Normal Cardiac Anatomy & Physiology Flashcards
What is the normal anatomy of the canine and feline heart?
- 4 chambers: 2 atria, 2 ventricles
- 2 great vessels: aorta, pulmonary artery
- 4 valves: tricuspid, mitral, pulmonic, aortic
What is cardiac conduction and function like?
electrical —> fill ventricles during diastole and eject during systole
What is cardiac output?
volume in liters pumped by the left ventricle each minute
How do the atria and ventricles compare?
ATRIA = reservoirs for ventricular filling during systole and conduits during diastole with a normal pressure of 0-12 mmHg
VENTRICLES = develop pressure necessary to open semilunar valves and expel blood into the great arteries
How do the right and left ventricles compare?
R = act as a bellow to eject blood into the pulmonary circulation at a relatively low pressure (0-8/15-25 mmHg)
L = conical-shaped chamber that must generate pressure 5-6x higher than pulmonary circulation at 4-12/110-130 mmHg) —> thicker myocardium
What happens in the ventricles during diastole?
both have very low pressure (<12 mmHg) and usually close to 0 mmHg
Heart chambers, pressure:
How does blood flow through the cardiovascular system?
arteries —> small arteries —> arterioles —> capillaries —> venules —> veins
- each circuit delivers the same volume of blood each minute to the opposite side of the heart
What part of the cardiovascular system represents the major storage compartment of blood in the body?
veins
What determines blood pressure?
BP = CO x SVR
- arterial pressure and vascular resistance are much higher on the systemic side
How does pulmonary veins’ limited capacity to store blood matter clinically?
increasing blood or plasma volume elevates venous pressure more rapidly in the pulmonary circulation than in the systemic circulation —> when the left heart fails, pressure builds up in the pulmonary circulation and results in fluid leaking out of the capillaries and into the interstitium = PULMONARY EDEMA
What kind of pressure system is pulmonary circulation? Why?
LOW - 15-25 mmHg systolic, 8-12 mmHg diastolic
allows for flow equal to systemic flow
At what 3 levels does pulmonary vascular resistance occur?
- left atrium
- arterioles, precapillary
- capillaries
What are some pre-capillary, capillary, and post-capillary causes of pulmonary hypertension?
arterial thromboembolism, reactive vasoconstriction
pulmonary parenchymal disease
left heart disease
What kind of pressure system is systemic circulation? Why?
HIGH - 110-140 mmHg systolic, 70-80 mmHg diastolic
high diastolic pressure must be maintained in the aorta so regional circulations can be perfused (CO is the same as the right ventricle = high systemic vascular resistance)
What is the major level of systemic vascular resistance?
arterioles
What does persistent hypertension indicate?
abnormally high SVR or CO
What is the cross-sectional area of pulmonary capillaries like? How does blood flow?
larger
flows slow to allow for gas exchange
(total blood in capillaries is small, much larger in veins)
What determines CO?
CO = HR x SV (stroke volume)
What is Ohm’s law?
flow = pressure difference / resistance
If cardiac output remains the same, how does HR affect the heart?
determines how much it can fill
What is blood pressure maintenance important for?
provides constant flow to vital organs
What 7 things happen during systole?
- AV valves close (S1)
- ventricular depolarization
- isovolumetric contraction
- aortic/pulmonic valves open
- maximal/rapid ejection
- ventricular pressures fall with repolarization
- aortic and pulmonary valves close (S2, end of T wave)
systole = LV contraction
What 6 things happen during diastole?
- isovolumetric relaxation, ventricular pressures drops
- atria fill with blood
- mitral valve opens
- LV fills rapidly
- slow LV filling (diastasis)
- atrial systole (kick)
diastole = LV relaxation
What is diastolic function? What 3 things determine diastolic ventricular volume (preload)?
ability of the LV to fill with blood during diastole
- venous pressure
- atrial contraction
- properties of the ventricle
What 2 things can reduce cardiac filling and preload?
- heart rhythm - shortened interval shortened by high HR
- atrial fibrillation - loss of atrial contraction reducing cardiac filling
What 2 things does diastolic function determine?
- preload - ventricles relax, reduce intraluminal pressure, and fill
- coronary perfusion
What diseases commonly limit ventricular filling?
- decreased myocardial distensibility = hypertrophy, chamber dilation, myocardial fibrosis, myocardial ischemia
- external compression = pericardial disease
What 7 factors affect diastolic function?
- HR and rhythm - influences filling time
- atrial function - must contract correctly to fill ventricles
- pericardial function - heart must be able to relax and fill
- sympathetic activity - beta stimulation improves active relaxation
- venoconstriction and venous return - filling and preload
- ventricular wall thickness and compliance - ease of ventricle distention
- coronary perfusion - oxygen and energy needed for active relaxation
What does systolic function determine? What 3 things does it depend on?
ventricular stroke volume —> what the heart can pump out
- preload
- contractility
- afterload
What is preload? When does it decrease? Increase?
volume of blood in ventricles at the end of diastole
- DECREASE - plasma volume loss (dehydration, diarrhea) reduces venous pressure (decreased CO)
- INCREASE - increased circulating volume (fluid overload, fluid retention, regurgitation/shunting of blood)
What is afterload? What happens when it’s high? What is it a major component of?
resistance in the aorta that the left ventricle must overcome to eject blood
limits the velocity and magnitude of ventricular contraction and decreases stroke volume
myocardial oxygen demand
Preload vs. afterload:
What is contractility? How is it measured?
ability of the myocardium to contract independently of change in preload or afterload
- cardiac catheterization
- echocardiogram
What 3 factors can increase contractility?
- exercise
- adrenergic stimulation
- medication - Pimobendan, digitalis
What is the Frank-Sterling Law?
increasing myocyte stretch leads to increased force of contraction in the normal heart, where stretch is directly related to preload of the ventricle or end diastolic volume (EDV)
- helps heart compensate under normal stressful circumstances, but eventually it will not work in a failing heart
