CVS anat, physio, patho Flashcards
(139 cards)
1
Q
What is the significance of the transverse pericardial sinus
A
Separates aorta & SVC
1
Q
What are 3 features found in the right atrium
A
SA node
AV node
Fossa ovalis
1
Q
What is the function of Fossa ovalis
A
Opened in foetus -> allows blood flow from RA to LA to bypass fluid filled lungs
1
Q
Where is the AV node found?
A
RA, above coronary sinus opening; interatrial septum
1
Q
Where is the SA node found?
A
RA, upper end of crista terminalis
2
Q
What is the function of papillary muscle
A
Attached to chordae tendinae -> prevent regurgitation
2
Q
How is the pulmonary valve kept close
A
Blood back flow fills cusps causing them to meet and fuse
2
Q
Name 5 features found in the right ventricle
A
Trabecular tendinae
Papillary muscles
Septomarginal trebaculae (moderator band)
Tricuspid valve
Pulmonary valve
3
Q
Where is the PV auscultated
A
2nd IC space, parasternal, left
3
Q
Where is the AV auscultated
A
2nd IC space, parasternal, right
3
Q
Where do the LCA and RCA originate from
A
L/R aortic sinus
3
Q
Explain how cardiac referred pain comes about
A
O2 deficiency & metabolic products stimulate pain nerve endings in myocardium
Heart supplied by sympathetic trunk T1-T4
Visceral afferent pain fibres accompany sympathetic fibres referred to T1-T4 region
Skin afferent pain fibres enter same T1-T4 ganglion
Pain is perceived by brain coming from dermatomes
3
Q
Where is the MV auscultated
A
5th IC space, mid-clavicular line, left
3
Q
Where is the TV auscultated
A
5th IC space , parasternal, left
3
Q
Describe the arterial blood supply of the heart
A
RCA (SA/AV nodes, RA, RV)
- marginal branch (anterior surface)
- PDA (posterior 1/3 IV septum)
LCA
- LAD (RV, LV, anterior 2/3 IV septum)
- LCX (LA, LV)
3
Q
How would tachycardia affect filling of coronary arteries
A
Decrease in filling time
3
Q
What is coronary dominance
A
Coronary artery that supplies PDA
3
Q
When are the left coronary arteries filled
A
During diastole only
4
Q
Name the structures found in superior mediastinum
A
Brachiocephalic vein
Oesophagus
Azygos vein
Trachea
Thoracic duct
Nerves (phrenic, vagus)
4
Q
Describe venous drainage of the heart
A
Great cardiac vein (runs w LAD), Middle cardiac vein (runs w PDA), Small cardiac vein (runs w marginal)
Drain into coronary sinus
Drain into right atrium
4
Q
Which veins directly drain into right atrium
A
Anterior cardiac veins
4
Q
What are the structures found at the sternal angle
A
Aortic arch
Rib 2
Trachea
Pulmonary trunk
Ligament arteriosus
Azygos vein
Nerves
Thoracic duct
4
Q
What structure is found in the anterior mediastinum
A
Thymus
5
Q
What structures are found in the middle mediastinum
A
Heart & great vessels
6
Which structures are found in posterior mediastinum
Sympathetic chain
Oesophagus
Descending thoracic aorta
Azygos vein
6
How does the aorta branch out after leaving the heart
Aortic arch
- Left carotid/subclavian artery
- Right brachiocephalic -> Right carotid/subclavian
- Descending aorta
6
What is the function of ductus arteriosus
Allows blood flow from pul. trunk to aorta to bypass fluid filled lungs
6
Describe venous drainage into the right atrium
Internal jugular/subclavian veins
Brachiocephalic
SVC
RA
6
How do signals flow in the conducting system
SA node -> AV node -> Bundle of His -> L/R branches -> Purkinje fibres
6
What is the primary pacemaker of the heart
SA node
6
What are the backup pacemakers of the heart
AV node and AV bundle
6
What is the purpose of AV nodal delay
Allows for complete ventricular filling before contraction
7
What allows for AV nodal delay
Fibrous rings separating atria and ventricles
7
What are the phases of ventricular depolarisation
0 - Depolarisation, Na+ (in)
1 - Initial repolarization, K+ (out)
2 - Plateau, Ca2+(in), K+ (out)
3 - Repolarization, K+ (out)
4 - Resting membrane potential
7
What is starling's law
Increased ventricular volume -> Increased stroke volume until a limit
7
Define contractility
Strength of contraction for given diastolic V
8
How is contractility regulated
Pain/chemo/baroreceptors/H+ => Vasomotor center in medulla => Autonomic Nervous System => Heart
Catecholamines/Thyroxine/Temp => Heart
8
How does parasympathetic activity affect the heart
More positive resting potential & increase depolarisation duration -> Decrease SAN firing freq -> Decrease HR
8
How does sympathetic activity affect the heart
More negative resting potential & decrease depolarisation duration -> Increase SAN firing freq -> Increase HR
8
Describe the different components of the PQRST wave
P - Atrial depolarisation
QRS - Ventricular depolarisation
Q - AV bundle
R - L/R bundles
S - Purkinje fibres & ventricles
T - Ventricular repolarisation
8
What is RR interval
Heart rhythm
8
How is HR calculated based of the ECG
60/RR
8
What is PR interval
AV nodal delay time
8
What is the abnormal range of PR interval values and what can cause it
>0.2s
Heart block
9
What is QRS complex
Ventricular depolarisation time
9
What is QT interval
Time taken for ventricular depolarisation & repolarisation
10
What does tall QRS-complex suggests
Ventricular hypertrophy
10
What does a tall T-wave suggests
Hyperkalaemia
11
What does ST elevation suggests
Myocardial infarction
11
What does ST depression suggests
Myocardial ischemia
12
What are the leads facing the anteroseptal part of the heart
V1, V2, V3, V4
12
Which coronary artery supplies the anteroseptal part of the heart
LAD
12
What are the leads facing the anterolateral part of the heart
I, aVL, V5, V6
13
Which coronary artery supplies the anterolateral part of the heart
LCX
13
What are the leads facing the inferior part of the heart
II, III, aVF
13
Which coronary artery supplies the inferior part of the heart
RCA
13
What are the leads reciprocal to the posterior part of the heart
V1, V2, V3, V4
13
Which coronary artery supplies the posterior part of the heart
PDA
13
Describe the pressure-volume loop during the cardiac cycle
Diastole begins = ventricles relax in close chamber = isovolumetric relaxation as P rises
Filling phase = MV opens = Increase in V w little increase in P
Systole begins = MV close = Increase P isovolumetric contraction
Ejection = AV opens = less rapid increase in P, decrease V
Ventricular P < Aorta P = AV close
13
Which heart sounds are normal and which are abnormal
Normal = S1, S2
Abnormal = S3, S4
13
What causes S1 and S2
S1 = MV close (systole start)
S2 = AV close (diastole start)
13
What causes the splitting of S2
During inspiration PV closes after AV
13
What causes S3
Early rapid filling of ventricles
Possible HF
13
What causes S4
Late filling of ventricles
Stiffening of ventricles eg LVH
13
Murmur heard over upper left sternal edge, coincident w carotid pulse
PV stenosis
13
Murmur heard over upper right sternal edge, coincident w carotid pulse
AV stenosis
13
Murmur heard over upper left sternal edge, not coincident w carotid pulse
PV regurgitation
13
Murmur heard over upper right sternal edge, not coincident w carotid pulse
AV regurgitation
13
Murmur heard over lower left sternal edge, coincident w carotid pulse
TV regurgitation
13
Murmur heard over lower left sternal edge, not coincident w carotid pulse
TV stenosis
13
Murmur heard over left 5th IC space, midclavicular line, coincident w carotid pulse
MV regurgitation
13
Murmur heard over left 5th IC space, midclavicular line, not coincident w carotid pulse
MV stenosis
14
What is the significance of the JVP
Reflects RA pressure
14
What is the normal range of measurement of the JVP
<4cm above sternal angle
15
What are the different components of the JVP wave
a-wave = Atrial contraction
x- wave = atrial relaxation
v-wave = atrial filling
y-wave = ventricle filling
16
What does a prominent a-wave suggests
Increase pressure to fill RV
Indicates RVH or tricuspid stenosis
17
What does a prominent v-wave represent
Tricuspid regurgitation
17
How is cardiac output calculated
HR x SV
17
What are the factors of cardiac output
Preload = amount of blood returning to heart
Heart = contractility & HR
Afterload = Arteriole resistance
18
What is ejection fraction
SV / EDV
18
What causes HFrEF
Impaired pumping
MI, Hypertension, Arrythmias
18
What causes HFpEF
Impaired relaxation
LVH
19
How do you treat HFrEF
ACE inhibitors
Beta-blockers
Diuretics
19
How do you treat HFpEF
Diuretics
20
What are the components of starling's forces
Colloid osmotic pressure
Hydrostatic pressure
20
Explain how oedema occurs with reference to starling's forces
Capillary hydrostatic pressure exceed colloid osmotic pressure -> Starling's forces favour filtration of fluid into interstitium - > filtrated fluid outweighs removal by lymphatics
20
What does circulatory shock mean
Hypoperfusion
20
What are the symptoms of shock
Sweating
Pale & cold
Decreased urine output
20
What are the types of shock
Hypovolemic
Cardiogenic
Obstructive
Distributive
20
What are the physiological changes due to ageing
Decreased responsiveness to sympathetic activation -> decreased HR and contractility
Stiffening of heart -> increased filling P -> back pressure on lungs
Stiffening of blood vessels -> Increases systolic BP and loss of elasticity -> Decreased diastolic BP
Baroreceptor reflex degeneration -> postural hypotension
21
Which hypertension is more common
Primary hypertension
21
What are the causes of secondary hypertension
Renal artery stenosis
Endocrine
Neurogenic
Aortic & arterial coarctation
Labile
21
Explain how the RAAS contribute to hypertension using the RAA pathway
Renin release from kidney increases from
- Hypotension triggering JG cells
- Hyponatremia triggering macula densa
- Increase sympathetic tone of B1 R
Increased renin -> angiotensinogen => Ang I -> Ang II (ACE)
Ang II causes the following to increase ECF V and BP:
- Increased aldosterone release from adrenal cortex -> Increases fluid and salt reabsorption @prox tub
- Increases fluid and salt reabsorption @prox tub
- Increase ADH release from pituitary gland and thirst @hypothalamus
- Act on Ang II receptors causing arteriolar constriction
21
What are the complications of hypertension
Athero/Arteriosclerosis
Aneurysm & Dissection
Renal disease
Heart eg HF, IHD, hypertrophy
21
What are the risk factors of atherosclerosis
Modifiable
- Hypertension
- Dislipidemia
- Diabetes
- Smoking
Non-modifiable
- Age
- Sex
- Genetics
21
What is the pathogenesis of atherosclerosis
Endothelial damage
Increase permeability and leukocyte/monocyte adhesion
Macrophage activation & SM cell recruitment
Macrophages and SM cells engulf lipids
SM proliferation + collagen + ECM + Extracellular lipids => Fibrofatty atheroma
21
Compare the features of a stable & unstable plaque
Stable = Thick, hard and calcified fibrous cap with minimum inflammation
Unstable plaque = Thin fibrous cap w scant collagen content, high inflammation & large lipid core
21
What organism can cause an aneurysm
Tertiary syphillis
21
What are the complications of atherosclerosis
Stenosis of medium sized vessels -> decreased blood flow and schema -> angina (coronary) & ischemic bowel disease (mesenteric)
Plaque to rupture
- Thrombosis -> MI (coronary)/ stroke (cerebral)
- Embolisation
Loss of structural integrity of aortic wall -> widening -> aneurysm
21
What is the pathogenesis of an aortic dissection
Vasa vasorum hypertrophy -> weakness -> dissection
a/w medial degeneration of elastic tissue & mucopolysaccharide deposition
21
What can cause an aortic dissection
Weightlifting
Hypertension
Aortic valve issue
CABG
21
How does aortic dissection present
Sharp shooting pain between scapulae w sudden severe stomach ache
Beck's triad
- Hypotension
- Distended neck veins
- Distant heart sounds
21
What are the complications of an aortic dissection
Blood flows from aorta into pericardium cavity -> hemoperricardium/ cardiac tamponade
21
Compare between stable and unstable angina
Stable
- Caused by stable plaque
- Chest pain on exertion radiates to left arm, diaphoresis, SOB
- Relieved by nitro and rest
Unstable
- Caused by unstable plaque
- Chest pain at rest, sweating, SOB
- Relieved by nitro only
- Progresses to MI
21
What is the basis of ischemic heart disease
O2 demand > O2 supply
21
What are some factors that can cause IHD
High O2 demand
- Ventricular hypertrophy
- Tachycardia
Low O2 supply
- Anaemia
- Hypertension
- Aortic dissection
- Occlusion
21
What is the pathophysiology of MI
Coronary artery occlusion due to plaque/ thrombosis / Lumen occlusion
21
What type of necrosis is present in MI
Coagulative necrosis
- Ghost cellular outlines
- Neutrophil invasion
21
What are the histological and microscopic changes of MI
12-24h = pale w blotchy discolouration; Infarcted muscle highly eosinophilic, loss of nuclei & intercellular oedema
1-3 days = yellow, soft, pale infarct; Neutrophilic infiltrate
3-10 days = hyperaemic border; granulation tissue
6-8 week = Dense fibrous scar; fibrosis
21
What are the complications of MI
Ventricles
- LV failure => HF
- Fibrosis
- Ruptured myocardium => cardiac tamponade
Conduction system = arrhythmia
Pericardium = Pericarditis
Valves = Ruptured papillary muscles
21
What are the symptoms of acute MI
Retrosternal chest pain, radiates to left arm
Sweating
SOB
21
What investigations are done for MI
Troponin = elevated
CXR = cardiomegaly
ECG
- V1-V4 = LAD => Anterior & anteroseptal LV
- II, III, aVF = RCA => Inferior & Inferoseptal RA/RV
- aVF, I, V5, V6 = LCX => Anteriorlateral & Iferolateral LV/LA
21
What are the causes of heart failure
RHF - LHF & right valve issues
LHF - MI, hypertension etc
21
Differentiate between concentric and eccentric HF
Concentric = Pressure overload eg HTN, stenosis
Eccentric = Volume overload eg mitral regurgitation
21
What are the effects of LHF
Backpressures = LA dilation (fibrillation risk) & Pul hypertension (oedema)
Forward failure
- Decreased CO and hypotension
- RAAS = peripheral odema and raised JVP
Poor tissue perfusion
21
What are the effects of RHF
Poor CO => increase pulmonary dead space
Backpressure on systemic
- Raised JVP
- Hepatosplenomegaly
- Bilateral pitting oedema
21
Explain the acute presentations of HF
Referred pain
Sweating and peripheral vasoconstriction (pallor) due to sympathetic activation from lowered BP
21
What is the pathophysiology of Pul. oedema for LHF
LV ejection fraction decrease -> Blood pools in left heart -> Increase LV/LA pressure -> Pul venous P -> Capillary hydrostatic P > colloid osmotic P -> Starling forces favour filtration -> fluid entering pul interstitium > removal by lymphatics
21
What are the imaging findings of HF
Alveolar oedema
Batwing opacities
Dilated pul vessels
Interstitial oedema
Cardiomegaly
Kerley B lines
21
What is the causative organism of Rheumatic Heart Disease and what is its nature
S. pyogenes
Grp A strep, B haemolytic
21
What is used to determine acute rheumatic fever
Joints
endOcarditis
Nodules
Erythema marginatum
Sydenham chorea
21
What is the pathophysiology of RHD
Molecular mimicry of M proteins resembling cardiac myosin -> antibodies cross react w self antigens (type II hypersensitivity)
21
What are the effects of RHD
Pericarditis = pain and rub
Endocarditis = MV/AV
Myocarditis = Decrease contractility
21
Differentiate between acute and subacute infective endocarditis
Acute
- Factors = IV drug abuse, Open heart surgery, Septicaemia
- Clinical = very ill, stormy course
- Organisms = S. aureus/epidermidis
Subacute
- Factors = Prosthetic valve, Valve abnormality, Dental/Surgical pricedures
- Clinical = insidious, pyrexia, longer course
- Organisms = Viridians, S.bovis
21
Which organism can cause infective endocarditis and is a/w colon cancer
S. bovis
21
What are the presentations of infective endocarditis
Vegetations on valve that contain RBCs, Inflame cells, platelets, fibrin and bacteria
Janeway lesions - microembolization of heart tissue due to infection
21
How does Libman sacks endocarditis differ from infective endocarditis
Sterile vegetations
21
What is the standard procedure of collecting a blood culture for infective endocarditis
- Aerobic/Anaerobic
- 8-10 ml bottle, one for aerobic & one for anaerobic
- x2 sets to increase chances of picking up organism
21
What are the complications of infective endocarditis
Local
- valve rupture
- myocardial ring abscess
- suppurative pericarditis
Distant
- septic emboli
- glomerulonephritis
- splenomegaly
21
Describe the characteristics of transient bacteraemia
a/w surgery
Asymptomatic/ mild fever
Bloodstream infection if immunity fails
21
Describe the characteristics of intermittent bacteraemia
Most common
a/w bacterial infections eg pneumonia
21
Describe the characteristics of sustained bacteraemia
a/w persistent endovascular infections
Occurs in 1st 2 weeks of typhoid fever
22
What are the common left to right shunt congenital heart diseases
VSD
ASD
Patent DA
Transposition of great vessels
23
Which part of the heart is affected in VSD
Membrane part of IV septum
24
Which part of the heart is affected in ASD
Failure to close FO -> septum secundum and primum do not fuse
25
What is heard when auscultating a person with patent ductus arteriosus
Machine like murmur
26
What is the most common right to left shunt congenital heart disease
Tetralogy of fallot
26
What is the pathologies of tetralogy of fallot
Overriding aorta
Pul. stenosis
VSD
RVH
27
What is the appropriate step to take when S. aureus is found in blood culture
Treat as S. aureus bacteremia search for foci of infection eg bones/heart
