Anatomy and physiology of heart failure

• Where does the pulmonary artery go?

  Sends blood to the lungs.
• Where does the aorta send blood?

  Everywhere
• Where does the vena cava take blood?

  Cranial vena cava and caudal vena cave - super low blood pressure as blood is deoxygenated ready to be sent to the lungs.
• What is needed to maintain perfusion?

  Normal systemic arterial pressure

  Cardiac output (HR and SV)

  Venous pressures.

  The priority is the maintainance of blood pressure
• What impacts blood pressure?

  The vascular resistance - force exerted on the blood by the vasculature, how much pressure is on the blood vessels as the blood goes through them.
• What is pre-load?

  The volume of blood/ hydrostatic pressure within the ventricles at the end of diastole.
• What is afterload?

  Systemic vascular resistance. Is the pressure the heart works against to open up the aorta in systole, arterial blood pressure is the primary factor.
• Pathophysiology of heart failure

  Whatever the cause of heart failure, it leads to fall in cardiac output which is detected as a fall in blood pressure. The brain then activates mechanisms to restore the blood pressure which actually makes the already damaged heart work harder. Sympathetic nervous system activation, Renin-angiotensin aldosterone system, cardiac enlargement.
• R.A.A.S

  Renin-angiotensin aldosterone system. When activated by the brain it causes systemic vasoconstriction (arteries and veins across the body gets tighter, causes the kidney to retain sodium and fluid, this increases the blood volume).

  This is a problem in heart failure as we have increased the pressure for the heart to pump and increased the amount of fluid for the damaged heart to pump. Aldosterone causes the kidneys to retain sodium and fluid.
• Consequences of CO and BP

  Fall in systemic blood pressure, increased sympathetic activity leads to and increased rate and force of myocardial contraction, peripheral vasoconstriction, refine secretion and activation of RAA system leading to peripheral vasoconstriction. This all leads to increased cardiac output and increased peripheral resistance leading ti an increased systemic blood pressure.
• Effects of vasoconstriction during heart failure

  vasoconstriction of veins means an increased volume of fluid returning to the heart, increase in atrial pressures and an increase in the liklihood of oedema
• Effects of salt and water retention in heart failure

  The volume returning to the heart increases, the volume of fluid in the vessels increases, the pressure in the capillaries goes up causing oedema to develop.
• Effect of cardiac enlargement in heart failure

  AV valves leak more, the atrium enlarges as blood from the valve shoots back and hits the atrial wall. Oxygen needs increase, but the oxygen supply decreases. Cells die, replaced with scar tissue causing the contractility fulls further.
• How to treat heart failure?

  Most of the patients present with oedema, typically pulmonary oedema (oedema within the alveoli) due to left sided disease. Oedema is a consequence of the compensatory mechanisms.

  To fix this we manipulate the compensatory mechanisms:

  Reduce the fluid build up with diuretics

  Antagonise the RAAS with ACE inhibitors +/- aldosterone antagonists

  Cause vasodilation with pimobendan.