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Medicine Sem 2 > Case 9 > Flashcards

Case 9 Flashcards

1
Q

what is alkalosis?

A

alkalosis refers to excess removal of H+ from the body fluids

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2
Q

what is acidosis?

A

acidosis refers to excess addition of H+ to the body fluids

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3
Q

the regulation of the acid-base control in the extracellular fluid in the body is carried out by what?

A

weak acids and bases

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4
Q

what is the normal pH of arterial blood?

A

7.4

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5
Q

what is the normal pH of venous blood?

A

7.35

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6
Q

what’s the normal pH within cells like?

A

it’s slightly lower than the arterial blood pH because cell metabolism of the cells produces acid, especially H2CO3 (carbonic acid)

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7
Q

what are normal sources of acid?

A
  1. CO2: this is converted to carbonic acid, leading to the dissociation into H+ ions
  2. metabolic acids: sulphuric acid; phosphoric acid; ketone acids (diabetic ketoacidosis); lactic acid (hypoxia and exercise)
  3. GI loss of HCO3-: this could be as a result of diarrhoea
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8
Q

how is acid removed?

A
  1. buffering (H+ ions and HCO3- ions)
  2. respiration
  3. renal control
  • the acid reacts with the bicarbonate ions (HCO3-) to form carbonic acid
  • the carbonic acid dissociates into water and carbon dioxide
  • the carbon dioxide is then expired
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9
Q

how is lactic acid removed?

A

the removal of lactic acid involves oxygen:

  • oxygen is involved in the breakdown of lactic acid
  • lactic acid is broken down into carbon dioxide and water in the liver
  • the carbon dioxide is expired
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10
Q

what happens to metabolic acids?

A

metabolic acids are broken down into an anion and H+ ions

  • the anion is excreted in the urine
  • the H+ ions are secreted from peritubular capillaries into the renal tubular lumen - this occurs at the distal part of the nephron in the kidneys
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11
Q

how long does each component of maintaining acid-base balance take?

A

buffering takes seconds; the respiratory control takes minutes and the renal control takes hours to days depending on the severity of the deviation from normal

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12
Q

what are the three main systems involved in the regulation of the H+ concentration in the body?

A
  1. chemical acid-base buffer systems
    - these function by combining the body fluid with acid or base to prevent excessive changes in H+ concentration
    - this looks to correct metabolic acidosis/alkalosis
  2. respiratory centre
    - this works quickly to regulate the removal of CO2 (and therefore H2CO3) from the extracellular fluid
    - this looks to correct respiratory acidosis/alkalosis
  3. kidneys
    - this works slowly by excreting either acid or alkaline urine, thereby readjusting the extracellular fluid H+ concentration
    - this is the most powerful system of the three
    - this looks to correct acidosis/alkalosis
    - there may be problems: excretion of excess acid can lead to metabolic alkalosis and excretion of excess base can lead to metabolic acidosis
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13
Q

what are inorganic mechanisms of buffering to maintain acid-base balance?

A 
bicarbonate:
HCO3- + H+  H2CO (-> CO2 + H2O) 
phosphate:
HPO42- + H+  H2PO4- 
(H2PO4- is excreted as a sodium salt (NaH2PO4), carrying with it the excess hydrogen 
ammonia: 
NH3 + H+  NH4+ 
(The NH4+ is secreted into the renal tubular and excreted from the body)
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14
Q

what is the organic mechanism of buffering to maintain acid-base balance?

A

protein

H+ + Hb HHb

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15
Q

what are the two main roles of the kidneys in regards to acid-base balance?

A
  1. filtration
    - HCO3- ions are freely filtered through the glomerulus and into the kidneys
    - 99.9% of HCO3- is reabsorbed
    - the reabsorption occurs mainly in the early proximal tubule
  2. secretion
    - secretion of H+ ions increases the plasma HCO3-
    - the kidneys mainly secrete two ions: NH4+ (ammonia buffering) and active (via H+-ATPase) secretion of H+ ions
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16
Q

describe the compensation of acidosis

A

this is compensated by excess secretion of H+ ions and the complete reabsorption of HCO3- ions

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17
Q

describe the compensation of alkalosis

A

this is compensated by excretion of HCO3- ions

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18
Q

what is HCO3- concentration regulated mainly by?

A

the kidneys

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19
Q

metabolic acid-base disorders result from a change in what?

A

HCO3- concentration

20
Q

respiratory acid-base disorders result from a change in what?

A

PCO2

21
Q

what is shock?

A

shock is a condition associated with circulatory collapse, when the arterial blood pressure is too low to maintain an adequate supply of blood to the tissues

shock is characterised by systemic hypotension as a result of reduced cardiac output or because of reduced effective circulating blood volume

22
Q

what are the signs of shock? and which shock are they associated with?

A
  • cold, sweaty pallid skin (hypovolemic shock)
  • warm, flushed skin (septic shock)
  • weak rapid pulse
  • irregular breathing (hyperventilation)
  • decreased level of consciousness
23
Q

what are they different ways in which shock may be caused?

A
  1. due to a decrease in the volume of blood (hypovolemic shock), as occurs after an internal or external haemorrhage (haemorrhagic shock)
  2. circulatory shock and haemorrhage shock fall under the category of hypovolemic shock
  3. by reduced activity of the heart (cardiogenic shock), as in coronary thrombosis, myocardial infarction or pulmonary embolism
  4. due to widespread dilation of blood vessels so that there is insufficient blood to fill them - this may be as a result of severe sepsis (septic shock) with a resultant systemic inflammatory response
  5. by a severe allergic response (anaphylactic shock) - in these situations, acute widespread vasodilation results in tissue hypoperfusion and hypoxia
  6. emotional shock due to a personal tragedy or disaster, or as a result of damage to the spinal cord (neurogenic shock)
24
Q

what are the consequences of shock?

A

impaired tissue perfusion and cellular hypoxia

  • at the onset of shock the cellular injury is reversible
  • prolonged shock eventually leads to irreversible tissue injury that often proves fatal
25
Q

what are the stages of shock?

  • what’s responsible for patient’s coolness of skin and pallor
  • which vessels are not affected
A
  1. non-progressive stage
    The normal circulatory compensatory mechanisms eventually cause full recovery without help from outside therapy
    - neurohumeral mechanisms help to maintain cardiac output and blood pressure
    - this results in: tachycardia, peripheral vasoconstriction and renal conservation of fluid
    - cutaneous vasoconstriction is responsible for the patient’s coolness and pallor of the skin in shock
    - coronary and cerebral vessels are not affected by the SNS so as to allow adequate blood flow and oxygen delivery to the heart and the brain
  2. a progressive stage
    Without therapy, the shock worsens until death
    - widespread tissue hypoxia, resulting in anaerobic glycolysis and subsequent build-up of lactic acid
    - this leads to ‘metabolic acidosis’, which causes dilation of the arterioles and subsequent pooling of blood in the microcirculation - this worsens the cardiac output by decreasing the venous return to the heart
    - widespread tissue hypoxia eventually leads to organ failure
  3. An irreversible stage
    - the shock has progressed to an extent where therapy is inadequate to save the person’s life, even though, for the moment, the person is still alive
    - lysosomal enzyme leakage results in widespread cell injury
    - nitric oxide release worsens myocardial contractile function
    - ischaemia of the bowel may cause intestinal flora to enter circulation and cause bacteraemic shock (septic shock)
    - at this stage the patient has complete renal shutdown and this leads to death
26
Q

explain how shock leads to death

A
  • the initial threat to life stems from the underling cause of the shock
  • rapidly, however, the cardiac, cerebral and pulmonary changes secondary to shock worsen the problem
  • eventually, the electrolyte disturbances and metabolic acidosis also exacerbate the situation
  • individuals who survive the initial complications may enter a second phase dominated by renal insufficiency and marked by a progressive fall in urine output as well as severe fluid and electrolyte imbalances
27
Q

what happens initially during haemorrhage?

A
  • initially blood pressure & cardiac output are maintained while blood is being lost
  • greater blood loss diminishes the cardiac output first and later the arterial pressure, until both fall to zero when around 45% of the blood is lost
28
Q

what do the sympathetic reflexes do during blood loss? (arterial pressure and cardiac output)

A
  • they maintain the arterial pressure at a higher level for longer than the cardiac output
  • the arterial pressure is maintained by increasing the total peripheral resistance (arteriole constriction), which has no effect on the cardiac output
  • the venous constriction prevents the decrease in venous return and cardiac output from falling too low, whilst still maintaining arterial pressure
29
Q

why is there a plateau in the graph of cardiac output and arterial pressure against percentage of total blood removed?

A

its due to the central nervous system’s ischaemic response, which provides extreme stimulation of the sympathetic nervous system

30
Q

which circulatory systems don’t undergo vasoconstriction?

A

the coronary and cerebral circulatory systems

31
Q

what is circulatory shock usually a result of?

A

inadequate cardiac output

- therefore, any condition that reduces the cardiac output far below normal will likely lead to circulatory shock

32
Q

what are the two types of factors that can severely reduce cardiac output?

A
  1. abnormalities that decrease the ability of the heart to pump blood
  2. factors that decrease venous return
33
Q

describe progressive shock

A

Cardiac Depression:

  • Fall in arterial pressure causes a decrease in the coronary blood flow to the myocardium, and consequently a decrease in the level of nutrition and oxygen delivered
  • This weakens the heart muscle and thereby decreases the cardiac output more
  • Thus, a positive feedback cycle has developed, whereby the shock becomes more and more severe

Vasomotor Failure:

  • Initially the sympathetic reflexes help maintain cardiac output and arterial pressure
  • Eventually, diminished blood flow to the brain’s vasomotor centre depresses the centre so much that it, too, becomes progressively less active and finally totally inactive

Acidosis:
- This results from anaerobic tissue metabolism continuing without tissue blood flow to remove the acidic by-products (lactate)

Blockage of Very Small Vessels:
- The acidic blood causes local blood agglutination, resulting in blood clots, leading to very small plugs in the small vessels, thus occluding them

Increased Capillary Permeability:

  • During prolonged capillary hypoxia, the capillary permeability gradually increases, and large quantities of fluid transude into the tissues
  • This decreases the blood volume even more.

Cardiac Depression Caused by Endotoxin:

  • Endotoxin is released from the bodies of dead gram-negative bacteria in the intestines
  • Diminished blood flow to the intestines causes enhanced formation and absorption of endotoxin
  • The circulating toxin then causes increased cellular metabolism despite inadequate nutrition of the cells
  • This causes cardiac depression

Generalized Cellular Deterioration

34
Q

what does bundle branch conduction delay produce on a ECG?

A
  • produces slight widening of the QRS complex (up to 0.11s) - it’s known as incomplete bundle branch block
  • complete block of a bundle branch - associated with a wider QRS complex (0.12s or more)
  • the shape of the QRS depends on whether the right or left bundle is blocked of
35
Q

what happens during a right bundle branch block? what causes the change in the QRS complex?

A
  • the right ventricle is not directly activated by impulses through the right bundle branch
  • the left ventricle however, is still normally activated by the left bundle branch
  • these impulses are then able to travel through the myocardium of the left ventricle to the right ventricle and depolarise the right ventricle this way
  • as conduction through the myocardium is slower than conduction through the bundle of His-Purkinje fibres, the QRS complex is seen to be widened
36
Q

what’s a hemiblock?

A

Blocks that occur within the fascicles of the left bundle branch are known as hemiblocks.
The left bundle branch consists of three fascicles:
1. The left anterior fascicle.
- Innervates the upper and anterior parts of the left ventricle.
2. The left posterior fascicle.
- Innervates the posterior and inferoposterior walls of the left ventricle.
3. The septal fascicle.
- Innervates the septal wall

A block of any of these fascicles is known as a hemiblock:

  1. Left Posterior Hemiblock (LPHB).
  2. Left Anterior Hemiblock (LAHB).
  3. Left Septal Hemiblock (LSHB).
37
Q

how is pulmonary artery pressure measured?

A

this is measured by inserting a catheter, the Swan-Ganz catheter, into the pulmonary artery

38
Q

what is the Swan-Ganz used for?

A
  • detect heart failure
  • monitor therapy
  • evaluate effects off drugs
39
Q

The Swan-Ganz catheter allows direct simultaneous measurement of which pressures?

A
  • right atrium
  • right ventricle
  • pulmonary artery
  • left atrium (filling pressure (‘wedge pressure’))
40
Q

describe the Swan-Ganz catheter

A
  • the catheter has two lumens and is equipped with an inflatable ballon at the tip, which facilitates its placement into the pulmonary artery through the flow of blood
  • the balloon, when inflated, causes the catheter to ‘wedge’ in a small pulmonary blood vessel
  • the catheter is so wedged that it can provide an indirect measurement of the pressure in the left atrium
  • it is monitored and guided by the pressure waveforms recorded from the distal
41
Q

what does fluid replacement therapy involve?

A

‘crystalloid’ (such as NaCl- also known as saline)
- these just add volume to blood as well as adding electrolytes
‘colloid’ (such as Gelofusine)
- colloids are volume expanders that is used as a blood plasma replacement if a significant amount of blood has been lost
- it causes an increase in the blood volume, blood flow, cardiac output and oxygen transportation.
- colloids are big molecules so when they are administered, they draw in extracellular fluid into to the blood as a result of osmosis

42
Q

what is diamorphine?

A
  • heroin

- narcotic analgesic

43
Q

what’s diamorphine’s mechanism of action?

A
  • it’s a mu-opioid agonist
  • it acts on endogenous mu-opioid receptors in the brain
  • diamorphine is converted into morphine before crossing the blood brain barrier and agonising the mu-opioid receptors
  • however, taken IV, diamorphine itself crosses the blood brain barrier - it’s rapidly metabolised into morphine once in the brain
  • morphine then agonises the opioid receptors
  • endorphins are released in the brain and nerves, attenuating pain
  • the body responds to diamorphine in the brain by reducing production of endogenous opioids when diamorphine is present
44
Q

what is the Glasgow Coma Scale?

A
  • a neurological scale that aims to describe the level of consciousness in a person following a traumatic brain injury
  • the patient is assessed against the criteria of the scale and the resulting points give a patient score between 3 (indicating deep unconsciousness) and 15
  • the elements of the GCS are: eye response, verbal response, motor response
  • cannot score lower than a 3
45
Q

what’s the primary survey in ATLS?

A 
A = airway maintenance and cervical spine protection 
B = breathing and ventilation 
C = circulation and haemorrhage control 
D = disability and neurological assessment 
E = exposure and environmental control
46
Q

what’s the Frank Starling curve?

A

as stroke volume increases, left ventricular end diastolic volume increases

47
Q

what are the immediate compensatory responses to shock?

A
  • tachycardia
  • venoconstriction: auto-transfusion
  • vasoconstriction
  • systemic and splanchnic (flow to mesentery, gut, liver, coeliac trunk)
  • cold peripheries (systemic vasoconstriction)
  • core-toe temperature gradient
  • reducing urine output

Medicine Sem 2 (10 decks)

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