Week 3 Cardiovascular Flashcards
1
Q
what is the pericardium
A
outermost layer of the heart, consisting of fibrous and serous pericardia
2
Q
what is the fibrous pericardium
A
strong connective tissue
3
Q
what is the serous pericardium
A
parietal and visceral pericardia
4
Q
list the layers of the pericardium from outermost to inner most
A
fibrous pericardium, serous (parietal) pericardium, pericardial fluid, serous (visceral) pericardium, adipose tissue
5
Q
function of the pericardium
A
-protect the heart
6
Q
list the layers of the heart, starting with the pericardium
A
pericardium (mesothelium)
epicardium (adipose, nerves, bv)
myocardium (cardiomyocytes, conduction system)
endocardium (inner ventricles and atria)
7
Q
what makes up the structure of a cardiomyocyte
A
sarcomeres
intercalated disks
couplons
axial tubules
8
Q
what are sarcomeres
A
the fundamental contractile unit within cardiomyocytes, separated by Z-lines
9
Q
what are intercalated disks
A
specialised cell junctions that facilitate electrical and mechanical coupling
10
Q
what are couplons
A
junctional complexes where T tubules and sarcoplasmic reticulum meet, crucial for calcium signalling
11
Q
what are axial tubules
A
intracellular tubules that assist in distributing calcium for excitation-contraction coupling within cardiomyocytes
12
Q
describe cardiac myocyte arrangement
A
-round cross section with central nucleus; longitudinal section joined end-end (branched)
-joined by junctions (intercalated disks) that appear as thin, dark stained linear structures dividing adjacent cells, perpendicular to muscle fibre direction
-lipofuscin; residual lysosomal substances that appears yellow-brown near nucleus of some cardiac myocytes
13
Q
features of lipofuscin pigment
A
-accumulates in cardiomycoytes in aged or stressed myocardial tissue
-excess can impair cellular function and contribute to pathophysiological age related cardiac diseases
14
Q
Describe how cardiac myocyte arrangement allows for the heart to contract in a twisting (wringing) motion
A
-contain myofilaments arranged into sarcomeres
-myosin and actin are arranged into 2 micrometer sarcomeres and subsequently striated
-cardiomyocytes are arranged in a helical manner which facilitates efficient and coordinated contraction
-intercalated disks between mycoytes contain gap junctions and desmosomes which synchronise contraction
15
Q
Outline sliding filament theory
A
-ATP binds to ATP binding site and Calcium binds to troponin
-Tropomyosin elicits conformational changes
-Actin binds to actin binding site on myosin
-actin pulls myosin towards M line, the Z disk moves towards M line; muscle contracts and sarcomere shortens
16
Q
role of actin
A
actin forms thin filaments in muscle fibres and serves as binding for myosin heads, enabling sliding of filaments and muscle contraction
17
Q
role of myosin
A
myosin is a motor protein that uses ATP energy to interact with actin, generating the force necessary for muscle contraction by pulling the actin filaments closer together
18
Q
role of troponin
A
troponin is a complex of proteins that regulates muscle contraction by controlling the position of tropomyosin on action filaments, allowing or preventing myosin binding to actin
19
Q
role of tropomyosin
A
tropomyosin is a protein that covers the active binding sites on actin in resting muscles, preventing myosin from binding until troponin releases it during muscle contraction
20
Q
function of AV valves
A
separate atria from ventricles and ensure unidirectional flow from atrial to ventricles
21
Q
function of SL valves
A
located on exit of ventricles and precent regurgitation of blood into ventricles
22
Q
location of aortic valve
A
2nd ICS, R Sternal border
23
Q
location of pulmonary valve
A
2nd ICS, L sternal border
24
Q
location of tricuspid valve
A
4th ICS, Left sternal border
25
location of mitral valve
5th ICS, L mid clavicular line
26
cusps of the aortic valve
non coronary, left, right
27
cusps of the pulmonary valve
anterior, left, right
28
cusps of tricuspid valve
septal, anterior, posterior
29
cusps of bicuspid valve
anterior, posterior
30
Gross anatomy of cardiac valves
-AV valves feature cusps anchored to the heart by chord tendinae, which connect to papillary muscles, preventing prolapse during ventricular contraction
-SL valves lack chord tendinae and papillary muscles, cusps open based on pressure gradients, preventing back flow of blood into ventricles after systole
31
list the layers of cardiac valves
fibrosa
spongiosa
superficial (Atrialis/Ventricularis)
32
describe fibrosa layer of cardiac valves
outermost layer composed predominantly of collagen fibres, provide structural integrity and rigidity
33
describe spongiosa layer of cardiac valves
middle layer with loose CT, rich in proteoglycans and glycosaminoglycans, acting as a shock absorber
34
describe superficial (A/V) layer of cardiac valves
innermost layer with abundant elastic fibres, offering flexibility and resilience to accommodate pressure changes
35
list the key structures of the cardiac valve musculature
chordae tendinae
papillary muscle
valve leaflets
valve annulus
36
describe chordae tendinae in cardiac valve musculature
fibrous chords that connect the valve leaflets to the papillary muscles, preventing prolapse during ventricular contraction
37
describe papillary muscle in cardiac valve musculature
ventricular wall muscles that anchor the chordae tendinae to help maintain valve leaflet tension
38
describe valve leaflets in cardiac valve musculature
thin, flexible flaps that open and close to regulate blood flow and prevent back flow
39
describe valve annulus in cardiac valve musculature
fibrous ring that provides structural support and attachment for the valve leaflets and maintains valve integrity
40
what are the main phases of the cardiac cycle
systole and diastole
41
what is systole
the ventricles contract, ejecting blood into the aorta and pulmonary artery, while the AV valves close to prevent back flow into the atria
42
what is diastole
involves ventricular relaxation and filling, SL valves close to prevent back flow into ventricles, and AV valves open allowing blood into ventricles from atria
43
Pressure in systole (atrial,ventricular and net flow)
atrial pressure is lesser than ventricular pressure (net flow FROM the ventricles)
44
Pressure in diastole (atrial,ventricular and net flow)
atrial pressure is greater than ventricular pressure (net flow INTO ventricles)
45
name the 7 stages of the cardiac cycle (starting in diastole)
isovolumetric relaxation
rapid filling
reduced filling (diastasis)
atrial contraction
isovolumetric contraction
rapid ejection
reduced ejection
46
Isovolumetric relaxation: P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=high (decreasing)
P(systemic)=high
47
rapid filling: P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=low
P(systemic)=high (decreasing)
48
reduced filling (diastasis): P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=low
P(systemic)=mid (decreasing)
49
atrial contraction: P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=low
P(systemic)=high (decreasing)
50
isovolumetric contraction: P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=high
P(systemic)=high
51
rapid ejection: P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=high (increasing)
P(systemic)=high (increasing)
52
reduced ejection: P(atrial), P(ventricular), P(systemic)
P(atrial)=low
P(ventricular)=high (decreasing)
P(systemic)=high (decreasing)
53
how many heart sounds
S1
S2
S3
S4
54
describe S1 sound
closure of av valves (normal)
55
describe S2 sound
closure of sl valves (normal)
56
describe S3 sound
blood striking compliant ventricle (systolic heart failure; regurgitation)
57
describe S4 sound
blood striking non compliant ventricle (left ventricular hypertrophy; aortic stenosis)
58
compliant vs non compliant ventricle
Compliant Ventricle:
Flexible, elastic, low filling pressure, efficient filling.
Non-Compliant Ventricle:
Stiff, rigid, high filling pressure, inefficient filling.
59
define CO
volume of blood ejected from LV in one minute
60
define preload
volume of blood stretching heart muscle for beginning of systole
61
define after load
measure of resistance against which heart must pump in order to eject blood from LV
62
describe frank starling law
increased cardiac preload will increase the stretch of the cardiac muscle, thus increasing the force with which blood is ejected during systole
63
How does the body respond to physiological stressor like exercise
-exercise (increased oxygen)
-detection of mechanical and metabolic stress by mechanoreceptors
-afferent signals sent to medullary control centre
-release of adrenaline (sympathetic innervation)
-vasocontriction of GI vasculature
-vasodilation of skeletal muscle vasculature
-muscle pumping
64
what does adrenaline and noradrenaline release do in response to physiological stress
increased HR-->increased CO
65
what does vasoconstriction of GI vasculature do in response to physiological stress
increased CO via the frank starling mechanism
66
what does vasodilation of skeletal muscle vasculature do in response to physiological stress
increased CO via the frank starling mechanism
67
what does muscle pump do in response to physiological stress
increases venous rerun
increased CO via frank starling mechanism
68
name some physiological stressors
emotional (anxiety, fear)
pain
extreme temperatures
infection/inflammation
exercise
69
Outline the baroreceptor reflex
1.Change in blood pressure (arterial stretch) are detected by mechanosensitive baroreceptors in aortic arch and carotid sinus
2.this sensory (afferent) message is sent to cardioregulatory centres of the medulla (AP sent out faster or slower depending) via afferent cranial nerves (9,10)
3.Cardioregulatory centres send out an efferent message that triggers the sympathetic or parasympathetic NS
4. Changes in CO (SV and HR) and constriction/dilation of blood vessels
5.Increase/decrease in BP
70
is vagal (parasympathetic) or sympathetic stimulation faster
vagal is much faster
71
what sub centres make up the Cardiovascular centre
cardioacceleratory
cardioinhibitory
vasomotor
72
what does the cardioacceleratory centre do
increase HR and increase HR contractility
(+chronotropic and +inotropic effect)
73
what does the cardioinhibitory centre do
decrease HR
74
what does the vasomotor centre do
changes blood vessel diameter
75
general functions of the cardiovascular centre
monitor joint movements
monitor BP
monitor blood acidity, H+, CO2 and O2
76
distinguish between short and long term mechanisms of blood pressure regulation
short term such as BR, quickly respond to acute changes in BP by adjusting HR, myocardial contractility and vascular tone, thereby preventing transient hypo/hypertension vs long term such as RAAS adjust blood volume and systemic vascular resistance to maintain BP over days/weeks
77
what is pressure diuresis
increased fluid output due to increased BP
78
whats pressure natriuresis
increased Na+ excretion with increased BP
79
Outline RAAS
-the macula densa (in the DCT) detects decrease in the NaCl concentration in the urine
-macula densa stimulates release of renin by JG cells
-renin acts on angiotensinogen and converts it into angiotensin I
-angiotensin I is further converted to angiotensin II by ACE
-angiotensin II stimulates release of aldosterone from adrenal glands, causing vasoconstriction of efferent arterioles
-aldosterone acts on DCT and collecting ducts, promoting sodium reabsorption and potassium excretion
-increased thirst and stimulation of pituitary gland to release ADH
-increased sodium reabsorption, increased water reabsorption and blood volume
-negative feedback loops work and Renin is inhibited
80
describe the control of blood flow for O2 delivery
increased tissue oxygen demand, such as during exercise, triggers vasodilation in the muscles through the release of vasodilators like adenosine and nitric oxide, enchanting blood flow to deliver more oxygen
81
describe the control of blood flow for CO2 removal
elevated levels of CO2 in the blood lead to vasodilation, particularly in the cerebral and muscular circulations, facilitating increased blood flow to remove excess CO2 through enhanced respiratory and renal processes
82
describe the control of blood flow for H+ removal
accumulation of H+ ions from metabolic processes lowers blood pH, prompting local vasodilation to increase blood flow and expedite the removal excess H+ and lactic acid from the tissues
83
describe the control of blood flow for hormone transport
The body responds to increased stress or metabolic changes by releasing hormones that regulate blood vessel tone and blood flow. This ensures that essential hormones, like insulin and adrenaline, are efficiently delivered throughout the body to meet heightened physiological demands.
84
describe the control of blood flow for nutrient transport
when there is high demand for nutrients, such as during digestion or growth, blood flow is redirected to the GI tract or growing tissues via vasodilation, optimising nutrient delivery and absorption
85
list the mechanisms for local blood flow control
tissue derived vasodilator
adenosine derivatives
endothelium-derived vasodilator
86
how does the tissue derived vasodilator work for controlling blood flow
substances released by tissues in response to increased metabolic activity that induce local blood vessel dilation
87
how do adenosine derivatives work for controlling blood flow
metabolic by-products of ATP, including adenosine, AMP, and ADP, that promote vasodilation by relaxing smooth muscle
88
how do endothelium derived vasodilators work for controlling blood flow
NO released from endothelial cells in response to shear stress or receptor activation, leading to vessel relaxation and increased blood flow
89
Define autoregulation of blood flow to the brain
describes the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure
90
list the common causes of systolic and diastollic heart dysfunction
hypertension
arrhythmias
cardiomyopathies
CAD
valvular disease
infiltrative disease
91
list the types of heart failure
heart failure with reduced ejection fraction
heart failure with moderately reduced ejection fraction
heart failure with preserved ejection fraction
92
what is heart failure with reduced ejection fraction classified by
LVEF <40%
93
what is heart failure with moderately reduced ejection fraction classified by
LVEF 41-49%
94
what is heart failure with preserved ejection fraction classified by
LVEF >50%
95
Describe a mechanism for the pathophysiology of HF (HFrEF)
-index event eg.MI
-myocardial damage and decreased LVEF
-decreased CO
-this triggers compensatory mechanisms eg nervous system activation (increased NE,renin,AT 2,aldosterone)
-these mechanisms initially help maintain perfusion and BP, but chronic activation of these compensatory pathways leads to maladaptive consequences, including increased after load, myocardial o2 demand and impaired cardiomyocytes and ECM
-this results in worsening HF, CO and end organ damage
96
examples of heart failure index events
cardiomyopathy
HTN
cardiac tamponade
MI or ishcemia
mitral/aortic regurgitation
advanced aortic stenosis
97
how does neurohormonal activation change with HF
-reduced SV leads to activation of sympathetic NS (increasing inotropy and chronotropy)
-renal hypoperfusion and sympathetic stimulation activate RAAS
-sustained RAAS activation provides short term support but long term adverse effects eg cardiac fibrosis
98
how do natriuretic peptides change with HF
Natriuretic peptides are hormones released by the heart in response to volume overload and stretching of the heart muscle. They help reduce fluid volume and blood pressure by promoting sodium excretion and inhibiting ADH release. Brain Natriuretic Peptide (BNP) is commonly used as a diagnostic marker for heart failure.
99
features of IHF
-begins with acute myocyte loss during MI, triggering remodelling (wall thinning, chamber dilation, increased wall stress)
-as infarcted areas heal, heart undergoes late remodelling, characterised by myocardial hypertrophy. increased fibrosis and increased wall stress due to RAAS and SNS
-these adaptive responses initially intend to compensate for function loss, ultimately worsening cardiac function-->HF
100
features of HFpEF
-50% of HF is HFpEF
-elevated Lv end diastole pressure
Dx:
-eleavted BNP and increased LV filling pressure
-clinical symptoms
-CV imaging
101
list the clinical symptoms of HF (history)
dyspnoea and PND
orthopnoea
swelling
exercise intolerance
fatigue
102
list the clinical signs of HF (exam)
pitting oedema
added s3 sound
raised JVP
103
why does HF present with dyspnoea (+PND)
reduced LV output (HFrEF) or elevated end diastolic pressure (HFpEF) leads to increased pulmonary pressure and pulmonary oedema, making it difficult for gas exchange--> SOB
104
why does HF present with orthopnoea
supine position results in blood displaced from extremities to thoracic compartment, along with the low LV output that increases pulmonary pressure makes it difficult for gas exchange --> SOB
105
why does HF present with swelling
caused by congestion due to low LV output
106
why does HF present with exercise intolerance
low CO, ventilation/perfusion mismatch within pulmonary circulation, leads to skeletal muscle dysfunction
107
why does HF present with fatigue
reduced O2 and nutrient delivery to tissues and brain (less pumping) causes decreased energy levels and fatigue
108
why does HF present with pitting oedema
caused by fluid accumulation in peripheral tissues due to compromised venous return and increased hydrostatic pressure from HF
109
why does HF present with S3 sound
resulting from rapid filling of LV during diastole, indicative of decreased ventricular compliance and increased filling pressures in HF
110
why does HF present with raised JVP
due to elevated central venous pressure from hearts inability to handle blood volume, leading to congestion in jugular veins
111
what is echocardiography
-non invasive diagnostic imaging technique that uses high frequency sound waves to visualise and asses structure and function of heart
112
how is echocardiography used in Dx HF
helps assess LVEF, Lv hypertrophy and enlarged chambers
113
how is echocardiography used in Dx valvular disease
helps assess valve leaflet abnormalities, regurgitation, stenosis, dilated annulus
114
why does HF present with nocturia
supine position redistributes fluid, increases fluid entry and reabsorption at nephron, increases production of urine and urge to urinate when lying flat
115
List the approach to HF diagnosis and management
history
physical exam
Investigations
116
describe use of history for HF diagnosis
comprehensive history, includes PHx, FHx, CV Sx
(chest pain
SOB (dyspnoea)
orthopnea
ankle swelling
palpitations
light headedness (presyncope) or fainting (syncope)
intermittent claudication
paroxysmal nocturnal dyspnoea
fatigue, sweating, N+V)
117
describe use of CV exam for HF diagnosis
physical exam taken, looking especially for elevated JVP, murmurs, added heart sounds, heaves, thrills, oedema, crackles
118
what do investigations look like for HF
CBE (lipids, EUC,ANP,BNP,CXR,ECG)
echocardiogram (<30% = HF)
119
Outline acute management of HF
furosemide: loop diuretic used to rapidly decrease fluid overload by promoting diuresis (reducing pulmonary congestion and peripheral oedema)
sublingual GTN: nitrate that provides rapid vasodilation, reducing preload and after load, decreasing cardiac workload and symptomatic relief
supportive care: measures eg O2 therapy, vitals monitoring and addressing underlying complications
120
Outline long term management for HF
beta blocker:reduced HR and o2 demand, improving cardiac function and mortality rates
ACE-i:reduces BP and cardiac workload, halting disease progression
ARB:reduces BP and fluid retention
121
list common conditions that present with dyspnoea
COPD
asthma
HF
PE
Pneumonia
Interstitial lung disease
122
differentiating features of COPD
chronic, smoking history, exposure to irritants, cough
123
differentiating features of asthma
seasonal, worse at night, triggered by allergens, cough
124
differentiating features of HF
chronic, sleep disturbances (PND/orthopnoea), fatigue, heart murmur
125
differentiating features PE
acute, sharp chest pain, worse on inspiration
126
differentiating features of interstitial lung disease
progressive, chronic, dry cough, exposure to toxins/irritants
127
list the exacerbating features of HF
non compliance
diet
infection
sedentary lifestyle
stress/anxiety
128
how does non compliance exacerbate HF
patients failing to take prescribed meds can lead to inadequate control of their HF Sx
129
how can diet exacerbate HF
consuming high sodium diet can result in fluid retention, increasing workload on heart and worsening symptoms
130
how can infection exacerbate HF
infections eg URTI, UTI's can increase body demand for O2, worsening HF Sx
131
how can sedentary lifestyle exacerbate HF
can lead go deconditioning and muscle atrophy making it more difficult for heart to pump effectively
132
how does stress exacerbate HF
emotional stress and anxiety can lead to increase in HR and BP, worsening Sx of HF
133
what are the common complications of HF
fluid retention
kidney dysfunction
HTN
liver dysfunction
134
describe fluid retention as a complication of HF
HF can cause body to retain excess fluid, eating to swelling in legs and ankles and sometimes abdomen
135
describe kidney dysfunction as a complication of HF
HF can impair kidneys unction, reducing urine output and accumulation of wastes in blood
-this is due to poor perfusion, increased venous pressure (congestion), chronic RAAS
136
describe HTN as a complication of HF
Compensation for the decreased CO and blood flow
RAAS Activation: Low blood flow in HF activates RAAS, increasing angiotensin II (vasoconstriction) and aldosterone (sodium/water retention), raising BP
Sympathetic Nervous System (SNS): HF triggers SNS to increase heart rate and vasoconstriction, elevating BP
Fluid Retention: HF leads to fluid buildup, increasing blood volume and BP
137
describe liver dysfunction as a complication of HF
congestion in the liver s blood vessels can result in liver dysfunction and elevated enzymes
138
139
what is regurgitation
back flow of blood through a valve due to its incomplete closure
140
what is stenosis
narrowing of a valve opening, restricting blood flow through the heart
141
list the causes of valvular disease
congenital heart defects
rheumatic fever
degenerative changes
infective endocarditis
CT disorders
medications
truma/injury
142
how do congenital heart defects contribute to valvular disease
valvular abnormalities that are present at birth
143
how does rheumatic fever contribute to valvular diseases
as a result of untreated streptococcal infection, valve damage arises
144
how do degenerative changes contribute to valvular disease
age related wear and tear on heart valves
145
how does infective endocarditis contribute to valvular disease
bacterial or fungal infection of heart valves
146
how do CT disorders contribute to valvular disease
conditions like marfans syndrome affecting valve structures
147
how does radiation therapy contribute to valvular disease
exposure to radiation that can affect heart valves
148
how do medications contribute to valvular disease
some meds, like ergotamine (treat migraines) derivatives can damage valves
149
how does trauma/injury cause valvular disease
physical injury to chest or heart affecting valve function
150
list the left sides valvular pathologies
aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation
151
what is aortic stenosis
narrowing of the aortic valve, which obstructs blood flow from the left ventricle to the aorta, leading to left ventricular hypertrophy and increased cardiac workload
152
what is mitral stenosis
narrowing of the mitral valve, restricting blood flow from left atrium to left ventricle
153
what is aortic regurgitation
occurs when the aortic valve fails to close properly, causing blood to flow back into the LV during diastole and leading to volume overload and ventricular dilation
154
what is mitral regurgitation
involves improper closure of the mitral valve, allowing for blood to flow back into the LA during systole, which can result in atrial enlargement and reduced CO
155
what symptoms do valve lesions cause
dyspnoea
chest pain
fatigue
palpitations
oedema
syncope
156
how do valve lesions cause dyspnoea
back flow or reduced forward flow of blood due to valve dysfunction leads to reduced oxygen supply, resulting in breathlessness
157
how do valve lesions cause chest pain
obstructed blood flow and increased pressure in the heart chambers cause chest pain
158
how do valve lesions cause fatigue
inefficient pumping due to valve lesions requires the heart to work harder leading to fatigue
159
how do valve lesions cause palpitations
irregular blood flow and turbulence can cause palpitations, especially in regurgitant valves
160
howdy valve lesions cause oedema
increased pressure in the heart chambers can lead to fluid retention and peripheral oedema
161
how do valve lesions cause syncope
reduced cardiac output from valve dysfunction can result in fainting episodes due to inadequate blood supply to brain
