Body Fluids Problems (Clinical) (Small & Ramchandra) Flashcards
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
Note that we can maintain BP with 10% blood volume lost.
Explain Findings At Time of Admission
His Blood Pressure And His Heart Rate At Time Of Admission
Explain Findings At Time of Admission
Summary
Findings recorded for this patient on admission are consistent with substantial blood loss that has been sustained for some time. They are a result of hypotensive haemorrhage the homeostatic responses triggered by it. These lead to “shut down” of cutaneous, skeletal muscle and renal circulations.
His Blood Pressure And His Heart Rate At Time Of Admission
Loss of blood volume has caused reductions in venous return, cardiac filling, stroke volume and cardiac output. This has resulted in decreased systemic arterial pressure to 90/60mmHg.
- Decreased systemic arterial pressure and reduced cardiac filling have led to a reduced firing of systemic arterial baroreceptors and cardiac receptors. This produces intense neural and hormonal responses that operate in short and medium term to maintain arterial pressure and restore extracellular fluid volume.
- In this patient, these r_eflex vasoconstriction_ may also be potentiated by chemoreceptor activation and by cerebral ischaemia (see notes on chemoreceptor reflexes and CNS ischaemic responses).
Heart rate is elevated (and cardiac inotropic state is increased) due to intense sympathetic activation and reduced vagal activity coupled with increased levels of circulating catecholamine (adrenaline and noradrenaline).
- Pallor and coldness is associated with _profound vasoconstrictio_n in and markedly reduced blood flow to cutaneous and skeletal muscle circulations.
- Sweatiness is often associated with high catecholamine levels and may also reflect sympathetic activation of sweat glands.
Note that we can maintain BP with 10% blood volume lost.
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
Describe His Blood Haemoglobin At The Time Of Admission (A Little Lower Than Normal)
Blood hemoglobin (122g/L) is a little below normal range (130-175g/L).
- Because haemorrhage occurred some hours before admission, there has been sufficient time for interstitial fluid to be translocated into circulation. This occurs because decreased capillary hydrostatic pressure as result of reduced arterial pressure, and is potentiated by intense constriction of precapillary resistance vessels.
- Because 5-800mL only can be translocated via this internal fluid shift, resultant haemodilution is relatively small.
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
Describe His Arterial pH, HCO3 And PCO2 At The Time Of Admission.
Reduced pH, HCO3 and PCO2 are consistent with metabolic acidosis and respiratory compensation.
- Metabolic acidosis is caused by:
- Its most likely to be anaerobic metabolism as a result of r_educed peripheral oxygen_ delivery leading to lactic acidosis.
- It can also be acute kidney injury (prolonged shut-down of kidney disturb acid-base balance)
- Respiratory compensation is seen in low PCO2.
Low pH is not life-threatening and bolus adminstration of bicarbonate has been linked with a number of undesirable effects. Therefore, administration of NaHCO3 to correct his acid/base status would not be approved.
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
Explain His Serum Creatinine At The Time Of Admission
Serum creatinine is a little elevated in this patient (0.19mmol/L (normal 0.06-0.12 mmol/L)).
Creatinine is a bi-product of muscle metabolism and its production is increased in ischaemia.
Creatine phosphate (PCr) buffers ATP v_ia ADP. If metabolic demand exceeds oxygen supply, ATP is maintained by c_reatine kinase reaction, hence results in increased creatinine (Cr) concentration.
Creatinine is freely filtered and not reabsorbed by kidney. However, when GFR is low, creatinine increases in plasma. In this patient, renal blood flow and GFR will have been very low for some hours.
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
Over the next three days he passed virtually no urine (i.e. shut down of kidney due to low blood flow, microvascular lesions)
Give a summary on what this means
Summary
The findings recorded for this patient several days after admission are consistent with renal failure.
- This is a direct result of _prolonged period of renal under-perfusio_n that occurred as a result of the blood loss. This has likely resulted in microcirculatory damage in the kidney.
- This could be due to r_eperfusion injury_ or disseminated coagulation.
- With reperfusion injury, cellular homeostasis is compromised as a result of decreased high energy phosphate stores (ATP and phosphocreatine).
- When oxygen is reintroduced, toxic reactive oxygen species are formed. This leads to expression of pro-inflammatory substances (ie cytokynes) and a_dverse bioactive agents (_i.e endothelin), which cause endothelial injury
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
On Day Four, His Serum Creatinine Was 0.31mmol/L (High)
On Day Five, His pH Was 7.15.
On Day Six His Serum K+ Was 5.8mmol/L (Normal 3.5-5.0mmol/L)
On Day Four, His Serum Creatinine Was 0.31mmol/L (High).
High serum creatinine suggests kidney failure. GFR has not been restored despite replacement of extracellular fluid volume.
On Day Five, His pH Was 7.15.
Acidosis is most likely due to _kidney failure a_nd patient’s inability to excrete acid produced as a result of metabolism (or to reconstitute bicarbonate). (Note that lactic acidosis has been treated.)
On Day Six His Serum K+ Was 5.8mmol/L (Normal 3.5-5.0mmol/L)
Serum potassium is high in part because of _kidney failur_e.
- Renal excretion of K+ is impaired.
- This is amplified by acidosis. H+ are buffered in cells are exchanged for K+ that move into ECF (H+ enters cells, K+ exits cells)
A 24 year old man had an accident in the bush and not found for some hours. When finally rescued it became evident that he had been bleeding. He was cold, pale and sweaty, and breathing rapidly.
On admission to hospital, his blood pressure was 90/60mmHg and his heart rate was 130/min.
Blood tests revealed the following: blood haemoglobin 122g/L (normal 130-175g/L): pH 7.15 (normal 7.36-7.44); HCO3 12mmol/L (normal 22-28mmol/L); PCO2 20mmHg (normal 36-44mmHg).
A saline drip was initially administered and, on completion of blood matching, the patient was given a transfusion of 1500mL of whole blood. His blood pressure returned to 120/80mmHg. Intravenous adminstration of 150mmol of NaHCO3 improved, but did not fully correct his acid/base status (we don’t give NaHCO3 anymore due to complications).
Twenty-four hours after admission, his serum creatinine was 0.19mmol/L (normal 0.06-0.12mmol/L).
Over the next three days he passed virtually no urine (i.e. shut down of kidney due to low blood flow, microvascular lesions)
He Became Progressively More And More Thirsty.
Six Days After Admission, He Drank A Large Volume Of Water.
Explain why this occured/why it is necessary to minimize fluid intake in this setting
Uncontrollable thirst often occurs in renal failure. There are a number of factors that could be responsible for this:
- Hypertonicity due to failure to maintain electrolyte balance; and
- Excessive release of renin by juxtaglomerular apparatus, and increased circulating [angiotensin II].
Both lead to stimulation of thirst centres in the hypothalamus.
Fluid and electrolytes are being retained as a result of renal failure.
- Because there is now no capacity to excrete water, water intake leads directly to expansion of ECF and BV.
- This will lead to increased venous pressures and in this case results in pulmonary oedema.
A Few Hours Later, He Became Very Short Of Breath And Chest X-Ray Revealed Pulmonary Oedema
Sustained elevation in circulating [renin] and [angiotensin II] are seen in circulatory shock (sustained renal hypoperfusion). This is thought to be result of _pre-renal (afferent) microcirculatory lesion_s that lower pressure at JGA (i.e. reduced perfusion pressure to kidney).
- Elevated [angiotensin II] contributes to reduced GFR under these circumstances and may exacerbate renal failure.
- In a clinical setting (with monitored blood biochemistry and controlled fluid intake), increased [angiotensin II] is most likely to be responsible for uncontrolled thirst.
The following physiological effects were observed in three Skylab astronauts during 28 days spent in earth orbit and immediately after their spaceflight.
While exposed to weightlessness in orbit, central venous pressure increased. After 28 day flight, there was a mean loss of red blood cells of 310ml and a mean reduction of total blood volume of 600ml (~10%). There were increases in both urinary excretion rates throughout flight, and plasma sodium and potassium concentrations were reduced. During the first four days post flight_, water intake was substantially increased and urine output was low._
Immediately after landing, Skylab crewmen exhibited an _increased tendency toward syncope on standin_g. This postural hypotension was abolished when crewmen wore a counter-pressure garment, which covered the lower body and, when inflated, imposed pressures against the skin of 85 to 90mmHg at the ankles and 10mmHg at the waist. The cardiovascular response to altered posture was completely restored a few days after returning to earth.
The exercise performance of the Skylab crewmen was examined before, during and after flight at workloads of 25, 50 and 75% of aerobic capacity (VO2 max) using a bicycle ergometer. No impairment of cardio-respiratory response was observed during flight. In contrast_, exercise capacity was markedly decreased_ immediately after returning to earth with r_eductions in stroke volume and cardiac output_. Return to pre-flight exercise levels required anything from 4 to 30 days.
Explain The Following Results
Reduction In Blood Volume During Spaceflight. Why Is Central Venous Pressure Increased In Flight, Despite Decrement Of Blood Volume?
Summary
Immediate cardiovascular responses to weightlessness are similar to those in supine subjects and adaptations to prolonged spaceflight and long periods of bed rest have many common features.
There are several factors lead to reduced extracellular fluid volume (decreased plasma volume and decreased red cell volume).
Loss of hydrostatic effects of gravity is accompanied by a translocation of blood and tissue fluid from lower body to interthoracic circulation. As a result, cardiac filling is increased and resting SV is increased (close to maximal level). This increases central blood volume, which leads to adjustment thus decreased plasma volume.
Mechanisms include:
- Atrial distension -> increased ANP release -> natriuresis
- Activation of cardiac (and pulmonary) stretch receptors -> trigger neural and neuro-humoral responses
- This include decreased renin release by kidney; decreased angiotensin II production; decreased aldosterone secretion from adrenal cortex
- This results in renal Na+ secretion (natriuresis) and K+ retention
- However, it should be noted that aldosterone levels are elevated after a day or two of weightlessness or bed rest.
- _Inhibition of pituitary ADH releas_e -> water diuresis
- Inhibition of thirst sensation -> r_educed water intake_
Decrease of red cell volume is a slower, secondary response which accompanies decreased plasma volume.
- This is due to inhibition of erythropoiesis.
- This may be stimulated by higher tissue PO2 levels due to initial increase in resting cardiac output caused by weightlessness.
The fact that central venous pressure remains slightly elevated indicates that:
- Venous return is preserved
- Blood volume in central thoracic compartment is still slightly elevated despite fall in total blood volume (i.e. high O2 delivery).
The following physiological effects were observed in three Skylab astronauts during 28 days spent in earth orbit and immediately after their spaceflight.
While exposed to weightlessness in orbit, central venous pressure increased. After 28 day flight, there was a mean loss of red blood cells of 310ml and a mean reduction of total blood volume of 600ml (~10%). There were increases in both urinary excretion rates throughout flight, and plasma sodium and potassium concentrations were reduced. During the first four days post flight_, water intake was substantially increased and urine output was low._
Immediately after landing, Skylab crewmen exhibited an _increased tendency toward syncope on standin_g. This postural hypotension was abolished when crewmen wore a counter-pressure garment, which covered the lower body and, when inflated, imposed pressures against the skin of 85 to 90mmHg at the ankles and 10mmHg at the waist. The cardiovascular response to altered posture was completely restored a few days after returning to earth.
The exercise performance of the Skylab crewmen was examined before, during and after flight at workloads of 25, 50 and 75% of aerobic capacity (VO2 max) using a bicycle ergometer. No impairment of cardio-respiratory response was observed during flight. In contrast_, exercise capacity was markedly decreased_ immediately after returning to earth with r_eductions in stroke volume and cardiac output_. Return to pre-flight exercise levels required anything from 4 to 30 days.
Increased Tendency To Postural Hypotension And Syncope Immediately After The Flight. How Does Counter-Pressure Suit Prevent This?
In normal gravity, a hydrostatic gradient is imposed on circulation when we move from a supine to an upright position.
- Vascular pressures at the ankles increase by 85-90mmHg
- Vascular pressures at the waist are 10-20mmHg greater.
Increase in intravascular pressure causes superficial veins in lower body to dilate. The resulting shift of 400-500mL of blood from “central” venous reservoir reduces venous return and cardiac filling. This leads to significant fall in stroke volume.
In general, well-developed homeostatic adjustments counter cardiovascular effects of altered posture.
- Increased autonomic “drive” to heart and vessels elevates heart rate, cardiac inotropic state and total peripheral resistance.
- These changes serve to maintain MAP.
Compensatory mechanisms outlined above may not prevent postural hypotension when:
- Blood volume is decreased, or
- Autonomic reflex responses are attenuated.
The mean loss of blood volume in crewmen was 600mL. In addition, possible adaptation of c_ardio-pulmonary receptors, central adaptation and stress relaxation_ in vascular smooth muscle during space flight may also alter normal homeostatic responses (attenuated autonomic reflex).
As a result, crewmen are not initially able to maintain arterial pressure on standing up. Therefore, cerebral perfusion is compromised and tendency to fainting or syncope is markedly increased.
Counter pressure suit overcomes this problem by physically preventing shift of blood volume into lower extremities.
The following physiological effects were observed in three Skylab astronauts during 28 days spent in earth orbit and immediately after their spaceflight.
While exposed to weightlessness in orbit, central venous pressure increased. After 28 day flight, there was a mean loss of red blood cells of 310ml and a mean reduction of total blood volume of 600ml (~10%). There were increases in both urinary excretion rates throughout flight, and plasma sodium and potassium concentrations were reduced. During the first four days post flight_, water intake was substantially increased and urine output was low._
Immediately after landing, Skylab crewmen exhibited an _increased tendency toward syncope on standin_g. This postural hypotension was abolished when crewmen wore a counter-pressure garment, which covered the lower body and, when inflated, imposed pressures against the skin of 85 to 90mmHg at the ankles and 10mmHg at the waist. The cardiovascular response to altered posture was completely restored a few days after returning to earth.
The exercise performance of the Skylab crewmen was examined before, during and after flight at workloads of 25, 50 and 75% of aerobic capacity (VO2 max) using a bicycle ergometer. No impairment of cardio-respiratory response was observed during flight. In contrast_, exercise capacity was markedly decreased_ immediately after returning to earth with r_eductions in stroke volume and cardiac output_. Return to pre-flight exercise levels required anything from 4 to 30 days.
The Exercise Capacity Of Crew Members Was Normal During Spaceflight, But Significantly Decreased Immediately Afterwards
This is not the case immediately after the flight.
- Gravity -> reduced venous return -> lower maximum cardiac output
- Reduced blood volume diminishes venous return in upright exercise, thus crewmen cannot maintain or increase stroke volume. As a result, maximum cardiac output is reduced and exercise performance is impaired.
- Finally, despite exercise regime, there is some muscle atrophy which may also contribute to reduced exercise capacity
The following physiological effects were observed in three Skylab astronauts during 28 days spent in earth orbit and immediately after their spaceflight.
While exposed to weightlessness in orbit, central venous pressure increased. After 28 day flight, there was a mean loss of red blood cells of 310ml and a mean reduction of total blood volume of 600ml (~10%). There were increases in both urinary excretion rates throughout flight, and plasma sodium and potassium concentrations were reduced. During the first four days post flight_, water intake was substantially increased and urine output was low._
Immediately after landing, Skylab crewmen exhibited an _increased tendency toward syncope on standin_g. This postural hypotension was abolished when crewmen wore a counter-pressure garment, which covered the lower body and, when inflated, imposed pressures against the skin of 85 to 90mmHg at the ankles and 10mmHg at the waist. The cardiovascular response to altered posture was completely restored a few days after returning to earth.
The exercise performance of the Skylab crewmen was examined before, during and after flight at workloads of 25, 50 and 75% of aerobic capacity (VO2 max) using a bicycle ergometer. No impairment of cardio-respiratory response was observed during flight. In contrast_, exercise capacity was markedly decreased_ immediately after returning to earth with r_eductions in stroke volume and cardiac output_. Return to pre-flight exercise levels required anything from 4 to 30 days.
Plasma Sodium And Potassium Levels Of Crew Members Were Reduced During Spaceflight
Explain this
Acute Condition
- increased ANP -> Na+ excretion
- decreased aldosterone -> high K+ retention
Chronic Condition
- increased ANP maintained -> Na+ excretion
- increased aldosterone rises toward normal (adaptation) -> K+ excretion
s[Na+] and s[K+] were reduced during spaceflight, which is also observed in patients after periods of prolonged bed rest.
Firstly, the balance of these endocrine systems is altered such that sodium remains low, but potassium is excreted. This is due to:
- ANP release from heart remains elevated after a few days of space flight, thus still natiuresis.
- However, after a few days of space flight, there is resetting of cardiac volume receptors and neuro-humoral response to their activation over a period of days. Therefore, circulating aldosterone levels are elevated (from initial reduction). This results in K+ excretion.
A further factor that should be noted here is that there is loss of bone mass and total body calcium (demineralisation) with prolonged weightlessness and bed rest.
The following physiological effects were observed in three Skylab astronauts during 28 days spent in earth orbit and immediately after their spaceflight.
While exposed to weightlessness in orbit, central venous pressure increased. After 28 day flight, there was a mean loss of red blood cells of 310ml and a mean reduction of total blood volume of 600ml (~10%). There were increases in both urinary excretion rates throughout flight, and plasma sodium and potassium concentrations were reduced. During the first four days post flight_, water intake was substantially increased and urine output was low._
Immediately after landing, Skylab crewmen exhibited an _increased tendency toward syncope on standin_g. This postural hypotension was abolished when crewmen wore a counter-pressure garment, which covered the lower body and, when inflated, imposed pressures against the skin of 85 to 90mmHg at the ankles and 10mmHg at the waist. The cardiovascular response to altered posture was completely restored a few days after returning to earth.
The exercise performance of the Skylab crewmen was examined before, during and after flight at workloads of 25, 50 and 75% of aerobic capacity (VO2 max) using a bicycle ergometer. No impairment of cardio-respiratory response was observed during flight. In contrast_, exercise capacity was markedly decreased_ immediately after returning to earth with r_eductions in stroke volume and cardiac output_. Return to pre-flight exercise levels required anything from 4 to 30 days.
It Takes Only A Few Days For The Tendency To Postural Hypotension To Be Reversed To Be After Returning To Earth, But Up To 30 Days For Normal Cardiovascular Exercise Responses To Be Restored
Time course of recovery of normal cardiovascular responses after returning to earth in large part reflects mechanisms in restoration of blood volume and body fluid volume. Under normal circumstances, moderate blood loss is compensated by:
-
Translocation of tissue fluid (ISF) into vascular compartment (plasma). It begins rapidly and can expand plasma volume by up to 800mL in a normal adult subject, but takes some hours to develop fully.
- This is associated with decreased capillary hydrostatic pressure (with blood loss).
- This is also facilitated by neurally mediated vasoconstriction, which accompanies blood loss.
-
Restoration of fluid volume is medium term process, which is completed over a period of days to hours.
- This is associated with neuro-humoral mechanisms involving RAAS and pituitary ADH release.
- This leads to decreased urine output, while f_luid intake is markedly increased._
- Restoration of red cell volume is a long term process, which operates over a period of days to weeks.
In this case:
- Effectiveness of mechanism (1) is limited, since there is a s_ubstantial reduction in total extracellular fluid volume._
- Therefore, time course for recovery of cardiovascular responses depends o_n mechanism (2) and (3)._
- Some “resetting” of cardiovascular control mechanisms may also be involved.
A 64 year-old man presented to hospital complaining of sudden onset of severe chest pain. He is a life-long smoker who has been treated for hypertension for more than 10 years.
He was cold, sweaty, pale and confused on admission. His blood pressure was 80/30mmHg and his heart rate was steady but elevated at 140/min. A chest X-ray is taken and the results are shown below.
His blood pH was 7.2, his haemoglobin is 140g/L (normal 135-180g/L) and plasma cortisol levels are markedly elevated.
Outline Possible Causes Of These Symptoms. What Does The Chest X-Ray Suggest?
There is wide range of possible causes that could give rise to circulatory collapse with symptoms of this kind. They include a larg_e myocardial infarction,_ massive internal haemorrhage, pulmonary embolism or cardiac tamponade (rapid and complete shutdown of heart).
However, chest X-ray suggests that this is a t_horacic aortic aneurysm_ that has ruptured (more likely in smokers due to endothelial dysfunction).
- White arrow indicates a large aneurysm of the descending aorta.
- Black arrows show a large left pleural effusion resulted from rupture (blood has spread outside pericardium).
A 64 year-old man presented to hospital complaining of sudden onset of severe chest pain. He is a life-long smoker who has been treated for hypertension for more than 10 years.
He was cold, sweaty, pale and confused on admission. His blood pressure was 80/30mmHg and his heart rate was steady but elevated at 140/min. A chest X-ray is taken and the results are shown below. His blood pH was 7.2, his haemoglobin is 140g/L (normal 135-180g/L) and plasma cortisol levels are markedly elevated.
Explain The Patient’s Blood Pressure And His Elevated Heart Rate
Patient’s very low mean arterial pressure is result of substantial blood loss.
- As a result, v_enous return is low_, stroke volume is reduced. Therefore, cardiac output is not sufficient to maintain arterial pressure despite reflex responses this elicits (see following).
- Continuing leakage of blood from ruptured aneurysm may also contribute to diastolic run-off.
Elevated heart rate reflects r_eflex response_, which includes increased sympathetic drive and reduced cardiac vagal activity. This increases inotropic state of heart as well as heart rate.
A 64 year-old man presented to hospital complaining of sudden onset of severe chest pain. He is a life-long smoker who has been treated for hypertension for more than 10 years.
He was cold, sweaty, pale and confused on admission. His blood pressure was 80/30mmHg and his heart rate was steady but elevated at 140/min. A chest X-ray is taken and the results are shown below.
His blood pH was 7.2, his haemoglobin is 140g/L (normal 135-180g/L) and plasma cortisol levels are markedly elevated.
Why Is He Cold, Sweaty, Pale and Confused?
He is cold and pale, as a result of markedly reduced tissue perfusion.
- This is partly due to reduced output.
- This also reflects intense autonomic drive to blood vessels, which causes widespread vasoconstriction (especially cutaneous vessels and skeletal muscle circulation)
He is sweaty due to catecholamine release from the adrenal medulla and sympathetic activation of sweat glands
He is confused due to decreased cerebral perfusion
A 73-year-old former smoker with a history of hypertension and dyslipidemia presented to
the emergency department with shortness of breath.
His blood pressure was 160/75 mm Hg, heart rate 60 beats per minute, and _respiratory rate 24 breaths per minut_e.
Chest auscultation revealed diffuse rales with pitting oedema. He was found to have a clear abdominal bruit.
His serum creatinine was 0.27 mmol.L-1 (normal 0.06-0.12 mmol.L-1), his 24 hour urinary Na+excretion was 15 mmol (normal 30-200 mmol in 24 hr) and his serumK+ was 3.2 mmol.L-1 (normal 3.5 – 5.3 mmol.L-1).
His condition improved after treatment with intravenous diuretics, but his blood pressure remained elevated A renal angiogram (below) revealed the following.
He was treated with an ACE inhibitor and his blood pressure returned to a normal level
(120/70 mm Hg) over the next few days, but his serum creatinine rose to 0.52 mmol.L-1.
What is the most probable cause of this man’s hypertension?
The renal angiogram shows narrowing at the origin of both renal arteries. This adds to the total resistance of blood flow in the afferent renal vascular circuit.
Thus pressure falls at the terminal end of the afferent arterioles which leads to _release of reni_n from the JGA activating the renin-angiotensinaldosterone
system (RAAS). AII acts directly to cause vasoconstriction and also affects the central nervous system and facilitates adrenergic neurotransmission.
_It increases thirs_t and also leads to increased release of ADH from the posterior pituitary.
AII is also associated with structural
remodelling of heart and blood vessels. These responses drive and sustain the hypertension. .
A 73-year-old former smoker with a history of hypertension and dyslipidemia presented to
the emergency department with shortness of breath.
His blood pressure was 160/75 mm Hg, heart rate 60 beats per minute, and _respiratory rate 24 breaths per minut_e.
Chest auscultation revealed diffuse rales with pitting oedema. He was found to have a clear abdominal bruit.
His serum creatinine was 0.27 mmol.L-1 (normal 0.06-0.12 mmol.L-1), his 24 hour urinary Na+excretion was 15 mmol (normal 30-200 mmol in 24 hr) and his serumK+ was 3.2 mmol.L-1 (normal 3.5 – 5.3 mmol.L-1).
His condition improved after treatment with intravenous diuretics, but his blood pressure remained elevated A renal angiogram (below) revealed the following.
He was treated with an ACE inhibitor and his blood pressure returned to a normal level
(120/70 mm Hg) over the next few days, but his serum creatinine rose to 0.52 mmol.L-1.
Explain the patient’s symptoms on admission and why treatment with diuretics improved them
The patients is exhibiting signs of pulmonary oedema: Difficulty in breathing, rales – discontinuous clicking, rattling or crackling sounds on auscultation.
Pulmonary disease may contribute to this, but it will be exacerbated by activation of the RAAS and retention of salt and water.
Finally, the patient will likely have LV dysfunction as a result of hypertension. Increased afterload and LV hypertrophy are associated with elevated LV end diastolic pressures, which will contribute to pulmonary oedema.
A 73-year-old former smoker with a history of hypertension and dyslipidemia presented to the emergency department with shortness of breath.
His blood pressure was 160/75 mm Hg, heart rate 60 beats per minute, and _respiratory rate 24 breaths per minut_e.
Chest auscultation revealed diffuse rales with pitting oedema. He was found to have a clear abdominal bruit.
His serum creatinine was 0.27 mmol.L-1 (normal 0.06-0.12 mmol.L-1), his 24 hour urinary Na+excretion was 15 mmol (normal 30-200 mmol in 24 hr) and his serumK+ was 3.2 mmol.L-1 (normal 3.5 – 5.3 mmol.L-1).
His condition improved after treatment with intravenous diuretics, but his blood pressure remained elevated A renal angiogram (below) revealed the following.
He was treated with an ACE inhibitor and his blood pressure returned to a normal level
(120/70 mm Hg) over the next few days, but his serum creatinine rose to 0.52 mmol.L-1.
Why did treatment with an ACE inhibitor reverse the patient’s hypertension? Explain the increase in serum creatinine.
This occurs for two reasons.
- Firstly, systemic arterial has been reduced as a result of treatment with ACE inhibitors.
- Secondly, the balance of resistance in afferent and efferent renal vessels is altered.
More detailed information about this is given below.
- Angiotensin II exerts a vasoconstrictive effect on both afferent and efferent arterioles, but because the efferent arteriole has a smaller basal diameter, the increase in efferent resistance exceeds that of the afferent side. Afferent vasoconstriction is further minimized by angiotensin II–mediated release of vasodilatory prostaglandins and nitric oxide. In addition, angiotensin II can constrict the glomerular mesangium, thereby reducing the surface area available for filtration.
- The net effect of angiotensin II on filtration invokes the opposing factors of reduced renal blood flow and mesangial surface area (causing a decrease in filtration) and the increase in glomerular capillary pressure (which tends to increase filtration). The end result depends on the clinical setting in which it occurs.
- In the healthy kidney,
- a fall in systemic blood pressure activates the renin-angiotensin system, which triggers a decrease in renal blood flow secondary to increased renal vascular (afferent) resistance. The preferential increase in efferent resistance mediated by angiotensin II results in increased glomerular capillary hydraulic pressure, which maintains the glomerular filtration rate (GFR).
- In the ischaemic kidney with reduced afferent blood flow,
- intraglomerular pressure and glomerular filtration are maintained by and depend upon angiotensin II–mediated efferent vasoconstriction. In this setting, removal of the efferent vasoconstrictive effect by angiotensin blockade, as achieved by angiotensin-converting enzyme (ACE) inhibitors, results in a decrease in intraglomerular pressure and GFR. Thus, in patients with renovascular disease, particularly those with bilateral renal artery stenosis, ACE inhibitors may cause a deterioration of renal function and azotaemia. Note that an acute such decline in renal function is reversible once the ACE inhibitor or the angiotensin receptor blocking agent is discontinued.
