Inability of the heart to maintain sufficient cardiac output to meet metabolic demands of the body.
Complex clinical syndrome that impairs the ability of the ventricles to be filled with or eject blood.
Resulting in congestion of blood flow in the systemic or pulmonary venous circulation.
Decreased tissue perfusion as a result of decreased cardiac output.
Etiology of heart failure
Congenital heart defects
Pathophysiology of Heart Failure?
Damaged to pump leads to decreased cardiac output, therefore, not meeting with oxygen body demands.
Dysfunctions: Diastolic and Systolic.
Systolic dysfunctions: When the ventricle is damaged and cannot contract effectively the stroke volume decreases leading to an increase n preload and the ventricle becomes distended.
Diastole dysfunctions: when the heart pumps against a high afterload, which leads to a decreased in the ability of the ventricles to comply, decreased filling of the ventricles which leads to decreased stroke volume.
What is the systolic dysfunction of heart failure?
It is the reduced myocardial contractility, evidence by low EF (ejection fraction) and inotropy (how quickly the ventricles can develop a forceful contraction), during ventricle systole.
Chronic over excitation of Beta1 receptors is thought to be another cause of the decreased in contractility.
Decreased ATP production.
Systole HF could cause diastole HF.
It is the disorder of myocardial relaxation such that the ventricle (Lt) is excessively noncompliant and does not fill effectively.
Causes: Coronary artery disease (CAD) and HTN are the 2 main causes.
More common in women, elderly, and those w/o history of MI.
Low CO, congestion, and edema formation with normal ejection fraction.
signs of failure, low CO but ejection fraction greater than 50%.
What are the compensatory Mechanisms in Heart Failure?
Baroreceptors response: decreased CO stimulates baroreceptors in the brain--> SNS activation (epi and norepi)--> increased HR and contractility --> increased CO.
* increased HR decreases Ventricular filling time compromising coronary artery perfusion, increases myocardial O2 demand, and this leads to inchemia and decreased CO.
RAS activation decreased GFR (glumerail flurtration rate): In the kidneys --> fluid retention --> increased preload --> increased CO.
Ventricular wall tension increased: in the heart --> myocyte growth --> hypertrophy --> Incresed CO.
Most often associated with: Diastole, Backwards effects and forward effects.
Backwards effect: which results in accumulation of blood within the pulmonary circulation, pulmonary convention, and edema. Unique finding is shortness of breath.
Forward effects: which results in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and organs.
Left sided effected more than right side.
Left ventricular and atrial end-diastolic pressures increase and CO decreases.
Impaired Lt ventricular filling results in congestion.
Backward effect: Blood goes back into the atrial and vena cava causing systemic venous congestion.
Forward effect: Causes low output to Lt ventricle leading to low CO. - Not enough blood goes to the lungs --> not enough blood goes to the Lt atrial/ventricle --> not enough blood in systemic circulation.
Causes: Pulmonary HTN and Lt-sided HF.
Rt ventricule hypertrophy and dilation.
Clinical Manifestations of HF
Lt ventricle failure is most common bc of high pressure in the lungs.
Forward failure: insufficient cardiac pumping manifested by poor CO.
Backward Failure: congestion of blood behind the pumping chamber.
backwards effects: hepatomegaly, ascites (in the abdomen), splenomegaly, anorexia, subcutaneous edema, jugular vein distention (JVD)
Forward effects: (same as Lt HF- bc the blood is not pushing over to the lungs) Fatigue, oliguria (decreased urine), increased HR, Faint pulse,
Principles of HF treatment:
Imporve CO while minimizing congestive symptoms and cardiac workload.
Obtained by manipulation preload, afterload, and contractility.
What are the 3 major typer of dysrhythmias?
abnormal rates of sinus rhythm
abnormal sites (ectopic) of impulse initiation.
Disturbances in conduction pathways.
What ar the 2 significant reasons why dysrhythmias are important?
They indicate an underlying pathophysiological disorder
They can disrupt normal CO.
What are the common causes of dysrhythmias?
disease of myocardium
What is the normal excitation of the heart?
SA node --> Atrial internodal pathways --> AV node --> bundle of his --> Ventricular bundle branches --> purkinje fibers.
What is a small box worth? a larger box?
small box: 0.04
larger box: 0.2
What id the p-wave, QRS interval, t-wave mean?
P-wave: Rt and Lt atrial depolarization (contraction).
QRS: Ventricle contraction.
T-wave: Repolarization of the ventricles (relaxation).
PR, QRS, QT intervals?
PR intervals: less than 0.20 or 5 little squares.
QRS: 0.12 or 3 little squares.
ST and QT: are not part of analysis, give you information about diastole.
What are the 5 things to analyze in a EKG?
Regular or irregular (looking at the R to R interval)
What is normal Sinus rhythm?
P wave precedes every QRS complex.
PR, QRS, QT intervals are of normal duration.
Normal P-R interval
What is a sinus Arrhythmia (dysrhythmia)?
Variability in the HR - SA is not firing correctly. Some are benign or serious.
what is Asystole?
Absence of heartbeat - Fatal without CPR.
What are the abnormal sites of impulse initiation?
It is the initiation of cardiac impulse other than the SA node.
Escape rhythm: Originzate in the AV nodal region in the Ventricular system and allows a slower pacemaker to take over (Do not see (see abnormal) a p-wave bc p-wave depends on atrial activity)
Premature beats and ectopic rhythms: enhanced excitability that cause a premature depolarization and over ride the SA node. (The impulse could come from the A, V, or the AV node- High risk for a code bc the V irritability dereases CO)
What are atrioventricular conduction disturbances?
Disturbance in conduction b/t sinus impulse and associated ventricular response. There are 3 degrees.
Intraventricular conduction defects: abnormal conduction of impulses through the intraventricular bundle branches-bundle-branch blocks. (Pt has blockage in the Rt or Lt side, the impulse takes too long and causes an MI. QRS longer than 0.12)
What are first degree, second degree, third degree atrioventricular conduction disturbances.
First degree: Prolongation of the PR ventricle (>0.20) - V premature beat. The danger is premature V contraction.
Second-degree block: More than one p-wave before a QRS. V doesn't pick the beat from the SA node, so the SA node fires again. Seen in MI or open heart surgery.
Third-degree block: Complete heart block- A and V are betting on their own. Prolonged QRS, irregular beating. (usually low pulse 40s or 30s)
What is atrial flutter? what is atrial fibrillation?
Flutter: It is typically manifested by a rapid atrial rate of 240-350 beats/min with a saw tooth pattern.
Fibrillation: It is a completely disorganized and irregular atrial rhythm accompanied by an irregular V rhythm. (prone to embolization).
Premature ventricular complexes (PVCs):
Arise from the ventricular myocardium.
Do not activate the atria or depolarize the sinus node.
Compensatory pause is common.
Begeminy (every other beat) or Trigeminy (every third beat).
With high frequency, CO may be compromised.
3 or more consecutive ventricular complexes at a rate greater than 100 beats/min.
P-wave are not associated with the QRS complex.
ECG depicts a series of large, wide, undulating waves.
Maybe fatal if not rapidly managed (antiarrhythmia drugs, CPR, Electrical Cardioversion)
Rapid, uncoordinated cardiac rhythm resulting in V quivering and lack of effective contraction.
ECG is rapid and erratic, with no identifiable QRS complex.
Results in death if not reversed within
What is EF (ejection fraction)? what are the normal values?