1. The Heart Flashcards
Heart blood flow
R side.
- Sup/inf vena cava
- R atrium
- Tricuspid
- R ventricle
- Pulmonary valve
- Pulmonary artery
L side
- Pulmonary vein
- L atrium
- Bicuspid/mitral
- L ventricle
- Aortic valve
- Aorta
Pulmonary circulation
Transports deoxygenated blood From the right side of the heart to the lungs
Pulmonary circulation is supported by right atrium and right ventricle
RIGHT side
Systemic circulation
Carries oxygenated blood from the left side of the heart to all the tissues in the body
Removes waste from tissues and returns deoxygenated blood to the right side of the heart
Supported by left atrium and left ventricle (major player in cardiac output)
Electrical system of the heart
Electrical impulse is generated by the sinoatrial node (SA node) generates 60-100 times per minute
Travels from SA node to AV node then travels to ventricle bundle via bundle of His
Bundle of His divides the right and left pathways to stimulate the right and left ventricles
Fine branching of bundle of His into the purkinje network which stimulated the right and left ventricles
Excitation / contraction
Excitation: generation of action potential trigged by electrical impulse
Contraction: shortening of muscle cells triggered by excitation
Single cardiac cycle divided into:
Diastole: period of time when ventricles are relaxed at the end of diastole both atria contract (time heart fills)
Systole: period of time when the ventricles contract and eject blood into the aorta and pulmonary artery
Three layers of the heart
Epicardium: outer layer
Myocardium: middle layer (cardiac muscle)
Endocardium: internal layer (CT and squamous cells continuous with endothelium)
Pericardium
Three layers are enclosed in a double lined membrane sac
Parietals : touches body
Visceral: touches heart
Acts as physical barrier
Contains pain receptors and mechanoreceptors
End-diastolic volume (EDV)
The filled volume of ventricle prior to contraction
Prior to diastole (Relaxation)
End-systolic volume (ESV)
The residual volume of blood remaining the ventricle after contraction
Prior to systolic (contraction)
Stroke volume (SV)
The volume of the blood pumped out by the left ventricle in one contraction
SV = EDV - ESV
Preload
The ventricle volume at the end of diastole, approximated by LVEDV
Amount of volume of blood before contraction, blood entering ventricles
Wind that makes biking easier
After load
The ventricular wall tension during contraction, depends on the arterial blood pressure and vascular tone. Resistance ventricles must overcome two circulate blood
Increase after load (resistance) = increase cardiac workload = Decrease SV
Rocky road that biker has to push against
Cardiac output
The amount of blood the heart pumps in 1 minute
Depends on HR,
contractibility (EDV, sympathetic stimulation, myocardial oxygen supply)
preload (end-systolic volume ESV, venous return - increase water = increase venous return)
After load (aortic pressure, total peripheral resistance)
CO (ml/min)= SV (ml) x HR (bpm)
Ejection fraction (EF)
The percentage of blood that’s pumped out of a filled ventricle with each heartbeat
Usually only measured in left ventricle (LVEF)
EF= SV/EDV %
Less then 40% bad
50-70% is normal
Used to measure hearts squeezing ability and assess heart failure
Chronotropic effect
Increase or decrease in HR
positive chronotropic: major effect increase HR (sympathetic stim norepi and epi)(increase CO2)
Negative chronotropic: decrease HR (parasympathetic stim -acetylcholine)(decrease O2 hypoxia)(increase calcium)
DIrect relationship with HR
Ionotropic effect
Force/strength of myocardial contraction
Positive ionotropic: strengthen force of heart
Negative ionotropic: weaken force of heart
direct relationship
Normal left ventricular pressure-volume relationship in association with SV
Preload (EDV) DIRECT- Increase in venous BP forces more blood to flow into the heart - increase SV increase stretch increase venous BP!
Myocardial contractibility: DIRECT -Higher contractibility allows the heart to pump out more blood into the vasculature - increased SV
After load: an inverse relationship - Decrease in after load (wall tension) can increase SV
Frank-Starling Law
Relationship between force and stretch (DIRECT)
SV rises in response to an increase in preload (EDV) - heart under influence of sympathetic nervous system (epi and norepi) = more force
Large volume of blood in ventricles - more stretch - more force from cardiac muscle
Increase stretch = increase force
Nervous control
Higher centers: medulla oblongata
Sympathetic nervous system (SNS) - Controls SA node, release epi and norepi, increase HR and contractibility
Parasympathetic nervous system (PNS) - Mainly controls AV noded, releases acetylcholine, decreased HR, little effect on contractibility
Hormonal control
ADH and aldosterone - affect BP (where salt goes water goes)
ADH decrease excretion of fluid increase BP
Epi and angiotensin II - affect BP , increase BP and vasoconstriction
Cardio vascular disease occurs as a consequence of one more more mechanism
Pump failure - poor contractibility or relation of heart
Blood flow obstruction atherosclerotic plaque, aortic valve stenosis
Regurgitating flow - output form each contraction directed backwards - volume overload and decreased forward blood flow
Shunted flow - abnormal blood flow
Abnormal cardiac conduction - uncoordinated myocardial contractions
Rupture of the heart of major vessel
Ischemic Heart Disease (IHD)
IHD frequently referred to as coronary heart disease - Mismatch between cardiac demand and supply of oxygenated blood
Etiology:
In more then 90% of cases IHD is due to atherosclerotic disease - reduced blood flow to coronary arteries
Myocardial ischemia in the absence of chest discomfort is “silent ischemia”
Pathophysiology of myocardial ischemia
Mismatch between supply and demand
Demand determined by HR, systolic BP, myocardial tension, myocardial contractibility
Supply determined by oxygen carrying capacity of the blood, the degree of unloading from the hemoglobin to tissues
Coronary artery blood flow delivered to the myocardium which is determined by:
Perfusion pressure
Collateral blood flow
HR
