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Vitals

There are four vital signs which


are standard in most medical
settings:
Pulse rate (or heart rate)

Body temperature
Blood pressure
Respiratory rate
Pulse
Rate
Rythm
Amplitude

Compare: left and right


Alternative sides
Pulse: Rate

 Bradycardia: Less than 60/min (Myxedema,


heart block, raised IC tension)

 Tachycardia: Faster than 100/min. (Sinus


tachycardia, PAT, atrial flutter, ventricular tach)
Pulse: Rhythm
 Irregular:(Sinus arrhythmia, extra
systoles, atrial fib, pulses bigemini)
 Pulses bigemini: Normal beat
alternating with extra systole (Dig
toxicity)
 Double systolic peak: Bisferiens
pulse (Aortic regurgitation)
Pulse: Amplitude
 Alternating weak and strong pulse
 Pulses alternans: Normal beat alternating with low
amplitude beat
 Slow small sustained (Aortic stenosis)
 Large bounding pulse: Water hammer pulse: (Aortic
insufficiency, high output states, slow heart rates)
 Decrease in amplitude during inspiration:
Paradoxical pulse: Exaggerated in Pericardiac
tamponade, obstructive lung disease.
Watson's water hammer
pulse
 is the medical sign which describes a pulse that is
bounding and forceful, as if it were the hitting of a
water hammer that was causing the pulse.
 This is associated with increased stroke volume of
the left ventricle and decrease in the peripheral
resistance leading to the widened pulse pressure of
aortic regurgitation.
Compare
 Missing or feeble on one side: (Prior
cath, Takayasu's disease, subclavian
steel syndrome)

 Femoral artery (caorctation of aorta)


Grading Pulse

 4 = Normal
3 = Slightly diminished
2 = About half
1 = Barely palpable
0 = Absent
Pulse: Rate
Rapid heart rate:
821medical conditions
Tachycardia

Paroxysmal tachycardia
Exercise or exertion
Paroxysmal supraventricular tachycardia
 Large meal
 Emotion Paroxysmal atrial tachycardia
 Nervousness Atrial fibrillation
 Anxiety (type of Neurosis) Ventricular fibrillation
 Excitement Electrical conduction disorders
 Anger Wolff-Parkinson-White syndrome
 Fever Heart disorders
 High blood pressure Heart failure
 Low blood pressure Congestive heart failure
 Arrythmias Prior heart attack
Myocarditis

Cardiomyopathy
 Asthma
 Anemia - see also causes of anemia and types of anemia
 Hyperthyroidism Vitamin B deficiency
 Sleep disorders
 Psychological disorders that may cause rapid heart beat Beri-beri
include:
 Panic attack
 Panic disorder Excessive dieting
 Certain stimulating substances that raise pulse include:
 Excess adrenaline Cancer



Nicotine
Caffeine
Illicit drugs
Hemorrhage
Liver disease
 Amphetamines
 Certain medications
Kidney disease



Blood loss
Internal bleeding
Potassium deficiency
Appendicitis
Certain drugs

Sinus tachycardia

Bowel obstruction
Febrile
conditions
Hypertension

Atrial and junctional tachycardia


Atrial flutter
Ventricular tachycardia
Supraventricular tachycardia
Caffeine poisoning
Rheumatic fever
Pulse: Rate

In its simplest formulation, HR is used to represent


sympathovagal balance.

Although this term is poorly defined, it is reasonable to


use it as a measure of the net effects of the
sympathetic and parasympathetic inputs into the sinus
node. This concept is captured by HR.
Heart Rate
 Heartrate is dominated by the activity of the
cardioinhibitory parasympathetic nervous system

 Inconscious and anesthetized humans there is a


tonic level of parasympathetic cardiac nerve firing
and little, if any, sympathetic activity to the heart
at rest.
THE ARTERIAL
BAROREFLEX
 is the primary short-term regulator of systemic
blood pressure via modulation of
parasympathetic and sympathetic nerve activity.
 Changes in arterial blood pressure result in
arterial baroreflex-mediated reciprocal changes
in heart rate (HR) and total peripheral resistance.
 During increases in arterial pressure, the initial
reflex-induced slowing of the heart is caused
primarily, if not exclusively, by increases in cardiac
vagal nerve activity.

 During decreases in arterial pressure, the baroreflex-


induced tachycardia is caused by decreases in
parasympathetic nerve activity in addition to
increases in sympathetic nerve activity .
Schematic diagram of the mathematical model for the baroreflex
feedback control of heart rate (HR).
 In many diseases, including hypertension and heart failure, cardiac vagal
activity is diminished and unresponsive.

 The relative absence of cardiac vagal activity, or a diminished respiratory


modulation of cardiac vagal activity, is often used clinically as an index of
pathophysiology and the likelihood of sudden cardiac death.

 Restoration of cardiac vagal activity lessens ischemia and reperfusion-


induced arrhythmias and decreases risk of sudden death after myocardial
infarction, suggesting that increases in cardiac vagal activity could be an
effective clinical target in heart diseases.

Neural cardiovascular control
during exercise
 Brain neural signals (central command)

 Aorta and carotid arteries (arterial baroreflex)

 skeletal muscle (exercise pressor reflex)


Exercise
Acombination of
sympathoexcitation and vagal
withdrawal

HR
Muscle metaboreflex
 skeletal muscle does not receive sufficient blood
flow to meet metabolic demands

 metabolites accumulate (e.g., lactic acid, H+, and


diprotonated phosphate)

 metabolites stimulate afferent neurons, which evoke


a reflex increase in sympathetic nerve activity
(SNA) and mean arterial pressure (MAP).
The nucleus of
the solitary
tract, or NST, is
located along
the length of the
medulla
Figure Legend

 It is proposed that a population of GABAergic NTS cells


is the synaptic target for spinal dorsal horn neurones
that transmit sensory feedback from skeletal muscle.
Corelease of glutamate and SP from dorsal horn fibres
depolarize second order GABA interneurones that, in
turn, hyperpolarize barosensitive NTS neurones. In this
manner, barosensitive neurones in the caudal aspect of
the NTS are inhibited, which may contribute to
baroreflex resetting. It is proposed that reflex resetting
may limit the degree of baroinhibition to the heart and
vascular smooth muscle and may contribute to exercise-
induced excitation of the cardiovascular system.
NO directly decreases
both glutamatergic
and glycinergic
neurotransmission to
CVPNs, and this is
likely mediated by
actions ofNO at
presynaptic terminals,
In contrast, NO
facilitates GABAergic
activity in CVPNs,
which is likely
because of excitation
of GABAergic
neurons at their cell
bodies, with no action
at presynaptic
terminals, because this

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