Heart Failure and Dysrhythmias.

• 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.

• Congenital heart defects
• Valvular disorders 
• Anemia
• Hyperthyroidism 
• Dysrhythmias 
• water intoxication 
• Medications

• 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.

• 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%.

• 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.

• Pulmonary disorders: increased pulmonary vascular resistance - high afterload - Rt ventricular hypertrophy (corpulmonale) - Rt ventricular failure. 
• 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.

• 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: (all lung related) Dyspnea on exertion, orthopnea, cough, paroxysmal nocturnal dyspnea, cyanosis, basilar crackles. 
• Forward effects: (Systemic circulation related) fatigue, oliguria (low urine output), increased HR, faint pulses, restlessness, confusion, anxiety.

• 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,

• Imporve CO while minimizing congestive symptoms and cardiac workload. 
• Obtained by manipulation preload, afterload, and contractility.

• abnormal rates of sinus rhythm 
• abnormal sites (ectopic) of impulse initiation. 
• Disturbances in conduction pathways.

• They indicate an underlying pathophysiological disorder
• They can disrupt normal CO.

• hypoxia
• electrolyte inbalance
• trauma
• inflammation 
• CAD
• disease of myocardium
• anemia
• pain 
• exercise 
• etc.

SA node --> Atrial internodal pathways --> AV node --> bundle of his --> Ventricular bundle branches --> purkinje fibers.

• small box: 0.04 
• larger box: 0.2

• P-wave: Rt and Lt atrial depolarization (contraction). 
• QRS: Ventricle contraction. 
• T-wave: Repolarization of the ventricles (relaxation).

• 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.

• Rate: 60-100
• Regular or irregular (looking at the R to R interval)
• P-wave
• PR interval
• QRS interval

• Rate 60-100. 
• P wave precedes every QRS complex. 
• PR, QRS, QT intervals are of normal duration. 
• Normal P-R interval 
• Normal QRS.

Variability in the HR - SA is not firing correctly. Some are benign or serious.

Absence of heartbeat - Fatal without CPR.

• 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)

• 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)

• 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)

• 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. 
• Bizarre QRS. 
• 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
• minutes. 

• The amont of blood pump out with every beat. 
• Normal values are 60 - 70%.