Rest of Cardio

Different types of heart failure

1. Left-sided failure

   • Systolic and Diastolic

2. Right-sided

3. Congestive

Systolic left sided

Reduced LV contractility → reduced ejection fraction

• stroke volume/end diastolic volume

Diastolic left sided

Reduced LV compliance

• reduced diastolic filling → lower end diastolic volume

• same ejection fraction (both SV and EDV decreases)

Right sided

(left-sided causes right-sided)

Increased plasma volume

• right side cannot pump back to pulmonary vein

• blood backs up in the lungs (vena cava side)

• consequence of left sided failure → less blood pumped systemically → backlog in pulmonary circulation

Congestive

Congestion in body tissues due to slow blood flow (hypotension or lack of contractility)

• leads to oedema

Action of Atrial Naturetic Peptide

1. low pressure stretch receptors (volume receptors) in atria walls, detect high pressure

2. ANP and BNP released

3. stimulates glomerular afferent arteriole dilation

4. increased GFR

5. more excretion of Na+ and H20

6. decreased plasma volume (peeing more)

7. vasodilation (stimulation cGMP formation)

8. inhibits RAAS → decreases vasopressin (ADH) and aldosterone production

BNP generated in ventricular myocytes on heart failure

diagnostic marker

Major equations

CO = SV x HR

MAP = CO X TPR (total peripheral resistance)

Preload

• venous return

  • circulating blood volume → impacted by haemorrhage

  • blood distribution btw central and peripheral veins

    • symp NS → peripheral venous tone

    • muscle pumps (gastrocnemius) → propels blood peripherally → centrally

    • thoracic pump

      • negative thoracic pressure and positive abdominal pressire propels blood centrally

degree of cadiomyocyte stretch prior to contraction

Influencers of ventricular filling [5]

• VEDV → ventricular end diastolic volume = preload

1. circulating blood volume

2. venous tone

3. heart rate (reduced HR increases ventricular filling time)

4. myocardial compliance → preload (expansion when filling)

5. venous return → linked to circulating blood volume, blood distribution and venous tone

Heart rate

(Chronotropy)

beats per min (autonomic control)

Contractility (inotropy)

contractile strength at a given muscle length

Afterload

1. total force that opposes sarcomere minus the srtetching that existed before contraction

2. pressure that the ventricles mist overcome to eject blood (increasing systemic resistance increases afterload)

Pacemaker potential

4 → 0 → 3

phase 4 - funny current If - opening of slow Na+ ions channels

phase 0 - rapid depol → vgated Ca2+

phase 3 - vgK+ channels repolarisation

Ventricular Action Potential

4 → 0 → 1 → 2 → 3 → 4

ventricular - constant resting membrane potential = phase 4

• when receives AP from AV node

  phase 0 - vgated Na+ (fast) - rapid depol

• phase 1 vg Na+ close → ito current

  • slow release K+ current

  • small drop in membrane channel triggers phase 1

• phase 2 - plateau phase

  • Ca2+ influx balances K+ efflux

  • due to opening of vg L-type Ca2+ channels (slow)

• phase 3 - repolarisation

  • Rapid delayed rectifier K+ channels open

  • slow Ca2+ channels close

• phase 4 - resting potential reached again