CVS Module Flashcards
A patient was brought to the emergency unit following sudden onset of difficulty in breathing. He had extensive anterior myocardial infarction 2 years back. Further examination revealed a respiratory rate of 30 breaths per minute.
Blood pressure of 80/60 mmHg (30 marks)
Normal blood pressure of a healthy adult is 120/80 mmHg. Therefore, a blood pressure of 80/60 mmHg is low.
The patient has suffered from an anterior myocardial infarction in which the anterior descending artery (a branch of the left coronary artery) is blocked. This has led to the death of cardiac muscles of the left ventricle due to deprivation of O2. The force of contraction produced by the left ventricle to eject blood into the aorta is reduced. Thus, the SV (stroke volume) is low resulting in a low cardiac output.
Cardiac output= stroke volume × heart rate
Blood pressure = Cardiac output × Total peripheral resistance
Therefore, the blood pressure is reduced in this patient.
A patient was brought to the emergency unit following sudden onset of difficulty in breathing. He had extensive anterior myocardial infarction 2 years back. Further examination revealed a respiratory rate of 30 breaths per minute.
Elevated jugular venous pressure (30 marks)
Jugular venous pressure reflects the right atrial pressure and is measured by visualizing the internal jugular vein. Elevated JVP indirectly indicates an increase in the right atrial pressure.
This patient has congestive cardiac failure developed over time. As the patient suffered from myocardial infarction 2 years back, blood accumulates within the right ventricle due to the left ventricular failure. The workload on the right ventricle is increased leading to right ventricular failure as well with time.
The force of contraction produced by the cardiac muscles of the right ventricle to eject blood into the pulmonary trunk is reduced. This leads to accumulation of blood within the right ventricle.
The end systolic volume and pressure of the right ventricle rises, reduces pressure gradient for blood flow from atrium to ventricle thus reducing the blood flow from right atrium to right ventricle.
The right atrial pressure also increases due to the high back pressure.
The rise in the right atrial pressure is transmitted to the internal jugular vein resulting in an elevated JVP.
A patient was brought to the emergency unit following sudden onset of difficulty in breathing. He had extensive anterior myocardial infarction 2 years back. Further examination revealed a respiratory rate of 30 breaths per minute.
Ejection fraction of 40% (30 marks)
Ejection fraction is the percentage of ventricular end diastolic volume which is ejected with each stroke. It is expressed as.
SV/EDV ×100%
Where SV is stroke volume; the volume of blood ejected by each ventricle per heartbeat, and EDV is the end diastolic volume; the volume of blood in each ventricle at the end of diastole. The ejection fraction is a good index of the systolic function of ventricles. The normal range is 60-65%, therefore an ejection fraction of 40% is low. As the patient has suffered from myocardial infarction the cardiac muscle mass is reduced due to the death of cardiac muscles as a result of O2 deprivation. The force of contraction produced by the cardiac muscles to eject blood into the great vessels is reduced. Thus. the SV is low, resulting in a low ejection fraction.
Splitting of the second heart sound during inspiration in a healthy adult
The second heart sound is produced as a result of the vibrations set up by the closure of aortic and pulmonary valves at the end of ventricular systole.
During inspiration the venous return increases due to the increased negative intra thoracic pressure created. Volume of the right ventricle increases. This delays the emptying time and closure of pulmonary valve.
Pooling of blood in the pulmonary veins reduces the filling of left atrium which makes the closure of the aortic valve slightly earlier than in expiration. So, the aortic valve closes before the pulmonary valve.
Thus, there is a physiological splitting of the second heart sound during inspiration in a healthy adult.
Elevated jugular venous pressure (JVP) in right heart failure
Jugular venous pressure reflects the right atrial pressure and is measured by visualizing the internal jugular vein.
Elevated JVP indirectly indicates an increase in the right atrial pressure.
In right heart failure, the right ventricle fails to eject sufficient blood into the pulmonary trunk.
The end systolic volume and pressure of the right ventricle rises, reducing the blood flow from right atrium to right ventricle.
The right atrial pressure also increases due to the high back pressure and accumulation of blood within the atrium.
The rise in the right atrial pressure is transmitted to the internal jugular vein via the central veins; i.e Superior vena cava resulting in an elevated JVP.
Compare the mechanisms of the following:
Cyanosis following exposure to cold and in right to left cardiac shunt (35 marks).
Cyanosis following exposure to cold:
Cyanosis is the bluish discoloration of the skin and mucous membranes as the deoxyhemoglobin levels increase more than 5g/dL. It occurs in the presence of hypoxia, where the tissues extract more oxygen from hemoglobin to compensate, causing more reduced hemoglobin to be formed.
On exposure to cold, the thermoregulatory center in the posterior hypothalamus responds and activates heat preservation mechanisms. Peripheral vasoconstriction of the blood vessels supplying the skin occurs to prevent heat loss by evaporation, reducing blood flow to peripheral regions. This leads to an accumulation of deoxyhemoglobin molecules, causing peripheral cyanosis in areas like fingertips and ear lobes. This cyanosis can be relieved by exposing the patient to heat.
Cyanosis in right to left cardiac shunt:
In a right to left cardiac shunt, there is mixing of deoxygenated blood from the right side with oxygenated blood from the left side of the heart. This results in more deoxyhemoglobin molecules entering the systemic circulation, leading to central cyanosis. Central cyanosis appears in areas like the tongue, nail tips, and ear lobes. It’s warm to touch.
Difficulty in breathing when lying down in Congestive Heart Failure (25 marks)
Difficulty in breathing when lying down, known as orthopnea, is caused by the worsening of pulmonary edema. In this patient, the left ventricle fails to eject sufficient blood into the aorta due to reduced cardiac muscle mass from recent myocardial infarction. This leads to increased left ventricular end systolic volume and pressure, elevating left atrial pressure and transmitting it to the pulmonary veins. When hydrostatic pressure at the venular end increases, reabsorption decreases, leading to accumulation of excess tissue fluid in the pulmonary interstitium, causing pulmonary edema. In the supine position, venous pooling decreases, increasing venous return and exacerbating pulmonary edema.
Ejection fraction of 40% in Congestive Heart Failure (25 marks)
The ejection fraction, the percentage of ventricular end-diastolic volume ejected with each stroke, is a good index of ventricular systolic function. In this patient, the ejection fraction of 40% is low due to reduced cardiac muscle mass from a recent myocardial infarction, leading to decreased force of contraction and stroke volume.
Treating the above patient (CHF) with ACE inhibitor and Digoxin.
a. ACE inhibitor (25 marks)
Angiotensin-converting enzyme (ACE) inhibitors reduce intravascular volume by inhibiting the conversion of angiotensin I to angiotensin II, decreasing sodium and water reabsorption in the proximal convoluted tubule and stimulating aldosterone secretion, increasing preload and afterload on the heart.
b. Digoxin (15 marks)
Digoxin inhibits the Na/K ATPase pump, indirectly inhibiting the Na/Ca exchanger, leading to intracellular calcium accumulation and enhanced cardiac contractility, aiding in ejecting sufficient blood into the great vessels.
Difficulty in breathing in CHF (35 marks)
Difficulty in breathing (35 marks)
In congestive cardiac failure, the left ventricle fails to eject sufficient blood into the aorta. This leads to an increase in left ventricular end-systolic volume and pressure. Consequently, the left atrial pressure rises, transmitting this pressure elevation to the pulmonary veins. As a result, the hydrostatic pressure at the venular end increases, reducing reabsorption. When the lymphatic system’s capacity is exceeded, excess tissue fluid accumulates in the pulmonary interstitium, leading to pulmonary edema.
The accumulated fluid thickens the alveolar capillary membrane and reduces lung compliance by increasing surface tension. This decrease in compliance hampers ventilation, causing a ventilation-perfusion (V/Q) mismatch. Additionally, gas diffusion across the alveolar capillary membrane is impaired, reducing the partial pressure of oxygen (PaO2) in arterial blood. Although the partial pressure of carbon dioxide (PaCO2) is not greatly affected due to its higher solubility compared to oxygen, the low PaO2 stimulates peripheral chemoreceptors in the aortic and carotid bodies. Nerve impulses from these chemoreceptors are transmitted via the vagus and glossopharyngeal nerves to the respiratory center in the medulla oblongata. Consequently, nerve impulses are sent to the diaphragm and intercostal muscles via the phrenic and intercostal nerves, increasing the rate and depth of ventilation, thus leading to dyspnea.
Rapid thready pulse in hypovolemic shock (30 marks)
Hypovolemic shock occurs due to inadequate tissue perfusion resulting from low blood volume. A normal pulse rate falls within the range of 60-100 beats per minute. A pulse exceeding this range is termed rapid, while a thready pulse refers to a weak pulse with reduced pulse pressure.
In hypovolemic shock, low blood pressure (BP) leads to decreased stimulation of baroreceptors in the aortic arch and carotid sinus. This results in reduced nervous discharge via the vagus and glossopharyngeal nerves. Consequently, there is less inhibition of the vasomotor center and decreased stimulation of the cardiac inhibitory center in the Medulla Oblongata.
The decreased inhibitory input and increased sympathetic nervous output result in enhanced sympathetic activity. Sympathetic activation acts on beta-1 receptors in the sinoatrial (SA) node of the heart, increasing heart rate and causing the pulse rate to become rapid.
Additionally, due to the reduced cardiac output (CO) in hypovolemic shock, systolic blood pressure (SBP) decreases. However, increased sympathetic discharge leads to heightened vasoconstriction, increasing total peripheral resistance (TPR) and consequently diastolic blood pressure (DBP). This results in a reduction in pulse pressure (PP), defined as SBP minus DBP, leading to a thready pulse.
Increased risk of developing heart failure when ventricles are dilated (20 marks)
According to the Law of Laplace, the pressure within a ventricle (P) is directly proportional to the wall tension (T) produced by cardiac muscle contraction, and inversely proportional to the radius (r) of the ventricle, divided by the wall thickness (W). Mathematically, it can be expressed as P = TW/r.
In normal healthy adults, a ventricular pressure of approximately 120 mmHg is generated during systole to eject blood into the aorta. This pressure is maintained by the wall tension produced by cardiac muscle contraction.
When the ventricles are dilated, the radius (r) increases while the wall thickness (W) decreases. As a result, the tension required to maintain normal ventricular pressure significantly increases. The ventricles must contract more forcefully to generate the higher tension, thereby increasing the workload on the cardiac muscles. Over time, this heightened workload can lead to an increased risk of developing heart failure, characterized by the heart’s inability to maintain sufficient cardiac output to meet tissue needs.
Ejection fraction of the left ventricle is reduced in myocardial infarction (35 marks)
Ejection fraction is a crucial measure of cardiac function, representing the percentage of ventricular end-diastolic volume ejected with each stroke. It is calculated as the stroke volume (SV) divided by the end-diastolic volume (EDV) multiplied by 100%.
In the context of myocardial infarction, there is a reduction in the ejection fraction due to several underlying physiological mechanisms.
Firstly, myocardial infarction results in the death of cardiac muscle cells due to oxygen deprivation. This reduction in viable cardiac muscle mass directly impacts the heart’s ability to contract effectively.
Consequently, the force of contraction produced by the remaining healthy cardiac muscle in the left ventricle is diminished. As a result, the stroke volume, which represents the volume of blood ejected per heartbeat, is decreased. This reduction in stroke volume leads to a decrease in ejection fraction.
Moreover, myocardial infarction contributes to systolic dysfunction in the left ventricle. This dysfunction manifests as an increase in the end-systolic volume (ESV), which refers to the volume of blood remaining in the ventricle after ejection. The accumulation of blood within the left ventricle over time further exacerbates systolic dysfunction.
The increased workload on the heart, resulting from both the reduced contractility and the accumulation of blood within the left ventricle, exacerbates the impairment in ejection function. This vicious cycle perpetuates a decline in ejection fraction, indicative of worsening cardiac function in the context of myocardial infarction.
Explain the physiological basis of:
Difficulty in breathing in HF (25 marks)
Congestive cardiac failure leads to inadequate pumping by both ventricles, resulting in reduced ventricular contractility.
With reduced contractility, ventricular end-systolic volume increases, leading to blood accumulation in the left ventricle and increased pressure in the left atrium.
Elevated pressure in the left atrium backs up into the pulmonary veins, increasing hydrostatic pressure in the alveolar capillaries and altering Starling forces.
This leads to fluid accumulation in the lung interstitium, causing pulmonary edema.
Pulmonary edema thickens the alveolar capillary membrane and reduces surface area for gas exchange, decreasing lung compliance and PAO2.
Impaired ventilation and gas exchange increase the work of breathing, resulting in difficulty breathing (dyspnea).
Low PAO2 stimulates peripheral chemoreceptors in the carotid and aortic bodies, leading to increased respiratory drive.
Increased respiratory drive stimulates the Pre-Botzinger complex, increasing efferent impulses to the diaphragm and intercostal muscles, thereby increasing the rate and depth of breathing and worsening dyspnea.
Cyanosis in CHF (15 marks)
Cyanosis is characterized by bluish discoloration of the skin due to elevated levels of deoxygenated hemoglobin (Hb) in capillary blood.
In congestive cardiac failure, pulmonary edema decreases PAO2, contributing to cyanosis.
Stagnant hypoxia occurs due to slowed circulation in congestive heart failure, further exacerbating cyanosis.
Increased extraction of oxygen from Hb by tissues leads to increased levels of reduced Hb.
Central cyanosis occurs when there is failure in the heart, presenting symptoms such as bluish lips, tongue, nail tips, and earlobes, which are warm to touch.
Blood pressure of 100/90 mmHg in CHF (25 marks)
In a healthy adult, normal blood pressure is around 120/80 mmHg.
In this patient, systolic blood pressure is reduced while diastolic blood pressure is increased.
Cardiogenic shock caused by heart failure results in insufficient blood pumping by the heart.
Reduced stroke volume leads to decreased cardiac output.
Since systolic blood pressure depends on cardiac output, it decreases due to reduced cardiac output.
Blood pressure is a product of cardiac output and total peripheral resistance.
With low blood pressure, baroreceptors in the aortic arch and carotid sinus are less stimulated, resulting in reduced nervous discharge via vagus and glossopharyngeal nerves.
Decreased inhibition of the vasomotor center and decreased stimulation of the cardiac inhibitory center lead to increased sympathetic nervous output.
Increased sympathetic activity causes vasoconstriction of peripheral vessels, increasing total peripheral resistance and, consequently, diastolic blood pressure.
A person has a cardiac output of 5.6 L/min, heart rate of 80 beats/min and ventricular end diastolic volume of 140mL. Calculate the ejection fraction. (10 marks)
1.1 Ejection Fraction Calculation:
Cardiac output = Stroke volume . Heart rate
Stroke volume = Cardiac output / Heart rate = 5.6 L/min / 80 beats/min = 0.07 L
Ejection fraction = (Stroke volume / Ventricular end diastolic volume) * 100%
= (0.07 L / 140 mL) * 100%
= 50%
The following are arterial blood pressure values for two persons ( A and B ) in supine position and at 5 minutes after standing up. Explain the physiological basis for the above findings in person A and B. (40 marks)
Person A:
In supine position, normal blood pressure is maintained. Upon standing, venous pooling occurs, reducing venous return to the heart, decreasing preload. According to the Frank-Starling law, reduced preload leads to decreased stroke volume and cardiac output. Reduced cardiac output decreases blood pressure, triggering baroreceptor inhibition and subsequent sympathetic discharge, increasing heart rate and restoring blood pressure to normal.
Person B:
In supine position, increased venous return elevates preload, leading to increased stroke volume and cardiac output, hence higher blood pressure. However, upon standing, reduced venous return decreases preload, lowering stroke volume and cardiac output. Due to cardiac autonomic insufficiency, baroreceptor reflex fails to compensate, causing postural hypotension.
1.3 Explain the physiological basis of the following:
a) Sub-endocardial portion of the left ventricle is relatively more prone to ischaemia compared to the rest of the myocardium. (25 marks)
b) Blood flow varies with arteriolar diameter (25 marks)
a) Sub-Endocardial Ischemia: During systole, left ventricular pressure rises, compressing coronary arteries, and reducing blood supply. In diastole, relaxation relieves this compression, allowing rapid blood flow. Sub-endocardial areas experience greater compression, receiving blood only during diastole, making them prone to ischemia.
b) Arteriolar Diameter and Blood Flow: Blood flow through arterioles is directly proportional to the fourth power of their radius, as per the Poiseuille-Hagen formula. Smooth muscle in arteriole walls allows efficient regulation of blood flow by adjusting diameter, demonstrating significant flow variations based on arteriolar diameter changes.
Anterior MI - Treatment with intravenous furosemide. (30 marks)
In congestive cardiac failure, cardiac workload should be reduced.
For that, furosemide is given to offload the heart.
Furosemide is a loop diuretic.
It acts by inhibiting Na+K+ 2Cl- transporters in the thick ascending limb of loop of Henle.
Osmotically active solutes remain in the renal tubules. Na holds water in tubules.
Due to reduced reabsorption of Na and other ions, medullary hypertonicity is not reached. Urine concentrating mechanisms are affected. Results in osmotic diuresis.
Reduced intravascular volume.
Reduced venous return to heart.
Reduced VEDV
Reduced SV
Cardiac Output (CO) = Stroke volume (SV)* Heart Rate (HR)
Thus reduced CO
This reduces cardiac workload and myocardial O2 consumption.
Question: Explain the five phases of the cardiac cycle with the aid of a diagram taking the following into consideration.
ECG changes
Pressure changes
Volume changes
Opening and closure of valves
JVP changes
-
Atrial Systole:
- Triggered by the SA node, atrial contraction follows the P wave (atrial depolarization).
- Atrial pressure rises, indicated by the ‘a’ wave in JVP.
- Ventricular end-diastolic volume reaches 130 ml, elevating ventricular pressure.
- Closure of AV valves occurs, marking the first heart sound (“lub”).
-
Isovolumetric Ventricular Contraction:
- Both aortic and pulmonary valves are closed, maintaining constant ventricular volume.
- Ventricular contraction raises pressure (up to 80 mmHg in the left heart), causing AV valves to bulge into the atria (represented by the ‘c’ wave in JVP).
-
Ventricular Ejection:
- Ventricular pressure exceeding 80 mmHg (aortic pressure) opens aortic and pulmonary valves.
- Blood is ejected from the left ventricle, reaching peak pressure of 120 mmHg (left heart).
- AV valves are pulled downward, and atrial pressure decreases (indicated by the “x” descent in JVP).
- Closure of aortic and pulmonary valves generates the second heart sound (“dub”).
-
Isovolumetric Ventricular Relaxation - Early Diastole:
- All valves are closed, maintaining ventricular volume at 50 ml.
- Ventricular pressure drops until it falls below atrial pressure, prompting AV valve opening.
-
Ventricular Filling - Late Diastole:
- AV valves are open, allowing ventricular filling (constituting 70% of ventricular blood flow).
- Passive reduction in right atrial pressure occurs (“y” descent in JVP) as blood flows from the right atrium to the right ventricle.
Physiological Basis of Korotkoff Sounds in Blood Pressure Measurement:
Physiological Basis of Korotkoff Sounds in Blood Pressure Measurement:
- Blood pressure measurement involves the use of a sphygmomanometer over the brachial artery, gradually inflating and deflating the cuff to alter blood flow and detect Korotkoff sounds.
- Initially, the cuff pressure exceeds systolic pressure, leading to complete arterial compression and silence.
- As cuff pressure decreases, turbulent blood flow occurs when systolic pressure exceeds cuff pressure, generating Korotkoff sounds.
- Systolic pressure is measured when Korotkoff sounds first appear, and diastolic pressure when sounds disappear.
Arm Position and Blood Pressure Measurement:
Arm Position and Blood Pressure Measurement:
- Blood pressure measurement in the brachial artery is influenced by arm position due to gravitational effects.
- The arm must be supported at heart level to ensure accurate measurement, as gravitational effects can alter blood pressure.
- Blood pressure increases when the arm is below heart level and decreases when above heart level.
Phasic Blood Flow in Ascending Aorta vs. Continuous Flow in Renal Artery:
Phasic Blood Flow in Ascending Aorta vs. Continuous Flow in Renal Artery:
- Blood flow in the ascending aorta is phasic due to cardiac ejection during systole and transient backflow during diastole before aortic valve closure.
- Elastic recoil of the arterial walls aids in blood propulsion during diastole, contributing to phasic flow.
- In contrast, the Windkessel effect in distal aorta and large arteries ensures continuous forward flow.
- In the renal artery, elastic recoil of vessel walls helps drive blood forward during diastole, resulting in continuous flow.
