HF Flashcards
HF
An abnormal clinical syndrome involving impaired cardiac pumping and/or filling
Heart is unable to produce an adequate cardiac output to meet metabolic needs
Characterizations of HF
Ventricular dysfunction
Reduced exercise tolerance
Diminished quality of life
Shortened life expectancy
Cardiac output is
HR x Stroke Volume
Main primary Risk Factors for HF
CAD
HTN (Vessels less elastic, heart must work harder)
Secondary Risk factors for HF
DM
Smoking
Obesity
High serum cholestoral
HF is caused by any interference with normal mechanisms regulating cardiac output - what are these mechanisms?
Preload
Afterload
Myocardial Contractility
HR
Preload
The initial stretching of cariac myocytes
What happens BEFORE contraction
Volume of blood at end of Diastole
Afterload
The resistance the left ventricle must overcome (In the aortic valve) to circulate blood
Ventircular reistance
Myocardial contractiliity
The capacity of the heart to pump effectively
HFrEF
HF with reduced dejection fraction
What is ejection fraction (+ what is a normal one)
% of total amount of blood in LV that is ejected druing each ventircular contraction; normal EF is >55% of ventricular volume
What causes HFrEF?
Myocardial ischemia, increased afterload AKA HTN, cardiomyopathy, or mechanical abnormality (Valvular disease)
Most common type of HF
HFrEF
Hallmark finding of HFrEF
Decreases in LV EF
Pts with an EF of ____ require specialist intervention
40% or less
HFpEF (Heart Failure with preserved ejection fraction
Inability of the ventricles to relax and fill during diastole
Results in decreased stroke volume and CO
What causes HFpEF
Poorly compliant ventricle - LV hypertrophy, myocardial ischemia, valvular disease (aortic or mitral), Cardial myopathy
Diagnosis of HFpEF is?
Based on presence of HF symptoms with an EF of 50% or greater
Compensatory mechanisms for HF
Increased SNS stim (increase HR, vasocontstriction) - Quick response, least effective - Effort to increase CO
Neurohormonal: Renal system is particularly senesitive to reductions in BF - activates RAA mechanisms - causes vasoconstriction and leads to aldosterone secrtion
Causes retention of salt and water - increasing preload - eventually results in systemic venous congestion and peripheral edema
ADH is secreted to retain water to increase preloadddddddddd
What is cardiac decompensation
When compensatory mehs can no longer maintain adequate CO and insufficient tissue perfusion
Ventricular Remodeling
Hypertrophy of cardiac myocytes - large abnormal cells (Less efficient pump)
Eventually leads to vent mass, changes in ventricular shap and impared contractillity
Results in a bigger but less effective pump
Ventricular dialation
Enlargement of chambers of heart due to elevated pressure over time
Initially an adaptive mechanism to cope with increased blood volume - decreased elasticity in muscle fibers resuts in decreased CO
Ventricular hypertrophy
Increase in muscle mass and cardiac wall thickness due to overwork and straindd
Counterregulatory mechanisms
If the compensatory mechs work TOO well
Atrial Naturuetic peptide (released from atria)
Beta-type natriuretic peptide (released from ventricles)
Both released in repsonse to increased blood volume in heart, effect renal, CVS and hormones
Types of HF
Left sided (Most common)
Right sided HF
Left sided HF
Back up of blood into LA and pulm veins manifested as
(acute) Pulmonary edema (flash)
Resp symptoms
3rd Heart sound
Decreased output
Right sided HF
Causes backward blood flow to the RA and venous circulation
Peripheral edema (halmark), enlargement of spleen, liver, JVD
Acute decompensated HF (ADHF)
Comp mechs fail
Manifests as PE, often Life threatneing (Flash PE)
Often happens secondary to MI
Symptoms of ADHF
Acutely short of breath
Altered LOC
Anxiety
Clammy and cold skin
Increased HR + RR
Severe Dyspnea (Tripodding/ acc muscles)
Wheezing/coughing with frothing/blood tinged sputum (Crackles)
Changes in BP
Anasarca
Full body Edema
Why would Left sided HF result in nocturia
While sleeping, the Heart doesn’t work as ard, therefore, blood flow is restored to kidneys
Management of Acute DHF
Decrease intravascular volume - Diretics
Decreasing venous return (Preload) - Position (High fowlers, feet dangle)
Decreasing Afterload - (Balancing BP)
Improving gas exchange and Oxygenation - High flow Oxygen (IV lasix ONLY if BP is high enough)
- Positive Airway Pressure mask forces fluid out of lungs into vascular space (improving Oxygenation)
Improving Cardiac Function (ICU, HACU) - Inotropes etc.
Reducing anxiety (morphine/hydromorphone - reducing sensation of breathlessness)
Care of Chronic HF
O2 administration (specifically with exertion) - shooting for 92 + SPO2
Self Management + teaching (monitoring, daily wt, sleep positioning)
Regular Exercise
Supportive device for Chronic HF
Cardiac resynchronization therapy
Implantable Cardioverter-Defibrillator (PM)
Mechanical Circulatory Support
Mechanical Circulatory Support
Dysrythmias associated with which part of heart are most deadly?
Ventricle
Therpeutic objective of medication therapy
Identify type of HF and causes
Correction of NA and H2O retention and volume overload
Reduction of cardiac workload
Improve myocardial contractility
Control of precipitating and complicating factors
Common meds for HF
Directics - Loop diretic Lasix etc. Thyaside diurectics
- Reduce intravascular volume in order to reduce preload
ACE inhibs: Ramabpril or analapril
- Vasodialt 9BP, decreased afterload, CO
Some pts can’t tolerate angioedema or cough and are put on ARBs instead
Beta-Adrenergic Blockers
- Reduces cardiac oxygen demand by decreasing HR and BP
Neprilsyn Inhibs - Combines ARB with Neprilsyn inhibitor (new drug)
Inotropic Drugs - Management of ADHF - improve cardiac contractililty for increased CO, and afterload
For pts with HFrEF
Nitrates: Reduces afterload by dilating peripheral BV
Increases myocardial O2 supply by dialting coronary BC
First line med in management of chest pain
- In acute PE with adequate BP
Digitalis: i.e. Digoxin. Small thereapeutic window
- Increases CO (decrease HR, increas V filling and contractility)
- Monitor Apical rate (should be>60BPM)
Who are inotropics given to
Pts who are hemodynamically unstable, those with HFrEF unless it’s end of life
Nutritional therapy for outpts with HF invovles
Diet education
- Na restriction
-Fluid restriction (1.5-2L)
Wt management
Report gains of 2 kg/24hr or 2.5 kg a week
Nursing Diagnoses for HF
Inadequat CO
Reduced gas exchange
Excess fluid volume management
Use of Diuretics
Monitor wt
Monitor for HypoK
Limit Na intake (+I&O)
Digitalis toxicityu
Bradycardia, tachycardia; irregular pulse/arrhythmia
GI: anorexia, nausea, vomiting, diarrhea, abdominal pain
Neuro: headache, drowsiness, confusion, insomnia, muscle weakness, double vision, blurred vision, visual halos
Patients have regular serum digoxin levels taken to make sure they are in the therapeutic range.
Successful HF mgmt. depends on these principles:
HF is progressive; QoL is paramount
Pt self-mgmt. needs to be emphasized
Na+ and H2O need to be restricted
Regular exercise should be maintained
Use of supports is essential to success of tx plan
Med adherence is important (education)
How is a persons EF determined?
Echocardiogram
Why does every HF pt need a Saline lock
Iv access in case anything needs to be done quickly
When do you withold a beta blocker?
For HR less than 50 or symptomatic HOTN
Two most common reasons for HF
Chronic HTN
CAD (MIs are a significant cause bc they can cause part of the muscle to die )
ADHF occurs when?
Often caused by MI, sepsis, an acute event
Paraoxym nocturnal dyspnea
Waking up suffocating in the morning because of fluid flowing back to lungs
What is a concerning amount of wt gain in HF pts
2kg in a day or 2.5 kg in one week
