High output CHF Flashcards
Regulators of IV volume
- 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
Homeostasis of arterial circulation: 2 main determinants
CO and PVR
What is arterial underfilling and physiologic response
o ↓BP from ↓CO +/- vasodilation → ARTERIAL UNDERFILLING
o Neurohormonal response: retain Na+ and H2O
Maladaptive with heart disease → volume overload and failure
What is the most common cause of ventricular underfilling and c/s
Cardiac tamponade
Intracardiac mass lesions → obstruction of blood flow
o C/s: episodic weakness (↓ CO and forward flow)
What defines high output CHF
- 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
Etiology of high output CHF
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 –
Thyrotoxicosis: pathophys of high output
→ most common cause in vetmed (cats)
* May cause reversible cardiomyopathy
* ↑ metabolic rate and tissue O2 consumption + ↓ peripheral resisatance
Thyrotoxicosis: factors influcencing dev of high output CHF
o Chronicity and rate of development of thyrotoxicosis (most important factors)
o Underlying cardiac disease
Anemia: pathophys of high output. On what depends its development?
- 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
Large/multiple AV fistula: pathophys high output
- 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
Cause of Beriberi syndrome
Thiamine or vitamin B1 deficiency → ↓ systolic function
Beriberi pathophys
↑ 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
Clinical manif high output CHF
o Hyperkinetic femoral pulses
o Soft systolic cardiac murmur
o Gallop rhythm
o Eccentric cardiac hypertrophy/generalized cardiomegaly
Thyroid hormones
- 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
Action site of thyroid hormones
intranuclear
o Bind to chromatin-bound nonhistone nucleoprotein
o Alterations in protein synthesis
Biological response to T4 in tissues
o Changes in myocardial contractility
o Stimulation of myocardial hypertrophy
o ↑ responsiveness to ∑ stimulation
o ↑ myocardial O2 consumption: ↑ protein synthesis + glucose/Ca2+ transport
How does T4 affect myocardial contractility
↑ 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
Describe ventricular myosin isoenzymes types and regulation w/ T4
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
How does ca2+ handling changes w/ hyper T4
- ↑# of L-type Ca2+ channels in sarcolemma
- ↑SR efficiency for Ca2+ uptake/release
Clinical recognizable effects of T4
o ↑HR
o ↑ inotropic state
o ↑ ventricular size/mass
HypoT4 and effect on heart
- Thyroid hormone deficiency → ↓ myocardial contractility
o Reversible
o Controversial if can cause alone DCM and CHF
Molecular changes in heart w/ hypoT4
o Adrenergic R system: ↓ responsiveness to catecholamines
↓# of β-R by 30-40% in rats
↓ physiologic responsiveness: ↓max response
No change in R affinity
Cause of K9 hypoT4
Commonly recognized endocrinopathy in dogs
* Cause: idiopathic atrophy or IM thyroiditis
K9 hypoT4: c/s
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
K9 hypoT4: ECG changes
severe hypoT4, reverse with supplementation
Sinus bradycardia
Conduction disturbance → PR prolongation
↓QRS voltage and ↑ duration
MEA deviation
Flattened, inverted T waves
K9 hypoT4: echo changes
Thinning of LVFW and IVS
↓FS%
↓LVFW excursion
Alteration of systolic and diastolic function parameters
Direct effect of hyperT4 on heart/vasculature
o Tachycardia
o Hypertrophy
o ↑ contractility
o Arrhythmias
o ↓ reserve capacity if ↑ cardiac work necessary
effect of hyperT4 on myocardial prot synthesis
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
Myocardial hypertrophy results from
Chronic volume overload
↑ ∑ tone
Systemic hypertension → ↑ afterload
Stimulation of myocardial protein synthesis
Response of adrenergic system to hyperT4
o ↑ ∑ activity
o ↑ responsiveness of cardiac tissue to ∑ stimulus
o Upregulation of β-R
Electrophysiologic changes hyperT4
o ↑ rate of spontaneous depolarization by SA node cells
o Shortened action potential duration
Most common endocrinopathy cats
HyperT4
Pathophys hyperT4 and heart
- 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
Feline HyperT4: signalment/hx
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
Feline HyperT4: PE
thyroid nodules
o Soft – moderate systolic murmurs +/- gallop
o Tachycardia
o Hyperkinetic pulse
Feline HyperT4: BW
o CBC: leucocytosis, eosinopenia, ↑PCV
o Chem: ↑ALT (83%), ALP (58%), AST (43%)
Feline HyperT4: ECG
Resolve after euthyroid state
o Sinus tachycardia (38%)
o ↑ R wave amplitude (8%)
o Atrial (3%), ventricular (4%) arrhythmias
o IV conduction disturbances: RBBB
Feline HyperT4: echo
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
Feline HyperT4: thyroid imaging
- 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
Feline HyperT4: tx
- Antithyroid drug
- Surgical thyroidectomy
- Radioactive iodine I-131
Feline HyperT4: thyroid fct testing
↑ 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)
Effects and options for anti thyroid drugs
o ↓circulating [T3/T4] by inhibiting thyroid hormone synthesis w/o destroying thyroid tissue
Propylthiouracil
Methimazole
Carbimazole
Ca2+/Na+ ipodate
Side effects Propylthiouracil
high incidence of side effects: anorexia, V+, lethargy, IMHA, thrombocytopenia
Side effects methimazole
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
Carbimazole features
carbethoxy derivative of methimazole
* Alternative if methimazole not available, TID
* Similar side effects, ↓ incidence
Why use B blockers for hyperT4
- Used to block some cardiovascular effects of thyroid hormone
- Not for routine tx
Sx for hyperT4
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
Post op complications thyroidectomy
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
Radioactive I131
o Selectively destroy hyperplastic/neoplastic thyroid tissue
o Long hospitalization, iodine regulations
What can influence tx modality
Coexistent cardiovascular disease, renal failure
Pheochromocytoma: etiology
- 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
Pheochromocytoma: more common in
- Dogs»_space;> cats
Pheochromocytoma: pathophys
- 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
Pheochromocytoma: myocardial injury
from coronary vasoconstriction, ischemia, ↑SR permeability, Ca2+ overload
* Multifocal cardiomyocyte necrosis/degeneration
* Contraction band
* Interstitial fibrosis
* Myocardial hemorrhage
* Lymphohistiocytic myocarditis
Pheochromocytoma: resp distress
similar to ARDS
Pulmonary edema
Capillary micro-hemorrhage
Capillary shrinkage
Pheochromocytoma: malignancy
- Local vascular invasion:
o Renal, adrenal, hepatic vessels
o Metastasis
Pheochromocytoma: c/s
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
Pheochromocytoma: PE
o Hypertension (50% of dogs)
o Auscultation: arrhythmias, systolic murmur, pulmonary crackles, tachycardia
Pheochromocytoma: BW
o Neutrophilic leucocytosis
o ↑liver enzymes
o Hypercholesterolemia → catecholamine induced lipolysis → conversion of free fatty acid → cholesterol
Pheochromocytoma: dx testing
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
Pheochromocytoma: ECG
o Short PR
o Short QRS
o LVE
o Atrial/ventricular arrhythmias
o T wave inversion, ST segment deviation
Pheochromocytoma: Abd Xrays
tumor visualized in 33% of cases
Pheochromocytoma: echo
o LVH
o SAM
o Normal function
o Myocarditis
o Reversible CM and CHF
Pheochromocytoma: gold std dx
- AUS or CT
Pheochromocytoma: tx
- 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
