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Physiology Flashcards

1
Q

Pressures in Chambers with PHTN and RCHF

A
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2
Q

What echocardiographic changes may be seen with cardiac tamponade?

A
  1. Diastolic (and early systolic) compression/collapse of the RA and somtimes RV
  2. LV often appears small with walls that look hypertrophied (pseudohypertrophy) because of poor cardiac filling
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3
Q

What are classic echocardiographic findings in dogs with MMVD?

A
  • Left ventricular and left atrial dilation
  • Hyperdynamic LV wall motion
  • Thickened mitral valve leaflets (or prolapse)
  • Leaflet flail (protrusion of the leaflet margin into the atrium during systole)
  • Ruptured chordae tendinae
  • LaAO >2.0 in patients with left sided CHF secondary to MVD (normal should be <1.5)
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4
Q

Describe serotonin’s action with respect to the heart and vasomotor tone.

A

Synthesized by the chromaffin cells; also present in platelets and mast cells.

Important in local control of the circulation.

Binds to 5-H2a/b receptors, causing vasoconstriction.

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5
Q

What is pulsus paradoxicus?

A
  • Inspiration typically lowers intrapericardial and right atrial pressures slightly, which enhances right sided heart filling and pulmonary blood flow.
    • Left sided heart filling diminishes as more blood is held in the lungs and the inspiratory increase in RV filling pushes the IVS outward.
  • LV output and systemic arterial pressure NORMALLY decrease slightly during inspiration.
  • Pulsus paradoxicus is an exaggeration of this normal pressure difference with respirations; patients with this condition exhibit a fall in arterial pressure during inspiration of 10mmHg or more.
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6
Q

Where are the high-pressure baroreceptors located?

The low pressure?

A
  1. High Pressure: Aortic arch, carotid sinus
  2. Low Pressure: pulmonary artery, junction of atria with their corresponding veins, atria themselves, ventricles (distention depends largely upon venous return to the heart and detect the “fullness” of the circulation; part of the system that control effective circulating volume).
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7
Q

Describe conditions that may lead to a diastolic dysfunction and subsequent development of cardiogenic shock.

A

Diastolic failure is due to inadequate ventricular filling; will result in a decreased preload and therefore a reduced stroke volume.

  1. Hypovolemia (most common cause of decreased preload resulting in inadequate CO; not truly cardiogenic shock as can be corrected with fluid resuscitation)
  2. Cardiac tamponade (secondary to pericardial effusion preventing diastolic ventricular filling)
  3. Hypertrophic cardiomyopathy (failure of myocardium to relax; decreased end-diastolic ventricular volume leads to decreased stroke volume and poor cardiac output)
  4. Tachyarrhythmias (inadequate time for diastolic filling to occur before systole)
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8
Q

In dogs with valvular disease, the degree of valvular insufficiency is dependent upon what three things?

A
  1. The regurgitant orifice area
  2. The pressure gradient across the valve
  3. The duration of systole (for AV valves) and diastole (for semilunar valves)
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9
Q

What are some risk factors for the development of FATE?

What locations do FATE commonly arise in?

A
  • Left atrial enlargement (although can develop in patients with normal LA size)
  • Spontaneous contrast
  • Systolic myocardial dysfunction
  • Aortic trifurcation, brachial artery, renal artery, mesenteric arteries, CNS
  • Leads to an ischemic neuromyopathy
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10
Q

What is the benefit of the cardiac refractory periods?

A

They prevent the development of ectopic beats that may be triggered by extraneous pacemakers.

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11
Q

What is stroke volume dependent upon?

A

Preload, afterload, contractility

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12
Q

Give examples of common causes of ventricular failure (primary/secondary/extracardiac)

A
  • Primary: LV failure (DCM), RV failure (ARVC)
  • Secondary to other cardiac disease: advanced degenerative valve disease with systolic dysfunction, tachycardia-induced cardiomyopathy
  • Extracardiac: sepsis, adriamycin toxicity, malnutrition
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13
Q

Describe the role the SNS has in development of heart failure.

A
  • In the short term, norepi/epi release increase HR, CO, and increase blood flow
  • With chronic activation, leads to adrenergic receptor downregulation, persistent tachycardia, increased myocardial oxygen demand, and myocyte necrosis–>ultimately leads to further cardiac damage.
  • In humans with heart disease, increased NE concentrations are a significant risk factor for mortality.
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14
Q

Describe what happens during phase 3 (ejection/outflow) of the cardiac cycle.

A

Opening of the aortic valve at the end of phase 2 triggers this phase.

  • During the first portion of the phase (rapid ejection), the ventricular pressure continues to rise, followed closely by aortic pressure.
  • A rapid decrease in ventricular volume occurs as blood flows into the aorta, causing aortic pressure to eventually exceed ventricular pressure just before both pressures begin to fall.
  • During the latter part of phase 3 (decreased ejection) the decrease in ventricular volume becomes less rapid and both the ventricular and aortic pressures decrease.
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15
Q

What is the formula for calculating fractional shortening?

A

FS=(LVIDd-LVIDs)/LVIDd

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16
Q

List the major criteria for diagnosis of infective endocarditis in dogs.

Minor criteria?

Ways to reach a definite or a possible diagnosis?

A

Major criteria:

  • Positive echocardiogram (vegetative or erosive lesion, abscess)
  • New valvular insufficiency (>mild aortic insufficiency wihout SAS)
  • Positive blood culture (>-/= 2 positive cultures; >/= 3 if skin contaminant)

Minor Criteria:

  • Fever
  • Medium to large dog
  • SAS
  • Thromboembolic disease
  • Immune-mediated disease (PLN, polyarthritis)
  • Positive blood culture not meeting major criteria)
  • Bartonella serology >/=1:1024

Diagnosis

  • Definite: histopath of valve OR 2 major criteria OR 1 major and 2 minor criteria
  • Possible: 1 major and 1 minor criteria OR 3 minor criteria
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17
Q

Describe AVP’s actions with respect to the heart and vasomotor tone.

A

Released by the posterior pituitary (also known as ADH)

Binds to V1a receptors, causing vasoconstriction, but only at concentrations that are strongly anti-diuretic.

Hemorrhagic shock causes enhanced AVP release and a vasoconstriction that contributes to a transient restoration of arterial pressure.

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18
Q

What is the normal PA systolic pressure and pressures with mild, moderate and severe pulmonary hypertension?

A
  • Normal 20-30mmHg
  • Mild PH >35-50mmHg
  • Moderate PH >50-80mmHg
  • Severe PH >80mmHg
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19
Q

List 5 humoral factors involved with control of pulmonary vascular tone and the effect each has on PAP, platelet aggregation, and endothelial proliferation/vascular remodeling.

A
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20
Q

How do catecholamines cause an increase in the strength of myocardial contraction (i.e. have a positive inotropic effect)?

A
  1. The increased Ca influx leads to a greater local increase in Ca and a greater Ca induced Ca release from the SR.
  2. Increase the sensitivity of the SR Ca release channel to cytoplasmic Ca.
  3. Enhance Ca pumping into the SR by stimulation of the SERCA Ca pump, which increases Ca stores for later use.
  4. The increased Ca influx presents more Ca to SERCA so that SR Ca stores increase over time.

**The combination of the 4 mechanisms make more Ca available to troponin C, enabling a more forceful cardiac contraction**

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21
Q

Define heart failure.

A

The heart’s inability to meet the metabolic needs of the peripheral tissues or instances where the heart can only do so in the presence of increased venous filling pressures.

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22
Q

Describe what happens during phase 4 (isovolumetric relaxation) of the cardiac cycle.

A

Very late in the ejection phase, blood flow across the aortic valve decreases and briefly reverses direction.

  • The aortic valve then closes, signifying the onset of diastole.
  • The aortic blood flow then again becomes very briefly positive, leading to a brief increase in pressure, signified by the presence of the dicrotic notch.
  • Because both the mitral AND the aortic valves are closed, no blood can enter the LV= isovolumetric relaxation.
  • Pressure in the LV decreases rapidly.
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23
Q

Describe the electrophysiologic mechanisms of V-tach (3 main)

A
  1. Reentry: requires an impulse to leave a point of departure and return to its starting point with a sufficient delay that the cardiac tissue has recovered its excitability.
  2. Enhanced automaticity: property of spontaneous depolarization with altered myocardial environment; less negative membrane potential, which gives it the ability to generate an AP similar to that of the sinus node
  3. Triggered activity: small membrane depolarizations that appear after and are dependent on the upstroke of the AP; trigger an AP when they reach the threshold potential
    1. Early afterdepolarizations (occur during the process of repolarization;) hypokalemia and drug induced QT prolongation
    2. Delayed afterdepolarizations (occur after full repolarization); occur secondary to intracellular Ca overload associated with sustained tachycardia and digoxin toxicity
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24
Q

Define cor pulmonale.

A

Development of right sided heart enlargement or failure due to pulmonary hypertension due to lung disease (eg chronic bronchitis/COPD/interstitial lung disease)

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25
Q

Describe low output versus congestive heart failure.

A
  • Congestive failure arises with pulmonary venous pressures greater than 25mmHg and systemic venous pressures >20mmHg; sufficient to produce congestion that manifests as pulmonary edema, pleural effusion or ascites.
  • Severe myocardial dysfunction can lead to insufficient cardiac performance and an inability to provide adequate cardiac output; patients present with signs of low output failure (wekaness, depressed mentation, cardiac shock, syncope)
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26
Q

What causes each of the heart sounds?

A
  • First heart sound: (S1)
    • Closure of the AV valves
  • Second heart sound: (S2)
    • Closure of the semilunar valves at the end of systole (aortic/pulmonary)
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27
Q

Describe what happens during phase 1 of the cardiac cycle.

A

Diastasis period (middle phase 1): happens at the very beginning of the cycle diagram.

  • Mitral valve is open, but little blood flows from the RA–>RV, with the ventricular volume slowly rising and approaching a plateau (similar rise in both atrial/ventricular pressures)
  • The P-wave occurs at the end of this cycle and stimulates atrial contraction, leading to a slight rise in atrial pressure.
  • Aortic pressure is falling during this period.

Beginning phase 1 (rapid ventricular filling period): happens at the end of the cycle diagram.

  • The LV pressure drops below the LA pressure and the mitral valve opens again; immediately thereafter, the LV volume begins to increase rapidly and the LV and LA pressures rise in parallel because the MV is open. The aortic valve remains closed during this period with falling pressure as blood flows to the periphery.
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28
Q

How does the natriuretic peptide system function in heart disease?

A
  • Myocardial tissue produces atrial and B-type natriuretic peptide in response to stretch/stress of the tissue.
  • Induce natriuresis, diuresis, vasodilation, which seve as a counter-regulatory system to the RAAS and SNA.
  • In the later stages of disease, the beneficial activity of this system is overwhelmed.
    • Reasons for loss many; combination of natriuretic peptide receptor downregulation, inappropriate/inadequate production or processing of peptides, increased peptide clearance or degradation.
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29
Q

Explain the Frank Starling Mechanism.

A
  • The greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater the quantity of blood pumped into the aorta.
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30
Q

Compare sinus nodal membrane potential (RMP) to ventricular RMP.

A
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31
Q

How do catecholamines (epinephrine/norepinephrine) function to increase heart rate?

A

Act on B1-adrenergic receptors.

  1. Increase the Na/Ca leak in phase 4, increasing the steepness of phase 4 depolarization.
  2. Increase the amount of Ca in all myocardial cells; this increases in the AV/SA nodal cells steepens phase 4 depolarization and also lowers the threshold potential.
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32
Q

What is the formula for cardiac output?

A

CO=SV x HR

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33
Q

What are the highest risk factors for thromboembolic disease associated with infective endocarditis?

A
  • Mitral valve inovlvement
  • Large mobile vegetative lesions > 1 to 1.5cm
  • Increasing lesion size during antibiotic therapy
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34
Q

Describe ANP’s actions with respect to the heart and vasomotor tone.

A

Released by atrial myocytes in response to stretch; bind to ANP receptor.

Causes vasodilation.

BC ANP has powerful diuretic and natruietic actions, it ultimately reduces plasma volume and therefore blood pressure.

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35
Q

Supraventricular tachyarrhythmias (SVTs) are defined as rapid cardiac rhythms that….

A
  1. Originate in the atria or AV junction (above the bundle of His)
  2. Involve the atria or AV junction as a critical component of a tachyarrhythmia circuit
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36
Q

List indications for treatment of ventricular tachycardia (remember accelerated idioventricular rhythm)

A
  • Multiforme (polymorphic) complexes (more likely to result in hemodynamic collapse)
  • Sustained VT >180-200/bpm
  • R on T phenomenon (superimposition of an ectopic beat on the T-wave of preceding beat)
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37
Q

Define ventricular tachycardia

A
  • Broad QRS tachycardia (>180bpm) with complexes wider than 0.06 seconds in dogs and 0.04 seconds in cats
  • Three most reliable diagnostic criteria:
    • AV dissociation
    • Fusion beats
    • Capture beats
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38
Q

Describe ANGII’s actions with respect to the heart and vasomotor tone.

A

Part of the RAAS cascade; potent vasoconstrictor.

Liver secretes angiotensinogen into the blood; renin (released by kidney) then converts Ang to AngI, then ACE (present on endothelial cells, particluarly those in the lung) converts Ang I to Ang II.

Ang II binds to G-protein coupled AT receptors, activating phospholipase C, raising Ca concentrations and leading to vasoconstriction. **Not NORMALLY present in high enough concentrations to produce constriction, however, plays a major role in control during blood loss, exercise or other situations that lower renal blood flow.

Has wide range of other effects that indirectly increase MAP.

  1. Increases cardiac contractility
  2. Reduces renal plasma flow, enhancing Na reabsorption in kidney
  3. Stimulates aldosterone release by the adrenal cortex
  4. Stimulates thirst, leads to release of AVP
  5. Facilitates release of norepi
  6. Acts as cardiac growth factor
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39
Q

Describe myocyte calcium ion cycling.

A
  1. Contraction of actin/myosin sarcomere complex requires cytoplasmic Ca ions.
  2. Ions enter cytoplasm partly throu sarcolemmal Ca channels, but mostly from intracellular stores within the SR.
  3. Exit of Ca from SR is regulated by the ryanodine receptor.
  4. Once released, Ca binds to troponin C located on actin; initiating contraction of sarcomere.
  5. After contraction, Ca discharged from troponin, taken back up into the SR by ATP-dependent SERCA2a channel.
  6. Phospholamban intracellular Ca regulator of Ca and inhibits reuptake of Ca by SERCA2.
  7. In animals with CHF, maladaptive changes within the cycle include myosin isoform switching, impaired Ca transients and ryanodine function, phospholamban upregulation, SERCA downregulation/energy depletion; leads to inappropriate distribution of intracellular Ca, poor sarcomere contraction, cell injury, and apoptosis/necrosis
40
Q

What conditions does the end systolic volume (ESV) depend upon?

A
  • Preload (end-diastolic volume): increase of the EDV increases the stretch on the cardiac muscle and the force of contraction and thus the stroke volume. Only at a very large EDV does contraction begin to weaken as the muscle fibers are too stretched to generate maximal power.
  • Afterload (force against which the ventricle ejects its contents): the afterload of the LV is the mean systemic arterial pressure; the afterload of the right ventricle is the mean pulmonary artery pressure. Increased afterload impedes the heart’s ability to empty and thereby increases ESV.
  • Heart Rate: an increased heart rate leads to greater Ca entry into myocardial cells, increasing contractility and reducing ESV.
  • Contractility: Positivive inotropic agents act by increasing Ca within the myocardial cells, enhancing the force of contraction and decreasing ESV.
41
Q

What role does vasopressin (AVP, ADH) play in the development of heart failure?

A
  • Causes increased reabsorption of free water within the renal collecting duct.
  • In patients with advanced heart disease, excessive vasopressin contributes to development of fluid overload, CHF, and dilutional hyponatremia.
  • Dilutional hyponatremia
    • Heightened free water retention to the extent that serum sodium concentrations are decreased, despite overall excess of body-wide sodium
    • Marker of severe neurohormonal activation
    • Poor prognostic sign
42
Q

What 2 findings in human trauma patients had a negative predictive value for cardiac complications?

A

Combination of a normal ECG and cTnI findings on admission

43
Q

Describe the 4 clinical classes/stages of heart failure.

A
  • A: Overtly healthy animals at risk for developing heart disease.
  • B: Animals with diagnostic evidence of heart disease but without clinical signs (asymptomatic dogs with a heart murmur or asymptomatic cats with an arrythmia)
    • B1: patients with no radiographic/echocardiographic evidence of cardiac remodeling.
    • B2: patients with radiographic/echocardiographic evidence of remodeling.
  • C: Animals with cardiac remodeling and current/historical clinical signs of heart failure.
  • D: patients with severe and debilitating signs of heart failure even at rest.

Transition between asymptomatic heart disease and symptomatic heart failure lies between class B1 and C/D.

44
Q

What is the most common electrolyte abnormality associated with v-tach?

A
  • Hypokalemia
    • increases phase 4 depolarization, increasing spontaneous automaticity and prolongs the AP duration, which promotes arrhythmias from triggered activity.
    • **Similar arrhythmias arise from hypomagnesemia, because Mg is necessary for proper functioning of the NaK ATPase pump**
  • Hypo and hypercalcemia also can cause…
45
Q

What is the formula for estimating pulmonary arterial pressure?

A

Estimated PA pressure= (TR Vmax)^2 x4 + estimated RA pressure

Estimated RA pressure:

5mmHg if not in heart failure

10mmHg if impending right heart failure

15mmHg if in right heart failure

46
Q

What changes will occur in a PV loop with increased afterload (arterial pressure)?

Draw the loop and describe the changes.

A

Decreases the SV and ejection fraction; cause loop to be taller and narrower.

47
Q

Describe DCM.

A
  • Characterized by chamber dilation and impaired systolic and often diastolic function of one or both ventricles
    • Reduced LV fractional shortening and ejection fraction
  • Adult onset disease except for in Porteguese Water Dogs (young as 2-32 weeks)
48
Q

Pressures in Heart Chambers in MODERATE Pulmonary Hypertension

A
49
Q

Describe concentric hypertrophy (development and limitations of)

A

Response to conditions causing pressure overload (increased afterload)-systemic hypertension, SAS.

Triggers replication of sarcomeres in parallel, resulting in an increase in relative thickness of ventricular walls.

Increased myocardial oxygen demand, endocardial ischemia, fibrosis, collagen disruption, injury to small coronary vessels.

50
Q

Describe conditions that may lead to a systolic dysfunction and subsequent development of cardiogenic shock.

A
  1. Failure of contractility
    1. Dilated cardiomyopathy (most common cause of cardiogenic shock from systolic dysfunction)
    2. Sepsis (even with increased CO, a decreased ejection fraction d/t reduction in ventricular compliance, biventricular dilation and decrease in contractile function)
    3. Endomyocarditis (rare condition in cats that occurs several days after a routine procedure; poor prognosis)
    4. Myocardial infarction (rare in animals)
  2. Mechanical failure
    1. Rare in dogs/cats–reduction in forward flow d/t an LVOT obstruction (aortic stenosis; HOCM)
      1. Chordae tendinae rupture leading to extensive mitral regurg reducing forward flow sufficiently to result in cardiogenic shock
51
Q

Define cardiac tamponade.

A

Develops when intrapericardial pressure rises toward and exceeds normal cardiac diastolic pressures.

External cardiac compression progressively limits RV filling and with increasing severity also reduces left ventricular filling.

Systemic venous pressure increases and forward cardiac output fails.

Tamponade is more likely to develop with acute, rapid accumulation of pericardial effusion.

52
Q

Draw/describe a normal left ventricular pressure volume loop.

A
53
Q

List the 5 groups of pulmonary hypertension.

A
  1. Pulmonary arterial hypertension (idiopathic, congenital heart disease, drug effects, connective tissue disorders)
  2. Left sided heart failure (most common cause of PHT in people, probably also in dogs)
  3. Chronic pulmonary disease (interstitial lung disease, chronic bronchitis)
  4. Pulmonary thromboembolism
  5. Miscellaneous (heartworm, polycythemia, vasculitis, masses)
54
Q

Which 2 dysrhythmias are most likely to result in arrest in an awake patient?

A

High grade AV block, Vtach

55
Q

Why do patients with infectious endocarditis tend to develop immune mediated disease?

A
  • IMPA and glomerulonephritis are the most common (75% and 36% of cases)
  • Continuous formation of circulating immune complexes are present in resopnse to the infectious endocarditis
  • Immune complex deosisition and further copmlementa ctivtation and tissue destruction in the glomerular basement membrane, joint capsule, or dermis
56
Q

If a pulmonary artery catheter is used for measurement, what changes may be seen in a patient with cardiogenic shock?

A

Decreased cardiac output with an increase in the preload parameters of CVP, pulmonary artery pressure, and pulmonary arterial occlusion (wedge) pressure.

57
Q

Effective Refractory Period

A

Inward currents of Na/Ca are largely inactivated by the membrane depolarization

During this period, an additional electrical stimulus has NO effect on the action potential

Normal ERP of ventricles 0.25-0.30 seconds

58
Q

How does acetylcholine function to lower the heart rate?

A
  1. It decreases the inward Na leak, reducing the steepness of phase 4 depolarization.
  2. It increases potassium conductance, which makes the maximum diastolic potential of the SA nodal cells more negative.
  3. Reduces the amount of Ca in the SA node, which decreases the steepness of phase 4 depolarization and moves the threshold to more positive values.

**ACH is released by the vagus nerve onto the heart; PARAsympathetic stimulation**

59
Q

Describe eccentric hypertrophy (development and limitations of)

A

Develops in response to volume overload (mitral regurg, DCM); sarcomeres replicate in series, leading to elongation of myocytes and dilatation of ventricular chamber.

Increased myocardial wall stress, myocyte injury/necrosis, myocyte slippage.

60
Q

What does the heart use as its main substrate for energy production under normal circumstances? In heart failure?

A
  • Normal–fatty acids
  • Heart failure–glucose; requires less oxygen to metabolize
61
Q

What is the formula for pulmonary vascular resistance?

A

PVR= (Mean pulmonary artery pressure-Mean left atrial pressure)/cardiac output

62
Q

Briefly discuss the pathogenesis of infectious endocarditis.

A
63
Q

List 5 recommended treatment options for pulmonary hypertension and the rationale for administering each.

A
64
Q

What are 5 indications for usage of cardiac biomarkers in ECC settings?

A
  1. To agument/refute suspicion of CHF (BNP/proBNP)
  2. Increase/decrease suspicion of cardiac neoplasia in a dog with pericardial effusion in which an obvious mass was not identified (cTnI)
    1. Study out of Tufts found dogs with HSA had significantly higher concentrations of cTnI than did dogs with idiopathic pericardial effusion
    2. cTnI >0.25ng/mL indicates cardiac HSA is likely in dogs with pericardial effusion
  3. Increase suspicion of cardiac involvement in a dog with splenic HSA and hemoabdomen (cTnI)
    1. cTnI >2.45ng/mL suggests that cardiac involvement is likely
  4. Better understand unexplained dysrhythmia (cTnI)
  5. Document myocardial injury due to any insult (cTnI)
65
Q

What are 4 echocardiographic features of myocardial injury in the dog?

A
  1. Increased end-diastolic wall thickness
  2. Impaired contractility indicated by wall motion abnormalities and decreased fractional shortening
  3. Increased echogenicity
  4. Localized areas of echoluceny consistent with intramural hematomas
66
Q

What conditions does the end-diastolic volume (EDV) depend upon?

A
  • Filling Pressure: ventricular filling pressure depends to a large degree on atrial filling pressure. When increased venous return causes atrial filling pressure to rise, EDV rises as well.
  • Filling Time: the longer the filling time, the greater the EDV. As heart rate rises, diastole shortens to a greater extent than does systole, thereby decreasing EDV.
  • Ventricular Compliance: As compliance increases, a given filling pressure will produce a greater increase in ventricular volume, thereby resulting in a greater EDV.
67
Q

What role does endothelin I play in development of heart disease?

A
  • Potent vasoconstrictor produced by vascular endothelial cells in response to sheer stress, angiotensin II and other vaarious cytokines.
  • Causes vasoconstriction and increased cardiac afterload.
  • Elevated in dogs and cats with heart failure.
  • Also alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes.
68
Q
A

P Wave: depolarization of the atria

QRS: depolarization of the ventricles

T: repolarization of the ventricles

69
Q

Describe a Jugular Pressure Wave (CVP)

A
  • A peak: contraction of right atrium. Typically the right atrial pressure increases 4-6mmHg during atrial contraction and left atrial pressure increases 7-8mmHg
  • AV minimum: d/t relaxation of right atrium, closure of tricuspid valve
  • C wave: pressure rise in the right ventricle early during systole, resultant bulging of the tricuspid valve (which has just closed) into the right atrium
  • X minimum: occurs as the ventricle contracts and shortens during the ejection phase, later in systole. The shortening heart (with tricuspid valve still closed) pulls on and elongates the veins, lowering their pressure.
  • V wave: related to filling of the right atrium against the closed tricuspid valve, causing right atrial pressure to rise. As the tricuspid valve opens, the v peak begins to wane.
  • Y descent: fall in right atrial pressure during rapid ventricular filling as blood leaves the right atrium through the open tricuspid valve and enters the right ventricle.
70
Q

What changes will occur in a PV loop with an increased preload (filling)?

Draw the loop and describe the changes.

A

Increased stroke volume; shift curve to the right.

71
Q

What are the most commonly reported arrhythmias secondary to canine myocardial injuries?

A
  • VPCs, ventricular tachycardia, non-specific ST segment elevation/depression
72
Q

What is LaPlace’s law in regards to cardiac wall stress?

A

Wall stress=(pressure x radius)/2x wall thickness

73
Q

Relative Refractory Period

A

At the end of the plateau, the cell begins to repolarize as outward potassium conductance increases.

Na/Ca efflux begin to recover from inactivation

During this period, an additional electrical stimulus can produce an AP, but will generate only a smaller AP than usual

RRP for atrial muscle much shorter than ventricles–0.15 seconds for atria, 0.30 for ventricles)

74
Q

Describe the SA Node Action Potential

A

Phase 0: Upstroke; dependent on Ca influx when threshold potential is reached

Phase 3: Repolarization component; depends on K+ efflux

Phase 4: Diastole; slow depolarization, dependent upon Na and Ca leak until threshold is reached and phase 0 commences

75
Q

Name causes of a trend of a low/falling CVP

Name causes of a trend of a high/rising CVP

A
  1. Low/falling: shock, vasodilation
  2. High/rising: volume overload, vasoconstriction/hypertension, right heart disease, pericardial disease, vena caval obstruction, pulmonary disease, increasing intrathoracic pressure, increasing intra-abdominal pressure
76
Q

Describe the changes to the Frank-Starling curve and why they develop.

A
  • A. Describes increased CO in response to increased preload. During exercise, sympathetic tone elevates the curve, and cardiac disease lowers the curve. In the diseased stage, change in preload effects relatively little change in CO bc of the flat slope of the curve.
  • B. Neurohormonal activation and excessive Na/H2O rention lead to elevated intracardiac/venous pressure. Pressures >25mmHg typically lead to development of congestion.
    • Diuretics reduce preload, and move performance leftward along the curve, and to a position below threshold for congestion. Have little detrimental effect on CO bc of flat slope of line.
  • C. Injury can also result in low cardiac output. Positive inotropes shift the curve upward, so that CO at any preload is improved.
  • D. Patients with severe CHF can exhibit signs of BOTH congestion AND low output. Need both diuretics, positive inotropes to improve function.
    • Mixed vasodilators (both venous/arterial dilation) will shift the curve upward and leftward, used if BP will allow.
77
Q

What echocardiographic changes may be expected with pulmonary hypertension?

Radiographic changes?

A

Echocardiography:

  • Paradoxical septal motion
  • Tricuspid regurgitation
  • Enlarged right heart
  • Flattened IVS
  • Thickened RV wall
  • Volume underloaded (small) left heart

Radiographic:

  • Right heart enlargement
  • Enlarged pulmonary artery
  • Tortuous pulmonary arterial vasculature
  • Regional oligemia (reduced blood flow to an area)
78
Q

Describe histamine’s actions with respect to the heart/vasomotor tone.

A

Binds to H2 receptors and causes vasodilation.

Causes vascular smooth muscle to relax, but causes visceral smooth muscle to contract.

79
Q

What is the primary determinant of preload? Afterload?

A

Preload (ventricular filling)=blood volume

Afterload=peripheral/arterial resistance

80
Q

What are the 4 classifications of cardiomyopathy?

A
  1. DCM
  2. HCM
  3. Restrictive cardiomyopathy
  4. Arrhythmogenic right ventricular cardiomyopathy
81
Q

A VHS of ___ predicts the development of CHF in 6-12 months…

A

>11.5

(<11.5 uncommonly associated with CHF)

82
Q

What was the major finding of the PROTECT study evaluating use of pimobendan in Dobermans with DCM?

A

Administration of pimo to Dobies with pre-clinical DCM prolongs the time to onset of clinical signs and extends survival, suggesting that pimo should be used early (in the pre-clinical phase) in Dobermans

83
Q

Describe the role that the RAAS has in development of heart failure.

A
  • Primary trigger is heart’s inability to provide normal renal perfusion. Decreased renal blood flow and sodium delivery to the distal nephron induce renin release from macula densa.
  • Renin converts angiotensinogen to angI, which is converted to AngII by ACE in the pulmonary vasculature.
  • AngII important effoctor molecule for maladaptive response that promote further cardiac injury and heart failure–>renal Na/H20 retention, aldosterone production, myocardial apoptosis, cardiac/vascular remodling/fibrosis, increased thirst and vasoconstriction.
  • End result of circulating and tissue RAAS activation is retention of fluid (which promotes CHF development) and maladaptive myocardial and vascular remodeling.
84
Q

Pressures in Heart Chambers (NORMAL)

A
85
Q

Describe forward or backward ventricular failure.

A
  • Backward flow failure occurs secondary to elevated venous pressures
  • Forward flow failure (left ventricular failure) occurs secondary to reduced forward flow into the aorta and systemic circulation.
86
Q

Describe the types of AV Block.

A
  • First Degree: all impulses conducted to the ventricles; PR interval is prolonged on ECG
    • Results from AV node fibrosis, increased vagal tone, or drugs that delay AV node conduction
  • Second Degree: some P waves are not followed by a QRS complex
    • Mobitz type I: progressive increase in PR interval duration ending by a blocked P wave
      • Results from combination of AV node fibrosis and progressive increase in vagal tone; typically benign, does not require tretment
    • Mobitz type II: unexpected occurrences of blocked P waves
      • PR intervals before and after are identical
      • More likely to worsen and result in clinical signs
    • Atropine response test–type I usually improves after atropine and type II worsens or does not change
  • Third degree: absence of conducted P waves to ventricles; independent atrial and ventricular activities
    *
87
Q

Describe the phases of the ventricular action potential.

A

Phase 0: Upstroke of AP. Rapid influx of Na, with K conductance dropping to 0. Positive transmembrane potential and Ca channels open.

Phase 1: Rapid repolarization. Na influx ceases/closure of Na channels. There is a transient outward K current and a brief drop in transmembrane potential.

Phase 2: Plateau phase/sustained depolarization. Leads to increased strength and duration of contractuion. The plateau is a balance between the outward K+ currents and inward Ca movement through L-type Ca channels.

Phase 3: Final repolarization. Rapid drop in TMP, with Ca/Na conductance dropping to 0. There is an outward K+ current to rectify the TMP.

Phase 4: Resting phase. The cell membrane is relatively permeable to K+ (with open K+ channels and an inwardly rectifying K+ current) and is impermeable to Na/Ca. Na is pumped out by NaKATPase–wants to maintain a negative charge inside as compared to out.

88
Q

What does the presence of a gallop sound on cardiac auscultation in cats signify?

A
  • Diminished ventricular compliance in association with high atrial pressure
  • More specifically identifies cats with heart disease than does a murmur
89
Q

Describe epinephrine’s action with respect to the heart and vasomotor tone.

A

Source is the adrenal medulla.

Binds to alpha-1 receptors, causing vasoconstriction or B-2 receptors, causing vasodilation. Because the B-2 receptors are largely confined to the blood vessels of skeletal muscle, the heart, the liver and the adrenal medulla, it is NOT a systemic vasodilator.

Also binds to the B1 receptors on the heart, increasing heart rate and contractiliy.

90
Q

What is the Bainbridge reflex?

A

Tachycardia caused by an increase in venous return.

An increase in blood volume leads to increased firing of low-pressure B fibers during atrial filling.

Acts as a counterbalance to the baroreceptor reflex in the control of heart rate.

In general, during volume loading, the Bainbridge reflex prevails, whereas during volume depletion, the high-pressure baroreceptor reflex dominates.

Heart rate is at its minimum when effective circulating volume is normal.

91
Q

What changes will occur in a LV PV loop with an increase in contractility?

(Draw the loop and describe the effective change)

A

Increased stroke volume

92
Q

Define cardiogenic shock.

A

Inadequate cellular metabolism secondary to cardiac dysfunction when there is adequate intravascular volume.

“Failure of forward flow”

93
Q

Describe what happens during phase 2 (isovolumetric contraction) of the cardiac cycle.

A
  • Ventricular depolarization occurs at the beginning of this phase, generating the QRS complex of the ECG.
  • The ventricles contract and the pressure in the LV exceeds that of the LA, leading to closure of the mitral valve (remember the aortic valve has always been closed).
  • BC BOTH valves are closed, isovolumetric contraction leads to a rapid rise in ventricular pressure (with little change in ventricular volume).
  • Ventricular pressure ultimately exceeds aortic pressure at the end of this phase, leading to opening of the aortic valve.
94
Q

How can the SA node slow the firing rate of the pacemaker (negative chronotropic effect?)

A
  1. The steepness of the depolarization during phase 4 can decrease, which lengthens the amount of time it takes the membrane potential to reach threshold. This way, diastole is longer and the heart rate falls.
  2. The maximum diastolic potential can become more negative–beginning at a lower value, the membrane potential takes longer to reach threshold.
  3. The threshold can become more positive.

**Conversely, the SA node can use each of these three mechanisms in the opposite way to increase their firing rate–>positive chronotropic effect**

95
Q

How do the following affect the Frank Starling Curve:

1 . Diuretics

  1. Positive Inotropes
  2. Arterial Vasodilators
  3. Venous Vasodilators
  4. Mixed Vasodilators
A
  1. Diuretics: reduce preload and intravascular pressure, shifting the curve leftwards
  2. Positive inotropes (dobutamine, dopamine, pimo): improve contractility; shift curve upwards resulting in improved cardiac output even as preload is reduced
  3. Arterial vasodilators (hydralazine, amlodipine): shift curve upwards
  4. Venous vasodilators (nitrates): reduce preload by increasing venous capacitance, shift curve leftwards
  5. Mixed vasodilators (ACEI): move both left and up

Cardiology (3 decks)

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