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Medical Studies 1 > Week 3 Cardiovascular > Flashcards

Week 3 Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

what is the pericardium

A

outermost layer of the heart, consisting of fibrous and serous pericardia

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2
Q

what is the fibrous pericardium

A

strong connective tissue

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3
Q

what is the serous pericardium

A

parietal and visceral pericardia

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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

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5
Q

function of the pericardium

A

-protect the heart

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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)

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7
Q

what makes up the structure of a cardiomyocyte

A

sarcomeres
intercalated disks
couplons
axial tubules

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8
Q

what are sarcomeres

A

the fundamental contractile unit within cardiomyocytes, separated by Z-lines

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9
Q

what are intercalated disks

A

specialised cell junctions that facilitate electrical and mechanical coupling

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10
Q

what are couplons

A

junctional complexes where T tubules and sarcoplasmic reticulum meet, crucial for calcium signalling

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11
Q

what are axial tubules

A

intracellular tubules that assist in distributing calcium for excitation-contraction coupling within cardiomyocytes

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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

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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

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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

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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

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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

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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

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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

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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

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20
Q

function of AV valves

A

separate atria from ventricles and ensure unidirectional flow from atrial to ventricles

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21
Q

function of SL valves

A

located on exit of ventricles and precent regurgitation of blood into ventricles

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22
Q

location of aortic valve

A

2nd ICS, R Sternal border

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23
Q

location of pulmonary valve

A

2nd ICS, L sternal border

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24
Q

location of tricuspid valve

A

4th ICS, Left sternal border

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25
Q

location of mitral valve

A

5th ICS, L mid clavicular line

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26
Q

cusps of the aortic valve

A

non coronary, left, right

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27
Q

cusps of the pulmonary valve

A

anterior, left, right

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28
Q

cusps of tricuspid valve

A

septal, anterior, posterior

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29
Q

cusps of bicuspid valve

A

anterior, posterior

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30
Q

Gross anatomy of cardiac valves

A

-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

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31
Q

list the layers of cardiac valves

A

fibrosa
spongiosa
superficial (Atrialis/Ventricularis)

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32
Q

describe fibrosa layer of cardiac valves

A

outermost layer composed predominantly of collagen fibres, provide structural integrity and rigidity

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33
Q

describe spongiosa layer of cardiac valves

A

middle layer with loose CT, rich in proteoglycans and glycosaminoglycans, acting as a shock absorber

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34
Q

describe superficial (A/V) layer of cardiac valves

A

innermost layer with abundant elastic fibres, offering flexibility and resilience to accommodate pressure changes

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35
Q

list the key structures of the cardiac valve musculature

A

chordae tendinae
papillary muscle
valve leaflets
valve annulus

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36
Q

describe chordae tendinae in cardiac valve musculature

A

fibrous chords that connect the valve leaflets to the papillary muscles, preventing prolapse during ventricular contraction

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37
Q

describe papillary muscle in cardiac valve musculature

A

ventricular wall muscles that anchor the chordae tendinae to help maintain valve leaflet tension

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38
Q

describe valve leaflets in cardiac valve musculature

A

thin, flexible flaps that open and close to regulate blood flow and prevent back flow

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39
Q

describe valve annulus in cardiac valve musculature

A

fibrous ring that provides structural support and attachment for the valve leaflets and maintains valve integrity

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40
Q

what are the main phases of the cardiac cycle

A

systole and diastole

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41
Q

what is systole

A

the ventricles contract, ejecting blood into the aorta and pulmonary artery, while the AV valves close to prevent back flow into the atria

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42
Q

what is diastole

A

involves ventricular relaxation and filling, SL valves close to prevent back flow into ventricles, and AV valves open allowing blood into ventricles from atria

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43
Q

Pressure in systole (atrial,ventricular and net flow)

A

atrial pressure is lesser than ventricular pressure (net flow FROM the ventricles)

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44
Q

Pressure in diastole (atrial,ventricular and net flow)

A

atrial pressure is greater than ventricular pressure (net flow INTO ventricles)

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45
Q

name the 7 stages of the cardiac cycle (starting in diastole)

A

isovolumetric relaxation
rapid filling
reduced filling (diastasis)
atrial contraction
isovolumetric contraction
rapid ejection
reduced ejection

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46
Q

Isovolumetric relaxation: P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=high (decreasing)
P(systemic)=high

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47
Q

rapid filling: P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=low
P(systemic)=high (decreasing)

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48
Q

reduced filling (diastasis): P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=low
P(systemic)=mid (decreasing)

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49
Q

atrial contraction: P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=low
P(systemic)=high (decreasing)

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50
Q

isovolumetric contraction: P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=high
P(systemic)=high

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51
Q

rapid ejection: P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=high (increasing)
P(systemic)=high (increasing)

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52
Q

reduced ejection: P(atrial), P(ventricular), P(systemic)

A

P(atrial)=low
P(ventricular)=high (decreasing)
P(systemic)=high (decreasing)

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53
Q

how many heart sounds

A

S1
S2
S3
S4

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54
Q

describe S1 sound

A

closure of av valves (normal)

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55
Q

describe S2 sound

A

closure of sl valves (normal)

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56
Q

describe S3 sound

A

blood striking compliant ventricle (systolic heart failure; regurgitation)

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57
Q

describe S4 sound

A

blood striking non compliant ventricle (left ventricular hypertrophy; aortic stenosis)

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58
Q

compliant vs non compliant ventricle

A

Compliant Ventricle:
Flexible, elastic, low filling pressure, efficient filling.

Non-Compliant Ventricle:
Stiff, rigid, high filling pressure, inefficient filling.

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59
Q

define CO

A

volume of blood ejected from LV in one minute

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60
Q

define preload

A

volume of blood stretching heart muscle for beginning of systole

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61
Q

define after load

A

measure of resistance against which heart must pump in order to eject blood from LV

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62
Q

describe frank starling law

A

increased cardiac preload will increase the stretch of the cardiac muscle, thus increasing the force with which blood is ejected during systole

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63
Q

How does the body respond to physiological stressor like exercise

A

-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

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64
Q

what does adrenaline and noradrenaline release do in response to physiological stress

A

increased HR–>increased CO

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65
Q

what does vasoconstriction of GI vasculature do in response to physiological stress

A

increased CO via the frank starling mechanism

66
Q

what does vasodilation of skeletal muscle vasculature do in response to physiological stress

A

increased CO via the frank starling mechanism

67
Q

what does muscle pump do in response to physiological stress

A

increases venous rerun
increased CO via frank starling mechanism

68
Q

name some physiological stressors

A

emotional (anxiety, fear)
pain
extreme temperatures
infection/inflammation
exercise

69
Q

Outline the baroreceptor reflex

A

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
Q

is vagal (parasympathetic) or sympathetic stimulation faster

A

vagal is much faster

71
Q

what sub centres make up the Cardiovascular centre

A

cardioacceleratory
cardioinhibitory
vasomotor

72
Q

what does the cardioacceleratory centre do

A

increase HR and increase HR contractility
(+chronotropic and +inotropic effect)

73
Q

what does the cardioinhibitory centre do

A

decrease HR

74
Q

what does the vasomotor centre do

A

changes blood vessel diameter

75
Q

general functions of the cardiovascular centre

A

monitor joint movements
monitor BP
monitor blood acidity, H+, CO2 and O2

76
Q

distinguish between short and long term mechanisms of blood pressure regulation

A

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
Q

what is pressure diuresis

A

increased fluid output due to increased BP

78
Q

whats pressure natriuresis

A

increased Na+ excretion with increased BP

79
Q

Outline RAAS

A

-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
Q

describe the control of blood flow for O2 delivery

A

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
Q

describe the control of blood flow for CO2 removal

A

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
Q

describe the control of blood flow for H+ removal

A

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
Q

describe the control of blood flow for hormone transport

A

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
Q

describe the control of blood flow for nutrient transport

A

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
Q

list the mechanisms for local blood flow control

A

tissue derived vasodilator
adenosine derivatives
endothelium-derived vasodilator

86
Q

how does the tissue derived vasodilator work for controlling blood flow

A

substances released by tissues in response to increased metabolic activity that induce local blood vessel dilation

87
Q

how do adenosine derivatives work for controlling blood flow

A

metabolic by-products of ATP, including adenosine, AMP, and ADP, that promote vasodilation by relaxing smooth muscle

88
Q

how do endothelium derived vasodilators work for controlling blood flow

A

NO released from endothelial cells in response to shear stress or receptor activation, leading to vessel relaxation and increased blood flow

89
Q

Define autoregulation of blood flow to the brain

A

describes the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure

90
Q

list the common causes of systolic and diastollic heart dysfunction

A

hypertension
arrhythmias
cardiomyopathies
CAD
valvular disease
infiltrative disease

91
Q

list the types of heart failure

A

heart failure with reduced ejection fraction
heart failure with moderately reduced ejection fraction
heart failure with preserved ejection fraction

92
Q

what is heart failure with reduced ejection fraction classified by

A

LVEF <40%

93
Q

what is heart failure with moderately reduced ejection fraction classified by

A

LVEF 41-49%

94
Q

what is heart failure with preserved ejection fraction classified by

A

LVEF >50%

95
Q

Describe a mechanism for the pathophysiology of HF (HFrEF)

A

-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
Q

examples of heart failure index events

A

cardiomyopathy
HTN
cardiac tamponade
MI or ishcemia
mitral/aortic regurgitation
advanced aortic stenosis

97
Q

how does neurohormonal activation change with HF

A

-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
Q

how do natriuretic peptides change with HF

A

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
Q

features of IHF

A

-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
Q

features of HFpEF

A

-50% of HF is HFpEF
-elevated Lv end diastole pressure
Dx:
-eleavted BNP and increased LV filling pressure
-clinical symptoms
-CV imaging

101
Q

list the clinical symptoms of HF (history)

A

dyspnoea and PND
orthopnoea
swelling
exercise intolerance
fatigue

102
Q

list the clinical signs of HF (exam)

A

pitting oedema
added s3 sound
raised JVP

103
Q

why does HF present with dyspnoea (+PND)

A

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
Q

why does HF present with orthopnoea

A

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
Q

why does HF present with swelling

A

caused by congestion due to low LV output

106
Q

why does HF present with exercise intolerance

A

low CO, ventilation/perfusion mismatch within pulmonary circulation, leads to skeletal muscle dysfunction

107
Q

why does HF present with fatigue

A

reduced O2 and nutrient delivery to tissues and brain (less pumping) causes decreased energy levels and fatigue

108
Q

why does HF present with pitting oedema

A

caused by fluid accumulation in peripheral tissues due to compromised venous return and increased hydrostatic pressure from HF

109
Q

why does HF present with S3 sound

A

resulting from rapid filling of LV during diastole, indicative of decreased ventricular compliance and increased filling pressures in HF

110
Q

why does HF present with raised JVP

A

due to elevated central venous pressure from hearts inability to handle blood volume, leading to congestion in jugular veins

111
Q

what is echocardiography

A

-non invasive diagnostic imaging technique that uses high frequency sound waves to visualise and asses structure and function of heart

112
Q

how is echocardiography used in Dx HF

A

helps assess LVEF, Lv hypertrophy and enlarged chambers

113
Q

how is echocardiography used in Dx valvular disease

A

helps assess valve leaflet abnormalities, regurgitation, stenosis, dilated annulus

114
Q

why does HF present with nocturia

A

supine position redistributes fluid, increases fluid entry and reabsorption at nephron, increases production of urine and urge to urinate when lying flat

115
Q

List the approach to HF diagnosis and management

A

history
physical exam
Investigations

116
Q

describe use of history for HF diagnosis

A

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
Q

describe use of CV exam for HF diagnosis

A

physical exam taken, looking especially for elevated JVP, murmurs, added heart sounds, heaves, thrills, oedema, crackles

118
Q

what do investigations look like for HF

A

CBE (lipids, EUC,ANP,BNP,CXR,ECG)
echocardiogram (<30% = HF)

119
Q

Outline acute management of HF

A

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
Q

Outline long term management for HF

A

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
Q

list common conditions that present with dyspnoea

A

COPD
asthma
HF
PE
Pneumonia
Interstitial lung disease

122
Q

differentiating features of COPD

A

chronic, smoking history, exposure to irritants, cough

123
Q

differentiating features of asthma

A

seasonal, worse at night, triggered by allergens, cough

124
Q

differentiating features of HF

A

chronic, sleep disturbances (PND/orthopnoea), fatigue, heart murmur

125
Q

differentiating features PE

A

acute, sharp chest pain, worse on inspiration

126
Q

differentiating features of interstitial lung disease

A

progressive, chronic, dry cough, exposure to toxins/irritants

127
Q

list the exacerbating features of HF

A

non compliance
diet
infection
sedentary lifestyle
stress/anxiety

128
Q

how does non compliance exacerbate HF

A

patients failing to take prescribed meds can lead to inadequate control of their HF Sx

129
Q

how can diet exacerbate HF

A

consuming high sodium diet can result in fluid retention, increasing workload on heart and worsening symptoms

130
Q

how can infection exacerbate HF

A

infections eg URTI, UTI’s can increase body demand for O2, worsening HF Sx

131
Q

how can sedentary lifestyle exacerbate HF

A

can lead go deconditioning and muscle atrophy making it more difficult for heart to pump effectively

132
Q

how does stress exacerbate HF

A

emotional stress and anxiety can lead to increase in HR and BP, worsening Sx of HF

133
Q

what are the common complications of HF

A

fluid retention
kidney dysfunction
HTN
liver dysfunction

134
Q

describe fluid retention as a complication of HF

A

HF can cause body to retain excess fluid, eating to swelling in legs and ankles and sometimes abdomen

135
Q

describe kidney dysfunction as a complication of HF

A

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
Q

describe HTN as a complication of HF

A

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
Q

describe liver dysfunction as a complication of HF

A

congestion in the liver s blood vessels can result in liver dysfunction and elevated enzymes

138
Q
A
139
Q

what is regurgitation

A

back flow of blood through a valve due to its incomplete closure

140
Q

what is stenosis

A

narrowing of a valve opening, restricting blood flow through the heart

141
Q

list the causes of valvular disease

A

congenital heart defects
rheumatic fever
degenerative changes
infective endocarditis
CT disorders
medications
truma/injury

142
Q

how do congenital heart defects contribute to valvular disease

A

valvular abnormalities that are present at birth

143
Q

how does rheumatic fever contribute to valvular diseases

A

as a result of untreated streptococcal infection, valve damage arises

144
Q

how do degenerative changes contribute to valvular disease

A

age related wear and tear on heart valves

145
Q

how does infective endocarditis contribute to valvular disease

A

bacterial or fungal infection of heart valves

146
Q

how do CT disorders contribute to valvular disease

A

conditions like marfans syndrome affecting valve structures

147
Q

how does radiation therapy contribute to valvular disease

A

exposure to radiation that can affect heart valves

148
Q

how do medications contribute to valvular disease

A

some meds, like ergotamine (treat migraines) derivatives can damage valves

149
Q

how does trauma/injury cause valvular disease

A

physical injury to chest or heart affecting valve function

150
Q

list the left sides valvular pathologies

A

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

151
Q

what is aortic stenosis

A

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
Q

what is mitral stenosis

A

narrowing of the mitral valve, restricting blood flow from left atrium to left ventricle

153
Q

what is aortic regurgitation

A

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
Q

what is mitral regurgitation

A

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
Q

what symptoms do valve lesions cause

A

dyspnoea
chest pain
fatigue
palpitations
oedema
syncope

156
Q

how do valve lesions cause dyspnoea

A

back flow or reduced forward flow of blood due to valve dysfunction leads to reduced oxygen supply, resulting in breathlessness

157
Q

how do valve lesions cause chest pain

A

obstructed blood flow and increased pressure in the heart chambers cause chest pain

158
Q

how do valve lesions cause fatigue

A

inefficient pumping due to valve lesions requires the heart to work harder leading to fatigue

159
Q

how do valve lesions cause palpitations

A

irregular blood flow and turbulence can cause palpitations, especially in regurgitant valves

160
Q

howdy valve lesions cause oedema

A

increased pressure in the heart chambers can lead to fluid retention and peripheral oedema

161
Q

how do valve lesions cause syncope

A

reduced cardiac output from valve dysfunction can result in fainting episodes due to inadequate blood supply to brain

Medical Studies 1 (15 decks)

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