CVS Answers
1) State the anatomical location of the heart
Middle mediastinum
2) Where is the transverse sinus of the heart located?
Posterior to the ascending aorta and pulmonary trunk as they exit the heart
3) Describe the layers of the pericardium from outside to inside, including the cavity
Fibrous pericardium  parietal pericardium  visceral pericardium
Serous pericardium
The pericardial cavity lies between the parietal and visceral layers of the serous pericardium
Remember that –itis means inflammation, so pericarditis is inflammation of the pericardium!
4) What is meant by cardiac tamponade?
Cardiac tamponade is a type of pericardial effusion. Fluid from pericardial capillaries leaks into the
pericardial cavity and compresses the heart, which can’t expand fully. This leads to congestive heart failure
– the heart is being compressed so much that it can’t pump blood out at the same time that it receives it.
You do need to learn the coronary arteries & veins & also the regions which they supply/drain
5) Do you understand the difference between systole & diastole?
Remember s for systole & squeezing – the heart is squeezing & ejecting blood during systole. The aortic
& pulmonary valves are closed during diastole – the heart is relaxed & filling
Systole = 280ms
Diastole = 700ms
6) Which property of arteries allows them to recoil?
Elastic tunica media & intima
7) Describe the structure of arteries from outside to inside
Tunica adventitia  tunica media  tunica intima (subendothelium & endothelium)
8) What is an end artery?
End artery = a terminal artery supplying all of the blood to a region of an organ without significant
9) What are venae comitantes?
Paired veins which accompany an artery. Blood pulsing through the artery enhances venous return. The
3 vessels are wrapped in 1 sheath.
10) The heart contracts isovolumetrically. What is meant by this?
Pressure in the ventricles increases, but the volume inside the ventricle stays the same.
11) What is heard during the 1st, 2nd and sometimes 3rd heart sounds?
1st (sounds like lup) – both atrio-ventricular valves close
2nd (sounds like dup) – the aortic & pulmonary valves close. This sound is shorter, higher in frequency
and lower in intensity than the 1st heart sounds
3rd – may be heard in early diastole after the 2nd sound. The heart will sound like the syllables of the
word “Kentucky”! Normal in athletes, but may also indicate heart failure.
12) What is a heart murmur?
A heart murmur is an audible disturbance in blood flow. This may be due to a narrowed (stenotic) valve
or backflow through a leaky (incompetent) valve
13) Give the equation for cardiac output
Cardiac output = stroke voume x heart rate
CO = SV x HR
Go to the LUSUMA embryology talk! Our housemate’s doing it and it will be much better than these
questions 
14) Label the primordial heart
15) Match the atria on the left with the embryological parts which make them up on the right

Left atrium



Right atrium


Develops from most of primitive atrium
Develops from a small portion of primitive
atrium
Absorbs proximal part of pulmonary veins
Sinus venosus
16) Arteries of the body begin as bilaterally symmetrical arched vessels. These remodel to create the
major arteries of a newborn. Be aware that the 5th arch isn’t present in humans
Which arch forms the arch of the aorta & the proximal part of the right subclavian artery? 4th
Which arch forms the right pulmonary artery and the left pulmonary artery? 6 th
17) The left recurrent laryngeal nerve loops around the arch of the aorta. Why is this clinically
significant?
Aneurysms in the aorta which compress the left recurrent laryngeal nerve may present with a hoarse
voice. This is because the recurrent laryngeal nerve also supplies the pharynx.
18) Briefly describe atrial septation
 Septum primum grows downwards towards fused dorso-ventral endocardial cushions
 Ostium primum is the hole present in the septum primum before it fuses with endocardial
cushions
 Ostium secundum appears in the septum primum
 Septum secundum grows
 Resulting hole through the septum is called the foramen ovale
19) Briefly describe ventricular septation
 Ventricular septum has 2 components: muscular & membranous
 Muscular portion grows upwards towards the fused endocardial cushions
 Membranous portion is an extension of the endocardial cushions, which fills the gap
20) How is foetal circulation different to that
of a newborn?
Lungs are non-functional in a foetus. Instead
it receives oxygenated blood from its mother
via the placental umbilical vein, which enters
the right atrium. Blood bypasses the lungs and
returns to the placenta via the umbilical
arteries. The ductus arteriosus allows blood
from the pulmonary trunk to enter the aorta.
When the first breath is taken, respiration
begins and pressure in the left atrium
increases. This causes the foramen ovale to
closes.Be aware that umbilical arteries and veins are named opposite to how you’d expect.
21) What are the names of the remnants of the following embryological structures when in an adult?
Foramen ovale – fossa ovalis (atrial septal defect)
Ductus arteriosus – ligamentum arteriosum
Ductus venosus – ligamentum vinosum
Umbilical vein – ligamentum teres of the liver
22) How do left to right heart shunts and right to left heart shunts differ?
Left to right – requires a hole between the left and right side. Results in an acyanotic defect (cyan =
blue)
Right to left - requires a hole between the left and right side, but also a distal obstruction. Results in a
cyanotic defect, so deoxygenated blood contaminates the arterial system
23) Match the following congenital defects with their descriptions:

Patent ductus arteriosus

Pulmonary atresia

Aortic lumen is narrow in the region of the
ligamentum arteriosum. This increases the
afterload on the left ventricle and can lead
to left ventricular hypertrophy

Blood flows from the higher pressure aorta
into the lower pressure pulmonary artery.
This can overload the pulmonary
circulation

Blood cannot leave the right ventricle
because the pulmonary valve is absent.
Blood moves from the right to the left
atrium, into the aorta and though the
ductus arteriosus into the lungs

4 factors: ventricular septal defect,
overriding aorta, pulmonary stenosis &
right ventricular hypertrophy, leading to a
cyanotic defect
(atresia means it’s not there)

Coarctation of the aorta
(coarctation means narrowing)

Tetralogy of Fallot
24) Draw and label the ventricular action potential
25) Draw and label the SAN action potential
26) Explain how Ca2= causes cardiac muscle contraction
 Ca2+ binds to calmodulin
 Calmodulin activates myosin light chain kinase
 Myosin light chain kinase phosphorylates myosin, allowing it to interact with actin
 Filament theory from ToB
27) Give 3 examples of the effects of increased sympathetic activity on the CVS
 Peripheral vasoconstriction (α1 adrenoceptors) to direct blood flow to major organs & muscles
 ↑HR
 ↑Force of contraction of heart
28) Define flow and velocity and describe the two types of flow
F=volume of liquid passing a given point per unit time, determined by resistance
V=rate of movement of fluid particles along a tube, varies is radius changes. Laminar flow has high
velocity in middle and stationary plasma at edges. Turbulent flow when above critical velocity so fluid
tumbles over each other causing bruit sound
29) Fill in blanks: resistance increases as viscosity …increases… or radius …decreases…
30) Explain how arteries can adapt to prevent turbulent flow
They have distensible walls so the radius can increase therefore reducing the velocity and reducing the
resistance before it reaches the critical velocity
31) Why is there a high pressure in arteries?
Need pressure to drive blood through small arterioles
32) Draw a graph of pressure against to show a distensible and rigid tube
33) Define total peripheral resistance
Integrated measure of body’s need for blood/combined activity of ALL vessels. TPR is proportional to
1/body’s need
34) At what stage of the cardiac cycle does blood flow into the arteries?
Systole-pulsatile flow
35) What is pulse pressure and therefore if a patient has a blood pressure of 130/85mmHg, what is their
pulse pressure?
Difference between systolic and diastolic pressures to show load on heart. 130-85=45mmHg
36) What would be the average pressure of this patient?
2/3 Diastolic + 1/3 systolic= 85*2/3 + 130/3= 100mmHg
37) How is blood supply to tissues autoregulated?
Balance between flow and metabolism because increased metabolism means increased vasodilator
metabolites so more blood flow.
38) What is central venous pressure and what does it show clinically?
Pressure in RA but same as pressure in great veins (IVC and pulmonary)
39) What happens to arterial and venous pressures and therefore cardiac output when you eat a meal?
Digestive system needs more blood so vasodilates causing decreased TPR. Therefore decreased ap,
increased vp so increased CO
40) How do IV fluids increase blood pressure and where would adrenaline enter this pathway?
Fluids increase vp so increase end diastolic vol so increase FOC so increase stroke vol so increase CO so
increase bp. Adrenaline increases FOC
41) Give equations for CO and BP
CO=SV x HR
BP=COxTPR
42) To increase ventricular filling would you increase arterial pressure or venous pressure?
Venous as ventricles only connected to veins in diastole (ventricular compliance curve)
43) Define Starling’s Law and draw curve
More the heart fills, the more it is stretched so the more it contracts. If stretched too far (heart failure) the
fibres cross over less so less cross-bridges form so reduced contractility and reduced stroke vol.
44) When we exercise, venous pressure increases due to muscle contraction. What protective
mechanism does the body use to stop this overfilling the heart and causing pulmonary oedema?
Increase HR just before exercise so SV kept stable when vp increases
45) How does our body stop postural hypotension from happening?
Fall in arterial pressure causes increase in CO and increased TPR to skin and gut so more blood to brain.
46) What is auto-tranfusion?
Body’s response to haemorrhage by bringing fluid from ECF into blood to increase blood vol.
47) What is the total CO of an average person?
5L/min
48) Give some adaptations of pulmonary circulation
High oxygen and CO2 transport capacity down conc gdt, lots of capillaries for large SA, short
diffusion path, hypoxic vasoconstriction so if low oxygen levels the gas exchange is optimised.
49) Describe tissue fluid formation using Starling’s forces
Hydrostatic pressure of blood in capillary pushes fluid out at arterial end, oncotic pressure from large plasma
proteins draws fluid into capillary at venous end.
50) Why does a patient with pulmonary oedema sit up and how is it treated?
Fluid sits at bottom so less pressure on lungs. Diuretics and treat cause
51) Give some adaptations of cerebral circulation
High oxygen extraction, high basal flow rate, reduced diffusion distance, lots of capillaries, anastomoses,
regulates other circulations by myogenic and metabolic regulation
52) Hypercapnia causes vaso…dilation.. Hypocapnia causes vaso…constriction..
53) Explain basis of ECG-why and what can we see
Myocardium is large mass of muscle undergoing electrical changes detected as changing membrane
potentials by electrodes outside the body so see combined effect of depol, repol and their spread over the
heart
54) List the 8 things to look at when interpreting an ECG
Rate, rhythm, axis, p wave, p-r interval, qrs complex, qt interval, t wave
55) Explain what is happening in heart at p wave, qrs and t wave
P: atrial depol and AVN delay-small bump up as little depol to electrode. Q: small depol out of septum. R:
Large depol to electrode during ventricular depol. S: depol up from base. T: ventricular repol away from
electrode so up wave
56) Draw where 6 limb leads view heart from
57) Where are 4 limb cables and 6 chest cables placed on
body?
Anterior wrist and front of ankles (start on your left and go
clockwise)
V1: RHS 4th intercostal space
V2: LHS 4th ICS
V4: Mid-clavicular line 5th ICS
V6: axillary 5th ICSV3: between V4 and V2
V5: between V6 and V4
58) Name four types of rhythmic disturbances of the heart
Atrial flutter, atrial fibrillation, ventricular fibrillation, ventricular tachycardia
59) Give two causes of these arrhythmias
Ectopic pacemaker activity-pacemaker in damaged myocardium is activates by ischaemia. Triggered
activity-premature depolarisation after an action potential as high intracellular Ca2+. Re-entry loopdamaged area causes conduction delay so accessory pathway set up so potential can spread to
ventricle.
60) Name the four classes of anti-arrhythmic drugs with an example of each
Block voltage-gated Na+ channels-lidocaine. B-adrenoreceptor antagonist-propanolol. Block K+
channels-amiodarone. Block Ca2+ channels-verapamil.
61) Explain the mechanism of action of lidocaine
Blocks open/inactive channels but rapidly dissociates in time for next AP, therefore, stops an extra AP
within that time
62) Why would you give propranolol after an MI?
An MI causes sympathetic stimulation to increase so B-blockers prevent this so ventricular tachycardia
doesn’t occur.
63) How does a Ca2+ channel blocker work?
Decreases upstroke of pacemaker AP at SAN, decreases AVN conduction, negative inotropy as less Ca2+
into myocytes and causes vasodilation of blood vessels.
64) Give two conditions in which there’s an increased risk of thrombus formation
Atrial fibrillation, acute MI, prosthetic heart valves
65) Define hypertension and explain two ways of treating it
Sustained blood pressure of >140/90
Want to reduce blood volume to reduce CO, reduce TPR or reduce CO directly:
Diuretics reduce water retention by kidneys to reduce vol and CO. ACE-inhibitors do the same and also
reduce TPR. B-blockers reduce CO. Ca2+ channel blockers and a1-adrenoceptor antagonists cause
vasodilation so reduce TPR.
66) Why does a patient with angina experience chest pain on exertion?
Coronary arteries fill in diastole. Diastole is shortened in exercise so gets less O2 to heart anyway but a
person with angina has narrowed coronary arteries due to atheromas therefore even less O2-> pain.
67) What is the primary action of GTN spray?
Venodilation to reduce preload to heart so fills less therefore reduced force of contraction and less O2
demand.
68) Define heart failure
Chronic failure of the heart to maintain adequate circulation for body’s requirements despite adequate
filling pressure
69) Would right or left heart failure present with shortness of breath and pulmonary crackles?
Left as blood backs up to lungs and causes pulmonary oedema
70) What is systolic dysfunction and what are some consequences of it?
Inability to contract. Increased LV capacity and reduced CO, thinning of myocardial wall
71) How do neuro-hormonal systems respond to heart failure?
Increase in sympathetic nervous system to increase CO therefore increase BP. RAAS activation to cause
H2O retention and increase TPR therefore increase BP and CO. Prostaglandins and endothelin increase
effects of RAAS. Natriuretic hormones are promoted by bradykinin and inhibit RAAS.
72) Give two ways to treat heart failure by increasing inotropy to increase CO
Cardiac glycosides-digoxin-block Na-KATPase so increased intracellular Na+ meaning NCX reverses and
more Ca2+ in cell for CICR so increased FOC->increased CO.
B1-agonists
73) How else could you treat heart failure?
Reduce workload using B-blocker, ACE-inhibitor, diuretics, Ca2+ channel blockers
74) A 45 year female presents to A and E with chest pain. Give 5 differential diagnoses
Angina, MI, burst aortic aneurysm, pulmonary embolism, pneumothorax, acid reflux, rib fracture, aortic
dissection
75) What are the modifiable risk factors for ischaemic heart disease?
Hyperlipidaemia, smoking, hypertension, diabetes
76) What is chronic stable angina?
Stable plaque in coronary artery causing narrowing but no thrombus formation as plaque has thick cap
so unlikely to rupture. Blood flow sufficient to meet needs at rest but ischaemia when exercise.
77) Describe an exercise stress test
Patient runs/walks on treadmill until they have chest pain, reach target HR or see ECG changes
78) Complete table
Degree of
occlusion
ECG
changes
Presence of
biomarkers
Treatment
Stable
Minimal
Unstable
Partial
Non-STEMI
Partial
STEMI
Complete
ST
depression
ST depression
and
T
inversion
No
ST depression
and T inversion
ST elevation
and
T
inversion
Yes
No
GTN,
Bblockers,
statins,
aspirin
Yes
Anti-thrombotic
drugs,
angiography,
nitrates,
Bblockers
79) If an ECG has ST elevation in views V1-V4, which coronary artery is occluded?
LAD
Emergency
PCI
or
fibrinolytic
drugs
80) What does this ECG show?
Atrial fibrillation as lack of p waves, irregularly irregular
81) What does this ECG show?
Inferior STEMI-RCA occlusion due to ST elevations in II, III, aVF and pathological Q wave in III and
aVF
82) Shock is a caused by poor perfusion throughout the body due to a fall in arterial pressure. What
conditions can cause poor regional perfusion?
Peripheral arterial disease from diabetes, peripheral venous disease from varicose veins or DVT
83) Name three types of circulatory shock with examples
Cardiogenic-MI so heart fails to maintain CO. Mechanical shock-cardiac tamponade so heart fills less.
Hypovolaemic-haemorrhage
84) What is disruptive shock?
Profound peripheral vasodilation so decreased TPR. Toxic shock from bacteria or anaphylactic shock
from allergic reaction releasing histamine to cause vasodilation, reduced TPR and reduced BP and
bronchoconstriction.