pbl 2

  • Created by: hadar
  • Created on: 27-05-15 20:30
Pale and sweating in shock?
1. BP drops → reduced cardiac output → baroreceptors → results in vasoconstriction → redistribute blood 2. Pain → sympathetic nervous system activated → autonomic hyperactivity → activation of sweat glands → and causes vasoconstriction
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Pale, sweating and clammy
Talk about pain and decreased cardiac output and baroreceptors// RAAS system → kidney → explain pale
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Crackle/ Crepitations
pop open of small airways when inhale (presence of oedema or mucus or anything that constricts the small airways) airways close on exhalation
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narrowing of airways (exudate/transudate/mucus plugging/ anything compresses the airways)
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Expiratory wheeze
lower distal lung → small bronchial → lower (most common)
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Inhalation wheeze
upper airways → compression
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Why would you get tachycardia in hypovolemic shock?
Low cardiac output → compensation mechanism → low blood volume →low blood pressure → baroreceptors activation→ firing to cardiac centre increased→ increase heart rate and contractility
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FRANK- STALIN → law of capillaries
Oedeoma → hydrostatic pressure overcomes the oncotic pressure Increased central venous pressure → pooling of blood in extremities e.g. right heart failure/ pulmonary emboli/ chronic renal disease
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Hypovolemic shock
rapid fluid loss resulting in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion.
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Cardiovascular system response to hypovolemic shock
increasing the heart rate, increasing myocardial contractility, and constricting peripheral blood vessels. occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors)
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Renal system response to hemorrhagic shock
mulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I to angiotensin II. Angiotensin II has 2 main effects - vasoconstriction of arteriolar smooth muscle, and aldosterone secretion
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Neuroendocrine system responds to hemorrhagic shock
increased ADH, response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased reabsorption of water and salt
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Cardiogenic shock
failure of the pump action of the heart, resulting in reduced cardiac output. acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume.
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Signs and symptoms of shock
• Cool, clammy skin • Pale or ashen skin • Rapid weak pulse • Rapid slow breathing •Nausea/vomiting •Weakness/fatigue •Dizziness/fainting
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Physiological consequences of blood loss on heart
increasing the heart rate, increasing myocardial contractility, reduced cardiac output, EDV and ESV decrease
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Physiological consequences of blood loss on blood vessels
constricting peripheral blood vessels, lowers total blood volume,
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3 phases of cardiac cycle
isovolumetric contraction --> ventricular filling --> ventricular systole (contraction)
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End systolic volume (ESV)
the volume of blood in each ventricle at the end of systole (residual volume).
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End diastolic volume (EDV)
the volume of blood within a ventricle immediately before a contraction.
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Stroke volume
the volume of blood ejected from a ventricle with each heartbeat.
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Ejection fraction
the fraction of the end diastolic volume that is ejected with each beat.
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Cardiac output
the volume of the blood ejected by each ventricle per minute.
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Cardiac reserve
the work that the heart is able to perform beyond that required of it under ordinary circumstances. the difference between the rate at which the heart pumps blood and its maximum capacity for pumping blood at any given time.
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the end diastolic pressure that stretches the right or left ventricle of the heart to its greatest geometric dimensions under variable physiologic demand. It’s the initial stretching of the cardiomyocytes prior to contraction.
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the pressure against which the heart must work to eject blood during systole. Afterload is the tension or stress developed in the wall of the left ventricle during ejection.
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Appreciate how cardiac output and total vascular resistance determine blood pressure.
Blood pressure= cardiac output x total peripheral resistance
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Normal RR
16–20 breaths per minute
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Normal pulse
60 to 100 beats per minute.
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Normal BP
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Other cards in this set

Card 2


Pale, sweating and clammy


Talk about pain and decreased cardiac output and baroreceptors// RAAS system → kidney → explain pale

Card 3


Crackle/ Crepitations


Preview of the front of card 3

Card 4




Preview of the front of card 4

Card 5


Expiratory wheeze


Preview of the front of card 5
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