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SAM Exam 2 and final Cardio, Resp, Infectious DZ > SAM Cardio Baller > Flashcards

SAM Cardio Baller Flashcards

1
Q

How does the SNS respond to a decrease in CO?

A
  1. Increase contractility ( +inotrope)
  2. Increase HR (+chronotrope)
  3. Veno/Arterio constriction
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2
Q

How is the RAAS activated?

A

Decreased Renal Blood flow

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3
Q

Functionality of the RAAS System?

A
  1. Angiotension 2 ===> Peripheral vasoCONSTRICTION of arteries/veins
  2. Aldosterone ===> Increased Na & H2O retention
  3. OVERALL ======> INCREASE venous return to heart
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4
Q

Brief description of DCM?

A
  1. Pump FAILURE

2. Ventricular walls become thinner & SYSTOLIC force is decreased ====> Lowered CO

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5
Q

Brief description of chronic valve dz?

A
  1. MITRAL valves thickened & contracted ===> Mitral regurg
  2. L-Ventricle contracts ===> 70% SV regurgs through faulty mitral valve into the LA==========»> Decreased CO
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6
Q

Effects of sustained activity on HF?

A
  1. INCREASE peripheral resistance ===> DECREASED flow + signs of HYPOtension
  2. +chronotrope effect increases heart O2 demand
  3. Since HR is INCREASED = Time in Diastole is DECREASED ===> reduced coronary perfusion
  4. Can cause arrhythmias b/c coronary vasospasm & myocardial damage
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7
Q

Animals with HF have elevated levels of ________ which shortens their survival time

A

Norepinephrine

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8
Q

Problem with long term stimulation of RAAS system?

A
  1. Failing heart Frank starling curve = LESS steep and the increase in CO is NOT as pronounced as normal heart
  2. Increased PRELOAD ===> Pulmonary Edema
  3. Chronic vasoCONSTRICTION increases AFTERLOAD ====> Hypotension
  4. Aldosterone causes
    - myocardial fibrosis
    - direct vasculature damage
    - BARORECEPTOR dysfunction
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9
Q

Cause of Eccentric Hypertrophy?

A
  1. Chronic INCREASED diastolic pressure

2. VOLUME Overload

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10
Q

Characteristics of Eccentric Hypertrophy?

A
  1. Addition of sarcomeres ===> Cells elongating
  2. Large ventricle w/ INCREASING chamber size but walls of NORMAL thickness
  3. Results in INCREASED end Diastolic volume & afterload
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11
Q

Describe afterload

A

The ventricular RESISTANCE encountered as it tries to eject blood during systole

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12
Q

Describe preload

A

After Diastole (filling) occurs ===> MAXIMUM ventricular volume/pressure that occurs

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13
Q

Characteristics of Concentric Hypertrophy

A
  1. Sarcomeres replicate side by side resulting in WIDER cells & THICKER/STIFFER ventricular wall
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14
Q

Cause of Concentric Hypertrophy

A
  1. Response to INCREASED Systolic Ventricular Pressure
  2. Aortic Stenosis or Systemic Hypertension
  3. “PRESSURE OVERLOAD”
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15
Q

Physiology responsible for the clinical signs of HF?

A
  1. Chronic compensatory mechanisms occurring
  2. Cause INCREASED Preload ===> Edema
  3. Vasoconstriction increases workload of heart
  4. Results in cardiac hypertrophy ===> increased MVO2 requirement
  5. Eventually cannot compensate enough ===> DECREASED efficiency of heart muscle contraction
  6. Leads to arrhythmias
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16
Q

Why does increased preload cause pulmonary edema in the failing heart?

A
  1. Increase in preload causes drastic INCREASE in Systolic volume
  2. Dz’ed heart cannot compensate so SV is only slightly elevated
  3. Causes high pressure buildup in the vessels filling the heart forcing fluid into interstital space ===> Interstitial Edema
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17
Q

Signs of excessive LEFT Ventricular Preload?

A
  1. Pulmonary Edema
  2. Hypoxemia/Cyanosis
  3. Excessive RIGHT Ventricular Preload
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18
Q

Signs of excessive RIGHT Ventricular Preload?

A
  1. Jugular & peripheral vein distension
  2. Pleural effusion
  3. Hepatomegaly
  4. Ascites
  5. SC Edema
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19
Q

What are the general signs of HF?

A
  1. Low CO, weakness/syncope, dyspnea, severe hypotension (cardiogenic shock)
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20
Q

Physiology behind LEFT HF?

A

DECREASED forward Stroke Volume ===> Hypotension & high End Diastolic pressure

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21
Q

Classic L-HF clinical signs?

A
  1. Coughing
    Dyspnea
    Orthopnea
    Tachypnea & Cyanosis
2. LETHARGY & DEPRESSION
    Synchope
    Hypotension/ Tachycardia
    Weak pulses
    Pre-renal azotemia
22
Q

Physiology behind R-HF?

A
  1. High End Diastolic pressure in R-ventricle ===> INCREASED pressure in posterior/anterior vena cava
  2. DECREASE in forward stroke volume from right heart ===> DECREASED venous return to LV = lowered CO
23
Q

Signs of R-HF

A
  1. Jugular & peripheral vein distension
  2. Ascites, hepto, splenomegaly
  3. Pleural effusion (peripheral edema rare)
  4. Hypotension
    Depression/weakness
    Synchope
    Azotemia
24
Q

Describe the Phases of L-CHF and each ones clinical signs associated

A

Phase I- Murmur but no clin. signs

Phase II- Cough, Fatigue, Dyspnea, w/ normal or strenous exercise

Phase III- Same as II but at night with activity

Phase IV- Same as II & III but also cyanosis at rest w/ signs exacerbated by exercise

25
Q

What is the ultimate goal for treating HF?

A

Lessening the neuroendocrine response and decreasing vagal tone

26
Q

Morphine is contraindicated in CHF why?

A

Can cause nausea and vomiting

27
Q

Drugs used for CHF Px?

A

Diazepam & Butorphanol ( Dog/Cat)

28
Q

What can be a problem seen w/ ventilatory support?

A
  1. In + pressure vent., venous return is decreased as air ir pushed into lungs
  2. Can cause severe systemic hypotension
29
Q

Drug used to reduce edema in CHF?

Why?

A

Furosemide

Prolongs/ improves quality of life

30
Q

Possible complications with Furosemide?

A
  1. RAAS activation
  2. Decreased CO, hypotension, dehydration, azotemia, electrolyte imbalance
  3. Use as lowest dose possible with reduced Na diet and ACE inhibitor
31
Q

What drugs are used to reduce preload by trapping blood in the peripheral venous system & away from the heart & lungs?

A

2% nitroglycerine cream
Nitroprusside
ACE inhibitors

32
Q

What is the most commonly used venodilator in the acute situation?

A

Topical 2% nitroglycerine cream

33
Q

What are ACE inhibitors?

A
  1. Angiotensin converting enzyme inhibitors
  2. Mixed dilator, but have relatively weak effects w/ a slow onset of action (weeks)
  3. Very effective maintenance therapy of HF
34
Q

What drug is the cornerstone in the management of CHF?

A

ACE inhibitors

35
Q

How do ACE inhibitors manage HF?

A
  1. Slow progression
  2. Blunten pathological remodeling & fibrosis from angiotensin 2 & aldosterone
  3. Allow an up to 50% reduction in furosemide dosage & reduce electrolyte abnormalities
  4. Prolonge & improve the quality of life
36
Q

What are the side effects of ACE inhibitors ?

A
  1. Hypotension: weakness, lethargy, synscope

2. Azotemia if used in early tx & on high doses of furosemide

37
Q

If an animal is on ACE inhibitors & furosemide & the BUN and Cr are 3x normal or are showing signs of uremia, what should your do?

A
  1. Decrease dose of furosemide by 30%

2. Can reverse the azotemia & hypotension

38
Q

What is the function of ACE inhibitors on the cardiovascular system?

A
  1. Arteriodilation
  2. Increase stroke volume
  3. Decrease regurgitation
  4. Increase myocardial shortening
39
Q

What is pimobendan?

A
  1. Phosphodiesterase inhibitor which causes arterio & venodilation
  2. Ca sensitizer
  3. Has + inotropic & vasodilatory effect
  4. Can be used as outpx tx
40
Q

What is hydralazine?

A

Good arteriodilator, but has a complicated dosing schedule based on blood pressure measurements & GI side effects

41
Q

What is amlodipine?

A
  1. Ca Channel blocker
  2. Arteriodilator

No proven efficacy

42
Q

What drug can be used if animal is in cardiogenic shock (improve cardiac contractility)?

A

CRI of IV dobutamine

43
Q

What drug is very effective in the management of HF in dogs w/ dilated cardiomyopathy or mitral insufficiency?

A

Pimobendan

44
Q

What characteristics should fluids have that are being used for CRI therapy in CHF?

A

–Low in Na (5% dextrose in water or 1/3 to ½ strength saline & dextrose)

45
Q

What should you do with regards to arrhythmias in HF?

A
  1. Tx them if they are the cause of HF

2. Then Tx underlying causes f the HF

46
Q

What is the purpose of the Na restricted diet in HF Px?

A
  1. Will decrease Na & water retention which lowers drug requirements
  2. May be unpalatable
  3. Intake should be around 12 mg/kg/day or 220 mg/100g dry matter (kidney & senior diets)
  4. Beware of drinking water (use distilled if over 150 ppm)
47
Q

What are the side effects of severe Na restriction diets?

A

Hypotension
Renal dysfunction
Especially in ACE inhibitors

48
Q

What are beta blockers helpful in tx?

A
  1. Dilated cardiomyopathy

2. Block the deleterious effects of the sympathetic nervous system

49
Q

What beta blockers are commonly used?

A

Metoprolol

Carvedilol

50
Q

What is indicative of progression of HF?

A
  1. Reduction in serum Na levels
  2. Enlargement of the heart
  3. Reduction in echocardiographic function of the heart
51
Q

99% of SA murmurs occur when?

A

S1 Systolic murmurs

52
Q

Diastolic murmurs occur as a result of what problems?

A

Aortic or pulmonary valve insufficiency

SAM Exam 2 and final Cardio, Resp, Infectious DZ (6 decks)

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