HF, Afib and Pulmonary edema (EXAM 2) Flashcards
How does blood flow through the body
RA-> RV-> Lung -> LA -> LV
Electrical flow of the heart
SA-> AV-> Bundles of His-> Purkinjie Fibers
AV Node role
Signals the ventricles to contract
Sympathetic nervous system compensation HF
-Both increases contractility and HR, which increase SV
-Becomes less effective over time causing decompensation
Increasing preload compensation HF
Ejection fraction is low, heart fills more which allows the heart to contract harder
-ADH is released to fill heart more
-Uses more energy, requires more blood, which can cause tissue to die, if they dont die the muscles become buff to compensate further, These are stronger but again require more blood and oxygen or else they die. And if the muscles become too big the chambers get smaller
Frank starling law
Increased preload, increased stroke volume= increased CO
Myocardial hypertrophy
Ventricles gain muscles, leads to worse hF in the long run
Right sided HF: Definition
-Ineffective RV contraction, blood cannot effective pump into the lungs, this can be a failure of the ventricle or the pressure in the lung is too high
-Caused by, acute RV infarction, PE, COPD, Backward flow due to LV HF
Left sided HF: Definition
-Ineffective LV contraction
-LV has decreased pumping ability, fluid accumulates, which causes fluid to back up into the atrium and then the lungs. This can lead to pulmonary edema and right HF
-Leads to pulmonary congestion, pulmonary edema, decreased CO
-Caused by, LV MI, Hypertension, and aortic and mitral val stenosis or regurgitation
Systolic HF
-HF with lowered ejection fraction, LV cant pump enough blood into the systemic circulation during systole
-Blood backs up into the pulmonary circulation, pressure rises in the pulmonary venous system and CO fails
Diastolic HF
HF with preserved EF, Ventricles cant relax properly and fill with blood in diastole, which causes the EF to remain the same while SV falls
-LV is affected, needs larger ventricular volumes to maintain CO
Cardiac output (CO)
HR*SV=CO
Amount of blood pumped out in a min
Normal CO
5-6 L
HF ejection fraction
30% and below
Normal EF
50-75%
Acute HF
-Symptoms come on suddenly and compensatory mechanisms havent kicked in
-Could have chronic HF and this is an exasperation or something completely new
-PT decompensates
Chronic HF
S+S have been present for some time and compensatory mechanisms have taken effect. Fluid volume overload persist
-HF increases with age
-Most reasons for hospitalizations over 65 yr old are for HF
-Very high re admittance rate for the hospital
Patho of HF
-Systolic HF results in decreased Blood being ejected from the ventricle, this activates the sympathetic nervous system (Fight or flight)
-The sympathetic nervous system is stimulated which causes the release of Epi and norepi, which increases contractility and HR
-Due to the decreased blood from from the heart, renal perfusion is decreased, which prompts the formation of angiotensin I, which is converted to angiotensin II by ACE (enzyme), constricting blood vessels and stimulating aldosterone (ADH) leading to fluid and sodium retention
-There is a reduction in contractility of the muscle fibers of the heart as the workload increases , which the heart compensates in by increasing the thickness of the heart muscle (Helps for a lil but only makes the problem worse)
Clinical manifestations of HF: Right
-Pertains to the fluid build up, weight gain is very important
-Viscera and peripheral congestion
-Jugular vein distension
-Dependent edema
-Hepatomegaly
-Ascites
-Weight gain
Clinical manifestations of HF: Left
-Pertains more to impairment of function of lung and poor o2 status
-Pulmonary congestion
-S3 sound
-Dyspnea on exertion
-Low o2 sat (Fluid in lung, heart isnt pumping well)
-Dry non-productive cough initially
-Oliguria (Low kidney perfusion)
Mnemonic for right HF (AW HEAD): A
Anorexia and nausea
-From venous engorgement and venous stasis in the abdominal organs
-Ascites is putting pressure on organ and stomach making you feel full or nauseous
Mnemonic for right HF (AW HEAD): W
Weight gain, from retention of fluids
-Huge concern if you gain ~2lbs (most sources say 3, but professor said 2) in one day or 5 in a week
Mnemonic for right HF (AW HEAD): H
Hepatomegaly
-Venous engorgement of the liver, with the increased pressure impacting its ability to function
Mnemonic for right HF (AW HEAD): E
Edema (Pipedal)
-Edema affecting the feet and ankles and worsens when the pt stands or sits for a long period of time
Mnemonic for right HF (AW HEAD): A
Ascites
Accumulation of fluid in the peritoneal cavity, increased pressure within the portal vessels causes the fluid from the vessels to be forced into the abdominal cavity
Mnemonic for right HF (AW HEAD): D
Distended neck veins
-Increased venous pressure leads to distended neck veins
Mnemonic for Left HF (DO-CHAP): D
Dyspnea: Air hunger
-Precipitated by minimal to moderate activity; also occurs during rest
Mnemonic for Left HF (DO-CHAP): O
Orthopnea, Cant breath while lying flat
-Dyspnea develops in the recumbent position and is relived with elevation of heads
-Pt sleeps in recliner or on a bunch of pillows
Mnemonic for Left HF (DO-CHAP): C
Cough is initially, dry and nonproductive. Large volume of frothy sputum, which may be pink is produced later in to the disease which indicates pulmonary congestion (Blood from lung)
Mnemonic for Left HF (DO-CHAP): H
Hemoptysis: Pink of blood tinged sputum
Mnemonic for Left HF (DO-CHAP): A
Adventitious breath sounds: Crackles/rales in the lungs, usually starts being heard in the bottom of the lungs but as the disease progresses it can be heard throughout
Mnemonic for Left HF (DO-CHAP): P
Pulmonary congestion: Continual high pressure in the pulmonary veins eventually forces fluid into the lungs which occlude alveoli
Risk factors for HF
-Sleep apnea (Huge)
-CAD
-HTN
-MI
-Diabetes
-Viruses
-Alc
-Congenital heart issues
-Smoking
-High fat high sugar
-Obesity
-Inactive or poor self care
-Age
-Ethnicity
Causes of HF: Starts with A
-Anemia
-Arrhythmia
-Atherosclerosis with MI
Causes of HF: Starts with C
-Connective tissue disorders
-Constrictive pericarditis
-Cor pulmonale
Causes of HF: Starts with E
-Emotional stress
-Excessive salt or water intake
Causes of HF: Starts with I
Infections
Causes of HF: Starts with M
Mitral or aortic insufficiency
-Mitral stenosis secondary to rheumatic heart disease, constrictive pericarditis or a fib
-Myocarditis
-
Causes of HF: Starts with N
-Nonadherance to meds (BP)
-Nutritional deficicnies
Causes of HF: Starts with P
Polycythemia
-Pregnancy
-PE
Causes of HF: Starts with T
Thyrotoxicosis
Causes of HF: Starts with V
Ventricular and atrial septal defects
Class I heart Failure
-No symptoms, can have a low EF without knowing it
Class II Heart failure
-Some symptoms with activity but is comfortable resting, slight limitation on physical exercise needed
Class III HF
Symptoms with minor activity but is comfy at rest, more limits on activity
Class IV HF
Patient displays symptoms at rest and with any activity, severe limitations on activity
History of HF
-Dyspnea, orthopnea or paroxysmal nocturnal dyspnea (Wake up gasping for air)
-Peripheral edema
-Fatigue
-Weakness
-Insomnia
-Anorexia
-Sense of abdominal fullness (Right HF)
-Decreased exercise tolerance
-Weight gain or loss (can have gain from fluid and loss from not eating)
-Nocturia (Trying to get rid of fluid)
-Nausea
OLD CART
Lab value for HF/Pulmonary edema
Beta Natriuretic peptide (BNP)
-Will be increased in HF and Pulmonary edema
-Hormone released by the heart when there is pressure changes
Lab findings for HF
Increased BNP
-Decreased sodium
-Increased creatine and BUN (Kidney)
-Increased bilirubin (Sometimes) (From enlarged liver)
-LFT may be abnormal
-Arterial blood gas (ABG), may reveal hypoxia
-CBC may reveal anemia or leukocytosis (Infection)
-Lipid panel-HDL and LDL will be elvated
BNP in chronic HF
Constantly elevated
Diagnostic for HF
-Echocardiogram is best (Ventricular size and function, valvular function, diastolic function, PA hypertension, EF)
-Chest Xray (Enlarged heart, pleural effusion)
-CT or MRI (Size of heart, wall thickness, valves, calcifications)
-Cardiac Catherization (Shows altered function, coronary artery perfusion, blockages Heart pressure and EF)
Complications of HF
-Hypotension -> Poor perfusion -> Organ failure
-Cardiogenic shock
-Pulmonary edema (LV)
-MI (Can cause HF and be caused by HF)
-Cardiomyopathy (thicc muscle)
-Cardiac arrhythmias (Afib, V tach V fib )
-Sudden cardiac death
-Valvar insufficiency
- -Embolism
-Percardial effusion
-Hypoxia
-Fluid and electrolyte imbalance
-Malnutrition
mgmt of HF
-Treat underlying conditions
-Oral and IV meds
-Fluid restriction
-Lifestyle modification
-o2
-Surgery (For the underlying problems
-VTE prophylaxis
-Elevation of lower extremities
-Comprehensive education and counseling to pateint and family
Diet in HF mgmt
-Sodium and fluid restriction
-Calorie restriction, (Weight loss)
-Trans-fat restriction (Weight loss)
-Dash Diet
Dash diet
Eating clean,
-Fruits and veg, low fat dairy, whole grains, lean meat, nuts, low alc,
-Also a low sodium version
Inotropes
Affect the contractility of the heart, force and strength of heart contraction
-Positive increase, negative decrease
Chronotropes
-Influences the HR
-Chrono=time
-Positive increase, negative decrease
Dromotropic
-Affects conduction velocity through the conducting tissues of the heart, improves the state of heart impulse
-Positive increase, negative decrease
Angiotensin converting enzyme inhibitors (ACE inhibitors) (HF)
End in il
-Causes vasodilation (Decreasing afterload), decreasing BP, improves LV EF
-Monitor for hypotension, hyperkalemia and altered renal function
-Cough is a common side effect (Annoys some people)
-First line
Afterload
The resistance the heart is pumping against
Angiotensin II receptor blockers (ARBS) (HF)
-ENds in sartan
-Blocks receptors that hormones act on, found in heart, kidney and blood vessels
-Lowers BP and prevents dmg to the heart and kidneys
-Given if they dont like the ACE inhibitor cough
Diuretics (HF)
Torsemide, furosemide, bumetanide, Hydrochlorothiazide, Spirolactone (K sparing)
-Decreases Fluid volume
-Monitor serum electrolyes
Beta blockers (HF)
End in lol
-Blocks the effects of epi/norepi
-Slows and strengthens the heartbeat-> lowers bp
-Widens veins and arteries to improve blood flow
-Use with caution in patients with asthma, can increase airway reactivity
Sodium-glucose cotransporter 2 inhibitors (SGLT-2) (HF)
Ends in Flozin
-Used in diabetes type 2, preventing the reuptake of glucose in the kidneys, causing glycosuria
-Glucose in urine acts like diuretic, causing increased fluid loss, decreasing BP/weight
-Reduced HF and reduces cardiovascular death
-Used with pt with type 2 and HF
-Can lead to UTI/yeast infection from the glucose in the urine
Digoxin (HF)
Improves contractility
-Monitor for digital toxicity, especially if they are hypokalemic
-Positive ionotropic, negative chronotropic
-Monitor apical rate
Nitrates (HF)
Nitroglycerin
-Decreases LV filling pressure and systemic vascular resistance
Potassium supplements (HF)
Diuretic use cause loss of potassium
Anticoagulants (HF)
-High risk of stroke, LV thrombus and DVT in HF, used to prevent
-Risk of A fib which is concern
Morphine (HF)
Decreases dyspnea and pain
Mnemonic for treating HF (DAD BOND CLASH) D
Digitals, increases contractility, and diuresis
Mnemonic for treating HF (DAD BOND CLASH) A
ACE inhibitors
Mnemonic for treating HF (DAD BOND CLASH) D
Dobutamine, IV med for LV dysfunction and hypoperfusion, stim beta 1 adrenergic receptors
Mnemonic for treating HF (DAD BOND CLASH) B
Beta blockers
-Reduces mortality and morbidity by reducing effects of sympathetic nervous system
Mnemonic for treating HF (DAD BOND CLASH) O
Oxygen, may be needed based on degree of pulmonary congestion
Mnemonic for treating HF (DAD BOND CLASH) N
Nitrates, Causes venous dilation which reduces the blood return to heart and lowers preload
Mnemonic for treating HF (DAD BOND CLASH) D
Diuretics: Remove fluid by urine
Mnemonic for treating HF (DAD BOND CLASH) C
Calcium Channel blockers
-Causes vasodilation reducing vascular resistance
Mnemonic for treating HF (DAD BOND CLASH) L
Lifestyle changes , lowering sodium, fluid, weight and completing regular exercise
Mnemonic for treating HF (DAD BOND CLASH) A
Angiotensin II receptor blockers, used for those who cant tolerate ACE inhibitors, blocks angiotensin II
Mnemonic for treating HF (DAD BOND CLASH) S
Sodium restriction, Low sodium diet (2-3g)
Mnemonic for treating HF (DAD BOND CLASH) H
Hydralazine Lowers systemic vascular resistance and LV afterload
Which classification of medications play a pivotal role in the management of HF caused by systolic dysfunction?
ACE inhibitors
Beta-blockers
Diuretics
Digitalis
ACE inhibitors
ACE inhibitors play a pivotal role in the management of HF caused by systolic dysfunction. They slow the progression of HF, improve exercise tolerance, and decrease the number of hospitalizations in patients with HFrEF.
Ventricular assist device (VAD)
Helps with HR, with a peripheral pump that drains the blood from the heat and pumps it either into the aorta or the pulmonary artery
Implantable cardioverter defibrillator (ICD)
For pt with risk of sudden cardiac death, defibs them if they go into V fib
Planning and Goals for. pt with HF
-Promote activity and reduce fatigue
-Relive Fluid overload symptoms
-Decrease anxiety or increase pt ability to mgmt of anxiety
-Encourage the pt to verbalize his or her ability to make decisions and influence outcomes
-Educate pt and fam about mgmt of the therapeutic regimen
mgmt of fluid volume (HF)
-Assess for symptoms of Fluid volume overload
-Daily weight
-I+O
-Diuretics therapy and timing of meds
-Fluid intake and fluid restriction
-Sodium restriction
Promote activity tolerance (HF)
-Bed rest for acute exasperations
-Encourage regular physical activity, build up to about 30 min daily (take rest periods)
-Exercise training
-Pacing of activities, wait 2 hrs after eating for physical activity
-Avoid heat ,cold, or humid weather
-Modify activities to conserve energy
-Positioning, elevation of the head of bed to facilitate breathing and rest, support arms
-High fowlers
Which of the following is not an appropriate recommendation for an exercise program for the patient with HF?
Follow the exercise period with a cool-down activity
High-intensity training will provide the most benefit
Wait 2 hours after eating a meal before performing the physical activity
Begin with low-impact activities such as walking
High-intensity training will provide the most benefit
Pulmonary edema (Acute)
Emergent situation, breakdown of physiologic compensatory mechanism
-LV function fails , blood backs up into the lung, pressure forces it into the pulmonary interstitial and alveolar edema
-Causes severe resp distress and hypoxemia
-Can become chronic
-Can be life threatening
Causes of pulmonary edema
-Congestive heart failure
-Pneumonia
-Sepsis
-Exposure to certain chemicals
-Organ failure
-Near drowning
-Inflammation
-Trauma
-Reaction to certain meds
-Overdose of certain drugs
Complications of pulmonary edema
Pulmonary fibrosis (Lung is repaired with scar tissue)
-Hepatomegaly (from fluid overload)
-Resp and metabolic acidosis
-Resp failure
-Cardiac or respiratory arrest
-Death
-If not caught
Pulmonary edema diagnostics
-Elevated BNP
-Elevated Creatine
-ABG -> hypoxia
-Chest X-ray : diffuse haziness of the lung fields, cardiomegaly and pleural effusion
S+S pulmonary edema
-Restlessness , Anxiety
-Tachypnea
-Dyspnea
-Cool and clammy skin
-Cyanosis
-Weak and thready pulse
-Cough
-Lung congestion
-Increased sputum production (Pink)
-Confusion
-Decreased LOC (If not caught early, decreased o2 to brain)
Mgmt of pulmonary edema
Prevention is easier than treating
-Minimize exertion and stress
-Recognize early signs
-Acute mgmt
o2: Non rebreather
Diuretics (Furosemide)
Vasodilators (Nitro)
Morphine (dyspnea)
Early signs of pulmonary edema
-Lung sounds (Crackles)
-Decreased activity tolerance
-Fluid retention, (Pedal edema/weight)
mgmt of pulmonary edema
-Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP)
-Endotracheal intubation and mechanical ventilation for respiratory failure
-Intra-aortic balloon pump for cardiogenic shock– reduces the workload on the heart, allowing it to pump more blood; placed inside aorta and the balloon on the end of the catheter inflates and deflates with the rhythm of the heart.
-Extracorporeal membrane oxygenation for severe refractory hypoxia– (ECMO), blood is pumped outside of the body to a heart-lung machine that removes carbon dioxide and sends oxygen-filled blood back to tissues in the body.
-When possible, treat underlying cause
Loop diuretics, Pulmonary edema
Furosemide, decreases fluid
Nitrates, Pulmonary edema
Nitro: causes vasodilation decreases the LV filling pressure and SVR increasing CO
ACE inhibitors, Pulmonary edema
Decrease SVR, increase CO and improves renal perfusion which allows diuresis in a pt with fluid overload
Nesiritide Pulmonary edema
-recombinant human brain type natriuretic peptide (BNP)
-Reduces pulmonary artery pressure,RA pressure, and systemic vascular resistance
What is the most reliable sign of cardiac arrest in an adult and child?
Decrease in blood pressure
Absence of brachial pulse
Absence of breathing
Absence of carotid pulse
Absence of carotid pulse,
its cardiac arrest, not resp, and the brachial is used in infants not children
Atrial Fibrillation
-Irregularly irregular HR, possibly fast
-P wave is non existent, and is replaced by multiple ectopic foci in the atria (not SA node)
-QRS is normal
-Can have Paroxysmal and Persistent
-Rate can be over or under 100
Paroxysmal A-fib
Comes and goes
-Most dangerous: Blood pools in atria, forming clot which can then be sent to brain or lungs
Rate in A fib
Atrial: indiscernible
Ventricular is variable, and HR is counted by ventricular rate
Ventricular rate is what you hear when you auscultate
60<Rate>100 adequate in afib</Rate>
Afib with a rate of 100+
Rapid ventricular response
Super bad, pt can decompensate
Causes of A-fib
-Obesity
-Sleep apnea
-HF
-Age
-Htn
-Heart enlargement (Left)
-Ischemic heart disease
-Hyperthyroidism
-Chronic kidney disease
-Alc use/drugs
-Smoking
Complications of A-Fib
TIA
-Stroke
-HF (Can both cause and be caused)
-Thromboembolism
-Bleeding with anticoagulation
-Recurrence of afib, you take them out only for them to fall back in
Symptoms of A fib
-Asymptomatic (many people are)
-Palpations
-Fatigue
-Decreased exercise tolerance
-Dyspnea, with exertion
-Chest pain, discomfort, or pressire
-Dizziness, light headedness
-Syncope
-Nausea
-Diaphoresis, clammy skin
HR of 100+ with afib rapid response
Treatment of A-fib
Meds, (control rate, anticolagulation)
-Weight loss, sleep study
-Sleep apnea
-Avoid triggers
-Synchronized cardioversion
-Radio-frequency or cryoablation
-
Radiofrequency/ cryo-ablation
Create scaring by heat or cold energy in the atria
Meds used in a-fib: Calcium channel blockers
-Control ventricular rate (dont use if decompensated HF is present)
-Diltazem hydrochloride, verapamil hydrochloride
Meds used in a-fib: Beta blockers
Control ventricular rate
end in lol
Meds used in a-fib: Anticolagulants
Warfarin, dagigatran etexlate, apixban, endxaban, rivaroxaban
Meds used in a-fib: aspirin with clopidogrel
if a person isnt taking an anticoagulant
Meds used in a-fib: Statins
Control lipid levels
Nursing interventions for A-FIb
-Give medications, know potential side effects
-Assess heart rate and rhythm and auscultate heart and lung sounds for changes.
-Cardiac monitoring, as indicated, noting any changes.
-Obtain a 12-lead ECG, as ordered.
-Obtain and monitor blood coagulation studies if the patient is receiving anticoagulant therapy.
-Institute bleeding precautions to minimize the patient’s risk of injury if receiving anticoagulant therapy.
-Monitor for Stroke
-Psychosocial support and education for the patient and family.
-Prepare the patient for possible synchronized cardioversion, if indicated.
-Apply anti-embolism stockings or sequential compression stockings to prevent VTE while the patient is hospitalized.
Your patient suddenly feels clammy, diaphoretic and nauseous. You assess them and find they have an irregularly irregular heart rhythm with a HR >100.What is the probable cause?
A. Hypertension
B. Rapid Atrial Fibrillation
C. Hyperglycemia
D. Pulmonary Edema
B. Rapid Atrial Fibrillation
Digoxin Toxicity
Levels higher than 2.0
Can cause arrythmias and heart block
-Changes in vision HALOS around bright objects
-Overdose symptoms: Ventricular tachycardia, ventricular fib, Bradycardia, heart block, CA, hyperkalemia
-N+V diarrhea, headache, confusion, anxiety, hallucinations
-Restlessness, weakness and depression
