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Flashcards in Heart Failure Notes Deck (53)
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1

What are the two ways that can cause heart failure within the heart?

Defect in ventricular systolic function/ LV contraction (HFrEF)
Defect in ventricular diastolic functioning/filling (HFpEF)

2

2 main RF for HF

HTN
CAD

3

Pathophysiology of Left Sided HF Systolic (HFrEF)

LV does not have enough pressure to push blood out of the aorta.
Heart dilates and enlarges to compensate but the heart cannot generate enough Stroke Volume (SV) and Cardiac Output (CO).
LV pressure increases.
LV fails and blood is backed up into the LA.
Lungs will have too much fluid and it will spread into the alveoli and interstitium.

4

Pathophysiology of Left Sided HF Systolic (HFrEF)

LV does not have enough pressure to push blood out of the aorta.
Heart dilates and enlarges to compensate but the heart cannot generate enough Stroke Volume (SV) and Cardiac Output (CO).
LV pressure increases.
LV fails and blood is backed up into the LA.
Lungs will have too much fluid and it will spread into the alveoli and interstitium.

5

LVEF in HFrEF (Systolic)

<40%

6

Pathophysiology of Left Sided HF Diastolic (HFpEF)

LV is stiff and noncompliant, creating high filling pressure.
Decreased ventricular filling leads to decrease SV and CO.
Too much fluid in the lungs because they can't get into the heart and it will spread to alveoli and surrounding tissues.

7

LVEF in HFpEF (Diastolic)

41-49%

8

What are the 3 things that can determine if it is a HFrEF or HFpEF?

Based on
Signs and symptoms of HF
Normal LVEF
Evidence of LV diastolic dysfunction by echocardiography or cardiac catherization

9

Pathophysiology of Right Sided HF

RV does not pump effectively
Fluid backs up into the venous system aeb systemic symptoms (peripheral edema, abd ascites, etc.)

10

What is the most common cause of Right side HF?

Left sided HF

11

Pathophysiology of Biventricular HF

Both ventricles cannot pump ineffectively leading to fluid build up and systemic venous engorgement.

12

What are the compensatory mechanisms?

Renin Angiotensin Aldosterone System (RAAS)
Sympathetic Nervous System (SNS)
Ventricular Dilation
Ventricular Hypertrophy

13

RAAS purpose

Increase preload and ventricular contraction to maintain CO
Retains Sodium and Fluid, Excretes Potassium

14

Pathophysiology of RAAS

Decrease CO will let the kidneys activate Renin.
Renin will be converted to angiotensinogen to Angiotensin I.
Angiotensin I will be converted to Angiotensin II in the lungs.
Angiotensin II is a strong vasoconstrictor that stimulates water and sodium retention and allows aldosterone to be released from adrenal gland.
Aldosterone will also retain water and sodium, waste potassium and allow myocardial fibrosis (thickening of heart scar tissue).

15

Pathophysiology of SNS

Low arterial pressure will get the SNS to release Catecholamines (norepinephrine and epinephrine).
Catecholamines will stimulate B-adrenergic heart receptors into increasing HR and ventricular contractility.
This will increase O2 consumption of the heart.

16

What will happen with continuous neurohormonal responses (RAAS and SNS)?

High ADH (antidiuretic hormone) levels, endothelin and proinflammatory cytokines.

17

Endothelin and Proinflammatory purpose (Short and Long term use)

Reduce ventricular contraction.
Chronic use: Increase heart's workload, progressive LV dysfunction, myocyte hypertrophy and ventricular remodeling.

18

Dilation

Enlargement of heart chambers that allows an increases in preload but no increase in CO.

19

Frank-Starling Law

Strength of heart's contraction is directly proportional to its diastolic expansion.

20

Hypertrophy

Increase in muscle mass and heart wall thickness that develops slowly.
It leads to poor contractility, more O2 demand, poor coronary artery circulation and prone to dysrhythmias.

21

Remodeling

Change in heart structure due to pressure or volume overload, injury and compensatory mechanisms.
It increases ventricular mass, increased wall tension, increased O2 consumption, and impair contractility.

22

Renal effects of ANP and BNP

Increase GFR and diuresis
Sodium excretion

23

Cardiovascular effects of ANP and BNP

Vasodilation and decrease BP

24

Hormonal effects of ANP and BNP

Aldosterone Inhibition and Renin secretion
Interference with ADH release

25

Nitric Oxide (NO) and Prostaglandin

Relax arterial smooth muscle, vasodilation and decreased afterload.

26

Compensated HF

Compensatory mechanism can maintain adequate CO

27

Decompensated HF

Compensatory mechanisms can NOT maintain CO and inadequate tissue perfusion occurs.

28

Chronic HF C/M:

Fatigue - when doing daily activities and is an early symptom of Chronic HF
Dyspnea - most common manifestation of chronic HF
Orthopnea
PND- paroxysmal nocturnal dyspnea
Cough - chronic and nonproductive that’s worse in recumbent position
Tachycardia - early sign of HF
Palpitations - Atrial Fibrillation is the most common dysrhythmia associated with HF,
Edema - most common sign of HF
Decreased urine output
Nocturia
Mottling skin- blue or gray skin color
Coolness or clammy to touch
Dizziness, lightheadedness and Syncope
Sleep apnea
Insomnia
Chest Pain or Angina
Weight changes- due to fluid retention
Cardiac cachexia with muscle wasting and fat loss.

29

Interprofessional Care: ADHF stable

High Fowler's position with dyspnes
Assess v/s, pulse ox, q4hrs
Record I&O, daily weights
Treat underlying cause
Supplemental O2
Drug therapy
Circulatory Assist Device
Daily weights
Sodium and Fluid restricted diet

30

Interprofessional Care: ADHF unstable

Continual ECG and O2 saturation monitoring, v/s, urine output q1hr
Hemodynamic monitoring- arterial BP, pulmonary artery pressure
Continuous CO and Pulmonary Artery Wedge Pressure (PAWP)
Supplemental O2
Ultrafiltration
Mechanical Cardiac Assist Device
Intraaortic Balloon Pump (IABP)
Treat underlying cause