Cases Flashcards
Describe the events that occur in the four segments between numbered points on the pressure– volume loop. Correlate each segment with events in the cardiac cycle.
According to Figure, what is the value for left ventricular end-diastolic volume? What is the value for end-systolic volume?
What is the approximate value for stroke volume? What is the approximate value for ejection fraction?
Which portion, or portions, of the pressure–volume loop correspond to diastole? To systole?
Which portions of the pressure–volume loop are isovolumetric?
At which numbered point does the aortic valve open? At which numbered point does the aortic valve close? At which numbered point does the mitral valve open?
At which numbered point, or during which segment, would the first heart sound be heard?
At which numbered point, or during which segment, would the second heart sound be heard?
Superimpose a new pressure–volume loop to illustrate the effect of +++ left ventricular EDV (++preload). What is the effect on stroke volume?
Superimpose a new pressure–volume loop to illustrate the effect of an increase in contractility. What is the effect on ESV volume? What is the effect on ejection fraction.
Superimpose a new pressure–volume loop to illustrate the effect of an increase in aortic pressure (i.e., +++ afterload). What is the effect on ESV? What is the effect on ejection fraction?
1-2 isovolumetric contraction, 2-3 ventricular ejection, 3-4 isovolumetric relaxation, 4-1 ventricular filling
EDV is 140 ml, ESV is 70 ml
Stroke volume= End-diastolic volume - end-systolic volume = 140-70=70 ml, ejection fraction= stroke volume/end-diastolic volume= 70/140= 50%
Diastole: 3 →4 & 4 →1 Systole: 1 → 2 & 2→3
1 → 2 & 3 →4
aortic valve opens at point 2 ;
aortic valve closes at point 3 ; mitral valve opens at point 4
At point 1 and 1 → 2 segment
At point 3 & 3 →4 segment
An increase in ventricular EDV (preload) shifts the point 1 to the right.
When contractility is increased, the ventricle can develop greater tension and pressure during systole. As a result, SV increases and ESV decreases. If SV increases and EDV is unchanged, ejection
fraction must have increased.
if +afterload, the left ventricle must work harder than usual to overcome this higher pressure. Ventricular pressure increases to a higher level during isovolumetric contraction ; —-SV and more blood remains in the left ventricle after ejection →+++ESV. Because the EDV is unchanged, EF must have decreased
A 50 year old obese male complaining of constricting pain radiating to his left shoulder, arm and root of neck.
What is the possible diagnosis
What are the affected arteries and their number
Giver their origins
Name 2 branches of these arteries
Mention their distribution
Anginal pain
Coronary arteries right and left
Ascending aorta
Right coronary: posterior interventricular artery, right marginal artery
Left coronary: Anterior interventricular, circumflex
Left coronary: left atrium and ventricle
Right coronary: right atrium and ventricle SNA, posterior 1/3 of interventricular septum, muscular part containing atrio-ventricular bundle
Congestive heart failure:
Explain the presence of third heart sound
Explain the presence of crackles at the base of lung on auscultation
Draw the normal pressure-volume relationship for the left ventricle. Superimpose a second curve after the myocardial infarction, and use this relationship to predict changes in stroke volume and cardiac output
Which information provided in the case tells you that his stroke volume was decreased?
What is the meaning of the patient’s decreased ejection fraction?
Why was his pulmonary capillary pressure increased?
Why did pulmonary edema develop? (In your explanation, discuss the Starling forces involved.) Why is pulmonary edema so dangerous?
Why did he have dyspnea and orthopnea?
Why was his skin cold and clammy?
What was the rationale for treating him with a positive inotropic agent, such as digitalis?
What was the rationale for treating him with furosemide (a loop diuretic)?
Why was the patient sent home on a low-Na+ diet?
turbulent blood flow during atrial filling phase.
Pulmonary congestion and increased hydrostatic pressure lead to filtration of fluid into alveoli.
SV and EF decrease
Ejection fraction is 40%
Decreased stoke volume to the end-diastolic volume
Increased blood volume and pressure in left atrium which backwards to the lung
Increased hydrostatic pressure leads to fluid filtration out of capillaries
Pulmonary edema is dangerous as the fluid will impair the gas exchange and hypoxia develop.
When the patient lies down at night, the excess fluid redistributes from the base of the lung . Consequently, there is a greater deficit
in gas exchange and nocturnal dyspnea develops. The hypoxemia awakens the patient, preventing a restful sleep
Because of heart failure and decreased COP, sympathetic system is activated which causes vasoconstriction of cutaneous vessels and activation of sweat glands.
Digitalis decreases the heart rate and increases the contractility and hence SV
Prevent salt and water retention to decrease volume overload on the heart.
A man with difficulty of respiration. On x-ray there was plural activity
name the condition
What is the complication and why?
Give the parts of the pleura and their recesses
Mention the function of the pleura
Mention the condition if blood, air or pus accumulate in pleural cavity
Pleural effusion
Respiratory failure due to interference with lung expansion
Visceral and parietal, Costodiaphragmatic and costomediastinal recesses.
Allows lungs to move
Hemothorax, pneumothorax, pyothorax
Essential hypertension.
Describe the role of baroreceptors in regulation of acute changes in BP
Explain how anxiety can elevate the arterial BP
Explain the role of diabetes and obesity in elevation of arterial BP
What is meant by left axis deviation in this case?
Suggest how to treat this patient
What are the cardiac complications of persistent hypertension?
When blood pressure in the carotid sinus or aortic arch falls there is a reflex activation of sympathetic nervous system and inhibition of parasympathetic nervous system.
Anxiety can lead to an increase in sympathetic nervous system activity which can cause an acute increase in blood pressure
diabetes and obesity damages arteries and makes them targets for hardening, called atherosclerosis
Left ventricular hypertrophy
The treatment of hypertension with diuretics and Diminishing sodium intake
High blood pressure can cause hardening and thickening of the arteries (atherosclerosis), which can lead to a heart attack, stroke and ventricular hypertrophy
A man with stab wound in the 4th intercostal space induced accumulation of blood in the pericardial cavity.
Name the condition
How can it be treated
Give parts of the pericardium
Name the structures between pericardium and sternum
Name two arteries supplying the pericardium
Heamopericardium
By aspirating a fluid from the pericardial cavity at 5th intercostal space near sternum
Fibrous and serous pericardium
Sternopericardial ligaments, thymus gland remains, internal thoracic artery and its terminal branches
Pericardial branches of internal thoracic artery
Pericardial branches of descending aorta
Hemorrhagic shock
What is the definition of circulatory shock? What are the major causes?
After the blood loss, what sequence of events led to decreased arterial pressure?
Suggest why the arterial pressure will be lower in the upright position than in the lying (supine) position
Why the heart rate was elevated (120 beats/min)? Why the heart rate will be even more elevated in upright position?
If central venous pressure and pulmonary capillary pressure had been measured, would you expect their values to have been increased, decreased, or the same as in a healthy person?
Why was the skin pale and cold?
If urinary Na excretion had been measured, would you expect it to be higher than, lower than, or the same as that of a healthy person? Why?
How was the saline infusion expected to help his condition?
Why did the physicians consider monitoring his urine output? How do prostaglandins “protect” RBF after a hemorrhage? In this regard, why was it dangerous that he had been taking aspirin?
If blood loss had been more severe, he might have received a low dose of dopamine. In cerebral, cardiac, renal, and mesenteric vascular beds, dopamine is a VD; in muscle and cutaneous vascular beds, dopamine is a VC. Why is low-dose dopamine helpful in the treatment of hypovolemic shock
Circulatory shock is characterized by the inability of multi-organ blood flow and oxygen delivery to meet metabolic demands.
Major cause: bleeding
Blood loss → — venous pressure → — EDV (preload) → — SV & CO → — ABP
Gravity → more decrease in the venous return
— ABP → +++ Sympathetic → +++ HR
upright position → — ABP → — baroreceptors → more sympathetic stimulation
Decrease
+++ sympathetic to skin → VC (pale & cold skin)
Lower
Hemorrhage stimulates the release renin from the kidney, leading to angiotensin II synthesis which stimulate the renal retention of water and sodium
Restoration of arterial pressure after control of the hemorrhage and replacement of circulating blood volume allows normal urine production to resume and resulted in a complete recovery.
Urine production also depends on an adequate arterial pressure. Severe hypotension acutely causes a marked drop in urine production.
PGs antagonize the VC effect of sympathetic nervous system on the kidney vessels… aspirin may make the bleeding worse cause it reduces platelet aggregation
Low dose of dopamine directly dilates the mesenteric, renal, and cerebral vessels and redirects blood flow to essential viscera.
Following on attack of severe chest pain (anginal) the patient complained of frequent attacks of irregular heart beats, pain and respiratory distress.
Name the most frequently affected coronary artery
Name the damaged tissue causing the irregular heart beats
Describe the name of the different components of the damaged tissue
Describe the site, course and divisions of these tissues
Right coronary artery
Conduction system of the heart
SAN, AVN and AV bundle
SAN: junction of SVC to right atrium
AVN: membranous part of the interventricular septum
AV bundle: posterior third of the membranous interventricular septum
1) How a pressure gradient between the alveoli and the atmospheric air is created?
2) How a negative Intrapleural pressure in the thorax is created?
3) Define pneumothorax. Name 2 different causes for this situation.
4) Explain why the collapse is limited to one side of the lung?
5) Suggest why air moves through the knife wound during inspiration?
6) Comment on the patient’s pulse and respiratory rate. Explain
7) Explain the presence of difficult breathing and chest pain
8) Why the thoracic cage is asymmetrical, with the left side protruding more than the right side?
9) Explain why the left side shows much less movement than the right during breathing?
10) What is the significance of decreased breath sounds on the left side with hyperresonance on percussion?
11) Why oxygen saturation is low?
12) Comment on the Arterial blood gases of this patient. Give a reason.
13) Describe a strategy for treatment of this patient
1) By changing the volume of chest wall and then the volume of the lung:
During inspiration movement of diaphragm down and contraction of external inter-costal muscle → +++ chest volume → -ve IPP & -ve IAP → moving air in. During expiration chest volume decreases by elevation of diaphragm and relaxation of external inter-costal → ++ IAP → movement of air out.
2) negative Intrapleural pressure in the thorax is created by +++ chest wall volume & traction of chest wall on parietal pleura and traction of lung on visceral pleura.
3) Pneumothorax is presence of air inside pleural sac.
Open pneumothorax caused by penetrating thoracic injury and entrance of atmospheric air inside pleural sac. Closed pneumothorax caused by rupture of air bulla leading to entrance of lung air to pleural sac.
4) because each lung has its own pleural sac that is separate from the other one.
5) Because of the negative pressure created in lung during inspiration.
6) Pulse: tachycardia (sympathetic stimulation due to pain and hypotension) Respiratory rate: tachypnea (lung collapse causes decreased PO2 and increased PCO2 that stimulate respiration)
7) Difficult breathing is due to lung collapse and chest pain due to injury of pain sensitive pleura. With inspiration & lung expansion → pain → short inspiration.
8) Presence of air in left pleural sac ameliorates the negative intra-pleural pressure leading to lung collapse (as it has tendency to collapse) and chest expansion (as it has tendency to expand).
9) Because of lung collapse and pain.
10) Decreased breath sounds is an indicator for the amount of air in pleural sac and the degree of lung collapse.
11) Because of the non -functioning collapsed lung.
12) Low PO2 and high PCO2 due to decreased gas exchange in the non -functioning collapsed lung.
13) Placing the patient on a positive-pressure ventilator and surgical repair of injury.
A 15 year old teenage boy inhaled a foreign body
Which main bronchus and lung is likely affected and why?
Which lobar bronchus is frequently blocked by foreign body and why?
Which type of foreign body gives a more dangerous outcome if left for a long time and why?
What is the expected complication of blocking a lobar bronchus?
Right principle bronchus because its wider and shorter and more inline with trachea.
Medial basal bronchus as its more in line with right principle and right lobar bronchus.
Wood and seed as they hold water and swell
Lung abscess, segment collapse
CO poisoning
1) Explain why the arterial PO2 in this patient was normal
2) What does the arterial O2 content represent?
3) In healthy people, the percent O2 saturation of hemoglobin in arterial blood is 95%-100%. Why was the patient’s O2 saturation reduced to 50%
4) What percentage of the heme groups on his hemoglobin were bound to carbon monoxide (CO)?
5) Draw a normal O2-Hb dissociation curve, and superimpose the O2-Hb dissociation curve that would have been obtained for this patient. What effect did CO poisoning have on his O2 binding capacity?
6) What effect did CO poisoning have on the affinity of hemoglobin for O2?
7) How did CO poisoning alter O2 delivery to tissues?
8) Explain why the patient in spite of hypoxia has no rapid respiratory rate?
9) Explain why the patient complains of chest pain and weakness?
10) Suggest why the patient is hypothermic?
11) What was the rationale for giving the patient 100% O2 to breathe?
12) Why PO2 in pulmonary vein is slightly lower than alveolar PO2?
13) Patients with severe CO-poisoning, where carboxy-Hb levels exceed 70%, are treated in a hyperbaric O2 chamber. Explain
1) The arterial PO2 is normal, because the dissolved oxygen content came into equilibrium with the PO2 of the alveoli.
2) The arterial oxygen content represents the amount of oxygen bound to hemoglobin.
3) Carbon monoxide binds to hemoglobin with an affinity 200 times greater than that of oxygen. Carboxyhemoglobin can no longer bind oxygen and, consequently, diminishes
the total blood oxygen content.
4) 40%
6) CO shifting the oxygen dissociation curve to left
7) Because of the increased affinity between hemoglobin and oxygen during carbon monoxide poisoning, little will be released into tissue.
8) The aortic body and carotid body chemoreceptors sense the dissolved oxygen content, and, consequently, there is no ventilatory stimulus from hypoxia.
9) — oxygen delivered to tissues → myocardial ischemia causing chest pain & muscles hypoxia causing weakness).
10) CO inhibit mitochondrial oxidase enzyme so no ATP. Also lack of O2 for metabolism
11) Breathing 100% O2 would increase fivefold the amount of O2 dissolved in the plasma.
12) Blood in the pulmonary vein has a slightly lower PO2 because of venous mixture from bronchial circulation.
13) At the higher total barometric pressure, the dissolved O2 can be sufficient to support basal metabolism. Given time, CO will disassociate from Hb and Hb-carrying capability
can be restored.
An old man suffers from pulsatile retrosternal pain which increases following effort associated with irregular heart beats, dysphagia and horsiness of voice.
Name the affected organ and diagnosis of the disease
Explain the reason of irregular heart beats
Explain the reason of dysphagia
Why all the mentioned complains are pulsatile and increase after effort
Why there is horsiness of voice.
Aortic arch aneurism
Pulling stretching and pressure on cardiac plexus
Compression of esophagus
Due to increase of frequency and force of the heart beats
Pressing and stretching of the left recurrent laryngeal nerve.
