Clinical Cardiac and pulmonary physiology

Question 1

What are the physiological components of mean arterial pressure (MAP)?

Answer 1

Regulated by change in CO and SVR
CO is determined by HR x SV
Strove Volume determined by (preload, Afterload, and contractility)

Question 2

What are the 2 factors that control preload?

Answer 2

Venous compliance

Blood volume

Question 3

How does venous compliance increase or decrease preload ? How does BV increase or decrease preload(i.e constriction vs dilation)?

Answer 3

A decrease in venous compliance, as occurs when the veins constrict, increases ventricular preload by increasing central venous pressure. Total blood volume is regulated by renal function, particularly renal handling of sodium and water.

Question 4

Heart rate, inotropy, venous compliance, and renal function are all strongly influenced by

Answer 4

neurohumoral mechanisms.

Question 5

What factors increase or decrease SVR?

Answer 5

The most important mechanism for changing systemic vascular resistance involves changes in vessel lumen diameter.

Question 6

Poiseuille relationship shows that resistance is

Answer 6

inversely related to the fourth power of the vessel radius.

Question 7

Name 3 VASCULAR factors which have important influences on vessel diameter.

Answer 7

nitric oxide, endothelin, and prostacyclin

Myogenic mechanisms can also increase or decrease

Question 8

Neurohumoral mechanisms are regulated principally by

Answer 8

arterial baroreceptors and to a lesser extent by chemoreceptors.

Question 9

Chemicals released by parenchymal cells surrounding blood vessels and can significantly alter vessel diameter

Answer 9

Tissue factors (e.g., adenosine, potassium ion, hydrogen ion, histamine) are chemicals

Question 10

In general, tissue factors are more concerned with regulating___________ than systemic arterial pressure; however, any change in vessel tone will affect both organ blood flow and systemic arterial pressure.

Answer 10

organ blood flow

Question 11

The most important arterial baroreceptors are located in

Answer 11

the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch

Question 12

Explain Baroreceptors are what type of sensors (receptors)

Answer 12

Pressure sensors (sense arterial pressure)
If arterial pressure rises, the receptors increases their firing frequency of the receptors due to the stretching of the arterial walls
If arterial pressure decrease, the receptors decreases their firing

Question 13

What is the carotid sinus innervated by?

Answer 13

Sinus nerve of Hering, which is a branch of the glossopharyngeal nerve, IX

Question 14

Of these two sites for arterial baroreceptors, which is the most important for regulating arterial pressure and why?

Answer 14

carotid sinus is quantitatively. The carotid sinus receptors respond to pressures ranging from 60-180. Receptors within the aortic arch have a higher threshold pressure and are less sensitive than the carotid sinus receptors.

Question 15

Although the baroreceptors can respond to either an increase or decrease in systemic arterial pressure, their most important role is responding to

Answer 15

sudden reductions in arterial pressure (

Question 16

How does a decrease in Mean arterial pressure or both affects baroreceptors?

Answer 16

A decrease in MAP or pulse pressure results in decreased baroreceptor firing. Autonomic neurons within the medulla respond by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow.

Question 17

Long term firing and baroreceptors

Answer 17

It is important to note that baroreceptors adapt to sustained changes in arterial pressure. For example, if arterial pressure suddenly falls when a person stands, the baroreceptor firing rate will decrease; however, after a period of time, the firing returns to near normal levels as the receptors adapt to the lower pressure. Therefore, the long-term regulation of arterial pressure requires activation of other mechanisms (primarily hormonal and renal) to maintain normal blood pressure.

Question 18

3 Most common causes of tachycardia in the OR are?

Answer 18

severe hypovolemia, an inflammatory response or an inadequate anesthetic for surgical stimulus.

Question 19

Hemodynamic instability can occur with

Answer 19

tachycardia (typically HR >150bpm) for which cardioversion is indicated.

Question 20

Differential for tachycardia intraoperative

Answer 20

Light anesthesia
Hypovolemia/Anemia
Vasodilatation
Hypercarbia
Hyperthermia
Hypoxia
Auto-PEEP

Fever /MH
Sepsis

Question 21

Why is tachycardia bad for the patient in the OR?

Answer 21

Time for LV filling is also diminished with even mild tachycardia.

Question 22

Treatment of tachycardia when not to give beta blockers?

Answer 22

If patient is hypovolemic, decompensated HF, asthma

Question 23

Treatment of tachycardia with What beta blockers

Answer 23

Esmolol (50-300mcg/min)

Metoprolol/ Labetalol

Question 24

Other treatment for tachycardia other than beta blockers?

Answer 24

Deepen the anesthesia

Administer OPIOIDS

Question 25

How do bradycardia cause a low cardiac output?

Answer 25

Bradycardia

Question 26

3 causes on How tachycardia cause a low cardiac output?

Answer 26

The stroke volume becomes reduced because of decreased ventricular filling time and decreased ventricular filling (preload) at high rates of contraction.
Tachycardia: Another consequence of tachycardia is increased myocardial oxygen demand. This can cause angina (chest pain), particularly in patients having underlying coronary artery disease. Finally, chronic states of tachycardia can lead to systolic heart failure.

Question 27

Discuss the unique features of the coronary circulation.

Answer 27

As in all vascular beds, it is the small arteries and arterioles in the microcirculation that are the primary sites of vascular resistance, and therefore the primary site for regulation of blood flow.

Question 28

Why is the left ventricle mainly perfused during diastole?

What effect does tachycardia have on left ventricle perfusion?

Answer 28

• Left ventricular myocardial perfusion occurs in diastole rather than systole due to arrangement of the coronary anatomy.
  Coronary perfusion pressure is a significant determinant of myocardial oxygen supply; local factors regulate coronary flow across a range of coronary perfusion pressures.
  If coronary perfusion pressure becomes acutely reduced in patients with circulatory shock, type 2 myocardial infarction may occur; this has a different etiology to the widely known type 1 myocardial infarction.

Question 29

Explain how capillary blood flow end up draining to the Right Atrium?

Answer 29

Capillary blood flow enters venules that join together to form cardiac veins that drain into the coronary sinus located on the posterior side of the heart, which drains into the right atrium.

Question 30

Draining directly into the cardiac chambers?

Answer 30

There are also anterior cardiac veins and thesbesian veins drain directly into the cardiac chambers.

Question 31

In non-diseased coronary vessels, whenever cardiac activity and oxygen consumption increases

Answer 31

there is an increase in coronary blood flow (active hyperemia) that is nearly proportionate to the increase in oxygen consumption.

Question 32

Myocardial oxygen consumption (MVO2) of a resting heart?

Answer 32

8 ml O2/min

Question 33

Oxygen consumption in the brain

Answer 33

3.5 ml O2/min

Question 34

Oxygen consumption in the kidney

Answer 34

5 ml O2/min

Question 35

What is the Fick’s Principle ?

Answer 35

There is a unique relationship between MVO2, coronary blood flow (CBF), and the extraction of oxygen from the blood (arterial-venous oxygen difference, CaO2 - CvO2). This relationship is an application of the Fick Principle:

Question 36

What is the FICK principle formula?

Answer 36

MVO2 = CBF × (CaO2 − CvO2)
where CBF = coronary blood flow (ml/min), and (CaO2 – CvO2) is the arterial-venous oxygen content difference (ml O2/ml blood). For example, if CBF is 80 ml/min per 100g and the CaO2-CvO2 difference is 0.1 ml O2/ml blood, then the MVO2 = 8 ml O2/min per 100g.

Question 37

Oxygen supply is primarily determined by

Answer 37

FLOW

Question 38

Describe hypoxic pulmonary vasoconstriction.

Answer 38

Hypoxic pulmonary vasoconstriction is

Question 39

What are the west zones of the lung?

Answer 39

Zone 1 PA>Pa>Pv
Zone 2 Pa>PA>Pv
Zone 3 Pa>Pv>PA

Question 40

A pulmonary shunt is a pathological condition which results when the alveoli of the lungs are

Answer 40

perfused with blood as normal but ventilation fails to supply the region ventilation/perfusion ratio (the ratio of air reaching the alveoli to blood perfusing them) is zero.

Question 41

What is anatomic and alveolar dead space?

Answer 41

Dead space is the portion of ventilation inadequately exposed to perfusion, primarily altering carbon dioxide elimination.
Anatomical dead space, an absolute dead space, is the portion of ventilation to structures that are incapable of gas exchange, such as the pharynx, trachea, and large airways.
Alveolar dead space, which can be both absolute and relative, consists of ventilation to alveoli with suboptimal perfusion exposure. Approximately one-third of minute ventilation in spontaneously ventilating individuals is dead space. With positive pressure ventilation, dead space ventilation may further increase.

Question 42

HPV is decreased (causing increased shunt, worsening oxygenation) by:

Answer 42

●Metabolic and respiratory alkalosis
●Hypocapnia
●Hypothermia
●Increased left atrial pressure
●Administration of a volatile inhalation anesthetic at a dose >1 minimum alveolar concentration (MAC)
●Hemodilution

Question 43

Coronary Perfusion Pressure (CPP) =

Answer 43

Aortic Diastolic Pressure – Left Ventricular end-diastolic Pressure (LVEDP)

Question 44

What effect does tachycardia have on left ventricle perfusion?

Answer 44

Tachycardia increases the relative percentage of time spent during systole (shortening of diastole) and consequently the duration of restricted LV perfusion. In contrast to the LV, systolic intramyocardial pressure is low in the RV and thus does not produce compressive forces that impede blood flow.

Question 45

All inhaled anesthetics and ventilatory response to hypercabia?

Answer 45

depress the ventilatory response to hypercarbia in a dose-dependent fashion

Question 46

All inhaled anesthetics and ventilatory response to hypercabia?

Answer 46

depress the ventilatory response to hypercarbia in a dose-dependent fashion. High concentrations of volatile anesthetics may almost entirely eliminate hypercarbia-induced increases in ventilatory drive.

Question 47

CO2 response curve
Opioids 
Benzodiazepines
Propofol 
Hypoxemia

Answer 47

Opioids: right-shift the ventilatory response curves (slope may change at high doses)
Benzodiazepines: decrease the slope of the ventilatory response curves
Propofol: decrease the slope of the ventilatory response curves (58% reduction at 100 ucg/kg/min)
Hypoxemia: at less than 65 mm Hg paO2, the CO2 response curve is left-shifted

Question 48

Patients with mild acute hypercapnia frequently complain of dyspnea, which is thought to be due to the initial compensatory

Answer 48

increase in respiratory drive induced by elevated levels of arterial CO2 and the associated acidemia

Question 49

One of the physiologic effects of hypercapnia (and/or acidosis) includes a shift of the oxyhemoglobin dissociation right,

Answer 49

leading to increased release of oxygen to tissues (Bohr effect). on curve to the

Question 50

Hypoxic ventilatory response

Answer 50

Blunted by VA

Question 51

Hypercapnic and hypoxic ventilatory response

Answer 51

The chemoreflexes mediate the ventilatory response to hypoxia and hypercapnia, and they also exert important cardiovascular effects.

The peripheral arterial chemoreceptors, the most important of which are located in the carotid bodies, respond primarily to changes in the partial pressure of oxygen. HYPOXEMIC stimulation elicits an increase in respiratory muscle output, inducing hyperventilation, and an increase in sympathetic outflow to peripheral blood vessels, resulting in vasoconstriction. Hyperventilation in turn activates pulmonary stretch receptors, which buffer the increases in sympathetic and vagal outflow, thereby maintaining homeostasis under normal conditions. During apnea, when hyperventilation is absent or prevented, vasoconstriction is potentiated and occurs simultaneously with activation of cardiac vagal drive resulting in bradycardia, collectively termed the “diving reflex,” a protective mechanism which helps preserve blood flow to the heart and brain while limiting cardiac oxygen demand.

The central chemoreceptors are located in the brainstem and respond to changes in pH mediated primarily by carbon dioxide tension. Stimulation of central chemoreceptors by hypercapnia also elicits sympathetic and respiratory activation, but without the cardiovagal effects seen with hypoxia.2