Cardiovascular

Question 1

Describe the baroreceptor response.

Answer 1

See image

Question 2

Where are located the baroreceptors?

Answer 2

Carotid sinus and aortic arch

Question 3

Which nerves carry the impulse of the baroreceptors and to which nuclei?

Answer 3

Carotid sinus –> CN IX
Aortic arch –> CN X
To the Nucleus Tractus Solitarius

Question 4

What are the different central centers for the baroreceptor reflex arc?

Answer 4

Cardiac accelerator (Sympathethic, NE –> SA node activation and inotropy), cardiac decelerator (Parasympathetic) and vasoconstrictor center (SNS–> arteriolar and venous constriction)

Question 5

Draw and label a central venous pressure waveform.

Answer 5

A- Atrial contraction
C- Triscupid valve closure during ventricular contraction
X- Atrial relaxation
V- Atrial diastolic filling during ventricular contraction
Y- Atrial emptying

Question 6

What are common pathologies altering the CVP waveforms?

Answer 6

Pericardial effusion (Increased CVP baseline, prominent X-descent, lack of Y as atrium is unable to fill)
Atrial fibrillation (Lack of a-wave, prominent C-waves from tricuspid bulging with atrial overfilling)
Tricuspid regurgitation (Prolonged and prominent C-wave due to regurgitant flow during systole, prominent v-wave during ventricular systole)
Tricuspid stenosis (Prominent a-wave during atrial contraction, attenuated y-wave due to resistant to atrial emptying)

Question 7

What are determinants of CVP?

Answer 7

Venous return (Venous resistance, venous tone, venous compliance)
Right heart function (Heart rate, preload, afterload, contractility, structural disease)
Intrathoracic pressure (Pleural effusion, pericardial effusion, PEEP, mass, expiratory effort)

Question 8

What is the normal mean PAOP?

Answer 8

5-12mmHg

Question 9

Define preload

Answer 9

Ventricular stretch at the end of diastole, often referred to as end-diastolic ventricular volume

Question 10

Define afterload

Answer 10

Load that the heart must pump against to eject blood

Question 11

Define inotropy

Answer 11

Intrinsic ability of the myocardial cells to develop force at a given muscle length

Question 12

Define dromotropy

Answer 12

Cardiac conduction velocity

Question 13

What factors affect inotropy?

Answer 13

Preload, afterload (Anrep effect; increased afterload = increased inotropy), heart rate (Bowditch effect; increased HR = increased inotropy), sympathetic stimulation

Question 14

Explain the Bowditch effect

Answer 14

An increased in heart rate lead to intracellular calcium accumulation and increased muscle tension (Contractility) from calcium availibility

Question 15

Draw a normal pressure-volume loop. 
Identify the phases of the loop
Identify Sys, MAP and DAP
Identify the afterload
Identify ESV, EDV and stroke volume 
Draw EDPVR --> What does it represent? 
Draw ESPVR  --> What does it represent?

Answer 15

EDPVR –> Represent lusitropy (Cardiac relaxation)

ESPVR –> Inotropy

Question 16

How is calculated the ejection fraction based on a PV loop?

Answer 16

EJ (%) = 100x Stroke Volume / EDV

SV = ESD -ESV

Question 17

Describe the innervation of the heart.

Answer 17

Parasympathetic system releases acetylcholine to M receptors at SA and AV node through vagus nerve

Sympathetic efferent nerves throughout the SA node, conduction system/atria and ventricles.

Question 18

What is the principle factor of myocardial oxygen consumption?

Answer 18

Inotropy (So affected by afterload, HR and sympathetic innervation)

Question 19

Which mediators cause vasoconstriction?

Answer 19

Endothelin-1, vasopressin, catecholamines, angiotensin II, serotonin, thromboxane-2

Question 20

Which mediators cause vasodilation?

Answer 20

Nitric oxide, bradykinin, prostaglandins, histamine, severe alkalosis/acidosis, severe hypoxia, electrolyte abnormalities

Question 21

Draw and explain the action potential for nodal cells and myocardial cells

Answer 21

Nodal cells
Phase 4: Spontaneous depolarization (Influx of sodium by funny channels), longest part of the action potential, determinant of HR
Phase 0: Upstroke (Rapid calcium influx once membrane treshold is reached)
Phase 3: Repolarization (Potassium efflux)

Myocardial cells
Phase 0: Upstroke (Influx of sodium)
Phase 1: Initial repolarization (Influx of calcium)
Phase 2: Plateau (Slow influx of potassium with influx of calcium)
Phase 3: Repolarization (Rapid efflux of potassium, decrease influx of calcium)
Phase 4: Resting membrane potential (Inward current = Outward current)

Question 22

Describe excitation-contraction coupling.

Answer 22

1) Calcium enters the cell during the plateau phase during the action potential
2) Calcium induced calcium release by sarcoplasmic reticulum (through ryanodine receptors)
3) Calcium binds to troponin C
4) Tropomyosin retracts itself from myosin-binding sites on actin
5) Myosin-actin complexes form crossbridges, moving past each other (creating tension and contraction)
6) Calcium is actively transported back in SR and Ca is pumped out of the intracellular space
7) Tropomyosin blocks myosin binding sites (Muscle fiber releases/relaxes)

Question 23

What are the 5 most common echocardiographic views

Answer 23

Right parasternal short axis view, left apical 4 chamber view, left apical 5 chamber view, right parasternal long axis 4 chamber view,

Question 24

What is the equation for fractional shortening?

Answer 24

FS (%) = 100 x (LVEDD- LVESD ) /LVEDD

Question 25

Describe the placement of a pulmonary arterial catheter

Answer 25

The patient is sedated The neck over the external jugular is shaved and aseptically prepped The area is draped A local lidocaine block is applied and a small stab incision over the vessel is performed A sterile introducer sheath is introduced into the jugular vein The catheter is advanced through the introducer sheath The catheter is advanced to the pulmonary artery (Either confirmed by waveform analysis or fluoroscopy)

Question 26

What are potential complications of PAC placement?

Answer 26

Hemorrhage, infection, thrombosis, carotid artery laceration, pulmonary artery necrosis, air embolism, hemothorax, pneumothorax, arrhythmia, tricuspid valvular damage

Question 27

What are indications for CO monitoring?

Answer 27

Refractory hypotension, vasopressor, extensive third spacing losses, oliguria/anuria, hemorrhage/trauma, sepsis, burn

Question 28

What function can be performed with a PAC?

Answer 28

CPV, RAP, PAP, PAWP monitoring, mixed venous and central venous sampling (SvO2, ScVO2), estimation of cardiac output (Fick's method, thermodilution), pulse pressure variation calculation, hyperosmolar solute administration, pacing, angiography

Question 29

Described different methods of cardiac output monitoring

Answer 29

* *Fick's method: Gold standard. Patient is intubated. PAC required for SvO2. Inspired and expired oxygen are measured. Arterial and mixed venous oxygen concentration are calculated. CO = VO2 / (CaO2 - CmvO2). Less reliable with hemodynamic instability. * *NICO- Patient is intubated. CO is calculated based on CO2, either via complete rebreathing or partial rebreathing (NICO) Indicator dilution * Thermodilution- A set liquid at a set volume and temperature is quickly injected in the proximal port of the PAC. The temperature change is noted at the thermistor at the distal port of the PAC. An algorithm calculates the CO (Inversely proportional to area under the curve of temperature over time). Not reliable if valvular regurgitation or chamber shunting. * Transpulmonary thermodilution- A known volume/temperature of liquid is quickly injected through a central venous catheter and a thermistor in the femoral artery analyzes temperature changes. * Lithium dilution- A known volume of lithium is injected through a central venous catheter and an arterial sample is continuously obtained through a peripheral arterial catheter to measure concentration (Large volume of blood). * Transesophageal echocardiogram- Determine CO from aortic flow and area. Requires GA, experienced personal, must be calibrated from invasive CO method (Lithium, thermodilution), * Transthoracic impedance: Non-invasive, but animal conformation is too variable.

Question 30

List the pressures throughout the pulmonary and systemic circulation?

Answer 30

``` RA 4-6mmHg/ 0-4 RV- 15-30mmHg/0-4 PAP- 15-30mmHg/5-15mmHg PAOP 5-12mmHg (Mean pressure) LA - 10/2 (?) LV- 120/5 (?) Aorta- 120/80 ```

Question 31

What are potential causes of error in CO measurement (Thermodilution)?

Answer 31

Respiratory cycle, arrhythmia, low cardiac output, thermistor error, injectate error, multiple infusions at the same time

Question 32

What are the potential complications of arterial catheterization?

Answer 32

Infection, hemorrhage, thrombosis, necrosis of distal limb, air embolism

Question 33

Describe components of an arterial waveform.

Answer 33

Systolic blood pressure, diastolic blood pressure, pulse pressure, dicrotic notch (Rebound of the aortic valve at the time of closure, depend on the compliance of vessels and vascular tone).

Question 34

Describe distal pulse amplification

Answer 34

The further in the arterial tree the pressure is measured, the higher the systolic and lower the diastolic pressure will be. The dicrotic notch will also be later in the waveform.

Question 35

Describe a square test.

Answer 35

This test is used to evaluate the natural frequency and damping of a system. The fast flush valve is activated for 1 second. The waveform should make a plateau at 300mmHg, then form a 90 degree angle with a rapid downstroke. If the system is underdamped, the waves will have multiple sharp upstrokes and downstrokes (Excessive ringing) before returning to baseline (Cause: Long tubing). If the system is overdamped, there is less than one oscillation after square test. Low systolic, high diastolic, loss of dicrotic notch (Cause: Air bubble, kink, clot, overly compliant tubing).

Question 36

Describe pulse pressure variation

Answer 36

Dynamic measure of volume status under positive pressure ventilation derived from pulse variation during the respiratory cycle

Question 37

What is the equation for pulse pressure variation

Answer 37

PPV (%) = 100x (PPmax -PPmin)/ [(PPmax-PPmin)/2]

Question 38

Describe the Bainbridge reflex?

Answer 38

An increased in cardiac filling (Atrial stretch receptors) leads to SNS activation and increased heart rate

Question 39

Describe the Branham reflex

Answer 39

Transient bradycardia and increased blood pressure after ligation of a PDA.

Question 40

Describe the Anep effect.

Answer 40

An increased in afterload leads to an increased contractility

Question 41

Describe the Bowditch effect

Answer 41

An increased heart rate leads to an increased contractility

Question 42

Describe the mechanisms of cardiac injury

Answer 42

Alteration in intracellular calcium cycling Myocardial/vascular remodeling Deficiency in myocardial energy production

Question 43

Define cardiogenic shock

Answer 43

Inadequate cellular metabolism secondary to cardiac dysfunction despite adequate intravascular volume

Question 44

What are the two principal compensatory neurohormonal mechanisms involved in heart failure?

Answer 44

SNS activation RAAS activation (Also endothelin-1, ADH, ANP)

Question 45

What are the consequences of RAAS activation in heart failure?

Answer 45

Na and water retention leading to volume overload Cardiac remodeling/fibrosis Increased systemic vascular resistance (AgII, ADH, endothelin-1, catecholamines)

Question 46

What 3 substances lead to cardiac remodeling?

Answer 46

Aldosterone, angiotensin II, norepinephrine

Question 47

Describe the types of hypertrophy

Answer 47

Concentric hypertrophy: Thickening of the myocardium with increased myocardial oxygen demand and decreased relaxation (Diastolic dysfunction). Secondary to chronic pressure overload Eccentric hypertrophy: Dilation of the heart chamber with relative wall thinning secondary to chronic volume overload (or acquired disease). Systolic dysfunction.

Question 48

Define Laplace Law

Answer 48

Wall stress = Pressure x Radius / 2 x wall thickness Wall tension related to myocardial oxygen consumption Thicker ventricular wall means the stress is spread through a higher ventricular mass.

Question 49

What are the causes of cardiogenic shock (3) ?

Answer 49

Systolic dysfunction (Failure of contractility or outflow obstruction), diastolic dysfunction (Decreased RV filling --> HCM, RCM, tachyarrhythmia, cardiac tamponade) and bradyarrhythmias (Decreased cardiac output)

Question 50

What are the different causes of systolic failure?

Answer 50

``` Primary cardiac -Intrinsic failure of myocardial contractility (DCM) - ARVC Secondary cardiac - Severe MMVD - Tachycardia-induced cardiomyopathy ``` Extracardiac - Sepsis - Doxorubucin toxicity - Malnutrition

Question 51

Describe Frank-Starling relationship

Answer 51

Volume ejected by the heart is dependent on the volume present in the ventricle at the end of diastole, and cardiac output =venous return (Relationship between cardiac output/Stroke volume) and preload. In a healthy heart, an increase in preload should lead to an increased in cardiac output/stroke volume up to a physiology limit.

Question 52

Name three pathological characteristics of feline HCM

Answer 52

Diastolic dysfunction, systolic anterior motion of the mitral valve, feline aortic thromboembolism

Question 53

What breeds are predisposed to familial HCM

Answer 53

Maine coon, ragdoll

Question 54

What is the wall thickness associated with HCM?

Answer 54

Interventricular septum or free ventricular wall >6mm in a volume repleted patient

Question 55

What prognostic factors are associated with FATE?

Answer 55

Positive: One limb affected and temperature above 37.2 (<50% survival if below)

Question 56

Acute management of feline CHF?

Answer 56

Oxygen therapy, diuretics, sedation (opioid) | +/- nitroglycerin ointment (Reduced preload from venodilation) **Diastolic dysfunction

Question 57

Chronic management of feline CHF?

Answer 57

ACE inhibitor, furosemide, clopidogrel

Question 58

What are secondary causes of canine cardiomyopathy?

Answer 58

Drugs (Doxorubicin, catecholamines, ionophores), neoplasia, myocarditis (infectious/inflammatory), nutritional, infiltrative (Glycogen storage disease, mucopolysaccharidosis), Duchenne muscular dystrophy in golden, metabolic (Hypertension, hyperthyroidism, DM, acromegaly).