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
