chapter 20-heart(cardiovscular system) Flashcards
pulmonary circuit
right ventricle -> lungs -> left atrium
systemic circuit
left ventricle -> body -> right atrium
arteries
away from the heart
veins
toward the heart
capillaries
exchange vessels in between
heart
-left of midline, between 2nd rib & 5th intercostal space, posterior to sternum in pericardial cavity in mediastinum
-heart fist-sized, beats 10,000 times/day, 8000L of blood
-surrounded by pericardium (serous & fibrous layers)
serous membrane of the heart
visceral & parietal secretes pericardial fluid, reduce friction
pericarditis
inflammation of pericardium, usually due to infection, causes friction
cardiac tamponade
buildup of fluid in pericardial space restricts heart movement
2 atria (2 chambers of the heart)
-superior, thin walls, smooth posterior walls internally, pectinate muscles (ridges) anteriorly
-each has expandable flap called an auricle lateral & superior
-separated by interatrial septum
2 ventricles (2 chambers of the heart)
-inferior, thin walls, lined with trabeculae carneae (muscular ridges)
-left & right separated by interventricular septum
-left ventricle 3x thicker, 5x more friction while pumping, round shape
-right ventricle crescent shape, same volume as left
external divisions of heart
-coronary sulcus marks division between atria & ventricles
-anterior interventricular sulcus & posterior interventricular sulcus mark division between ventricles
epicardium (heart wall of the heart)
-thin
-visceral pericardium
-serous membrane with loose CT attached to myocardium
myocardium (heart wall of the heart)
-thick
-cardiac muscle tissue with CT, vessels & nerves
endocardium (heart wall of the heart)
-thin
-simple squamous epithelium lining with basal lamina, continuous with endothelium of blood vessels
cardiocytes
muscle cells
cardiac muscle tissue
-uses actin & myosin sliding filaments to contract
-rich in mitochondria, resists fatigue, dependent on aerobic respiration
-contraction all or none
-longer contractile phase
-fibrous skeleton of heart (tough CT) acts as tendon
heart valves
one way, prevent backflow
gap junctions + desmosomes =
intercalated discs that connect cardiocytes
atrioventicular valves (heart valves)
between atria & ventricles (flaps = cusps)
tricuspid valve
right atrium -> right ventricle, 3 cusps
bicuspid (mitral) valve
left atrium -> left ventricle, 2 cusps
cusps
-flaps
-attached to chordae tendineae from papillary muscles on ventricle wall
-contraction of papillary muscles prevent cusps opening backward during ventricle contraction
-hang loose when ventricle not contracting, allow ventricles to fill with blood
semiluniar valves (heart valves)
-between ventricles & arteries
-3 cusps
-no chordae tendineae or muscles
-forced open by blood from ventricular contraction
-snap closed to prevent backflow
valvular heart disease
valve function deteriorates to extent that heart can’t maintain adequate circulation
- ex: rheumatic fever
rheumatic fever
childhood reaction to streptococcal infection, chronic carditis, VHD in adults
heart murmur
leaky valve, born with
mitral valve prolapse
murmur of left AV valve, cusps don’t close properly, blood regurgitates back into left atrium
congestive heart failure (CHF)
decreases pumping efficiency (diseased calves, damaged muscle, blood backs up, fluid leaks from vessels & collects in lungs and tissues
blood flow through the heart: pulmonary circuit (right side)
deoxygenated blood -> superior vena cava (head, neck, upper limbs, chest) or inferior vena cava (trunk, viscera, lower limbs) -> right atrium -> tricuspid valve -> right ventricle -> pulmonary semilunar valve -> pulmonary trunk -> right pulmonary arteries -> right lung -> right pulmonary veins
blood flow through the heart: systemic circuit (left side)
pulmonary trunk -> left lung -> pulmonary veins -> O2 & CO2 -> left atrium -> bicuspid valve -> left ventricle -> aortic semilunar valve -> ascending aorta -> aortic arch -> brachiocephalic trunk, left common carotid artery, left subclavian artery (head, neck shoulders, upper limbs) or descending aorta (trunk, viscera, lower limbs)
fetal heart (adapted to bypass lungs)
- foramen ovale in right atrium, ~25% of blood bypass directly to left atrium: closes at birth -> fossa ovalis
-ductus arteriosus connects pulmonary trunk to aorta, ~90% of blood bypasses lungs, closes at birth -> ligamentum arteriosum
cyanosis “blue baby syndrome”
failure of the foramen ovale & ductus arteriosus of the fetus’s heart to close, leading to poor oxygenation of blood
coronary circulation
-heart: <1% body mass, requires 5% of blood
-too thick for diffusion
-coronary arteries -> capillary beds for diffusion
-blood returns via cardiac veins that empty into right atrium
coronary arteries
originated at base of ascending aorta, brach to capillary beds for diffusion (4 major coronary arteries)
coronary artery disease (CAD)
partial or complete block of coronary circulation, results in coronary ischemia
myocardial infarction (heart attack)
heart tissue denied oxygen dies
-can be from CAD
angina pectoralis
pain the chest, especially during activity, as a result of ischemia
-common symptom of CAD
coronary bypass surgery
use healthy veins (from legs) to create anatomizes around blockages
heart beat
-1% myocardial cells autorhythmic
-depolarization transmitted to other myocardial cells through cardiac conduction system
-cells of nodes can’t maintain resting membrane potential, drift to depolarization
autorhythmic (heart beat)
depolarize without neural or endocrine stimulation
sinoatrial (SA) node (heartbeat conduction)
right atrium wall near superior vena cava
- “natural pacemaker”
atrioventricular (AV) node (heartbeat conduction)
inferior portion of interatrial septum above tricuspid valve
AV bundle, bundle braches or Purkinjie fibers (heartbeat conduction)
-conducting cells
- connect nodes & myocardium, run-down interventricular septum & around apex
depolarization (heartbeat conduction)
SA node 80-100 action potential/min, AV node 40-60 action potential/min
sinus rhythm
-resting heart rate
- ~75bpm set by SA node + parasympathetic stimulation
electrical conduction & contraction events of the heartbeat (1-3)
- action potential is generated at SA node
- spreads across the atrial surface & reaches AV node
- atrial contraction begins during 100ms delay at AV node
how many times does the heartbeat chain of events occur?
~370ms
electrical conduction & contraction events of the heartbeat (4-6)
- impulse travels down the interventricular septum from AV node by way of AV heading toward Purkinje fibers
- Purkinje fibers signal papillary muscles to contract, the distribute impulse to ventricular myocardium, atrial contraction -> ventricular contraction
- ventricular contraction is finished
normal average heart rate
~70-80 bpm
max = ~230bpm, but inefficient about 180
bradycardia
-slow heart rate
-heart rate slower than normal <60
tachycardia
-fast heart rate
-heart rate faster than normal >100
electrocardiogram (EKG/ECG)
recording of electrical events of heart
EKG events
P-wave: depolarization wave from SA node through atria ~80ms
QRS complex: atrial depolarization & ventricle depolarization ~80ms
T wave: ventricle depolarization ~160ms
EKG used to diagnose heart problems:
- P-R longer than 200ms = damage to AV node or conducting cells
-large ORS = enlarged heart - Q-T longer than 380ms = coronary ischemia or myocardial damage
total heart block
damaged AV node, no impulses transmitted through, atria & ventricles beat independently (atria fast, ventricles slow)
cardiac arrhythmias
abnormal pattern of cardiac activity
fibrillation
rapid, irregular, out-of-phase contraction due to activity in areas other than SA node: defibrillation to stop all activity so SA node can resume control
cardiac cycle
alternating contraction & relaxation
-increase in heart rate = decreased cycle time, decreased diastole time = decreased time to fill
-atrial contraction adds ~30% more to ventricles
systole
contraction, high pressure, blood gets pushed to next chamber
diastole
relaxation, low pressure, chamber fills with blood
atrial systole begins (cardiac cycle event #1)
atrial contraction forces a small of additional blood into relaxed ventricles
-atrial systole ends atrial diastole begins
-0 mess & atrial systole
ventricular systole - first phase (cardiac cycle event #2)
ventricular contraction pushes AV valves closed but doesn’t create enough pressure to open semilunar valves
-atrial diastole & ventricular systole
-100-370 mesc
ventricular systole - second phase (cardiac cycle event #3)
as ventricular pressure rises & exceeds pressure in the arteries, the semilunar valves open & blood is ejected
-atrial diastole & ventricular systole
-100-370 mesc
ventricular diastole - early (cardiac cycle event #4)
as ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves & forces them closed, blood flows into relaxed atria
-ventricular diastole
-370-800mesc
ventricular diastole- late (cardiac cycle event #5)
all chambers are relaxed, ventricles fill passively
-ventricular diastole
-370-800mesc
“lubb” (heart sound)
S1: AV valves close at start of ventricular systole
“dubb” (heart sound)
S2: semilunar valves close at start of ventricular diastole
cardiac output
amount of blood pumped by each ventricle in 1 min, depends on heart rate & stroke volume: CO = HR * SV
-change HR to increase CO
-@160-180 bpm CO at max: increased HR = decreased time to fill ventricles, if not full = decreased SV & CO
stroke volume (SV)
amount of blood pumped by ventricle
-usually constant
HR (heart rate) triggers
- autonomic nervous input sympathetic = increased HR
- hormones
- venous return = more blood increases HR
- other factors: ions, drugs
heart conditioning:
conditioning can increase SV & decrease HR
-fit athletes can increase max CO by 700% & decrease resting HR by 50% with same CO due to increased SV
autonomic innervation (heart rate effector)
-SA node, AV node & atrial myocardium innervated by both sympathetic (NE) & parasympathetic (Ach) nerve fibers equally
-sympathetic dominates in ventricles
cardiac centers in medulla oblongata monitor BP & gasses to adjust HR:
a. cardioacceleratory center: sympathetic
b. cardioinhibitory center: parasympathetic
parasympathetic (autonomic innervation) tone reduces rate of SA node:
-72-80bpm females
-64-72bpm males
-40bpm athletes
hormones (heart rate effector)
-epinephrine, norepinephrine, thyroxine all increase HR by acting at SA node
-beta-blockers drugs to treat hypertension block B-receptors for E/NE, thus preventing sympathetic stimulation
caffeine (heart rate effector)
rapid depolarization of the SA node, increased HR
nicotine (heart rate effector)
stimulates sympathetic neurons, increases HR
hyperkalemia (heart rate effector)
high K+ inhibits repolarization, beats weak, and the heart can stop
hypokalemia (heart rate effector)
low K+, hyperpolarization, cells less responsive, decreased HR
hypercalcemia (heart rate effector)
high Ca+, muscle cells excitable, increases HR, can cause prolonged contraction, heart seizes
hypocalcemia (heart rate effector)
low Ca+, contractions weak, heart can stop
temperature (heart rate effector)
affects metabolic rate of cardiocytes
-high temp = increased HR
-low temp = decreased HR
a severe case of pericarditis could lead to a what where the fluid restricts movement of the heart?
cardiac tamponade
what of the heart has pectinate muscles?
atria
what are the expandable flaps of the heart intended to accommodate excess blood volume?
auricles
the visible branchy appearance of muscle lining the ventricles is called the what?
trabeculae carneae
you have a very thick chunk of heart, which you are told is from the inferior lateral
aspect. from which chamber wall did it come?
left ventricles
what is the layer of the heart wall where the cardiocytes are located?
myocardium
the abundance of mitochondria in cardiocytes tells you what about their method of ATP production?
aerobic respiration dependent
where is the tricuspid valve located?
right side between atrium & ventricle
the bumps in the ventricles where the chordae tendineae attached are called the what?
papillary muscles
name the valve that prevents backflow into the left ventricle.
aortic semilunar valve
what is the condition of
fluid accumulation in the thoracic cavity due to decreased heart pumping efficiency?
congestive heart failure (CHF)
blood from the right ventricle goes into what vessel next?
pulmonary trunk
what is the state of blood in the pulmonary veins: oxygenated or deoxygenated?
oxygenated
the first branch off the aorta is the what & it brings blood to the left or right side of the upper body?
brachiocephalic trunk, right side
two specializations of the fetal heart allow for bypass of the pulmonary circuit:
the ductus arteriosus & the what?
foramen ovale
the coronary sulcus, the anterior interventricular sulcus & the posterior
interventricular sulcus serve as handy anatomical landmarks but what are their importance to heart function?
contain the coronary vessels that bring blood to/from the heart tissue for diffusion of nutrients & wastes
ischema
lack of oxygen to the tissues
the collection of autorhythmic myocardial cells in the superior right atrium make up the what?
sinoatrial node (SA node)
cells of the what depolarize spontaneously 40-
60 times per minute?
atrioventricular node (AV node)
why are the papillary muscles stimulated to contract by the Purkinje fibers before the impulse is conducted throughout the myocardium?
to ensure AV valves stay closed during ventricular contraction (papillary muscles pull on chord tendineae to prevent back-flap of cusps into atria)
on an ECG, ventricular repolarization is represented by what wave?
T wave
during systole of a chamber, the pressure on the blood is what?
high
when heart rate is increased, the time spent in diastole is what?
decreased
considering the equation CO = HR x SV, why at a certain point does an increased heart rate not result in increased cardiac output?
SV decreases, not enough time to fill ventricles
