Facts about U wave.
The origin of the U wave is still in question,
although most authorities correlate the U
wave with electrophysiologic events called
"afterdepolarizations" in the ventricles.
U waves are usually best seen in the right
precordial leads especially V2 and V3.
Differential Diagnosis of U Wave Abnormalities
Prominent upright U waves
Sinus bradycardia accentuates the U wave
Hypokalemia (remember the triad of ST segment depression, low amplitude T waves, and
prominent U waves)
Quinidine and other type 1A antiarrhythmics
CNS disease with long QT intervals (often the T and U fuse to form a giant "T-U fusion
LVH (right precordial leads with deep S waves)
Mitral valve prolapse (some cases)
Negative or "inverted" U waves
Ischemic heart disease (often indicating left main or LAD
disease) Myocardial infarction (in leads with pathologic Q waves)
During episode of acute ischemia (angina or exercise-induced ischemia)
Post extrasystolic in patients with coronary heart disease
During coronary artery spasm (Prinzmetal's angina)
Nonischemic causes Some cases of LVH or RVH (usually in leads with
prominent R waves)
Some patients with LQTS (see below: Lead V6 shows giant negative TU
fusion wave in patient with LQTS; a prominent upright U wave is seen in
Sites where the heart sound are heard
Mitral area: 1st heart sound
Tricuspid area: 3rd and 4th heart sound
Aortic area: 2nd heart sound
Pulmonary area: 2nd heart sound
Abnormal heart sounds are called murmur.
1.Narrowing of valve or stenosis.
2. Incompetence (dilation) of valve.
3.Congenital defect: atrial septal defect, ventricular septal defect.
4. Increased flow through the normal valve.
Murmur that are produced outside heart in vascular system are called bruits.
Process of listening for sound within body usually sounds of thoracic or abdominal viscera by
Pulse is rhythmic dilation and elongation of arterial wall passively produced by pressure change during
ventricular systole and diastole.
Normal range: 60—90beats/min
Normal pulse tracing is called catacrotic pulse.
Pulse has upstroke and down stroke wave.
•The upstroke wave is ‘P’ and has no secondary wave. It is called percussion wave.
•Near the middle of down stroke there is sharp depression called dicrotic notch (D).
•This dicrotic notch is followed by small wave called dicrotic wave (d).
P or percussion wave
It is the wave from starting of the wave upto dicrotic notch
It coincides with ventricular systole.
It is due to sharp fall of arterial pressure.
It is due to rolling back of aortic blood to left ventricle at the beginning of ventricular diastole.
ATRIAL PULSE DEPENDS UPON
1. Intermittent discharge of blood from contracting left ventricles.
2. Resistance to the blood flow in its passage from arterioles into capillaries.
3.The elasticity of vessels wall.
Components of examination of Pulse
Rate: pulse/min, normally coincide with heart rate. Different in premature contraction.
Rhythm: Each beats are at equidistant or not.
Volume: Depends upon stroke volume. More the stroke volume more volume of pulse.
Condition of vessel wall: By feeling pulse we can know condition of blood vessels.
Soft and easily compressible pulse indicates: low CO.
Hard and not compressible pulse indicates atherosclerosis.
Character: normal or abnormal, anacrotic (aortic stenosis), water hammer etc.
Radio femoral delay Co-actation of aorta.
Site of feeling a pulse
Post. Tibial artery
Arteria dorsalis pedis
2. Venous pulse
Jugular vein only can be seen but not felt.
Procedure of feeling arterial pulse
Pulse is felt by placing three finger side by side on radial artery.
Fingers are index, middle and ring finger.
Anacrotic pulse: slow rising pulse
When secondary wave is found in upstroke of pulse tracing then it is called anacrotic pulse
Cause: aortic stenosis
Collapsing pulse (water hammer pulse):
It is characterize by rapid upstroke and descend of pulse wave.
Cause: Aortic Incompetence, PDA, Arteriovenous fistula.
Pulsus bisferiens (double peak):
Combination of slow rising pulse and collapsing pulse.
Cause: Aortic Stenosis and Aortic Regurgitation
Pulse volume smaller during inspiration and larger during expiration.
Causes: Cardiac temponade (pericardial effusion), severe acute asthma.
The amplitude of pulse become alternately large and small.
Cause: Left ventricular failure
When the frequency of pulse is increased during inspiration and fall during expiration, it is called sinus
Found in children but less commonly in adult.
It occurs due to alteration of vagal tone during inspiration.
BP means force exerted by blood against any unit area of the vessel
BP is also defined as lateral pressure exerted by blood on the vessels
wall by its contained blood while flowing through it.
Blood pressure 50 mm Hg, means that force exerted on the wall is
sufficient to push a column of mercury against gravity up to 50
1 mm Hg of mercury pressure equals to 13.6 mm of water.
of mercury is 13.6 times specific gravity than that of water.
Blood pressure = Cardiac Output X Peripheral Resistance
Importance of BP:
1. It is essential for the flow of blood through the circulatory tree.
2. It provides the motive force for filtration through the capillary bed which is essential for
b. Formation of urine
c. Formation of lymph
Basal blood pressure:
It is lowest blood pressure necessary for maintaining blood flow sufficient for the need of body at rest.
Causal blood pressure
Any pressure that is recorded under ordinary circumstances of life is called casual BP.
Types of blood pressure
It is maximum pressure in the artery during systole.
100-140 mm Hg
2. Diastolic BP
It is minimum pressure in the artery during diastole.
It is difference between systolic and diastolic pressure.
4. Mean pressure
It is diastolic pressure plus one third of pulse pressure
Significance of different types of BP
Systolic pressure indicates
1.The extend of work done by heart
2.The force with which heart is working
3.The degree of pressure, which the arterial wall has to withstand.
1.It indicates the constant load against which the heart works
2.Increased diastolic pressure indicates that the heart is approaching to failure.
It indicates the cardiac output.
Physiological variation of blood pressure
Age: With increasing age BP increases
Infant 60/30 mmHg
1 year 80/40
20 year 120/80
45 year 145/90
70 year 170/95
Sex: In female BP is slightly lower
Exercise: In heavy exercise systolic BP increases
During daytime pressure rises up to 2 o clock then there is a slight fall
During sleep: During sleep there is fall of BP by 15-20 mmHg
After meal: BP rises
Emotion and excitement: Raises systolic BP
Respiration: During inspiration BP fall and increases during expiration.
Factors controlling the blood pressure
1. Cardiac Output, which depend on
Force of contraction
2. Peripheral resistance, which depend upon
Elasticity of arterial wall
Velocity of blood
Viscosity of blood
1. Short-term regulation
A. Mechanism acting within seconds
I. Baroreceptor feedback mechanism
II. Chemoreceptor feedback mechanism
III. Central nervous system ischaemia mechanism
B. Mechanism acting within minutes
I. Renin angiotensin vasoconstrictor mechanism
II. Capillary fluid shift mechanism
III. Stress relaxation changes in vasculature
Baroreceptor are spray like nerve ending which are stimulated when stretched
Location: In wall of internal carotid artery above the bifurcation
In the wall of arch of aorta.
When blood pressure increased
When blood pressure rises above a critical value, the baroreceptor are stimulated
( the stimulation reaches maximum when pressure is 180 mm Hg)
Impulse is carried by Hering’s nerve and Glossopharyngeal nerve to tractus solitarius
This impulse cause inhibition of vasomotor center and excitation of Vagal center
Vasodilatation of peripheral vessels
Slowing of heart rate and force of contraction
Both these effect decrease the blood pressure back toward normal level.
Decrease in blood pressure
When blood pressure falls
Baroreceptor remain inactive
No inhibition to vasomotor center
No excitation to vagal center
Blood pressure increase back to normal
As baroreceptor system opposes either increase or decrease in original arterial
pressure it is called pressure buffer system.
Baroreceptor are unimportant in controlling blood pressure for long term
because baroreceptor reset to the pressure that they are exposed after 1 or 2
Chemoreceptor are chemosensitive cells
They are sensitive to lack of oxygen and to excess of H ion and CO2
Location: Carotid bodies in bifurcation of internal carotid arteries
Aortic bodies in arch of aorta
When blood pressure falls
There is decrease in blood supply to all tissue of body. So there is decrease in blood supply to
chemoreceptor. Decrease blood supply means decrease oxygen conc. and increase CO2 conc.
Decrease supply of oxygen and presence of more carbon dioxide and H+ in chemoreceptor
Stimulates these receptor
Impulse are carried by Hering’s and glossopharyngeal nerve to vasomotor center ‘
Which excites vasomoto pressure center
Increase blood pressure back to normal
CNS ischaemia mechanism
Decrease blood pressure
Decrease blood supply to vasomotor center in brain
Cause nutritional deficiency and decrease Carbondioxide removal
This leads to cerebral ischaemia
Cause stimulation of vasomotor sympathetic system
Increase BP back to normal
Mechanism acting within minutes
Works only after few minutes following an acute arterial pressure change, mostly activated within 30
min to several hours.
1. Capillary fluid shift mechanism
2. Stress relaxation mechanism
Capillary fluid shift mechanism
When BP increases
Increase capillary hydrostatic pressure
This cause increase fluid loss out of circulation into the tissue
This reduce ECF volume
This reduces blood volume
Reduces BP back to normal
Capillary fluid shift mechanism (cont)
When BP falls
Decrease in Capillary hydrostatic pressure
Capillary absorbs fluid from tissue
Increase blood volume
Increase BP back to normal
Stress relaxation mechanism
When pressure in blood vessels becomes too high
This Stress the blood vessels
This process keeps on stretching wall more and more
This stretch of wall of vessels cause fall of pressure toward normal
Vessel achieves a larger diameter.
This continuing stretch of vessels is called “stress relaxation”
Poiseuille’s law flow across the tube
Q= pai P r4/ 8nl
D= 1 flow 1ml/min
D= 2 flow 16ml/min
D= 4 flow 256ml/min.
Long-term control mechanism
1. Renal body fluid mechanism
2. Renin angiotensin mechanism
Renal body fluid mechanism
Increase in BP
Increase renal output of salt and water
(Pressure diuresis and pressure natriuresis)
Decrease ECF volume
Decrease Blood volume
Decrease Cardiac output
Decrease BP back to normal
When blood pressure decrease
Decrease renal water and salt output
Increase ECF volume
Increase blood volume
Increase venous return to heart
Increase Cardiac output
Increase blood pressure to normal
Importance of salt in renal body fluid system for arterial pressure regulation
Excess salt in body fluid
Increases osmolality of body fluid
This stimulate thirst center
Person drinks water to dilutes ECF salt to normal
Increase ECF volume
Increase salt -increase osmolality in ECF
Stimulates hypothalamic posterior pituitary glands
Increases ADH secretion
ADH stimulates kidney to reabsorb large quantity of water
Decreasing urinary loss of water
Increase ECF volume
Renin angiotensin mechanism
Renin is small protein enzyme released by the juxtaglomerular cell of kidney
when arterial BP falls too low.
Renin is synthesized and stored in an inactive form called prorenin in
juxtaglomerular cell of kidney.
When arterial pressure decrease in kidney prorenin molecules split and releases
J G cells secrete Renin, which is released in blood
Renin causes conversion of Angiotensiongen (plasma protein) into Angiotensin I
Angiotensin I is converted to Angiotensin II by Angiotensin converting enzyme
(ACE) located in endothelium of lungs vessels.
Angiotensin II has following effects:
1.It cause vasoconstriction of arteriole and veins which increase peripheral resistance---increase
2.It help to secrete aldosterone from adrenals-Aldosterone increase salt retention, which in turn
increase water reabsorption---- increase ECF volume --- increase blood pressure.
3.Angiotensin II itself can also cause salt and water retention by directly acting on kidney.
Renin persists in blood for 30min to 1 hour.
Angiotensin I is weak but angiotensin II is strong vasoconstrictor.
Angiotensin II persists in blood for 1-2 min, because it is rapidly inactivated by
multiple blood enzymes collectively called “ Angiotensinase”.
On the other hand increase blood pressure cause decrease Renin secretion that also decrease
the function of angiotensin. So salt and water output of kidney increases which cause
decrease ECF volume and ultimately causes decrease blood pressure back to normal.
Measurement of blood pressure
a. Palpatory method: can measure only systolic
b. Auscultatory method
Turbulent flow means that the blood flows in all the directions within the artery with
intermixing. Laminar flow pattern is lost. Due to this turbulent flow the a sound is heard
with each pulsation.
Blood flow through the smooth blood vessels produce normally no sounds.
But if the artery is partially occluded by inflated cuff then it creates turbulence of blood flow, the jet of
blood through the partially occluded vessel sets up the vibration and produce sound called
It has four different stages
1. Tapping sound: sudden appearance of faint but clear tapping sound-systolic pressure
2.Loud sound: On decreasing the pressure for (10mmHg) the sound becomes loud.
3.Dull sound: Further decreasing the pressure (10-15mmHg) the sound becomes dull.
4. Muffle sound: Further decreasing the pressure (10-15mm Hg) the sound becomes muffled
and gradually disappear .The point at which the muffled sound appears/disappear coincides
with diastolic blood pressure.
How to measure blood pressure
1. Patient should be relaxed, arm supported at the
level of heart, clothing removed from arm.
2. Cuff neatly applied, correct size (should cover
at least 2/3 of the circumference), no leaks.
3. Manometer upright, well supported, if aneroid regularly
4. Operator check systolic pressure by palpation, release pressure
, avoid parallax error.
1. The blood pressure should be measured in both
arms, patient in lying or sitting and standing
positions. (postural hypotension).
2. Report as 130/90 mmHg, right/left arm,
HTN is a clinical condition characterized by persistent rise of blood pressure above the normal range.
Normal BP 120/80mm Hg(100-140/60-90).
Pre HTN 120-140/80-90 mm Hg
Stage I HTN 140-160/ 90-100 mmHg
Stage II HTN > 160/100mm Hg
Effects of HTN
1.Excess workload on heart lead to early heart failure, it is a risk factor for CAD.
2.High pressure sometimes rupture major blood vessels in brain followed by death of major
portion of brain which is called stroke, which causes paralysis.
3.High pressure almost causes multiple hemorrhages in kidney producing many area of renal
destruction and eventually renal failure.
1.Primary / essential HTN
HTN for which no specific cause Is known.
It is due to some specific disease like
Coarctation of aorta
Volume loading HTN
HTN, which occurs due to excess ECF volume. It is due to salt intake or salt retention by kidney
It is due to continuous infusion of vasoconstrictor agent into blood or by excess secretion of
vasoconstrictor from endocrine glands
The vasoconstrictors are
concept of shock
Description of each type
Causes of each type
Shock and syncope
Shock refers to reduction to peripheral tissue
Syncope: Partial or complete loss of consciousness
with interruption of awareness of oneself and ones
surroundings. When the loss of consciousness is
temporary and there is spontaneous recovery, it is
referred to as syncope or, in nonmedical quarters,
fainting. Syncope accounts for one in every 30 visits
to an emergency room. It is pronounced sin-ko-pea.
Syncope is due to a temporary reduction in
blood flow and therefore a shortage of
oxygen to the brain. This leads to
lightheadedness or a "black out" episode, a
loss of consciousness. Temporary
impairment of the blood supply to the brain
can be caused by heart conditions and by
conditions that do not directly involve the
Shock is a Cardiovascular Derangement in
1. Deliver Oxygen and Metabolic Substrates
2. Remove Products of Cellular Metabolism
Definition:A physiological state characterized by a significant,
systemic reduction in tissue perfusion, resulting in decreased
tissue oxygen delivery and insufficient removal of cellular
metabolic products, resulting in tissue injury.
Shock can be caused by any condition that reduces
blood flow, including:
1.Heart problems (such as heart attack) or
2.Low blood volume (as with heavy
bleeding or dehydration).
3.Changes in blood vessels (as with
infection or severe allergic reactions).
Dizziness, light-headedness, or faintness.
Profuse sweating, moist, pale skin
Rapid but weak pulse
•Decreased preload->small ventricular end-diastolic volumes ->
inadequate cardiac generation of pressure and flow
-- bleeding: trauma, GI bleeding, ruptured aneurysms,
-- protracted vomiting or diarrhea, severe burn
-- adrenal insufficiency; diabetes insipidus-- dehydration
-- third spacing: intestinal obstruction, pancreatitis, cirrhosis
Signs & Symptoms: Hypotension, Tachycardia, Oliguria,
Markers: monitor UOP,CVP, BP, HR, Hct,CO, lactic acid
Treatment: ABCs, IVF (crystalloid), Transfusion,stop
ongoing Blood Loss
Patients on β-blockers, spinal shock & athletes may not
Mechanism: release of inflammatory mediators leading to
1. Disruption of the microvascular endothelium
2. Cutaneous arteriolar dilation and sequestration of blood in
cutaneous venules and small veins
1. Anaphylaxis, drug, toxin reactions
2. Trauma: crush injuries, major fractures, major burns.
3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis, meningitis,
cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic
shock syndrome, etc.
Signs: Early– warm vasodilation, often adequate urine
output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Early—hyperglycemia, respiratory
WBC typically normal or low.
Late – Leukocytosis, lactic acidosis
Very Late– Disseminated Intravascular
Coagulation & Multi-Organ
Tx : ABCs, IVF, Blood cx, Drainage (ie abscess)
Mechanism: Intrinsic abnormality of heart -> inability to
deliver blood into the vasculature with adequate power
1. Cardiac: myocardial ischemia, myocardial infarction, cardiomyopathy,
2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture, septal
defects, aortic stenosis
3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrial fibrillation,
atrial flutter, ventricular fibrillation)
4. Obstructive disorders: PE, tension peneumothorax, pericardial tamponade,
constrictive pericaditis, severe pulmonary hypertension.
1. Spinal cord injury
2. Regional anesthesia
4. Neurological disorders
Mechanism: Loss of autonomic innervation of the
cardiovascular system (arterioles, venules, small
veins, including the heart)
Bee or wasp sting, drugs as penicillin
Antigen antibody mediated type 1 hypersensitivity
reaction, systemic, in a previously sensitized person.
Ag + Ab mast cell, basophils-release inflamatory
mediators, as histamine, leukotrines, serotonine,
Typical early phase and late phase reactions.
Widespread vasodilatation leading to shock.
Renal, pulmonary and other system effects.
Monitoring Adjuncts in Shock
Central Venous Line
* Check the person's airway, breathing, and circulation. If necessary, begin
rescue breathing and CPR.
Even if the person is able to breathe on his or her own, continue to check
rate of breathing at least every 5 minutes until help arrives.
If the person is conscious and DOES NOT have an injury to the head, leg,
neck, or spine, place the person in the shock position.
Lay the person on the back and elevate the legs about 12 inches.
DO NOT elevate the head. If raising the legs will cause pain or
potential harm, leave the person lying flat.
Give appropriate first aid for any wounds, injuries, or illnesses.
Keep the person warm and comfortable. Loosen tight clothing.
The position that has the head and torso
(trunk) supine and the lower extremities
elevated 6" to 12". This helps to increase
blood flow to the brain; also referred to as
the modified Trendelenburg's position.
IF THE PERSON VOMITS OR
Turn the head to one side so he or she will not
choke. Do this as long as there is NO suspicion of
If a spinal injury is suspected, "log roll" him or her
instead. Keep the person's head, neck and back in
line and roll him or her as a unit.
DO NOT give the person anything by mouth, including anything
to eat or drink.
DO NOT move the person with a known or suspected spinal
DO NOT wait for milder shock symptoms to worsen before
calling for emergency medical help.
Learn ways to prevent heart disease, falls, injuries,
dehydration, and other causes of shock.
If you have a known allergy (for example, to insect
bites or stings), carry an epinephrine pen.
Once someone is already in shock, the
sooner shock is treated, the less damage
there may be to the person's vital organs
(like the kidney, liver, and brain).
Early first aid and emergency medical
help can save a life.
changes of tissues
Shock = hypoperfusion of microcirculation
humoral factors ↑
Shock is an acute, systemic fundamental
pathologic process in microcirculatory
disorder of perfusion .
drenaline, noradrenaline , angiotensin II,
Pale, cold and
Apathy or coma
Pathogenesis and typical
changes of shock
According to the different changes of
microcirculation, the typical shock is
usually divided into three phases :
Ischemic hypoxia phase
(Early phase of shock or Compensated phase)
phase of stagnant hypoxia
(phase of shock or Decompensated phase)
phase of microcirculatory failure
(Late phase of shock or Refractory phase of shock or phase of Disseminated
Microcirculation is the blood circulation between
the arterioles and venules. between arterioles and venules.