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MS1 > Week 3 Cardiology > Flashcards

Week 3 Cardiology Flashcards

1
Q

Layers of Heart wall (innermost to outermost)

A
  1. Endocardium
  2. Myocardium
  3. Epicardium
  4. Visceral layer of serous pericardium
  5. Pericardial Cavitity
  6. Parietal layer of pericardium
  7. Fibrous pericardium
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2
Q

Fibrous pericardium

A

Outermost layer, strong connective tissuse

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3
Q

Serous pericardium

A

Consists of the partial and visceral pericardium

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4
Q

Epicardium is made of

A

Adipose tissues, nerves, blood vessels

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5
Q

Myocardium is made of

A

Cardiomyocytes, conducting system

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6
Q

Endocardium

A

Innermost layer of the heart wall, signed cell thick

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7
Q

Structure of cardiac Myocytes

A
  • Sarcomeres (The fundamental contractile units within cardiomyocytes; separated by Z-lines)
  • Intercalated Disks (Specialised cell junctions that facilitate electrical and mechanical coupling)
  • Couplons (crucial for calculus signalling)
  • Axial tubules (Intracellular tubles that assist in s=distrubuting calcium for excitation contraction coupling within mycotyes)
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8
Q

How do Cardiomyocytes contract

A

Calcium induced calcium release (CICR), whereby extracellaurlar calcium flux triggers release from the SR

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9
Q

Lipofuscin

A

-pigment composed of lipid contains residues from lysomal digestion
-functions as an indicator of oxidative stress and cellular senescence, associated with various cardiomyopathies and het failure

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10
Q

Twisting wringing motions of Cardiomyocytes

A

-arranged in a helical range ent around the heart —> efficient contraction during systole
-coordinated

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11
Q

Sacromere shortening mechanism

A
  1. ATP binds to ATP binding site and calcium bonds to troponin
  2. Tropomyosin elicits a conformational change
  3. Actin binds to actin binding site on myosin
  4. Actin pulls myosin towards the M-Line, the Z-disk moves towards the M line, muscle contracts and the sacromere shortens
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12
Q

Semi lunar valves

A

-Arotic and pulmonary
-rely on pressure gradients to open and close as they lack papillary muscles and Chordae Tendineae

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13
Q

Atrioventricular valves

A

-Tricuspid and mitral valves
-have papillary muscles and chordae tendineae to control valve function
-Papilarry muscles attached to the walls contract to pull on the tendineae, ensuring proper closure
-then during distole they relax, allowing valve to open

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14
Q

Mitral Valve: Location, No. of cusps, Systole, Diastole

A

Location: Between La and LV
No. Of cusps: 2
Systole: closed
Diastole: open

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15
Q

Aortic Valve: Location, No. of cusps, Systole, Diastole

A

Location: Between LV and Aorta
No. Of cusps: 3
Systole: open
Diastole: closed

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16
Q

Pulmonary Valve: Location, No. of cusps, Systole, Diastole

A

Location: Between RV & Pulmonary trunk
No. Of cusps: 3
Systole: open
Diastole: closed

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17
Q

Tricuspid Valve: Location, No. of cusps, Systole, Diastole

A

Location: Between RA & RV
No. Of cusps: 3
Systole: closed
Diastole: open

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18
Q

When does papillary muscle contraction occur re ventricular muscle contraction

A

Slightly before

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19
Q

S1 heart sound

A

Closure of AtrioVentricular
Start of systole

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20
Q

S2 Heart sound

A

Closure of Semilunar valves
Just before start of diastole

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21
Q

S3 Heart sound

A

Blood striking compliant ventricle
Indicates systolic heart failure or regurgitation
Occurs mid diastolic

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22
Q

S4 heart sound

A

Blood striking non-compliant ventricle
Indicates ventricular hypertrophy or aortic stenosis
Is late diastolic

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23
Q

Frank-Starling law

A

Increased cardiac preload will increase the stretch of the cardiac muscle (myocardial fibres) during diastole, thus increasing the force with which blood is ejected during systole.

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24
Q

Describe the effect of physiological stressors, such as exercise, on cardiac function and haemodynamics.

A

-Overall increase heart rate and stroke volume —> higher cardiac output

• Sympathetic nervous system (SNS) activation leads to increased myocardial contractility (positive inotropy)
and faster heart rate (positive chronotropy), resulting in more efficient circulation of oxygenated blood.
• Exercise further induces vasodilation in skeletal muscle arterioles, reducing systemic vascular resistance and
optimising tissue perfusion.
• The increased venous return during exercise augments end-diastolic volume (preload), which, according to the
Frank-Starling mechanism, further boosts stroke volume.

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25
Q

Baroreceptor Reflex
(High Blood Pressure)

A

1.Mechanosensitive afferent nerve endings in the carotid artery sinuses and aortic arch detect arterial stretch
2.a signal is sent via the Vagus nerve (aortic) or the Glossopharyngeal Nerve (carotid) to the Medullary cardiovascular control center
3.After processing numerous Effects occur
* Sympathetic Inhibition –> negative ionotropic (reduces atrial contractility) and chronotropic (reduced firing in SA node –> lower HR) effect
* Parasympathetic activation via the vagus nerve –> decreased heart rate
* These lead to a decreased cardiac output
* Vasodilation also occurs due to sympathetic inhibition –> reduced peripheral resistance

4.Lower Blood pressure
5.Negative feedback loop

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26
Q

RAAS System

A
  1. Stimulus: Juxtaglomerular cells in the kidneys detect the decrease in BP or Na+
  2. These cells release renin
  3. Renin catalyses the conversion of angiotensinogen (released from the liver) to Angiotensin I
  4. ACE (Angiotensin converting enzyme) is released from the lungs and converts Angiotensin I to Angiotensin II
  5. Angiotensin II acts on smooth muscle of blood vessels to vasoconstrict
  6. Angiotensin II stimuluates release of Aldosterone from adrenal glands
  7. Aldosterone acts on the kidneys to increase the reabsorption of Na+ and water alongside the excertion of K+ in the DCT and collecting duct
  8. increased blood volume and resistance
  9. Higher Blood Pressure
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27
Q

Control of vascular resistance

A

-Sympathetic nervous system: controls the rate of firing across sympathies nerve fibres dictates extent of resistance vessel vasoconstriction
-Adrenaline and Noradrenaline secretes from the adrenal gland innate vasocontration
-Angiotensin II and vasopressin also cause Vasoconstriction

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28
Q

Autoregulation of Cerebral Flow

A

• The autoregulation of cerebral blood flow ensures that the brain receives a consistent blood supply despite fluctuations in systemic blood pressure; remember, the brain requires high levels of oxygen and glucose.
• This process is primarily mediated through the myogenic response, where cerebral blood vessels constrict in
response to increased intravascular pressure to prevent excessive blood flow.
• Conversely, in low-pressure conditions, these vessels dilate to maintain adequate perfusion.
• Additionally, metabolic factors, such as elevated levels of CO2 and H+, cause local vasodilation to increase
blood flow to active brain regions.
• This regulation hence maintains optimal cerebral perfusion and protects brain function from pressure-induced
damage.

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29
Q

HFrEF (Heart Failure with reduced Ejection Fraction) Consequences

A
  1. Diminished cardiac output
  2. Triggers compensatory mechanisms, such as SNS activation, and release of renin, noradrenaline, angiotensin II, and Aldosterone
  3. Higher Blood pressure and heart rate, maintaining perfusion
  4. Chronic activation of these pathways lead to maladaptive consequences such as increased; after load and myocardial oxygen demand
  5. This can lead to left ventricular hypertrophy, dilation, and fibrous, further impacting cardiac function
  6. Gets worse and worse, reduced cardiac output, end-organ damage
30
Q

Diagnostic marker for heart failure

A

-NT-ProBNP is biologically inert form of BNP with a longer half life
-BNP is Brain Natrutietic peptide, released from the ventricles during heart failure
-Their is also ANP from atrium

31
Q

Summary of HFrEF

A

An index event causes impaired myocardial contractility leading to a decreased ejection fraction, causing inadequate cardiac output and consequent symptoms of heart failure.

32
Q

Summary of HFpEF

A

Impaired diastolic filling of the heart due to elevated left ventricular end-diastolic pressure and reduced compliance, despite a normal ejection fraction.

33
Q

Summary of ischemic HF

A

Myocardial infarction-induced myocyte loss and subsequent maladaptive remodelling, which leads to progressive heart failure with either reduced or preserved ejection
fraction.

34
Q

Clinical features of Heart Failure

A
  • Dyspnoea + Paroxysmal nocturnal dyspnea
  • Orthopnoea
  • Pitting Oedema/swelling
  • Exercise Intolerance
  • Fatigue
  • Added S3 sound
  • Raised JVP
35
Q

How does HF cause Dyspnoea

A

Reduced LV output (HFrEF) or elevated end diastolic pressure leads to increased pulmonary pressure and pulmonary oedema, fluid is forced out of capillaries into the alveoli, which obstructs small airways
Fluid will accumulate in the bottom of the lungs first, explaining why crackling sounds can be heart at the base of the lungs

36
Q

How does HF cause Orthopnoea

A

Positional change due to lying flat redistributes fluid from extremities to the thoracic space; increased pulmonary fluid build-up exacerbates shortness of breath.

37
Q

How does Heart Failure cause swelling

A
  1. Reduced Ventricular Output
  2. Build up of pressure backlog in the veins
  3. Increased venous pressure raises capillary hydrostatic pressure
  4. Fluid moves out of the capillaries and into the interstitial space
    NB: if liver dysfunction is also occurring, their will be a lower cailairy oncotic pressure due to less proteins being made in the liver, so fluid moves out of the capililres via osmosis
38
Q

Left sided Heart Failure VS Right sided heart failure

A

Left= pulmonary congestion and odema
Right= Systemic

39
Q

How does Heart failure cause exercise intolerance

A

Low cardiac output, V/Q mismatching within pulmonary circulation, skeletal muscle dysfunction

40
Q

How does heart failure lead to fatigue

A

Reduced oxygen and nutrient delivery to tissues (less pumping) causes decreased energy levels, leading to fatigue

41
Q

How does Heart failure cause an Added S3 sound

A

Resulting from rapid filling of the LV during diastole, indicative of decreased ventricular compliance and increased filling pressures in heart failure.

42
Q

How does Heart Failure cause a raised JVP

A

Due to elevated central venous pressure from the heart’s inability to effectively handle blood volume, leading to congestion in the jugular veins.

43
Q

Role of Echocardiography in Diagnosis of heart failure and valvular disease

A

• For heart failure, echocardiography helps assess left ventricular ejection fraction, chamber sizes, and diastolic function to determine the extent of cardiac impairment.
• For valvular disease, echocardiography enables the detailed examination of valve morphology, function, and the presence of regurgitation or stenosis.

44
Q

Echocardiography findings in heart failure

A

Reduced ejection fraction; left ventricular hypertrophy; enlarged chambers

45
Q

Echocardiography findings in valvular disease

A

Valve leaflet abnormalities; regurgitation; stenosis; dilated annulus

46
Q

How does Heart Failure cause Nocturia

A

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

47
Q

How does Left sided heart failure cause right sided heart failure

A
  • over time left sided heart failure results in pulmonary hypertension, this means the right ventricle has to work harder and can be overexerted, resulting in heart failure
48
Q

Cardiomegaly

A

An enlarged heart

49
Q

Acute Management of Heart Failure

A
  • Furosemide
  • Sublingual GTN
  • Supportive Care
50
Q

Furosemide

A

A loop diuretic used to rapidly decrease fluid overload by promoting diuresis, which reduces pulmonary congestion and peripheral oedema, thereby alleviating symptoms of
acute heart failure.

51
Q

Sublingual GTN

A

A nitrate that provides rapid vasodilation, reducing preload and afterload, which decreases cardiac workload and improves symptomatic relief in acute heart failure.

52
Q

Supportive care in acute HF management

A

Measures such as oxygen therapy to enhance oxygenation, monitoring of vital signs and electrolytes, and addressing underlying conditions or complications, all crucial for
stabilizing the patient and preventing further deterioration.

53
Q

Long Term Management of Heart Faiure

A
  • Beta Blockers
  • Calcium Channel Blockers
  • Ace inhibitors
  • Angiotensin receptor Blocker
54
Q

Beta Blockers in long term management of heart failure

A
  • used to reduce sympathetic nervous system activation, thereby decreasing heart rate and myocardial oxygen demand, and improving overall cardiac function.
  • name ends in -olol eg Metoprolol
55
Q

Calcium Channel blockers in long term management of heart failure

A
  • primarily used to manage hypertension and angina, and they can help in cases where there is coexisting atrial fibrillation or significant vasospasm.
    -Lowers heart rate and reduces myocardial contractility, used primarily in heart failure with preserved ejection fraction to manage symptoms of hypertension and angina.
    -name ends in -dipine eg Amlodipine
56
Q

ACE inhibitors in long term management of HF

A
  • Blocks the conversion of angiotensin I to angiotensin II, reducing blood pressure, decreasing cardiac workload, and preventing disease progression in heart failure.
    -name ends in -pril eg perindopril
57
Q

Angiotensin receptor blockers in long term management of HF

A

Inhibits the effects of angiotensin II at its receptor, reducing blood pressure and decreasing fluid retention, offering an alternative to ACE inhibitors.
Name ends in sartan eg losartan
Can be used as an alternative to ACE inhibitors when they cause a cough

58
Q

Exacerbating factors for heart failure

A

-Non-compliance with medications
-Diet
-Infection
-Sedentary life
-Stress/anxiety

59
Q

Complications of heart failure

A

-fluid retention
-kidney dysfunction
-hypertension
-liver dysfunction

60
Q

Conditions that may cause a heart murmur

A

-pulmonary stenosis
-aortic stenosis or regurgitation
-mitral regurgitation or stenosis
-ineffective endocardiaitis
-RHD
-anemia

61
Q

Valvular disease types

A

Stenosis: Narrowing of a valve opening, restricting blood flow through the heart
Regurgitation: The backflow of blood through a vale due to its incomplete closure

62
Q

Causes of valvular disease

A
  • Congenital heart defects (birth defects)
  • Rheumatic fever
  • Age related wear
  • Infective endocarditis
  • Connective tissues disorders (eg Marfans)
  • Radiation
  • Medications
  • Trauma/injury
63
Q

Aortic Stenosis

A

Narrowing of the aortic valve, obstructing blood flow from the left ventricle to the aorta, leading to increased ventricular pressure and reduced cardiac output.

64
Q

Mitral Stenosis

A

Involves the backflow of blood from the aorta into the left ventricle due to inadequate closure of the aortic valve, resulting in volume overload and left ventricular dilation.

65
Q

Aortic regurgitation

A

The mitral valve becomes narrowed, impeding blood flow from the left atrium to the left ventricle during diastole, causing elevated atrial pressure and pulmonary congestion.

66
Q

Mitral Regurgitation

A

Backflow of blood from the left ventricle into the left atrium during systole due to improper closure of the mitral valve, leading to atrial enlargement and volume overload.

67
Q

Hopw does a valve lesion cause Dyspnoea

A

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

68
Q

How does valve lesions cause chest pain

A

Obstructed blood flow and increased pressure in the heart chambers can cause chest pain.

69
Q

How does valve lesions cause fatigue

A

Inefficient pumping due to valve lesions requires the heart to work harder, leading to fatigue.

70
Q

How do valve lesions cause palpitations

A

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

71
Q

How do valve lesions cause oedema

A

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

72
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 the brain.

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