see also:

• cardiology

• the heart is a 4 chamber pump which beats due to electrical impulses generated in the sino-atrial node in the right atrium which pass to the AV node then down the bundle of His, and then spreads out in a wave to excite myocardial fibres in the ventricles
• the pumping requires adequate myocardial contractility, relaxation and non-obstructed blood flows in the forward direction and valves to prevent back-flow
• the contractions of the atria help fill the ventricles and in normal people contribute some 25% to cardiac output - this is lost in patients with atrial fibrillation
• a key factor for myocardial contraction is adequate myocardial blood supply and oxygenation and this is dependent upon:
  • coronary blood flow which is determined by:
    • coronary perfusion pressure
    • coronary artery diameter which is determined by:
      • autoregulatory vasodilatation via adenosine, etc
      • physical obstructions such as atheroma, clot
  • oxygen levels in the blood which is dependent upon:
    • haemoglobin levels
    • oxygenation of the blood

• this is the volume of blood the heart is pumping out and at rest in adults it is 5 L/min
• cardiac output = stroke volume x heart rate
• stroke volume is normally 70mL in a health adult and is determined by:
  • myocardial contraction resulting in muscle shortening and this is determined by:
    • amount of blood able to feed into the ventricles (inadequate blood flows will also reduce preload)
      • low effective blood volume eg. shock states
      • poor venous return to heart eg. IVC compression in pregnancy, prolonged standing
      • cardiac tamponade
      • tricuspid or mitral stenosis
      • atrial fibrillation
      • pulmonary hypertension
      • pulmonary embolism (PE)
    • ejection fraction
      • the percentage of the total amount of blood in your heart that is pumped out with each heartbeat
      • normally 55-70% (if < 40% this indicates a failing heart, maybe > 75% as in hypertrophic cardiomyopathy (HCM or HOCM))
      • pre-load (see below)
        • the degree of lengthening of muscle fibres prior to contraction
      • after-load
        • resistance to pushing the blood out of the heart:
          • high diastolic blood pressure as in peripheral vasoconstriction / hypertension
          • outflow obstruction eg. aortic stenosis
      • inotropic factors affecting contraction
        • increasing the concentration of intracellular calcium or increasing the sensitivity of receptor proteins to calcium results in the action potential being sustained for longer and therefore, contractility increases
        • sympathetic state
        • inotropes
      • amount of functional myocardium
        • ischaemia, infarcts
        • excessively dilated ventricles do not contract as well (eg. dilated cardiomyopathy)
      • optimal excitation pattern of myocardium so that blood is pushed out from bottom to top
      • degree of back fill from leaking valves

• within limits, muscles can contract more strongly when they are already stretched prior to contraction
• LV preload can be defined as stretch of the LV cavity and is related to LV end diastolic volume (LVEDV)
• assuming no change in afterload or inotropy, the ventricle will eject blood to the same end-systolic volume despite an increase in preload thus increasing ejection fraction and stroke volume
• an adequate “preload” is thus necessary for optimum stroke volume
• preload, afterload and inotropy do not remain constant, and changing any one of these variables usually changes the other two variables

• the heart rate is normally determined by the pacemaker cell firing rate of the sinoatrial node in the RA
• it is modulated by the autonomic nervous system via two types of channel: Kir and HCN (members of the CNG gated channels)
• sympathetic nerves:
  • originate in T1-4
  • noradrenaline neurotransmitter acting upon beta-1 adrenoceptors resulting in cAMP which binds to the HCN channel which increases the flow of Na+ and K+ into the cell, speeding up the pacemaker potential and thus firing rate and heart rate
• parasympathetic:
  • via vagus nerve and acetylcholine neurotransmitter acting on M2 muscarinic receptor which blocks the cAMP pathway and also activates a potassium channel GIRK-1 and GIRK-4, which allows K+ to flow out of the cell, making the membrane potential more negative and slowing the pacemaker potential, therefore decreasing the rate of action potential production and therefore decreasing heart rate

• coronary arteries originate off the ascending aorta
  • left coronary artery arises from the aorta within the left cusp of the aortic valve and feeds blood to the left side of the heart via branches:
    • left anterior descending artery
      • perfuses the interventricular septum and anterior wall of the left ventricle.
    • left circumflex artery
      • perfuses the left ventricular free wall.
      • in a third of individuals, the left coronary artery gives rise to the posterior descending artery which perfuses the posterior and inferior walls of the left ventricle
  • right coronary artery (RCA) originates within the right cusp of the aortic valve and branches into:
    • the right marginal arteries
    • and in two-thirds of individuals, supplies the posterior descending artery
    • in most, it supplies the sinoatrial nodal artery (in others it is supplied by the circumflex artery)
  • almost half of individuals have the conus artery which provides collateral blood flow to the heart when the left anterior descending artery is occluded

• cardiac contraction compresses coronary blood vessels during systole hence coronary blood flow only occurs during diastole
• coronary blood flow which is determined by:
  • coronary perfusion pressure
  • coronary artery diameter which is determined by:
    • autoregulatory vasodilatation via adenosine, hypoxia, etc
    • physical obstructions such as atheroma, clot
• coronary perfusion pressure (CPP) = Aortic Diastolic Pressure – Left Ventricular end-diastolic Pressure (LVEDP)
  • in cardiac arrest:
    • a coronary perfusion pressure of at least 15 mmHg is thought to be necessary for ROSC
    • cardiac compressions helps to maintain coronary perfusion during the relaxation phase of CPR as it creates diastole-like conditions
      • (compression phase is primarily to maintain cerebral and other end organ perfusion)

• defined as the pressure just after the a wave and before the abrupt rise in systolic pressure coinciding with ventricular ejection.
• normal range is 0-25mmHg
• measured right atrial pressure can be used in place of LVEDP as the coronary sinus drains into the right atrium
• there is a curvilinear relationship between LVEDV and LVEDP, with the curve getting steeper at higher volumes
  • as an example in a healthy senior female, it may rise from almost zero levels at LVEDV of less than 60mL to 8mmHg at LVEDV of 90mL and 15mmHg at LVEDV of 120mL and then quickly rising to 20mmHg at LVEDV of 130mL ¹⁾
• LVEDP (either measured or estimated) provides useful information about where a current LVEDV lies within the range of possible LVEDVs for a given ventricle and also allows prediction of whether there is preload reserve, arguably the most important information for clinical purposes:
  • A low LVEDP, or a LVEDP in the normal range (4–12 mmHg), suggests the presence of preload reserve and, therefore, the likelihood of responsiveness to intravascular volume infusion, whereas a LVEDP >20 mmHg, and possibly >15 mmHg, indicates minimal preload reserve and, therefore, minimal volume responsiveness.
• heart failure causes an increase in left ventricular end-diastolic pressure (LVEDP) and reduced CPP