1
Q
What are the 3 layers of the heart’s wall?
A
1) epicardium: outer layer of squamous epithelial cells overlying connective tissue
2) myocardium: muscle
3) endocardium: innermost layer- endothelial tissue with small blood vessels and bundles of smooth muscle
2
Q
What makes up the pericardium that surrounds the heart?
A
fibrous pericardium + serous pericardium.
3
Q
What is the fibrous pericardium?
A
- composed of tough, white, fibrous tissue, fits loosely around the heart, protecting it.
- attaches to the great vessels, diaphragm, and sternum
4
Q
What is the serous pericardium?
A
the thin, smooth, inner portion, has two layers:
• the parietal layer, which lines the inside of the fibrous pericardium
• the visceral layer, which adheres to the surface of the heart.
5
Q
Where is the pericardial space?
A
It separates the visceral and parietal layers of the pericardium and contains 10 - 20 ml of thin, clear pericardial fluid that lubricates the two surfaces and cushions the heart
6
Q
The right atria receives deoxygenated blood from ?
A
blood returning from the body through the inferior and superior vena cavae and from the heart through the coronary sinus.
7
Q
The left atria receives oxygenated blood from ?
A
oxygenated blood from the lungs through the four pulmonary veins
8
Q
No of leaflets / cusps in mitral valve vs tricuspid?
A
Mitral: 2 vs tricuspid 3
9
Q
What stops the atrioventricular valve from bulging backward into the atria during ventricular contraction?
A
Chordae tendinae that anchor to the papillary muscles in the heart wall
10
Q
Why do the aortic and pulmonary valves not require chordae tendinae?
A
They open due to pressure within the ventricles and close due to the back pressure of blood in the pulmonary arteries and aorta, which pushes the cusps closed.
11
Q
When does coronary artery perfusion happen and why?
A
During diastole
- During systole, when aortic valve is open, the coronary ostium is partially covered. During diastole, aortic valve is closed and the coronary ostium is open, enabling blood to fill the coronary arteries.
12
Q
What is the opening through which blood enters from aorta to coronary arteries ?
A
The coronary ostium - located near the aortic valve
13
Q
How could tachycardia lead to less coronary perfusion
A
- With a shortened diastole -> less blood flows through the ostium into the coronary arteries.
2, contraction of the ventricles squeezes the arteries and lessens blood flow through them.
14
Q
What dos the right coronary artery supply?
A
- right atrium and ventricl, and part of the inferior and posterior surfaces of the left ventricle.
-In about 50%, sinoatrial (SA) node too
- bundle of His + the AV node
15
Q
What does the left anterior descending artery supply?
A
- anterior wall of LV
- inter ventricular septum
- the right bundle branch
- the left anterior fasciculus of the left bundle branch.
- it’s branches—the septal perforators and the diagonal arteries—help supply blood to the walls of both ventricles
16
Q
What does the left anterior descending artery supply?
A
- anterior wall of LV
- inter ventricular septum
- the right bundle branch
- the left anterior fasciculus of the left bundle branch.
- it’s branches—the septal perforators and the diagonal arteries—help supply blood to the walls of both ventricles
17
Q
What does the left circumflex artery supply?
A
- lateral walls of the LV
- LA
- in 50% the SA node
- the left posterior fasciculus of the left bundle branch
18
Q
where does deoxygenated blood from coronary veins drain into?
A
cardiac veins become the coronary sinus which drains blood into the right atrium
19
Q
what happens during diastole?
A
ventricles relax, atria contract
20
Q
what are the 5 events of the cardiac cycle?
A
- Isovolumetric ventricular contraction
- Ventricular ejection
- Isovolumetric relaxation
- Ventricular filling
- Atrial systole
21
Q
what happens during isovolumetric ventricular contraction?
A
- ventricular contract in response to ventricular depolarisation
- all valves are closed (rise in pressure within the ventricles leads to closure of the mitral and tricuspid valves, aortic and pulmonary valves remain closed)
22
Q
what happens during ventricular ejection?
A
when ventricular pressure exceeds aortic and pulmonary arterial pressure -> the aortic and pulmonary valves open and ventricles eject blood
23
Q
what happens during isometric relaxation?
A
- ventricular pressure falls below that of aorta and pulmonary artery
-> aortic and pulmonary valves close - all valves closed during this phase
- atrial diastole occurs as blood fills the atria
24
Q
what happens during ventricular filling?
A
- atrial pressure exceeds ventricular pressure
- blood flows passively into ventricles (70% of ventricular filling occurs during this phase)
25
what happens during atrial systole?
atrial systole (coincides with late ventricular diastole), supplies the ventricles with the remaining 30% of cardiac output
**certain arrhythmias e.g. AF can cause loss of atrial systole and thus drop in cardiac output
26
how may fast AF reduce cardiac output?
- lack of atrial systole/ atrial kick (30% of cardiac output generated by this)
- tachycardia causes shortened diastole-> less time for ventricles to fill -> less cardiac output
27
Cardiac output equation?
Heart rate x Stroke volume
28
what is cardiac output?
the amount of blood the heart pumps in 1 minute
29
what is stroke volume?
the amount of blood ejected with each ventricular contraction
30
what is normal cardiac output?
4-8L/min, depending on body size
31
what factors affect stroke volume?
preload, afterload and myocardial contractility
32
what is preload?
determined by the pressure and amount of blood remaining in the LV at end diastole
*according to Starling's law, the more the heart muscles stretch during diastole, the more forcefully they contract during systole
33
what is afterload?
the amount of pressure the left ventricle must generate to overcome the higher pressure in the aorta to pump blood into the circulation.
34
what is myocardial contractility and what affects it?
- the inherent ability of the myocardium to contract
- depending on how much the muscles fibres are stretched at end diastole (influenced by preload)
- overstretching/ understretching alters contractility (ie. rubber band concept)
35
what nerves supply the heart?
autonomic nervous system- sympathetic (adrenaline, noradrenaline and parasympathetic (vagus nerve)
36
how does vagus nerve help to slow heart rate?
vagus nerve is stimulated by baroreceptors in the aorta and internal carotid arteries
stretching of baroreceptors e.g. hypertension/ applying pressure to carotid artery like carotid massage can help to stimulate vagus nerve
37
generation and transmission of electrical impulses depend on 4 characteristics of cardiac cells
what are these 4 things?
- automaticity: ability to spontaneously initiate an impulse-> pacemaker cells
- excitability: ion shifts across cell membrane. how well a cell responds to electrical stimulus
- conductivity: ability of a cell to transmit an electrical impulse to another cardiac cell
- contractility: how well the cell contracts after receiving a stimulus
38
what makes up the cardiac conduction system?
impulse from SA node -> travels through internodal tracts and Bachmann's bundle -> AV node -> bundle of His -> bundle branches -> Purkinje fibres
38
what are the phases of depolarisation and repolarisation?
phase 0 - cell receive impulse and is depolarized
phase 1: early rapid repolarization
phase 2: plateau phase, slow repolarization
phase 3: rapid repolarisation
phase 4: resting phase
39
where is the SA node located?
upper right corner of the right atrium, where the SVC joins
40
why does the cardiac conduction system only flow forward like from SA node to AV node etc?
because it starts from SA node which has the pacemaker cells -> then follows the conduction system through the heart
usually can't flow backward because the cells can't respond to a stimulus immediately after depolarization
41
where is the AV node located?
the interior right atrium near the ostium of the coronary sinus
42
what happens at the SA node?
pacemaker cells generate impulses ~60-100 bpm
43
does AV node have pacemaker cells?
no
but the tissue surrounding it (the junctional tissue) contains pacemaker cells that can fire at ~40-60 bpm
44
what happens at the AV node?
main function is to delay impulses by 0.04 seconds to keep the ventricles from contracting too quickly -> allows the ventricles to complete their filling phase as the atria contract
this delay allows cardiac muscle to stretch to its fullest for peak cardiac output
45
where are there pacemaker cells in the heart?
- SA node
- junctional tissue surrounding AV node*
- Purkinje fibres*
*usually remain dormant unless they are not receiving impulses from above ie. when SA node damaged post MI
46
what is an escape rhythm?
a compensatory beat generated by a lower pacemaker site (not SA node)
47
how does the sympathetic nervous system affect the heart?
increases heart rate, automaticity, AV conduction and contractility through release of noradrenaline and adrenaline
48
how does parasympathetic nervous system affect the heart?
vagus nerve stimulation reduces HR and AV conduction through release of acetylcholine
49
what are the normal pressure waveforms seen along the path of an advancing swan ganz catheter
50
How to see if Swan Ganz catheter is in in the true wedge position?
1. atrial tracing (reflecting left atrial pressure) will be seen
2. if catheter is withdrawn, MAP should rise from wedge pressure (reflecting physiologic gradient between mean PA and mean wedge pressure)
3. gentle aspiration of blood from distal port should reveal highly oxygenated blood if catheter is truly wedged
4. in cath lab, Fluoro can be used to determine catheter is in distal pulmonary arteriole
51
what does pulmonary capillary wedge pressure signify?
- pressure transducer is measuring pressure distally in the pulmonary arterioles (as balloon is shielding tip from pressure in the PA)
- this pressure approximates left atrial pressure
- when mitral valve is open at end diastole, LVEDP is measured
- hence PAWP can be used to approximate LV preload
52
when is PAWP not able to approximate LVEDP?
if there is obstruction between catheter tip and LV
e.g. mitral stenosis and pulmonary vein stenosis
53
role of right heart catheterisation in pulmonary hypertension?
- for diagnosis and severity of pulmonary arterial hypertension
- used to assess for reversible PH in patients with post capillary and combined pre-post capillary PH. -> impt for those undergoing heart transplantation and valvular interventions
- in PAH, used to determine if patients are eligible for CCB
54
how does right heart cath measurements affect treatment options for patients with pulmonary arterial hypertension?
- reductions in mean PA pressures (with inhaled NO/ adenosine/ epoprostenol) by >/=10mmHg to eligibility for CCB
55
absolute contraindications of placement of Swan Ganz catheter?
- right sided endocarditis
- mechanical tricuspid or pulmonary valve prosthesis
- presence of thrombus or tumour in right sided heart chamber
56
relative contraindications to placement of Swan Ganz catheter
- coagulopathy
- recent implantation of a permanent pacemaker or ICD
- LBBB
- bioprosthetic tricuspid or pulmonary valve
57
Swan Ganz catheter tracing showing equalisation of diastolic pressures across all chambers?
pericardial tamponade
58
how can LGE imaging (cMR) be used to determine the likelihood of recovery of function with revascularization or medical therapy?
segments of myocardium with >50% transmural scar are less likely to recover/ improve fn with revascularization
59
which cardiovascular medications are associated with drug induced lupus erythematosus?
procainamide, hydralazine, diltiazem, quinidine, methyldopa
probable: BB, captopril, hydrochlorothiazide, amiodarone, ticlopidine
60
common CVD manifestations of HIV/AIDs?
- pericardial effusion /tamponade
- dilated CMP
- severe systolic dysfunction
- myocarditis
- marantic (thrombotic) or infectious endocarditis
- cardiac tumours (kaposi's, lymphoma)
- pulmonary arterial hypertension
- sudden cardiac death
- CAD, MI, HFpEF/rEF
61
when to assess cardiac function in patients receiving anthracycline therapy for cancer?
assess before therapy
then at 3, 6 and 9 months during tx, + 12 and 18 months after
if EF decreases to <40%, should discontinue anthracycline
62
in pt who previously received anthracycline therapy, how long to monitor cardiac function for?
lifelong cardiac monitoring
- LVEF assessment every 1-5 years
(freq depends on total dose, or if received radiation therapy in addition)
63
triad of findings suggestive of RV infarction?
Hypotension, distended neck veins, clear lungs
64
most common causes of syncope in young pts?
- most commonly neurally mediated e.g. vasovagal, reflex
less common:
conversion reactions
primary arrhythmic causes
obstructive structural heart disease
myocardial dysfunction
65
what are the major risk factors for the development of contrast nephropathy?
preexisting renal disease + Diabetes
66
most common secondary causes of hyperlipidaemia?
- hypothyroidism
- overt proteinuria (CKD, nephrotic syndrome)
- excessive ETOH intake
- uncontrolled DM
- obstructive liver disease
- weight gain, obesity
- pregnancy
- drugs e.g. corticosteroids, anabolic steroids, progestins
67
when to start statins?
- established ASCVD (ACS, stroke, stable/unstable angina, coronary or other arterial revasc, PAD)
- primary severe hypercholesterolaemia (LDL>/=190 ie 4.9, or FH)
- DM (aim <1.8)
68
causes of secondary hypertension?/
- Renal artery stenosis
- Renal parenchymal disease
- primary hyperaldosteronism
- phaeochromocytoma
- Cushing's disease
- HyperPTH
- aortic coarctation
- Sleep apnoea
69
what will constitute a patient as having a hypertensive emergency?
- hypertensive encephalopathy, ICH
- MI, pulmonary oedema
- dissection aortic aneurysm
- preeclampsia
70
most common cause of sudden cardiac death in young athletes?
1 HOCM
2 anomalous origin of a coronary artery
others: long QT, Brugada, CPVT, ARVD/C, PE
71
side effects of amiodarone?
- toxicity to lung, thyroid, liver
- worsen sinus Bradycardia
- photosensitivity, bluish discolouration of skin
- tremor
- peripheral neuropathy
- ocular deposits, ocular neuropathy
72
monitoring while on amiodarone?
- LFT, TFT
- CXR, Pulmonary function tests
73
what GDMT can be used in patients with HFrEF if they have renal failure and are unable to tolerate ACEi/ARB/ ARNIs or bc of angioedema?
Hydralazine, ISDN
74
when to consider ICD post MI?
if LVEF remains < 30-35% despite optimal medical tx or revascularisation (if life expectancy >1 year)
- for primary prevention of SCD
75
treatment duration in provoked PE with transient risk factors?
3 months
(can be extended up to 6-12 months)
76
treatment duration in patients with unprovoked PE or in the presence of ongoing risk factors e.g. active malignancy, immobility or inherited prothrombotic condition?
consider indefinite therapy
77
main echo criteria for severe mitral stenosis?
- mitral valve area <1.5cm2
- diastolic pressure half time of >/=150ms
- PASP >50mmHg
78
What arrhythmias may be caused by sleep apnoea
Ventricular pauses up to 15s
second-degree atrioventricular (AV) block
PVCs
nonsustained VT
Without significant intrinsic sinus or AV nodal disease
79
Findings suggestive of a hemodynamically significant coarctation
- small diameter (<10 mm or <50% of reference normal descending aorta at the diaphragm)
- presence of collateral blood vessels,
- gradient across the coarctation of >20 to 30 mm Hg.
Cardiology 101
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