Cardio 12 Flashcards
Describe heart failure.
-pathophysiological state where the heart is impaired in the ability to eject or receive blood
>physical disability w clinical signs that vary with cause & between species
>weakness, lethargy, exercise intolerance
>right X left side congestive heart failure
What can heart failure result from?
-heart valve dis function
-arrythmias
-myocardial disease
-pericardial disease
-increased resistance to ejection
What are the 4 functional classifications of heart failure?
- Impeded cardiac filling
- Increased resistance to ejection of blood (afterload)
- Impaired ejection or volume overload
- Arrhythmias & conduction disorders
Describe impeded cardiac filling.
-pericardial disease with restricted filling
(Ex: pericardial effusion)
-valvular inflow obstruction
(ex: AV valve stenosis)
-intrinsic myocardial disease with impaired diastolic function
(Ex: hypertrophic cardiomyopathy)
Describe increased resistance to ejection of blood (afterload).
Ex: pulmonic or aortic stenosis; pulmonary hypertension
Describe impaired ejection or volume overload.
-primary & secondary myocardial disease with impaired systolic function
>ex: dilated cardiomyopathy
-misdirected blood flow = volume overload
>ex: valvular insufficiency
Describe arrhythmias & conduction disorders.
-sustained tachyarrhythmias
>supraventricular tachycardia
>atrial fibrillation
-chronic bradyarrhythmias
>complete heart block
Describe compensatory mechanisms.
-when CO falls = BP falls = triggers compensatory mechanisms
-beginning = beneficial then contribute to clinical signs of heart failure
Which fast mechanism is activated & responds after a fall in BP?
-baroreflex
Describe neurohumoral responses.
-begin with detection of decrease in MAP by arterial baroreceptors
-increase sympathetic activity to heart, peripheral arterioles & veins
>vasoconstriction to skin, kidneys, spleen, resting muscles, mucosa
-decrease parasympathetic tone
>increase HR
Which receptors are involved with increase in sympathetic tone to the heart?
-beta adrenergic B1
Which receptors are involved with enhanced sympathetic outflow, vasoconstriction, & increase of TPR?
-alpha adrenergic A1&A2
Describe how the arterial baroreflex becomes counterproductive.
-Initially the arterial baroreflex maintains BP but as heart failure progresses & CO declines = counterproductive
-tissue ischemia to non vital organs
>skin, spleen, & kidneys = reduced perfusion activates RAAS
-rise in TPR = reduces SV
Why does the increase in TPR reduce SV?
-increase in afterload
Describe what happens when there’s an increase in blood volume.
-initially increase SV bc of frank starling mechanism
>compensates for low pumping ability of heart by increasing venous return
What are the volume overload physiological consequences?
-increase workload of heart
-overstretching of heart = weakens
>chronic excess stretch on actin-myosin cross bridges
>decreased ability to generate force of contraction
cardiac enlargement
Volume overload will increase capillary hydrostatic pressure. What is the consequence?
Movement of fluid from capillary to interstitial space
What happens when a failing ventricle is unable to pump all the blood returned to it?
-veins behind the failing ventricle becomes congested with blood
>filtration of fluid into lungs = pulmonary edema
>extensive edema in parts of the body
*increased venous congestion & capillary hydrostatic pressure
*pulmonary & systemic congestion
Describe L & R heart failure.
What are other neuroendocrine responses?
-induce alterations in heart failure
>natriuertic peptides (atrial, brain & C type)
>endothelin
>adrenomedullin (produced by adrenal medulla, heart, lungs, kidneys)
vasodilator & natriuretic action
>cytokine & integrins signaling
important role in inflammation ex. Myocarditis
Describe angiotensin II in heart failure.
-stimulates vascular & cardiac remodeling
>myocyte growth
>sm muscle growth
>collagen
cardiac & vascular hypertrophy
What is the vascular remodeling part of?
Long term control of local blood flow
What is the mechanism designed for acute loss in CO?
chronic activation of mechanism worsen the heart failure
