Cardiac 03: Heart Failure , Pacers Flashcards
Definition of Heart Failure
The heart’s inability to adequately supply blood to meet the metabolic demands of the tissues. This results in inadequate tissue perfusion and volume overload
What’s different about Acute HF compared to HF?
It occurs suddenly, frequently w/o time for compensatory mechanisms to be activated. If severe/rapid enough, this can result in cardiogenic shock.
What is the demographic of HF?
It can be anyone, even a young person who got COVID->cardiogenic shock to postpartum cardiomyopathy.
What response does the heart have when the CO drops in cardiogenic shock? (4 steps)
- Drop in CO -> drop in EF
- Increased in End Diastolic Volume, leading to myocardial fiber stretch
- Increased contractility (augmented sensitivity to Ca++)
- Activation of the neurohormonal system
! What are 4 systems within the compensatory neurohormonal system?
All 4 occurs at the same time
- Adrenergic System
- Renin-Angiotensin-Aldosterone System
- Hypothalamic- Neurohypophyseal System
- Endothelium activated Mediators
Read and recall:
In adrenergic response..
Baroreceptors in aorta sense low bp/co. The SNS is activated by brain and norephinephrine and epinephrine is released. Leads to beta stimulation and increase in HR and contractility.
Alpha stimulation occurs -> vasoconstriction
Read and recall:
In Renin-Angiotension response
Low BP/CO leads to lower filturation rate/GFR -> Renin Release ->Angiotensin I->Angiotensin II -> vasoconstriction.
Aldosterone is released, leading to Na & water retention
Read and recall:
In Hypothalamic Neurohypophyseal System. Basically vasopressin effect
Low BP/CO leads to release of vasopressin (ADH) from Posterior Pituitary -> Vasoconstriction -> Sodium and Water retention.
UOP decreases
Delete
When low BP/CO occurs, it leads to endothelin-1 vasoconstriction.
Nitric oxide, endothelium-derived relaxin
What does the systems of the compensatory response do in CO? (4)
- Increased HR
- Increased Contractility
- Vasoconstriction
- Sodium & water retention
Compensatory responses for low CO are good in situ where patient is bleeding out, but not when the heart is failing, why?
Compensatory responses are great with a good working heart in a bleeding patient. But in a person with a bad heart, a positive feedback loop occurs where the afterload increases, and the compensatory normal response continues. It becomes progressive heart failure.
Read about during the progression of heart failure and what ANP and BNP does
Continued activation of sympathetic system causes an increase in afterload and the release of natriuretic peptides: ANP& BNP.
These peptides promotes diuresis, vasodilation and inhibition of RAAS. Atrial is produced by a stretch atria and BNP produced by ventricles.
What is TNF Alpha?
TNF-alpha: Tumor necrosis factor. Produces secondary to hypervolemia and triggers both systemic and cardiac inflammatory responses.
Releases cytokinesis during HF
What occurs to the heart anatomy in progressive HF?
It actually hypertrophies and remodels. Initially adaptive in nature, it leads to hypertrophy, ventricular dilation and increased O2 demands. But with increased demand, it leads to a decrease in CO and ischemia
Cardiac signs of HF: (9) List five or so
- Tachycardia, arrhythmia
- Weak pulses
- Low CO & BP
- Jugular venous distension
- S3 diastolic gallop
- Displaced PMI
- C xray cardiomegaly and vascular prominence
- Peripheral edema
9 Positive hepatojugular reflux
Pulmonary signs and symptoms of HF: (3)
- Dyspnea
- Rales
- Paroxysmal Nocturnal Dyspnea
All are from the heart volume backing up into the lungs
Neurological signs and symptoms of HF (3)
- Fatigue, weakness, dizziness
- LOC Change
- Sense of impending doom from decrease O2, increased CO2. Anxious , confusion etc.
TIA, strokes could occur from lack of perfusion.
If poor coronary perfusion is the primary cause of HF, what are some possible interventions?
- Thrombolytics
- PCI
- CABG
- Cardiac Transplant
- Treat the physiological cause, i.e CAD, HTN, dysrhythmia
Why are vasodilators helpful in the management of HF?
They decrease preload, decrease afterload and increase renal perfusion. So it improves symptoms of failure and and symptoms related to the compensatory response.
How do Angiotensin Converting Enzymes Inhibitors work? (ACE) 3
ACE is now main drug used in HF management.
1. Dilate arterioles -> decreases afterload, increase SV, inscrease CO, improve regional flow
2. Dilate veins -> Decrease preload -> decrease pulmonary congestion -> decrease cardiac dilation -> increase renal perfusion which then increases sodium and water excretion. This will also stop encouraging the positive feedback loop of the compensatory response.
3. Decrease aldosterone release -> Retention of K. Release of Na and water.
