Endocardium
blood next to this layer in the chambers of the heart
Excitability
controlled by potassium (K +)
Conductivity
starts with the SA node ( 60-80 beats per minute)
SA node
sinoatrial node
AV node
atrioventricular node
What picks when the SA node fails?
AV node
What is another name for the Bundle of his?
AV bundle
bundle of branches
converts conduction to Purkinje fibers
ECG or EKG
Electrocardiogram
Arrhythmias
irregular heart beat rhythm
Chemoreceptors
found in the carotid arteries, detects oxygen and carbon dioxide (toxic at a certain level), arterial reception
Baroreceptors
stretch receptors, vessels in the body, detect the quantity of fluid, help the body to know fluid levels, when relaxation increases
Arterial
rhythmic ejection of blood from the left ventricle to the aorta
What is the average normal blood pressure?
120/80
What are the atria doing?
They are opening and filling with blood
systole
ventricular contraction
diastole
relaxation
Pulse pressure
difference between systolic and diastolic ( Example: 120-80= 40)
Cardiac output
Stroke volume x Heart rate
Blood pressure
cardiac output multiplied by peripheral vascular resistance ( If blocked the heart has to pump harder. )
Cardiac output
Have to have atrial filling during relaxation, venous return after systole
Preload
atrial filling occurs and blood comes through the veins
Lymphatic system
the network that returns fluid to the circulatory system, works with the immune system, it includes lymph nodes, spleen, thymus, tonsils
The blood coming into the atria from the veins is what?
deoxygenated
Afterload
the force of ejection, it is not the same as cardiac output but can be negative
What are the mechanisms of blood pressure regulation?
Neural mechanisms and humoral mechanisms
Neural mechanisms
intrinsic reflex receptors, the baroreceptors (stretch), arterial (chemoreceptors)
Extrinsic reflex receptors are activated by?
hypothalamus
Humoral mechanisms
the Antidiuretic hormone (vasopressin), renin, aldosterone secretion, and vasopressin is converted to vasocontriction
Renin
it is produced in the kidneys
Angiotensin 1
constrict to retain fluid
Angiotensin 2
the aldosterone secretion
blood vessels
have layers
Arteries can be subdivided into what?
arterioles, capillaries, venules, and veins
What are the layers of blood vessels?
Tunica intima, the tunica media, and the tunica adventitia
Tunica intima
The outside of a blood vessel.
Tunica media
The middle of a blood vessel.
Tunica adventitia
The inside of a blood vessel.
Pericardium
the double-layered serous membrane protecting the heart
Visceral pericardium
on the side next to the heart
parietal pericardium
the outside of the heart
What is the distance between the visceral and parietal pericardium?
There is 30-50 millimeters in between the two layers.
Effusion
accumulation of fluid in the pericardial cavity
Tamponade
The increase pressure returning fluid in the pericardial sac, so cardiac output decreases
Chronic tamponade
the lack of oxygenated blood
Acute tamponade
cyanosis occurs, which means blood pressure is decreased and heart rate is increased
Pulsus paradoxus
exaggerated decrease in systolic blood pressure, will have a decrease in diastolic blood pressure
The heart cannot fight against what?
fluid
Constrictive pericarditis
inflammation of all types and of all causes
Fibrous scar tissue
fibrin and collagen
What in the heart limits pumping?
Scar tissue it leads to decrease filling with blood and decreased cardiac output.
Pericarditis
inflammation of the pericardium
Acute pericarditis
has a triad of symptoms which include chest pain, friction rubbing (which can be heard with a stethoscope, the tissue is thickening and there is less serous fluid), and ECG changes
What are the other changes associated with pericarditis?
dyspnea, tachycardia, and flu like symptoms
Infective endocarditis
occurs within the heart valves, it is the bacterial infection of the heart valves, the infection can cause the heart valve to become inflamed
This bacterial infection is very common in who?
IV drug users
What are the risk factors for infective endocarditis?
valve replacements, prosthetics, and IV drug users
With infective endocarditis patients are adept to do what?
They are adept to go into septic shock.
What are the symptoms of infective endocarditis?
fever, petechial hemmorrhages
Myocarditis
inflammation of the heart muscle, anything can happen in the host, can potentially happen but is rare
Viral etiology
coxsackie, AIDS
What are the symptoms of myocarditis?
asymptomatic, flu-like or death
What is the prognosis of myocarditis?
It resolves in one to two months on its own.
Stenosis
the narrowing of blood vessels
Incompetence
regurgitant that allows blood to spit backwards
What are the Mitral valve disorders?
MV stenosis and MV regurgitation
Valvular disease
open and close and is suppose to prevent backflow
Mitral valve stenosis
the left atrium distends with the left ventricle causing impaired filling to occur, blood is not going through with each contraction
Mitral valve regurgitation
The stroke volume is divided between the aorta and the left atrium (blood squirts through the aorta and when concentrated pops back through the mitral valve
___________________ needs to be strong and contract with good symmetry.
Left ventricle
What are the aortic valve disorders?
AV stenosis and AV regurgitation
Aortic valve stenosis
asymptomatic unless less than 25% functioning
Aortic valve regurgitation
blood flows backwards into the left ventricle, there is adequate cardiac output until late in the disease
What hypersensitivity disorder is Rheumatic Heart Disease?
It is a type three hypersensitivity disorder.
Rheumatic Heart Disease
It is caused by group A beta hemolytic streptococcus bacteria ( 1st inflammation response to an antigen), immune system mediated multisystem inflammatory reaction, it occurs in children
Cardiomyopathies
The muscle wall of the heart thins out.
If this progresses to all chambers of the heart what does the patient need?
A heart transplant due to cardiomyopathy.
Dilated cardiomyopathy
progressive ventricular thinning in the ventricles and all four chambers are affected
Is the cause known?
Unknown causes Increased age,infections, etoh, cocaine/amphetamine use
Hypertrophic Cardiomyopathy
The chambers of the heart get smaller. This condition is more adept to be genetic. have hypertension and is a valvular disease
Restrictive cardiomyopathy
more international, endermicin, nutritional and infectious cause in underdeveloped countries
What are the compensatory mechanisms?
The heart does not stop working it only begins working harder. When the heart works harder it causes it to become bigger and hypertrophy making it slower.
SNS activity
perceives oxygen levels and heart rate, when heart rate is increased, then blood flow is increased to the brain
Fluid hormones
Renin, angiotensin, and aldosterone
Fluid hormones
increased production to retain fluid, stop once we reach normal levels
What do high blood pressure with fluid retention result in?
myocardial hypertrophy
Congestive heart failure
failing to pump (impaired pumping ability), it is like a traffic jam in the heart
Systolic versus diastolic
decreased contractility v. impaired filling
Left side failure
systolic
The Right side of heart
is filling with deoxygenated venous blood into the right atrium, this happens during relaxation
The left side of the heart
is supposed to contract and send oxygenated blood out to the rest of the body. If this does not occur organ failure is possiblle.
Pressure changes pore size or what?
permeability
All of the blood from the organs comes through ________________ to the heart.
vena cava
Arrhythmias can lead to what?
sudden death
Cyanosis
de-saturated hemoglobin
central cyanosis
deoxygenated arterial blood
peripheral cyanosis
the altered delivery of oxygen
What are the manifestations of heart failure?
fluid, edema, pulmonary congestion(left failure),respiratory (nocturnal on left side), fatigue, cachexia, and cyanosis
Acute heart failures
new onset of acute heart failure, the worsening of end stage heart failure
Aneurysm
localized abnormal dilation of a vessel (innate, aorta)
Aortic aneurysm
asymptomatic, have chest surgery or family history
Aortic aneurysm dissection
acute rupture, abrupt pain, ripping or tearing of the inner layers of the vessels
Lipoproteins
measure cholesterol
HDL
good guys, float along the bottom and take some LDL outside of the body
LDL
is more adept to float around in the blood stream, the further up the cholesterol the worse it is
Triglycerides
more genetic
How do lower LDL?
exercise, and decrease the amount of fat in the diet
Atherosclerosis
the hardening of plaque this is due to oxygen in the blood
Cell death in the heart occurs when?
90% during infarction
Scavenger cells
Encounter fatty deposits in the artery lining and try to destroy the fats by oxidizing them.
What bumps into plaque all the time?
platelets
Oxidized fats
injure the endothelium causing inflammation that creates fibrous plaque
Peripheral arterial vascular disease
have acute arterial occlusion
Acute arterial occlusion
thrombus occurs usually in the collateral circulation of the heart
Atherosclerotic occlusive disease
occurs in the lower extremities, over time with poor diet(high fat), smoking
Intermittent claudication
pain with walking better if standing
Thromboangitis obliterans
due to gravity, increased blood flow, (Buerger's) inflammation
Raynaud's disease
vasospasm of arteries in the fingers and toes, the vessel will constrict longer, hypoxia in finger tips (arteries)
Atherosclerosis
is the most common cause of coronary heart disease
Fixed stable plaques
lead to chronic ischemia
Acute plaques
unstable, vulnerable there is no warning to plaque adhesion
Angina pectoris
chest pain
What will cause a heart attack?
insufficient blood flow
Chronic coronary artery disease is comprised of what?
Ischemia, stable angina, variant angina, and silent ischemia
Ischemia
blood flow insufficient to meet the need of oxygen and there is a lack of oxygen to areas
Stable angina
chronic, over time and angina pectoris at 75% occlusion
Variant angina
vasospastic, occurs at rest (consistent oxygen going to the heart, Prinzmental's)
Prinzmental's
Demands energy so the heart complies can die in sleep
Silent ischemia
no anginal pain
What are two types of patients silent ischemia affects?
Diabetics and women (complain of fatigue later)
thrombus
stationary clot
embolus
moving clot an example of this is a pulmonary embolus
Endocardium
blood next to this layer in the chambers of the heart
Excitability
controlled by potassium (K +)
Conductivity
starts with the SA node ( 60-80 beats per minute)
SA node
sinoatrial node
AV node
atrioventricular node
What picks when the SA node fails?
AV node
What is another name for the Bundle of his?
AV bundle
bundle of branches
converts conduction to Purkinje fibers
ECG or EKG
Electrocardiogram
Arrhythmias
irregular heart beat rhythm
Chemoreceptors
found in the carotid arteries, detects oxygen and carbon dioxide (toxic at a certain level), arterial reception
Baroreceptors
stretch receptors, vessels in the body, detect the quantity of fluid, help the body to know fluid levels, when relaxation increases
Arterial
rhythmic ejection of blood from the left ventricle to the aorta
What is the average normal blood pressure?
120/80
What are the atria doing?
They are opening and filling with blood
systole
ventricular contraction
diastole
relaxation
Pulse pressure
difference between systolic and diastolic ( Example: 120-80= 40)
Cardiac output
Stroke volume x Heart rate
Blood pressure
cardiac output multiplied by peripheral vascular resistance ( If blocked the heart has to pump harder. )
Cardiac output
Have to have atrial filling during relaxation, venous return after systole
Preload
atrial filling occurs and blood comes through the veins
Lymphatic system
the network that returns fluid to the circulatory system, works with the immune system, it includes lymph nodes, spleen, thymus, tonsils
The blood coming into the atria from the veins is what?
deoxygenated
Afterload
the force of ejection, it is not the same as cardiac output but can be negative
What are the mechanisms of blood pressure regulation?
Neural mechanisms and humoral mechanisms
Neural mechanisms
intrinsic reflex receptors, the baroreceptors (stretch), arterial (chemoreceptors)
Extrinsic reflex receptors are activated by?
hypothalamus
Humoral mechanisms
the Antidiuretic hormone (vasopressin), renin, aldosterone secretion, and vasopressin is converted to vasocontriction
Renin
it is produced in the kidneys
Angiotensin 1
constrict to retain fluid
Angiotensin 2
the aldosterone secretion
blood vessels
have layers
Arteries can be subdivided into what?
arterioles, capillaries, venules, and veins
What are the layers of blood vessels?
Tunica intima, the tunica media, and the tunica adventitia
Tunica intima
The outside of a blood vessel.
Tunica media
The middle of a blood vessel.
Tunica adventitia
The inside of a blood vessel.
Pericardium
the double-layered serous membrane protecting the heart
Visceral pericardium
on the side next to the heart
parietal pericardium
the outside of the heart
What is the distance between the visceral and parietal pericardium?
There is 30-50 millimeters in between the two layers.
Effusion
accumulation of fluid in the pericardial cavity
Tamponade
The increase pressure returning fluid in the pericardial sac, so cardiac output decreases
Chronic tamponade
the lack of oxygenated blood
Acute tamponade
cyanosis occurs, which means blood pressure is decreased and heart rate is increased
Pulsus paradoxus
exaggerated decrease in systolic blood pressure, will have a decrease in diastolic blood pressure
The heart cannot fight against what?
fluid
Constrictive pericarditis
inflammation of all types and of all causes
Fibrous scar tissue
fibrin and collagen
What in the heart limits pumping?
Scar tissue it leads to decrease filling with blood and decreased cardiac output.
Pericarditis
inflammation of the pericardium
Acute pericarditis
has a triad of symptoms which include chest pain, friction rubbing (which can be heard with a stethoscope, the tissue is thickening and there is less serous fluid), and ECG changes
What are the other changes associated with pericarditis?
dyspnea, tachycardia, and flu like symptoms
Infective endocarditis
occurs within the heart valves, it is the bacterial infection of the heart valves, the infection can cause the heart valve to become inflamed
This bacterial infection is very common in who?
IV drug users
What are the risk factors for infective endocarditis?
valve replacements, prosthetics, and IV drug users
With infective endocarditis patients are adept to do what?
They are adept to go into septic shock.
What are the symptoms of infective endocarditis?
fever, petechial hemmorrhages
Myocarditis
inflammation of the heart muscle, anything can happen in the host, can potentially happen but is rare
Viral etiology
coxsackie, AIDS
What are the symptoms of myocarditis?
asymptomatic, flu-like or death
What is the prognosis of myocarditis?
It resolves in one to two months on its own.
Stenosis
the narrowing of blood vessels
Incompetence
regurgitant that allows blood to spit backwards
What are the Mitral valve disorders?
MV stenosis and MV regurgitation
Valvular disease
open and close and is suppose to prevent backflow
Mitral valve stenosis
the left atrium distends with the left ventricle causing impaired filling to occur, blood is not going through with each contraction
Mitral valve regurgitation
The stroke volume is divided between the aorta and the left atrium (blood squirts through the aorta and when concentrated pops back through the mitral valve
___________________ needs to be strong and contract with good symmetry.
Left ventricle
What are the aortic valve disorders?
AV stenosis and AV regurgitation
Aortic valve stenosis
asymptomatic unless less than 25% functioning
Aortic valve regurgitation
blood flows backwards into the left ventricle, there is adequate cardiac output until late in the disease
What hypersensitivity disorder is Rheumatic Heart Disease?
It is a type three hypersensitivity disorder.
Rheumatic Heart Disease
It is caused by group A beta hemolytic streptococcus bacteria ( 1st inflammation response to an antigen), immune system mediated multisystem inflammatory reaction, it occurs in children
Cardiomyopathies
The muscle wall of the heart thins out.
If this progresses to all chambers of the heart what does the patient need?
A heart transplant due to cardiomyopathy.
Dilated cardiomyopathy
progressive ventricular thinning in the ventricles and all four chambers are affected
Is the cause known?
Unknown causes Increased age,infections, etoh, cocaine/amphetamine use
Hypertrophic Cardiomyopathy
The chambers of the heart get smaller. This condition is more adept to be genetic. have hypertension and is a valvular disease
Restrictive cardiomyopathy
more international, endermicin, nutritional and infectious cause in underdeveloped countries
What are the compensatory mechanisms?
The heart does not stop working it only begins working harder. When the heart works harder it causes it to become bigger and hypertrophy making it slower.
SNS activity
perceives oxygen levels and heart rate, when heart rate is increased, then blood flow is increased to the brain
Fluid hormones
Renin, angiotensin, and aldosterone
Fluid hormones
increased production to retain fluid, stop once we reach normal levels
What do high blood pressure with fluid retention result in?
myocardial hypertrophy
Congestive heart failure
failing to pump (impaired pumping ability), it is like a traffic jam in the heart
Systolic versus diastolic
decreased contractility v. impaired filling
Left side failure
systolic
The Right side of heart
is filling with deoxygenated venous blood into the right atrium, this happens during relaxation
The left side of the heart
is supposed to contract and send oxygenated blood out to the rest of the body. If this does not occur organ failure is possiblle.
Pressure changes pore size or what?
permeability
All of the blood from the organs comes through ________________ to the heart.
vena cava
Arrhythmias can lead to what?
sudden death
Cyanosis
de-saturated hemoglobin
central cyanosis
deoxygenated arterial blood
peripheral cyanosis
the altered delivery of oxygen
What are the manifestations of heart failure?
fluid, edema, pulmonary congestion(left failure),respiratory (nocturnal on left side), fatigue, cachexia, and cyanosis
Acute heart failures
new onset of acute heart failure, the worsening of end stage heart failure
Aneurysm
localized abnormal dilation of a vessel (innate, aorta)
Aortic aneurysm
asymptomatic, have chest surgery or family history
Aortic aneurysm dissection
acute rupture, abrupt pain, ripping or tearing of the inner layers of the vessels
Lipoproteins
measure cholesterol
HDL
good guys, float along the bottom and take some LDL outside of the body
LDL
is more adept to float around in the blood stream, the further up the cholesterol the worse it is
Triglycerides
more genetic
How do lower LDL?
exercise, and decrease the amount of fat in the diet
Atherosclerosis
the hardening of plaque this is due to oxygen in the blood
Cell death in the heart occurs when?
90% during infarction
Scavenger cells
Encounter fatty deposits in the artery lining and try to destroy the fats by oxidizing them.
What bumps into plaque all the time?
platelets
Oxidized fats
injure the endothelium causing inflammation that creates fibrous plaque
Peripheral arterial vascular disease
have acute arterial occlusion
Acute arterial occlusion
thrombus occurs usually in the collateral circulation of the heart
Atherosclerotic occlusive disease
occurs in the lower extremities, over time with poor diet(high fat), smoking
Intermittent claudication
pain with walking better if standing
Thromboangitis obliterans
due to gravity, increased blood flow, (Buerger's) inflammation
Raynaud's disease
vasospasm of arteries in the fingers and toes, the vessel will constrict longer, hypoxia in finger tips (arteries)
Atherosclerosis
is the most common cause of coronary heart disease
Fixed stable plaques
lead to chronic ischemia
Acute plaques
unstable, vulnerable there is no warning to plaque adhesion
Angina pectoris
chest pain
What will cause a heart attack?
insufficient blood flow
Chronic coronary artery disease is comprised of what?
Ischemia, stable angina, variant angina, and silent ischemia
Ischemia
blood flow insufficient to meet the need of oxygen and there is a lack of oxygen to areas
Stable angina
chronic, over time and angina pectoris at 75% occlusion
Variant angina
vasospastic, occurs at rest (consistent oxygen going to the heart, Prinzmental's)
Prinzmental's
Demands energy so the heart complies can die in sleep
Silent ischemia
no anginal pain
What are two types of patients silent ischemia affects?
Diabetics and women (complain of fatigue later)
thrombus
stationary clot
embolus
moving clot an example of this is a pulmonary embolus