Cardiovascular physiology-passmed Flashcards
A 34-year-old woman presents to the emergency department with a sudden onset headache. She describes it as the worst headache she’s ever had. Her past medical history includes polycystic kidney disease (PKD) and hypertension.
The emergency doctor diagnoses a subarachnoid haemorrhage secondary to a common complication of her PKD.
Which one of the following investigations is the gold standard for the investigation of intracranial vascular disease?
Non-contrast CT of the head Flow-Sensitive MRI (FS MRI) Cerebral angiography Contrast CT of the head PET scan of the head
PKD increases the risk of cerebral aneurysms, which in turn increases the risk of subarachnoid haemorrhages.
Cerebral angiography is the gold standard investigation for diagnosing intracranial aneurysms and other vascular diseases. It can be used to view arteries and veins. Contrast dye injected into the bloodstream helps visualise the vessels. Cerebral angiogram images can be 3-D reconstructed so that the cerebral vessels and accompanying pathology can be rotated and viewed from all angles.
Flow-Sensitive MRI (FS MRI) combines functional MRI with images of cerebrospinal fluid (CSF) flow. FS MRI can be useful in planning the surgical removal of a skull base tumour, spinal cord tumour, or a tumour causing hydrocephalus (fluid buildup in the brain).
Contrast and non-contrast CT scans are commonly used as the first line of investigation for intracranial lesions but are superseded by the cerebral angiography and therefore are not the gold standard investigation.
An 80-year-old gentleman comes into the GP surgery, complaining of shortness of breath especially when lying down. His ejection fraction is normal. What could be a possible explanation for this?
He has increased atrial compliance He has diastolic dysfunction He has increased ventricular compliance He has systolic dysfunction He has decreased afterload
Ejection fraction measures of the proportion of blood leaving the ventricles with each beat. It is calculated by dividing stroke volume by end-diastolic volume. A healthy value for this is usually taken as remember 60% (based on stroke volume of 70ml and end-diastolic volume of 120ml).
In systolic dysfunction, stroke volume is decreased and this decreases ejection fraction. Ejection fraction is not a useful measure in someone with diastolic dysfunction, due to the fact that stroke volume may be reduced whilst end-diastolic volume may be reduced. Diastolic dysfunction may arise when there is reduced compliance of the heart.
A patient suffering from primary pulmonary hypertension is given bosentan to treat his condition. Bosentan is an endothelin receptor antagonist.
What is the action of endothelin?
Vasoconstriction and bronchoconstriction Vasodilation and bronchodilation Vasoconstriction and bronchodilation Vasodilation and bronchoconstriction Anti-thrombotic effects
Endothelin is a long-acting vasoconstrictor and bronchoconstrictor. It is secreted by vascular endothelium and has is thought to have a role in the pathogenesis of primary pulmonary hypertension, cardiac failure, hepatorenal syndrome and Raynaud’s.
Joanna is a 62-year-old female who has recently been diagnosed with hypertension. Her doctor explains to her that her average blood pressure is determined by multiple bodily processes, including action by the heart, nervous system, and blood vessel diameter. Theoretically, on average, Joanna’s cardiac output (CO) is 4L/min. On examination today, her mean arterial pressure (MAP) is measured at 140mmHg.
Given these figures, what is Joanna’s systemic vascular resistance (SVR)?
35mmHg⋅min⋅mL-1 136mmHg⋅min⋅mL-1 144mmHg⋅min⋅mL-1 400mmHg⋅min⋅mL-1 560mmHg⋅min⋅mL-1
The calculation used to calculate systemic vascular resistance is: SVR = MAP / CO. Therefore, in this case, SVR = 140/4 = 35mmHg⋅min⋅mL-1.
This is a simplified equation, as theoretically SVR = (MAP - CVP) ÷ CO. However, as CVP is usually at or near 0mmHg, the equation is often simplified.
However, in real life, MAP is not determined by the CO and SVR (as these cannot be routinely measured). Therefore, it is measured by direct or indirect measurements of arterial pressure. At a normal resting heart rate, this is calculated using the equation: MAP = pressurediastolic + 1/3(pulse pressure). Pulse pressure is calculated using the equation: Pulse pressure = pressuresystolic - pressurediastolic.
A 67-year-old man presents to his GP with shortness of breath on exertion and is found to have heart failure. Systolic function can become impaired in heart failure due to increases in afterload.
Which of the following exacerbate his condition due to increases in afterload?
Decreased systemic vascular resistance Increased venous return Mitral valve stenosis Ventricular dilatation Hypotension
Afterload is the ‘load’ that the heart must push against in contraction. Looking at each myocyte the afterload is represented by the amount each myocyte must contract. Therefore afterload is commonly expressed as a calculation of ventricular wall stress.
ventricular wall stress ∝ (ventricular pressure (P) x ventricular radius (r)) / 2 x wall thickness (h)
Ventricular dilatation is a common cause of heart failure, why this is can be demonstrated in the above equation. Looking at this equation as radius increases, wall stress also increases thus an increase in afterload. For a constant aortic pressure as the ventricle dilates each myocyte must contract with more force to eject the same amount of blood from the heart. At a point the heart will no longer be able to compensate for ventricular dilatation, leading to heart failure.
Decreased systemic vascular resistance and hypotension would decrease afterload.
Increased venous return increases preload.
Mitral valve stenosis would decrease preload.
A 34-year-old gentleman presents to the emergency department with bradycardia. Cardiac muscle is likely to remain in phase 4 of the cardiac action potential for a prolonged amount of time.
What occurs in phase 4 of the cardiac action potential?
Slow sodium influx Rapid potassium influx Na+/K+ ATPase acts Slow calcium influx Rapid sodium influx
Resting potential is restored by Na+/K+ ATPase
Slow sodium influx is not a part of the cardiac action potential.
Rapid potassium influx occurs during repolarisation, phase 3.
Slow calcium influx occurs during phase 2.
Rapid sodium influx occurs in phase 1.
What occurs in Phase 3 of cardiac action potential?
Final repolarisation
Efflux of potassium
What occurs in Phase 2 of cardiac action potential?
Plateau
Slow influx of calcium
What occurs in Phase 1 of cardiac action potential?
Early repolarisation
Efflux of potassium
What occurs in Phase 0 of cardiac action potential?
Rapid depolarisation
Rapid sodium influx
These channels automatically deactivate after a few ms
Which part of the ECG represents atrial depolarization?
P wave Q wave T wave QRS complex P-R interval
The P wave represents atrial depolarization. Note that atrial repolarization is obscured within the QRS complex.
Which part of the ECG represents time between the onset of atrial depolarization and the onset of ventricular depolarization? P wave Q wave T wave QRS complex P-R interval
P-R interval
Time from the onset of the P wave to the beginning of the QRS complex
Ranges from 0.12 to 0.20 seconds in duration
Represents the time between the onset of atrial depolarization and the onset of ventricular depolarization
Which part of the ECG represents ventricular depolarization? P wave Q wave T wave QRS complex P-R interval
QRS complex
Represents ventricular depolarization
Duration of the QRS complex is normally 0.06 to 0.1 seconds
Which part of the ECG represents period in which the entire ventricle is depolarized? P wave Q wave T wave QRS complex P-R interval ST segment
ST segment
Isoelectric period following the QRS
Represents period which the entire ventricle is depolarized and roughly corresponds to the plateau phase of the ventricular action potential
Which part of the ECG represents ventricular repolarization and is longer in duration than depolarization? P wave Q wave T wave QRS complex P-R interval ST segment
T wave
Represents ventricular repolarization and is longer in duration than depolarization
A small positive U wave may follow the T wave which represents the last remnants of ventricular repolarization.
Which part of the ECG represents time for both ventricular depolarization and repolarization to occur? P wave Q wave T wave QRS complex P-R interval ST segment
Q-T interval
Represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential.
Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-T interval. Therefore the Q-T interval is expressed as a ‘corrected Q-T (QTc)’ by taking the Q-T interval and dividing it by the square root of the R-R interval (interval between ventricular depolarizations). This allows an assessment of the Q-T interval that is independent of heart rate.
Normal corrected Q-Tc interval is less than 0.44 seconds.
A patient is diagnosed with first-degree heart block which is shown on his ECG by an elongated PR interval. The PR interval relates to a particular period in the electrical conductance of the heart.
Which of the following could cause the PR interval to decrease?
Increase the conductance of the atria
Decreased conduction velocity of the SA node
Increased conduction velocity across the AV node
Increased hyperpolarisation in the cardiac action potential
Decrease hyperpolarisation in the cardiac action potential
Sympathetic activation increases heart rate by increasing conduction velocity of the AV node
The PR interval relates to the period of time between the start of atrial depolarisation (P wave) and the start of ventricular depolarisation (start of QRS complex). Conduction across the atria is 1m/s however it is only 0.05m/s across the AV node. This means the rate limiting factor is the AV node, therefore a decrease in the PR interval would be dictated by conduction velocity across the AV node.
A patient has a cardiac output of 6 L/min and a heart rate of 60/min. Her end-diastolic left ventricular volume is 200ml.
What is her left ventricular ejection fraction (LVEF)?
15% 20% 25% 50% 75%
Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) * 100%
First, calculate the stroke volume:
Cardiac output = heart rate x stroke volume.
Stroke volume = cardiac output / heart rate.
= 6000/60 = 100ml.
Then calculate LVEF:
LVEF = (stroke volume / end diastolic LV volume) x 100.
= (100/200) x 100.
= 50%.
Abnormal conduction in the heart can lead to the development of arrhythmias. This can happen due to hypoxia caused by impaired blood flow in the coronary arteries. Depolarisation in phase 0 can be slowed, leading to slower conduction speeds.
What movement of ions causes rapid depolarisation in the cardiac action potential?
Calcium influx Potassium influx Potassium efflux Sodium influx Sodium efflux
Rapid sodium influx causes rapid depolarisation
Calcium influx is responsible for phase 2, the plateau period.
There is potassium influx in phase 4 to maintain the electrical gradient. This is due to the inward rectifying K+ channels and the Na+/K+ ion exchange pump
Potassium efflux mainly occurs in phase 1 and 3.
Sodium efflux occurs in phase 4 due to Na+/K+ ATPase
A 68-year-old man is admitted with central chest pain which is crushing in character. He has associated flushing.
ECG results:
ECG T wave inversion in II,III and AVF
Blood results:
Troponin T 0.9 ng/ml (normal <0.01)
Which substance does troponin T bind to?
Calcium ions Tropomyosin Actin Myosin Sarcoplasmic reticulum
Troponin T binds to tropomyosin, forming a troponin-tropomyosin complex
The clinical and electrographic features raise concerns over an inferior myocardial infarction which is confirmed by the raised troponin. Troponin T binds to tropomyosin, forming a troponin-tropomyosin complex. It is specific to myocardial damage.
Troponin C binds to calcium ions. It is released by damage to both skeletal and cardiac muscle making it an insensitive marker for myocardial necrosis.
Troponin I binds to actin to hold the troponin-tropomyosin complex in place. It is specific to myocardial damage.
Myosin is the thick component of muscle fibres. Actin slides along myosin to generate muscle contraction.
The sarcoplasmic reticulum regulates the calcium ion concentration in the cytoplasm of striated muscle cells
Troponin is a complex of three proteins involved in skeletal and cardiac muscle contraction
Subunits of troponin
troponin C: binds to calcium ions
troponin T: binds to tropomyosin, forming a troponin-tropomyosin complex
troponin I: binds to actin to hold the troponin-tropomyosin complex in place
A 72-year-old man attends the emergency department following a syncopal episode. He has an ECG which shows a prolonged PR interval, with every second QRS complex dropped. The width of the QRS complexes are normal.
In which part of the heart is the conduction delay likely to be coming from?
Apex Atrio-Ventricular node Bundle of His Sino-atrial node Left Ventricle
The PR interval represents the time between atrial depolarisation and ventricular depolarisation
This man has a 2:1 block, a form of second degree heart block.
As he has a prolonged PR interval the pathology must occur in the pathway between atrial and ventricular depolarisation. As he has a normal width QRS complex this points to the AV node, rather than the bundles of His.
Pathology in the sino-atrial node would not cause a prolonged PR with dropped QRS complexes.
A slowing of conduction anywhere in the ventricles would cause a wide QRS, but not a prolonged PR interval.
