1/80
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
Arteries
carry blood away from the heart
Veins
carry blood back to the heart
Capillaries
are sites of exchange
Between blood and air in lungs
Between blood and body cells
Pulmonary circulation
Carries deoxygenated blood from right side of heart
to lungs
At lungs, blood picks up oxygen and releases
carbon dioxide
Blood vessels return blood to left side of heart
Systemic circulation
Moves oxygenated blood from left side of heart to
systemic cells
At systemic cells (e.g., skin, muscles), blood
exchanges gases, nutrients, and wastes
Blood vessels return blood to right side of heart
Fibrous pericardium
Dense irregular CT
Protects and anchors the hear prevents overstreching
myocardium
cardiac muscle layer is the bulk of the heart
myocartditist:inflamation of the myocardium
Pericarditis
inflammation of the pericardium
Serous Pericardium
thin delicate membrane
contains parietal layer-outer layer
pericardial cavity with
pericardial fluid
visceral layer (epicardium)
Pericardial effusion
collection of fluid in the
pericardial space
Cardiac tamponade
Associated bleeding into the
pericardial cavity that compresses the heart and is
potentially lethal
chordae tendinae and papillary muscle funciton
to help open and close the AV valves
SL valves open with-
ventricular contraction-allow blood to flow from ven to pulmonary trunk or aorta
Sl valves close with-
ventricular relaxation-prevents blood from returinnig,blood fills valve cusps, tightly closing the SL valves
Stenosis
is a narrowing of a heart valve
which restricts blood flow.
Insufficiency or incompetence is a failure
of a valve to close completely.
Heart Murumurs
abnormal heart
sounds produced due to turbulence of
blood flowing through a narrowed or
incompetent heart valve.
Coronary Circulation
Coronary circulation is blood supply to the heart
Heart as a very active muscle needs lots of O2
When the heart relaxes, high pressure of blood in
aorta pushes blood into coronary vessels
Coronary Artery Disease (CAD)
Heart muscle receiving
insufficient blood supply
narrowing of vessels---
atherosclerosis, artery
spasm or clot
atherosclerosis--smooth
muscle & fatty deposits
in walls of arteries
Coronary Artery Disease (CAD) treatment
drugs, bypass graft,
angioplasty, stent
Risk Factors for Heart Disease
Risk factors in heart disease:
high blood cholesterol level (LDL & VLDL)
high blood pressure
cigarette smoking
obesity & lack of regular exercise
Other factors include:
diabetes mellitus
genetic predisposition
male gender
high blood levels of fibrinogen
left ventricular hypertrophy
Myocardial Ischaemia
Reduced blood flow through coronary arteries leading to less
oxygen supply to myocardial cells.
Myocardial Infarction
complete obstruction of flow in a coronary artery may
cause myocardial infarction (heart attack).
Working cells or Contractile cells
Wall of atria & ventricles
Responsible for contraction & relaxation of
the heart
Conducting cells or Autorhythmic cells
Specialised cardiac muscle cells
Capable of producing an electrical impulse
Autorhythmic cells
are self-excitable.
generate spontaneous action potentials that then
trigger heart contractions.
act as a pacemaker to set the rhythm for the
entire heart.
SA node
pacemaker of the heart
Generates electrical impulses at the fastest rate compared to other
parts of the conducting system
90 – 120 impulses/min
AV node
40 – 60 impulses/min
AV (His) Bundle & Purkinje fibres
20 – 40/min
Normal range for heart rate
60 – 90 beats / min
Tachycardia
HR > 100 beats / min
Bradycardia
HR < 60 beats / min
Factors affecting the increase in heart rate
Sympathetic nerves
increase HR and increase the force of contraction
increase body temperature: increase HR
Respiration
HR increase slightly during inspiration
Factors affecting the decrease in Heart rate
Parasympathetic nervers (vagus nerve)
Decrease HR and Decrease force of contraction
Body temp
Decrease body temp decrease HR
Respiration
HR decrease slightly during expiration
Hormones & Chemical substances :affecting heart rate
epinephrine, norepinephrine, thyroid hormones:
HR
Acetylcholine: HR
Electrocardiogram (ECG)
Record of the electrical activity of the heart
Records the spread of electrical impulse through the heart
during each heart beat
Can be recorded from the surface of the skin using
electrodes
Standard limb leads
Bipolar limb leads
Measures the potential difference between 2 active electrodes
placed on the limbs
Lead I, Lead II, Lead III
Augmented limb leads
Augmented unipolar leads
Measures the potential difference between an active electrode
and an indifferent electrode
aVR, aVL, aVF
Precordial or chest leads
Unipolar leads
V1 – V6
P wave
Atrial depolarization (spread of electrical
impulse through the atria)
QRS complex
ventricular depolarization (spread of
electrical impulse through the ventricles)
T wave
Ventricular Repolarization
R-R
entire duration of a cardiac action potential
P-R interval
time taken for conduction of electrical
impulse from atria to ventricles
Q-T interval
Entire duration of a ventricular action potential
Uses of ECG
Heart rate
Rhythmicity
Conduction abnormalities
Heart size
Effect of ionic changes and drugs on
heart (hypokalemia, hyperkalemia,
hypocalcemia, hypercalcemia)
Myocardial ischaemia or infarction
Heart diseases
Arrythmia
is an irregularity in
heart rhythm resulting from a defect in the
conduction system of the heart.
Categories are bradycardia, tachycardia, and
fibrillation.
stroke volume
the amount of blood pumped by each ventricle during a single heart beat 70-90mL
cardiac output
the amount of blood pumped by each ventricle during a single heart beat per minute
resting CO=5000-6000mL per min
how to calculate cardiac output
CO=stroke volume x HR(bpm
Cardiac Reserve
Capacity to increase cardiac output above rest level
HR accelerates and stroke volume increases during exercise
CO can increase four-fold in a healthy non-athlete and up to seven-
fold in athlete
Ejection fraction
percentage of blood (out of total amount) that is ejected with each
ventricular systole
equal to stroke volume divided by EDV
normal ejection fraction is about 50–65% for each ventricle
Cardiac Cycle
Is the period between the start of one heartbeat and the beginning
of the next
Includes both contraction and relaxation
Ventricular contraction
V valves pushed closed
Semilunar valves pushed open and blood ejected to artery
Ventricular relaxation
Semilunar valves close
No pressure from below keeping them open
AV valves open
No pressure pushing them closed
Ventricular filling phase
All heart chambers are relaxed
Atrial blood pressure forces AV valves
open and blood flows into ventricles
Semilunar valves remain closed since
arterial pressure is greater than ventricular
pressure
Atrial systole
SA node starts atrial excitation
Atria contract pushing remaining blood into ventricles
Ventricles filled to end-diastolic volume (EDV) (120-140ml)
Atria relax for remainder of cardiac cycle
Isovolumetric contraction phase
Purkinje fibers initiate ventricular excitation
Ventricles contract, pressure rises, and AV valves are pushed
closed
Ventricular pressure is still less than arterial trunk pressure, so
semilunar valves still closed
Ventricular ejection phase
Ventricles continue to contract so that ventricular
pressure rises above arterial pressure
Semilunar valves forced open as blood moves from
ventricles to arterial trunks
Stroke volume (SV)
is amount of blood ejected by
each ventricle (70 – 90 mL)
End systolic volume
(ESV) is amount of blood
remaining in ventricle after contraction finishes
Isovolumetric relaxation phase
Ventricles relax and start to expand, lowering
pressure
Arterial pressure greater than ventricular pressure
By sliding back toward ventricles, blood closes
semilunar valves
AV valves remain closed
When all valves are closed, blood neither enters nor
leaves and the time is called “isovolumetric”
At 75 beats/min, one cycle requires how many seconds
0.8sec
End diastolic volume (EDV)
volume in ventricle at end of diastole, about 130ml
End systolic volume (ESV)
volume in ventricle at end of systole, about 60ml
Stroke volume (SV)
the volume ejected per beat from each ventricle, about 70ml
SV = EDV - ESV
Auscultation of the Chest
act of listening to sounds within the body
usually done with a stethoscope
factors affecting CO = Where heart rate increases
Anxiety/stress(corisol)
pain
hyperthyroidism
exercise
fever
pregnancy medications
caffeine
factors affecting CO = Where heart rate decreases
sleep
hypothyroidism
hypothermia
hypokalemia hypocalcemia
myocardial infarction
Factors affecting C = where stroke volume increases
Venus return
and contractility of the Ventricles
Venus return
the amount of blood returning to the heart
in a heathy normal condition, it should be the same as the CO
Frank-Starling Law of the Heart
Relationship between preload and stroke volume is
explained by mechanism known as Frank-Starling law
Within physiological limits, the force of contraction of the
heart is directly related to the degree to which the
ventricular muscle is stretched during diastole
preload
Stretch of the ventricular walls before they contract
Contractility of the Ventricles
Force of contraction of the ventricles during
ventricular systole
Contractility can be affected by
Autonomic nerves
Hormones
Afterload on the Heart
refers to force that right and left ventricles must
overcome in order to eject blood into their respective
arteries
Elasticity
allows arteries to expand & receive blood
under great pressure during contraction of the
ventricles and to recoil back propelling the blood
through the system.
Contractility
smooth muscle in the tunica media,
allows arteries to increase or decrease lumen size
and to limit bleeding from wounds.