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11. Acquired heart dz > High output CHF > Flashcards

High output CHF Flashcards

1
Q

Regulators of IV volume

A
  • Complex interaction of regulators of IV volume in any low cardiac output states
    o Heart
    o Kidneys
    o SNS
    o RAAS
    o Cellular/inflammatory modulators
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2
Q

Homeostasis of arterial circulation: 2 main determinants

A

CO and PVR

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3
Q

What is arterial underfilling and physiologic response

A

o ↓BP from ↓CO +/- vasodilation → ARTERIAL UNDERFILLING
o Neurohormonal response: retain Na+ and H2O
 Maladaptive with heart disease → volume overload and failure

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4
Q

What is the most common cause of ventricular underfilling and c/s

A

Cardiac tamponade
 Intracardiac mass lesions → obstruction of blood flow
o C/s: episodic weakness (↓ CO and forward flow)

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5
Q

What defines high output CHF

A
  • CO is already elevated before CHF occurs
  • Chronic ↑ in venous return
    o ↑CO from ↑ peripheral demand
    o ↓ peripheral resistance → ↑ increased tissue metabolism and oxygenation
    o Potential for circulatory overload → ↑ LV end diastolic P
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6
Q

Etiology of high output CHF

A

o ↑ tissue metabolism/O2 demand
 Obesity
 Thyrotoxicosis
 Fever
 Pregnancy

o Hyperkinetic states
 Anemia
 Large or multiple small AV fistulas

o Excess H2O/salt → kidney pathology, fluid administration, steroids
o Liver cirrhosis
o Beriberi syndrome
o Septic shock via gram –

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7
Q

Thyrotoxicosis: pathophys of high output

A

→ most common cause in vetmed (cats)
* May cause reversible cardiomyopathy
* ↑ metabolic rate and tissue O2 consumption + ↓ peripheral resisatance

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8
Q

Thyrotoxicosis: factors influcencing dev of high output CHF

A

o Chronicity and rate of development of thyrotoxicosis (most important factors)
o Underlying cardiac disease

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9
Q

Anemia: pathophys of high output. On what depends its development?

A
  • Cardiovascular response depend on rate of development + magnitude
    o Slowly developing anemia: ↑CO from tachycardia with stable SV
    o Chronic severe anemia: ↑ CO from ↑SV
     ↓ blood viscosity
     ↓ BP → ↓ afterload
  • Tissue hypoxia and vasodilator metabolites
     ↑ preload
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10
Q

Large/multiple AV fistula: pathophys high output

A
  • Excessive venous return + normal systolic function
    o ↑CO with normal RAP
    o Little cardiac reserve: if acute ↑ demand (ie. exercise) → high output failure
     Heart already at max capacity with pumping extra blood volume
  • Mild signs of peripheral venous congestion
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11
Q

Cause of Beriberi syndrome

A

 Thiamine or vitamin B1 deficiency → ↓ systolic function

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12
Q

Beriberi pathophys

A

 ↑ venous return from ↓ vascular resistance + ↓ systolic function
* CO curve shifted L and downward
* ↓CO → ↓ blood flow to kidneys → RAAS activation → H2O/Na+ retention
 Slight ↑CO at ↑ venous pressures → high output failure

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13
Q

Clinical manif high output CHF

A

o Hyperkinetic femoral pulses
o Soft systolic cardiac murmur
o Gallop rhythm
o Eccentric cardiac hypertrophy/generalized cardiomegaly

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14
Q

Thyroid hormones

A
  • Thyroid gland → secrete 2 biologically active hormones
    o Triiodothyronine T3 → major mediator of thyroid actions
    o Thyroxine T4
     Less active
     Circulating reservoir for conversion into T3
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15
Q

Action site of thyroid hormones

A

intranuclear
o Bind to chromatin-bound nonhistone nucleoprotein
o Alterations in protein synthesis

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16
Q

Biological response to T4 in tissues

A

o Changes in myocardial contractility
o Stimulation of myocardial hypertrophy
o ↑ responsiveness to ∑ stimulation
o ↑ myocardial O2 consumption: ↑ protein synthesis + glucose/Ca2+ transport

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17
Q

How does T4 affect myocardial contractility

A

 ↑ activity in Na/K/ATPase pump → sarcolemmal pump
 ↑ synthesis in ventricular myosin
 Alteration of myosin isoenzyme → predominance of fast ATPase activity
 Changes in Ca2+ handling

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18
Q

Describe ventricular myosin isoenzymes types and regulation w/ T4

A

 Alteration of myosin isoenzyme → predominance of fast ATPase activity
* Ventricular myosin isoenzymes:
o Expression dictated by
 Stage of development
 Thyroid hormone status
o 3 types, each have α and β chains
 V1: α - α homodimer → highest ATPase activity
 V2: α - β heterodimer
 V3: β - β homodimer → lowest ATPase activity
* ATPase activity correlates with velocity of shortening
o Regulation of isoenzymes: control of gene coding for α and β chains

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19
Q

How does ca2+ handling changes w/ hyper T4

A
  • ↑# of L-type Ca2+ channels in sarcolemma
  • ↑SR efficiency for Ca2+ uptake/release
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20
Q

Clinical recognizable effects of T4

A

o ↑HR
o ↑ inotropic state
o ↑ ventricular size/mass

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21
Q

HypoT4 and effect on heart

A
  • Thyroid hormone deficiency → ↓ myocardial contractility
    o Reversible
    o Controversial if can cause alone DCM and CHF
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22
Q

Molecular changes in heart w/ hypoT4

A

o Adrenergic R system: ↓ responsiveness to catecholamines
 ↓# of β-R by 30-40% in rats
 ↓ physiologic responsiveness: ↓max response
 No change in R affinity

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23
Q

Cause of K9 hypoT4

A

Commonly recognized endocrinopathy in dogs
* Cause: idiopathic atrophy or IM thyroiditis

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24
Q

K9 hypoT4: c/s

A

usually middle age, variable
o Lethargy, mental dullness
o Exercise intolerance
o Dermatologic lesions
o Reproductive system
o Neuromuscular system
o Cardiovascular signs: bradycardia, weak apex beat, arrhythmias

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25
Q

K9 hypoT4: ECG changes

A

severe hypoT4, reverse with supplementation
 Sinus bradycardia
 Conduction disturbance → PR prolongation
 ↓QRS voltage and ↑ duration
 MEA deviation
 Flattened, inverted T waves

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26
Q

K9 hypoT4: echo changes

A

 Thinning of LVFW and IVS
 ↓FS%
 ↓LVFW excursion
 Alteration of systolic and diastolic function parameters

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27
Q

Direct effect of hyperT4 on heart/vasculature

A

o Tachycardia
o Hypertrophy
o ↑ contractility
o Arrhythmias
o ↓ reserve capacity if ↑ cardiac work necessary

28
Q

effect of hyperT4 on myocardial prot synthesis

A

o ↑ protein synthesis: mitochondrial, ion pump, contractile proteins
o Alteration of myosin subtype: slow V3 to fast V1
o ↓ efficiency of energy conversion from chemical (ATP) → mechanical force

29
Q

Myocardial hypertrophy results from

A

 Chronic volume overload
 ↑ ∑ tone
 Systemic hypertension → ↑ afterload
 Stimulation of myocardial protein synthesis

30
Q

Response of adrenergic system to hyperT4

A

o ↑ ∑ activity
o ↑ responsiveness of cardiac tissue to ∑ stimulus
o Upregulation of β-R

31
Q

Electrophysiologic changes hyperT4

A

o ↑ rate of spontaneous depolarization by SA node cells
o Shortened action potential duration

32
Q

Most common endocrinopathy cats

A

HyperT4

33
Q

Pathophys hyperT4 and heart

A
  • High output state:
    o ↑ metabolic rate and tissue O2 consumption
    o ↓ peripheral resistance
  • Compensatory cardiac remodelling
    o Changes in myocardial protein synthesis/degradation → hypertrophy
  • Direct action of thyroid hormones on heart muscle + interaction with ∑ nervous system
    o Stimulate cardiac hypertrophy
    o ↑plasma volume + systemic BP
    o ↑CO, filling pressures, HR, contractility
34
Q

Feline HyperT4: signalment/hx

A

o Middle aged – old cats
o Uncommon <6y/o
o C/s: weight loss, polyphagia, V+, PUPD, ↑ activity, unkept hair coat
 5% of cats can have weakness, profound depression, anorexia → apathetic syndrome in Hu

35
Q

Feline HyperT4: PE

A

thyroid nodules
o Soft – moderate systolic murmurs +/- gallop
o Tachycardia
o Hyperkinetic pulse

36
Q

Feline HyperT4: BW

A

o CBC: leucocytosis, eosinopenia, ↑PCV
o Chem: ↑ALT (83%), ALP (58%), AST (43%)

37
Q

Feline HyperT4: ECG

A

Resolve after euthyroid state
o Sinus tachycardia (38%)
o ↑ R wave amplitude (8%)
o Atrial (3%), ventricular (4%) arrhythmias
o IV conduction disturbances: RBBB

38
Q

Feline HyperT4: echo

A

mimic HCM, resolve after euthyroid state
o LVH
o LA/LVE
o Hypercontractile state: ↑FS% and Vcf
o ↑Ao root dimension
o DCM phenotype reported → ↓ systolic function, ventricular dilation

39
Q

Feline HyperT4: thyroid imaging

A
  • Radionuclide thyroid imaging
    o Delineates functioning thyroid tissue
     Extent of thyroid gland involvement
     Metastatic/ectopic thyroid tissue
     1 or both thyroid involved
     Detect functional thyroid adenocarcinoma metastasis
    o Pertechnetate: shorter ½ life, rapid uptake
40
Q

Feline HyperT4: tx

A
  • Antithyroid drug
  • Surgical thyroidectomy
  • Radioactive iodine I-131
41
Q

Feline HyperT4: thyroid fct testing

A

 ↑ baseline T3 and T4
 Occult hyperthyroidism: normal T4 and T3
* Suppression of high T4/T3 because of concurrent nonthyroidal illness
* Fluctuation in and out of normal range
 T3 suppression test → thyrotropin releasing hormone (TRH) stim test
 Basal free T4 (unbounded)

42
Q

Effects and options for anti thyroid drugs

A

o ↓circulating [T3/T4] by inhibiting thyroid hormone synthesis w/o destroying thyroid tissue

Propylthiouracil
Methimazole
Carbimazole
Ca2+/Na+ ipodate

43
Q

Side effects Propylthiouracil

A

high incidence of side effects: anorexia, V+, lethargy, IMHA, thrombocytopenia

44
Q

Side effects methimazole

A

better tolerated, safer
* Side effects: usually anorexia, lethargy, V+ transient
o V+/D+/anorexia
o Facial pruritus
o Hepatotoxicity
o Hematologic abnormalities: thrombocytopenia, IMHA, agranulocytosis

45
Q

Carbimazole features

A

carbethoxy derivative of methimazole
* Alternative if methimazole not available, TID
* Similar side effects, ↓ incidence

46
Q

Why use B blockers for hyperT4

A
  • Used to block some cardiovascular effects of thyroid hormone
  • Not for routine tx
47
Q

Sx for hyperT4

A

o Medical tx prior → euthyroid state for 1-2 wks
 ↓ anesthetic risks (arrhythmias, CHF)
o Removal of abnormal thyroid tissue + preserve parathyroid gland
 Intracapsular technique: thyroid parenchyma dissected from capsule
* Preserves external parathyroid gland
* Risk of small remanants remaining attached to capsule
 Extracapsular technique: thyroid gland + capsule removed
* Risk of hypoparathyroidism
* Modified technique: capsule adjacent to parathyroid gland incised and left attached

48
Q

Post op complications thyroidectomy

A

 HypoCa2+/hypoparathyroidism 1-3 days post op
 Hypothyroidism 2-3mo post op
 Horner’s syndrome
 Renal failure (↓GFR)
 Laryngeal paralysis
 Recurrent hyperthyroidism if ectopic tissue, incomplete resection

49
Q

Radioactive I131

A

o Selectively destroy hyperplastic/neoplastic thyroid tissue
o Long hospitalization, iodine regulations

50
Q

What can influence tx modality

A

Coexistent cardiovascular disease, renal failure

51
Q

Pheochromocytoma: etiology

A
  • Endocrine tumor of adrenal medulla
    o Chromaffin cells → pheochromocytes
    o Most often solitary
    o Functional neoplasms → ability to secrete NE/epi/dopamine
     Epinephrine = 85% of adrenal gland secretion in normal gland in dogs/Hu
     Norepi = primary secretory product in cats
  • Distinguished from normal gland by lack of innervation
    o Hormone secretion NOT mediated by neural impulse
    o Exocytosis of storage granules
52
Q

Pheochromocytoma: more common in

A
  • Dogs&raquo_space;> cats
53
Q

Pheochromocytoma: pathophys

A
  • Excess in catecholamines:
    o Secreted constantly, episodically or both
     Hypertension
     Overload cardiomyopathy
     Arrhythmias
     Ischemic myocarditis
    o NE/epi → α1, β1, β2 stimulation → dominant effect depend on R density
     α1 → venous/arteriolar vasoconstriction
     β1 → positive chronotropic, dromotropic, inotropic
     β2 → venous/arteriolar vasodilation
  • α1 and β1 respond to Epi + NE
  • β2 respond to epi
54
Q

Pheochromocytoma: myocardial injury

A

from coronary vasoconstriction, ischemia, ↑SR permeability, Ca2+ overload
* Multifocal cardiomyocyte necrosis/degeneration
* Contraction band
* Interstitial fibrosis
* Myocardial hemorrhage
* Lymphohistiocytic myocarditis

55
Q

Pheochromocytoma: resp distress

A

similar to ARDS
 Pulmonary edema
 Capillary micro-hemorrhage
 Capillary shrinkage

56
Q

Pheochromocytoma: malignancy

A
  • Local vascular invasion:
    o Renal, adrenal, hepatic vessels
    o Metastasis
57
Q

Pheochromocytoma: c/s

A

mainly from systemic hypertension
o Anorexia, hyperT
o Panting, cough, dyspnea, cyanosis
o Weakness, trembling
o Mydriasis, hypertensive retinopathy
o Proteinuria, PUPD
o Neurologic signs
o Epistaxis
o Abdominal distension
o Collapse/death

58
Q

Pheochromocytoma: PE

A

o Hypertension (50% of dogs)
o Auscultation: arrhythmias, systolic murmur, pulmonary crackles, tachycardia

59
Q

Pheochromocytoma: BW

A

o Neutrophilic leucocytosis
o ↑liver enzymes
o Hypercholesterolemia → catecholamine induced lipolysis → conversion of free fatty acid → cholesterol

60
Q

Pheochromocytoma: dx testing

A

o Plasma or urinary catecholamine
 Episodic secretion
o Metanephrines: metabolites
 Production of metanephrine in tumor cells is autonomous and continuous
* Accurately reflect tumor mass
o Urinary ratios to creatinine can be calculated

61
Q

Pheochromocytoma: ECG

A

o Short PR
o Short QRS
o LVE
o Atrial/ventricular arrhythmias
o T wave inversion, ST segment deviation

62
Q

Pheochromocytoma: Abd Xrays

A

tumor visualized in 33% of cases

63
Q

Pheochromocytoma: echo

A

o LVH
o SAM
o Normal function
o Myocarditis
o Reversible CM and CHF

64
Q

Pheochromocytoma: gold std dx

A
  • AUS or CT
65
Q

Pheochromocytoma: tx

A
  • α adrenergic blocking agent → control hypertension
    o Phenoxybenzamine
    o Phentolamine
    o Medical tx 3-4wk prior to sx ↑ success rate
  • β adrenergic blocking agent → control arrhythmias
    o Propanolol
    o Atenolol
  • Surgical removal = only definitive cure

11. Acquired heart dz (18 decks)

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