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ECC boards > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Describe the baroreceptor response.

A

See image

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2
Q

Where are located the baroreceptors?

A

Carotid sinus and aortic arch

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3
Q

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

A

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

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4
Q

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

A

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

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5
Q

Draw and label a central venous pressure waveform.

A

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

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6
Q

What are common pathologies altering the CVP waveforms?

A 
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)
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7
Q

What are determinants of CVP?

A 
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)
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8
Q

What is the normal mean PAOP?

A

5-12mmHg

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9
Q

Define preload

A

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

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10
Q

Define afterload

A

Load that the heart must pump against to eject blood

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11
Q

Define inotropy

A

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

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12
Q

Define dromotropy

A

Cardiac conduction velocity

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13
Q

What factors affect inotropy?

A

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

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14
Q

Explain the Bowditch effect

A

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

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15
Q 
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?
A

EDPVR –> Represent lusitropy (Cardiac relaxation)

ESPVR –> Inotropy

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16
Q

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

A

EJ (%) = 100x Stroke Volume / EDV

SV = ESD -ESV

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17
Q

Describe the innervation of the heart.

A

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.

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18
Q

What is the principle factor of myocardial oxygen consumption?

A

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

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19
Q

Which mediators cause vasoconstriction?

A

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

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20
Q

Which mediators cause vasodilation?

A

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

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21
Q

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

A

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)

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22
Q

Describe excitation-contraction coupling.

A

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)

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23
Q

What are the 5 most common echocardiographic views

A

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

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24
Q

What is the equation for fractional shortening?

A

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

25
Q

Describe the placement of a pulmonary arterial catheter

A

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)

26
Q

What are potential complications of PAC placement?

A

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

27
Q

What are indications for CO monitoring?

A

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

28
Q

What function can be performed with a PAC?

A

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

29
Q

Described different methods of cardiac output monitoring

A
  • *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.
30
Q

List the pressures throughout the pulmonary and systemic circulation?

A 
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
31
Q

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

A

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

32
Q

What are the potential complications of arterial catheterization?

A

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

33
Q

Describe components of an arterial waveform.

A

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).

34
Q

Describe distal pulse amplification

A

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.

35
Q

Describe a square test.

A

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).

36
Q

Describe pulse pressure variation

A

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

37
Q

What is the equation for pulse pressure variation

A

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

38
Q

Describe the Bainbridge reflex?

A

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

39
Q

Describe the Branham reflex

A

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

40
Q

Describe the Anep effect.

A

An increased in afterload leads to an increased contractility

41
Q

Describe the Bowditch effect

A

An increased heart rate leads to an increased contractility

42
Q

Describe the mechanisms of cardiac injury

A

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

43
Q

Define cardiogenic shock

A

Inadequate cellular metabolism secondary to cardiac dysfunction despite adequate intravascular volume

44
Q

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

A

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

45
Q

What are the consequences of RAAS activation in heart failure?

A

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

46
Q

What 3 substances lead to cardiac remodeling?

A

Aldosterone, angiotensin II, norepinephrine

47
Q

Describe the types of hypertrophy

A

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.

48
Q

Define Laplace Law

A

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.

49
Q

What are the causes of cardiogenic shock (3) ?

A

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

50
Q

What are the different causes of systolic failure?

A 
Primary cardiac
-Intrinsic failure of myocardial contractility (DCM)
- ARVC
Secondary cardiac
- Severe MMVD 
- Tachycardia-induced cardiomyopathy

Extracardiac

  • Sepsis
  • Doxorubucin toxicity
  • Malnutrition
51
Q

Describe Frank-Starling relationship

A

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.

52
Q

Name three pathological characteristics of feline HCM

A

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

53
Q

What breeds are predisposed to familial HCM

A

Maine coon, ragdoll

54
Q

What is the wall thickness associated with HCM?

A

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

55
Q

What prognostic factors are associated with FATE?

A

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

56
Q

Acute management of feline CHF?

A

Oxygen therapy, diuretics, sedation (opioid)

+/- nitroglycerin ointment (Reduced preload from venodilation) **Diastolic dysfunction

57
Q

Chronic management of feline CHF?

A

ACE inhibitor, furosemide, clopidogrel

58
Q

What are secondary causes of canine cardiomyopathy?

A

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

ECC boards (4 decks)

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