Cardiology

• label the image

  A) vascular resistance

  B) cardiac output

  C) heart rate

  D) stroke volume

  E) preload

  
• label the image

  A) left atrium

  B) aorta

  C) left ventricle

  
• label the image

  A) aorta

  B) left atrium

  C) left ventricle

  
• label the image

  A) right ventricle

  B) right atrium

  C) caudal vena cava

  D) pulmonary artery

  
• label the image

  A) right ventricle

  B) right atrium

  
• label the image

  A) aorta

  B) pulmonary artery

  C) left atrium

  D) left ventricle

  E) right ventricle

  F) right atrium

  
• Four heart sounds can potentially be auscultated: First heart sound (S1): closure of the atrioventricular (AV) valves (mitral and tricuspid valves) at the onset of systole· Second heart sound (S2: closure of the semilunar valves (aortic and pulmonic valves) at the end of systole·Third heart sound (S3): vibration of the ventricles during diastole, specifically during rapid ventricular filling (E wave on an echocardiogram) Fourth heart sound (S4): vibration of the ventricles during late diastole, or atrial systole
• A gallop rhythm is the event associated with a relatively rapid rate of ventricular filling and is characterized by a ventricular bulge and a low-frequency sound. This creates a triple rhythm (S3, S4 or both) This is due to a decrease in ventricular compliance e.g in CHF, HCM, DCM
• Blood pressure = cardiac output x vascular resistance
• Cardiac output = stroke volume x HR
• An increase in cardiac output = increased hypertension
• The thickening and/or stiffening of the heart walls as well as the narrowing of blood vessels caused by high BP is a common non-cardiac cause of heart failure.

  • Hypertension often causes hypertrophy of the left ventricle which leads to diastolic dysfunction.
• what are the common causes of heart failure in dogs, cats and horses?

  mitral valve insufficiency, hypertrophic cardiomyopathy and dilated cardiomyopathy
• moderator band aka trabecula septomarginalis
• what ion movements are responsible for the generation of the cardiac action potential?

  calcium and sodium as well as chloride and potassium
• Central cyanosis = desaturation of arterial blood or the presence of a Hb derivative.
• Peripheral cyanosis = desaturation of blood due to a regional reduction in blood flow.
• Cyanosis is an insensitive indicator of the state of oxygenation because it is difficult to recognise until oxygen saturation of Hb in arterial blood reaches 80% or less.
• If an animal is cyanotic, they must be severely hypoxaemic. They may be normocapnic, hypercapnic or hypocapnic
• The left hand side pumps the blood around the body and hence is the most muscular however the right ventricle is larger in size and wraps around the left.
• Vascular resistance = the force exerted on the blood via the vasculature
• Cardiac output = how much force the heart is sending around the body (CO = HR x SV)
• Stroke volume = the volume of blood that is in the heart when it beats
• Pre-load = the volume of blood/hydrostatic pressure within the ventricles at the end of diastole
• After load (systemic vascular resistance) is the pressure the heart works against to open up the aorta in systole, arterial blood pressure if the primary factor
• Whatever the cause of heart failure is, this usually causes a drop in cardiac output which is detected as a fall in blood pressure.
• In chronic degenerative valve disease, the regurgitation means fall in forward flow and cardiac output
• In dilated cardiomyopathy, systolic failure leads to a fall in stroke volume and therefore cardiac output
• In hypertrophic cardiomyopathy/restrictive cardiomyopathy, the ventricle cannot fill causing a fall in cardiac output
• The mechanisms the body has to restore blood pressure include…

  • The sympathetic nervous system
  • The renin-angiotensin aldosterone system (RAAS)
  • Cardiac enlargement
  • This mechanism only occurs in heart disease not when there is a trauma
• • When the kidneys release renin (due to blood pressure drop and a decrease in renal blood flow)this combines with angiotensinogen to produce angiotensin I. This is then converted via ACE to produce angiotensin II which has a couple of effects such as systemic (arteries and veins) vasoconstriction, increases blood volume but also renal sodium and fluid retention.
  • Fluid retention can also occur via aldosterone
• Sensors in the arteries signal to the brain that the blood pressure has dropped causing noradrenaline to be released. Noradrenaline acts on the beta receptors in the heart to increase rate and vigour as well as the beta receptors on the kidney to release renin. It can also act on the alpha receptors in the arteries to cause vasoconstriction

  • In fact, a study revealed that the higher the patient's noradrenaline the sooner they are likely to die
• This is what causes the clinical signs of HF.

  • Vasoconstriction of arteries increases after load causing CO to fall and valves to leak more
  • Vasoconstriction of veins increases the volume returning to the heart causing an increase in atrial pressure and an increased risk of oedema
  • Increased salt and h20 retention means the volume returned to the heart and the volume of fluid in the vessels increases causes pressure in the capillaries to go up contributing to oedema formation
• Most of heart failure patients present with oedema, this is typically a pulmonary oedema due to left-sided disease. As this oedema is a consequence of the compensatory mechanisms, treatment aims to manipulate those mechanisms…

  • Reduce fluid build-up via diuretics
  • Antagonise RAAS via ACE inhibitors +/-aldosterone antagonists
  • Vasodilation via pimobendan

  But we must be careful as these mechanisms are designed to maintain blood pressure so we shouldn’t overdo treatment and cause further harm.
•  Diastole - the period of relaxation of the heart muscle, accompanied by the filling of the chambers with blood
•  Forward failure - the inability of the heart to pump an adequate volume of blood to supply the tissues (LHS heart failure, systolic failure)
• Backwards failure - filling pressures are raised causing a backflow of blood (RHS heart failure, diastolic failure)
• systolic failure = not able to contract fully so not enough blood pumps around the body
• diastolic failure = the heart doesn't fill adequately due to a lack of dilation e.g., in HCM
• RHS heart failure can be linked to backwards failure. This leads to an excess fluid accumulation in the body and hence oedema