic volume, which in turn reduces the stroke volume
86
Q

Give the symptoms of left and right heart failure

A
  • Left = Pulmonary oedema, dyspnoea, orthopnoea, paroxysmal nocturnal dysponoea, fatigue, reduced exercise tolerance, wheeze (cardiac asthma)
  • Right = sacral, thigh and ankle oedema, hepatosplenomegaly, ascites, raised JVP, nausea
87
Q

What investigations would you undertake if you suspect hf?

A
  • Bloods -> FBCs, U+Es, BNP, TFTs, glucose, lipids
  • CXR -> Cardiothoracic ratio, alveolar oedema (bats wing), prominant upper pulmonary veins, pleural effusion
  • ECG -> AF, ischaemia, hypertrophy
  • Echo
88
Q

What is the difference between acute and chronic heart failure?

A
  • Acute is new onset or decompensation of chronic characterised by pulmonary/peripheral oedema with or without signs of peripheral hypoperfusion -> medical emergency
  • Chronic is stable heart failure which is developing slowly and arterial pressure being maintained.
89
Q

Describe the compensatory mechanisms which occur in heart failure

A
  • Starling effect dilates the heart to enhance contractility
  • Hypertrophy to increase contractility
  • RAS in order to increase blood volume to try increase CO
  • ANP/BNP to decrease fluid volume due to stretch of atria and ventricles
  • Sympathetic activation to increase contranctility and CO
90
Q

What happens in decompensation of heart failure to cause presentation?

A
  • Heart cannot sustain contractility and loss of function causes decreased CO
  • Dilation of the heart due to remodelling leads to valve reguritation
  • Hypertrophy leads to relative cardiac ischaemia as too much heart tissue to perfuse
  • RAS activation causes excessive oedema due to venous congestion
  • Excessive sympathetic stimulation causes increased afterload which heart cannot overcome causing further decrease in CO
91
Q

Give the common causes of RVF?

A
  • LVF
  • Cor pulmonale
  • Tricuspid or pulmonary valve disease
92
Q

What are the most common causes of LVF?

A
  • IHD
  • Idiopathic dilated cardiomyopathy
  • Systemic HTN
  • Mitral/aortic valve disease
93
Q

Give some secondary causes of HTN

A
  • Glomerulonephritis (increased H2O retention)
  • Hyperthyroid, cushings, pheochromocytoma, Conn’s
  • Coarctation of aorta
94
Q

What is ischaemic heart disease? Give some risk factors for IHD

A
  • A spectrum of disease which includes stable angina, unstable angina and MI
  • Non-modifable = age, male gender, family history
  • Modifable = smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle
95
Q

How do you tell the difference between a STEMI and a NSTEMI

A
  • STEMI -> MI with tall t waves ST elevation on ECG

- NSTEMI -> MI with ST depression and T wave inversion or normal

96
Q

What is the difference between unstable angina and NSTEMI? How can you differentiate the two clinically?

A
  • No myocyte necrosis in unstable angina

- Troponin levels will be raised in NSTEMI as released due to myocyte necrosis

97
Q

What are the most common causes of acute coronary syndrome?

A

-Plaque rupture, thrombosis and inflammation

98
Q

How does ischaemic heart disease differ from ACS?

A

-IHD includes stable angina

99
Q

What is the difference between stable and unstable angina?

A
  • Stable angina = chest pain only occurs on exertion and is relieved by rest of GTN spray
  • Unstable angina occurs at rest or with increasing frequency or severity
100
Q

What are the associated symptoms of an MI?

A

-Nausea, vomiting, dyspnoea, palpitations, sweating

101
Q

Give some differential diagnoses of an MI

A

-Angina, pericarditis, aortic dissection, PE

102
Q

How is MI induced bradycardia commonly treated? How does this work?

A
  • Atropine

- Anti-muscarinic to decrease parasympathetic activation

103
Q

What is angina pectoris?

A

-Chest pain caused by a reduction in bloodflow to the heart secondary to atheromatous plaque formation. Pain often felt on exertion due to inability to vasodilate narrowed vessels. This means bloodflow cannot be increased in times of myocardial O2 demand. Also on exertion heartrate rises and shortens diastole which reduces bloodflow to the already narrowed vessels

104
Q

Does the chest pain in unstable angina differ from than of an MI?

A

-No it is the same central tight chest pain which radiates but less intense in angina as only partial occlusion

105
Q

How do you make a diagnosis of angina if you are clinically unsure?

A

-Exerceise Stress ECG test -> stop when target heart rate reached, show signs of chest pain or ECG changes

106
Q

What is the preferred treatment for an MI?

A

-Percutaneous Coronary Intervention

107
Q

What is the pathophysiological difference between STEMI and NSTEMI?

A
  • STEMI is a persistant complete occlusion of a coronary vessel without collaterals
  • NSTEMI is caused by brief occlusion or in an area with collaterals
108
Q

Which creatine kinase isotype is the cardiac kind?

A

-CK-MB

109
Q

Which MI markers are the most specific for an MI?

A

-Troponins

110
Q

Describe the ECG changes during a STEMI

A
  • Hyperacute T waves
  • ST Elevation
  • Prominent Q wave
  • T wave inversion
  • Pathological Q waves 4lyf
111
Q

Describe which leads will show which MIs

A
  • Inferior (RCA) by II, III, AVF
  • Anterior (LAD) by I, V2,3,4
  • Lateral (Circumflex) by I, AVL, V5, V6

PPE (15 decks)

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