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Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Cardiac cycle: Systole

1. Atrial systole

A

Beginning of cardiac cycle
Initiated by atrial excitation and follows crest of P wave on ECG
At the end of diastole, atrial contraction forces small blood bolus into LV chamber –> atrial kick
Heart sound: S4

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2
Q

Cardiac cycle: Systole

2. Isovolumic ventricular contraction

A

Mitral valve closure –> ventricular systole (occurs during QRS complex)
~50ms for ventricle to develop sufficient pressure to force aortic valve open. Myocytes are contracting around a fixed volume of blood until LVP meets and exceeds aortic pressure.
Heart sound: S1
*LV volume (LVEDV) is highest during this phase

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3
Q

Cardiac cycle: Systole

3. Rapid ventricular ejection

A

Aortic valve opens and blood exits the arterial system at high velocity
Pressure continues to climb even though blood is being ejected because the LV myocytes are still actively contracting
Atrium relaxes and begins to fill
*Highest pressure in LV is reached during this phase

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4
Q

Cardiac cycle: Systole

4. Reduced ventricular ejection

A

Ejection velocity decreases as ventricular systole nears completion.
Ventricular myocytes begin repolarising, contraction wanes and LVP falls rapidly
Aortic valve closure marks the end of this phase

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5
Q

Cardiac cycle: Diastole

5. Isovolumic ventricular relaxation

A

Isovolumic relaxation begins as LV contraction ends
Atrium continues to fill with venous blood
Heart sound: S2 (AV valve closure)

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6
Q

Cardiac cycle: Diastole

6. Rapid ventricular filling

A

LVP drops below L atrial pressure and the mitral valve opens
Rapid passive ventricular filling occurs
Heart sound: opening snap of MV (if stenotic), S3

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7
Q

Cardiac cycle: Diastole

7. Reduced ventricular filling (diastasis)

A

Cardiac cycle ends with reduced filling
This phase typically disappears when HR increases because cycle length is shortened at the expense of diastole
Arterial pressure continues to fall as blood flows through capillary beds (diastolic pressure of ~80mmHg)

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8
Q

Aortic pressure: Dicrotic notch

A

Aortic pressure dips briefly immediately following aortic valve closure
Caused by aortic valve bulging backward into LV under the weight of aortic pressure when it closes

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9
Q

Jugular venous pressures: a, c and v waves

A

a wave: R atrial contraction at the beginning of systole generates a pressure wave that forces blood into R ventricle and also causes the a wave

c wave: ventricular contraction causes ventricular pressure to rise sharply –> AV valve bulges back into atrium –> backward deflection of tricuspid valve generates jugular venous pulse

v wave: during ventricular systole, blood flows from venous system into R atrium and dam against closed TV. Pressure builds as atrium fills = upslope of v wave. Downward slope of v wave corresponds to rapid atrial emptying once TV opens

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10
Q

S3

A

Low intensity rumbling HS during early diastole

Rapid ventricular filling –> turbulence that makes LV walls reverberate and rumble (can be normal in children)

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11
Q

S4

A

Associated with atrial contraction - reflects blood being forced into ventricle at high pressure by hypertrophied atrium

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12
Q

Preload

A

Load that is applied to a myocyte and establishes muscle length before contraction begins
In LV, preload = volume of blood entering the chamber during diastole (EDV)

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13
Q

Afterload

A

It is the load against which a myocyte must shorten

  • Aortic pressure (for LV)/mean arterial pressure (MAP)
  • Vascular resistance
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14
Q

3 determinants of stroke volume

A

Preload, afterload and contractility

Contracility: measure of muscle’s ability to shorten against afterload. Equates with sarcoplasmic free Ca concentration

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15
Q

LV preload is determined by end diastolic pressure. Surrogate markers for EDP are… (2)

A

Right atrial pressure

Central venous pressure

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16
Q

Frank-Starling Law of the Heart

A

Stretching the sarcomeres of myocyte increases the amount of force that muscle is able to generate on next beat. Therefore, stroke volume increases with increased blood volume entering the ventricles.

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17
Q

Short-term and long-term adjustments to cardiac output involving preload

A

Short term: SNS activation vasoconstricts and forces blood out of veins –> ventricle to increase preload –> increased stroke volume –> increased CO
Long term: activation of RAAS leads to fluid retention by kidneys –> sustained increased in circulating blood volume which increases preload –> increased SV –> increased CO

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18
Q

Changes associated with increased afterload

A

Increeased afterload = increased aortic pressure
Short term = SNS activation and modulation of Ca release
Long term = ventricular remodelling

19
Q

Effects of increased afterload

A
  • Ventricle needs to generate greater pressure to sustain ejection against higher afterload
  • Prolonged isovolumetric contraction, truncated ejection, AV valve closes prematurely
  • Reduced stroke volume, increased ESV and EF reduced
  • Myocytes consume more ATP to generate greater pressures to force AV open, less ATP subsequently available to sustain ejection
20
Q

Agents with positive inotropic effects

A

Epinephrine, norepinephrine, digoxin

- Causes myocardium to contract faster, develop higher peak systolic pressures, then relax faster

21
Q

Vessels that are under control of autonomic nervous system

A

Small arteries and arterioles

  • Carry blood at modest pressures
  • Thick, muscular walls
  • Muscles contract and relax under influence of ANS and local factors
  • Controls blood flow to tissues

Veins

  • Carry blood at very low pressures
  • Walls contain thin layer of muscle - under control of ANS
  • Wide lumen accommodates large volume of blood, function as blood reservoirs that are used to adjust ventricular preload
22
Q

Blood vessel structure

A

All have common structure, but thickness and composition vary with vessel function and location

  • Tunica intima: single layer of endothelial cells
  • Tunica media: vascular smooth muscle cells which regulate diameter by contracting/relaxing
  • Elastin: ability to stretch/expand; elastin covered by microfibrils composed of glycoproteins
  • Collagen fibres: resist excessive stretching and limit expansion when internal pressures rise
  • Tunica adventitia: connective tissue - maintains vascular integrity and provides strength
23
Q

Primary determinant of vascular resistance

A

Vessel radius

24
Q

Systemic vascular resistance

A

(MAP - CVP)/CO

MAP - CVP = represents pressure difference between aorta and vena cavae
Rearrangement of modified Omh law = Q = P/R where Q is blood flow (CO), P is pressure gradient across vascular circuit and R = vascular resistance

25
Q

Mean arterial pressure

A

DBP + [(SBP - DBP)/3]

26
Q

Turbulent flow

A
  • Likelihood of turbulence predicted using Reynold’s number = (velocity x diameter x density)/viscosity
  • Turbulence occurs in regions where large volumes of blood are moving at high velocities e.g. heart, vessels entering and leaving the heart
  • Other factors increasing turbulence: stenotic valves, anaemia (decreased viscosity)
  • Inefficient, chaotic movements –> wastes energy
27
Q

Compliance

A

change in volume/change in pressure

- Measure of vessel’s ability to accommodate volume when filling pressure increases

28
Q

Sympathetic nervous system innervation of resistance vessels leads to…

A

Release of norephinephrine onto vascular smooth muscle cells –> activation of a1-adrenergic receptors via IP3 transduction pathway –> increased intracellular [Ca] –> contraction of VSMCs –> vasoconstriction to increase arterial pressure

29
Q

Hormonal control of resistance vessels

A
  1. ADH: stimulated by increased tissue osmolality or reduced blood volume; renal water retention or with sufficiently high levels –> vasoconstriction via ADH V1 receptors on VSMCs
  2. Ang II: triggered by reduced renal artery pressure and SNS activation; potent vasoconstrictor
  3. Adrenaline: produced by adrenal gland during SNS activation; inotropic and chronotropic effects, binds a1-adrenoreceptors to cause vasoconstriction to potentiate SNS effects
30
Q

Endothelial control of resistance vessels

A
  1. NO: potent vasodilator acting on both arteries and veins, produced by eNOS following a rise in intracellular [Ca2+]; binds to and activates soluble guanylyl cyclase –> increased cGMP –> protein kinase activation –> phosphorylates + inhibit myosin light-chain kinase and phosphorylates SERCA pump to reduced intracellular [Ca]
  2. Other vasodilators: prostaglandins (PGE, PGI2)
  3. Vasoconstrictors: PGF, thromboxane A2, endothelins
    - Endothelins are produced in response to e.g. Ang II, hypoxia, trauma. ET1 is a potent vasoconstrictor and binds to ETa receptors –> triggers intracellular Ca release via IP3 pathway
31
Q

Arterial pressure control: fast activating sensors for short term control

A
  1. Arterial baroreceptors
    - Aortic and carotid BRs detect change in MAP - fibres travel in aortic + vagus nerve and sinus + glossopharyngeal nerve
    - Responds to stretch when MAP increases/inactive when MAP decreases
  2. Cardiopulmonary receptors
    - Low pressure regions, detect “fullness” in vessels
    - Maintains MAP and controls renal function
  3. Chemoreceptors
    - Brainstem medulla and aortic + carotid bodies
    - Peripheral receptors activate when arterial O2 <60mmHg or when CO2/H+ rise
    - Medullary CR sensitive to pH of brain interstitial fluid (arterial CO2) - involved in respiratory control
32
Q

RAAS System

A
  1. Decreased NaCl in renal tubule detected by macula densa –> renin release from granular cells in afferent arteriole –> formation of Ang I from angiotensinogen
  2. Ang I coverted to Ang II by ACE in lungs
  3. Ang II effects: vasoconstriction of resistance vessels, ADH release, stimulates thirst and promotes aldosterone release
  4. Aldosterone promotes increased ENaC activity (Na reabsorption), increased ROMK activity (K secretion) and H+ secretion –> Na and H2O reabsorption
33
Q

How long does it take for RAAS system to take full effects?

A

~48hrs
- Aldosterone modifies expression of genes that encode ENaC, which promote recovery of Na and osmotically obligated water from tubules

34
Q

Sympathetic nervous system promotes release of…

A

ADH

Renin

35
Q

Pulmonary wedge pressure

A

Assesses pulmonary venous pressure = L atrial pressure

36
Q

Indications for prophylactic ABx in CHD

A
  1. Unrepaired cyanotic heart disease (inc. palliative shunts and conduits)
  2. Previous history of infective endocarditis
  3. Previous rheumatic heart disease (Indigenous)
  4. Completely repaired heart disease with prosthetic material for first 6/12
  5. Repaired heart disease with residual defect at, or adjacent, to site of prosthetic patch/device
  6. Prosthetic heart valve
  7. Cardiac transplant recipients who develop cardiac valvulopathy
37
Q

Diagnostic criteria for recurrent acute rheumatic fever

A
  • 2 major criteria, OR
  • 1 major + 2 minor criteria, OR
  • Severeal minor criteria
    PLUS
  • Evidence of preceding GAS infection
38
Q

Which major manifestation of ARF can be stand-alone for diagnosis?

A

Chorea

39
Q

Mild rheumatic heart disease

A
  • Any valvular lesion graded mild clinically or on echo

- No evidence of HF or cardiac chamber enlargement on CXR, ECG or echo

40
Q

Moderate rheumatic heart disease

A
  • Any valvular lesion graded moderate severity clinically (mild-mod cardiomegaly) or on echo
  • Any echographic evidence of chamber enlargement
41
Q

Difference between ARF criteria on NZ and Aus guidelines

A
  • NZ:
  • -> aseptic monoarthritis = new major criteria
  • -> Polyarthralgia = minor criteria
  • -> Monoarthralgia = not a criteria
  • Aus:
  • -> Polyarthralgia = major criteria
  • -> Monoarthralgia = minor criteria
42
Q

Severe rheumatic heart disease

A
  • Any severe valvular lesion clinically (sig cardiomegaly or heart failure)
  • Any severe lesion on echo
  • Any impending or previous cardiac surgery for RHD
43
Q

Valve repair vs valve replacement in severe RHD

A
  • Repair has better outcomes for survival
  • Less morbidity in terms of late valve-related events e.g. late death, re-operation, IE, thrombotic or embolic events
  • By 7 yrs, almost all bioprosthetic valves require further replacements
  • Mechanical mitral valve replacement = highest risk of thromboembolic event

Paediatrics (16 decks)

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