Exam 1 : Cardiovascular Chronicity Flashcards
Congestive heart failure
Congestive heart failure is a condition in which your heart can’t pump enough oxygen-rich blood to meet your body’s needs. When your heart doesn’t pump efficiently, blood may back up into your lungs and other tissues.
The severity of congestive heart failure depends on how much pumping capacity your heart has lost. As they age, most people lose some pumping capacity. However, in congestive heart failure, your heart has very little pumping capacity. Congestive heart failure often results from damage caused by a heart attack, high blood pressure, diabetes or other conditions.
Classifications of heart failure
Class I – ordinary activity does not cause concern
Class II – slight limitation of activity
Class III – comfortable at rest. Marked limitation with activity
Class IV – unable to carry on any physical activity without discomfort
Stroke volume
The larger the stroke volume the more it fills the ventricles and therefore it has to work harder, the more the work load of the heart ht emore the oxygen consumpition
True or false
Faster HR the higher the cardiac demands
True
What is the goal of medication therapy in HF?
Goal of medication therapy is to decrease cardiac workload through SV, HR, Preload, after load and contractility
What is cardiac output?
Stroke volume * heart rate
What is Preload?
Preload is the filling pressure of the RV-LV and is influenced by venous return
True or False
In a healthy heart, as you ↑Preload…You will INCREASE SV increasing the force of contraction . . . . . up to a certain point-then further stretching may actually DECREASE contractility
True
What decreases Preload?
Drugs that cause venous dilation (nitrates)- DECREASE preload . (gives fluid more space to disperse)
Diuretics that eliminate excess fluid volume- DECREASE preload
What are some labs you would check when giving a diuretic?
Labs you would check when giving diuretics: creatine, potassium, sodium
CHF exacerbation
CHF exacerbation: give alittle bit of morphine because it lowers anxiety and relieves chest pain and most importantly it’s a peripheral vasodilator…fluid can sit out there for a bit so the heart doesn’t have to deal with it
Low dose nitroglycerin drip: also a vasodilator
Starlings law of the heart
The greater the PRELOAD, the greater quantity of blood that can be ejected during systole due to INCREASED stretch of myocardium.
There is a limit! Greatest force of contraction is when the muscle fibers are stretched 2 ½ times their normal length.
The overstretch of cardiac muscle is like an overstretched rubber band-will DECREASE cardiac contractility and efficiency over time
What is after load?
Force of resistance that the LV must generate to open aortic valve
Influenced by resistance of blood vessels in the body-are the arteries dilated or constricted? –hypothermic constricted, running a temp its dilated
How does after-load correlate with systolic bp
Correlates with systolic blood pressure.. How much pressure is needed to push blood out of the heart into the aorta and into the entire systemic circulation
What medications decrease after-load
Arterial vasodilators (Ca++ channel blockers (CCB), ACE inhibitors) DECREASE afterload
What is contractility?
Ability of heart to change force of inherent contraction strength
Influenced by Ca++ in action potential…therefore Calcium Channel Blockers will do what to contractility?
Negative inotropic meds?
Negative inotropic meds: Calcium channel blockers, beta blockers
What is ejection fraction?
65-70% normal, reflects that with each contraction 65-70% of the blood in the LV is ejected into circulation
As this % goes down it reflects the loss of cardiac contractility and degree of CHF
35% EF is half the normal cardiac output with each contraction
Etiology heart failure
Heart failure is caused by systemic hypertension in 75% of cases.
About one third of clients experiencing myocardial infarction also develop heart failure.
Structural heart changes, such as valvular dysfunction, cause pressure or volume overload on the heart.
Left sided heart failure manifestations
Weakness, fatigue, dizziness, confusion, pulmonary congestion, dyspnea on exertion, orthopnea, paroxysmal nocutnal dypnea, oliguria, renal failrue
Right sided heart failure manifestations
Jugular distention, enlarged liver and spleen, anorexia, nausea, dependent edema (legs and sacrum), distended abdomen, swollen hands and fingers, polyuria at night, weight gain, increased BP
True or false
B NATURETIC PEPTIDE IMPORTANT IN DIAGNOSING HEART FAILURE
True
ONE OF THE BEST WAYS TO DIFFERENTIATE BETWEEN PNEUMONIA AND HEART FAILURE IS B NATURETIC PEPTIDE
ONE OF THE BEST WAYS TO DIFFERENTIATE BETWEEN PNEUMONIA AND HEART FAILURE IS B NATURETIC PEPTIDE
BMP vs BNP
BMP : basic metabolic panel
BNP: brain naturetic peptide
Why would BNP be elevated in heart failure?
BNP would be elevated when the ventricles are being stretched and having to work too hard
Could happen during heart failure, marathon runner in training, genetic makeup can also play in affect,
Normal BNP ranges
Normal range for BNP: 0-100
Elevated BNP: anything above 100
Sympathetic nervous system stimulation: arteries constricts resulting in increased afterload
Sympathetic nervous system stimulation: arteries constricts resulting in increased afterload
Key assessment sin heart failure
Lab assessment: electrolytes, renal panel, ABGs, BNP
Radiographic assessment: chest xray: cardiomegaly (enlarged heart)
Echocardiography: diagnoses valvular function, Ejection fraction
Pulmonary artery catherization: diagnose and manage HF
Impaired gas exchange interventions
Interventions include:
Ventilation assistance – vent or nasal.
Goal O2 sats: ________
Hemodynamic regulation – Swan Ganz
Energy management (conservation), positioning
Diet therapy
Drug therapy
Optimizing cardiac output
Interventions are aimed at optimization of: Stroke volume Preload Afterload Contractility
Why would you give coreg for the a low bp?
the bp went up because the heart didnt have to work as hard
Drugs that reduce after load
ACE inhibitors, ARBs, Nitrates - Human B-type natiuretic peptides for acute HF.
Drugs that enhance contractility
Digitalis
Digitalis toxicity includes anorexia, fatigue, changes in mental status.
Valvular diseases
Mitral stenosis: Stenotic means stiff, possible calcium buildup..too stiff for blood to go through it
Regurgitant valve: blood get regurgitated or sent back up
Mitral valve prolapse: valve is limp and falls through ventricles
Assesment for valvular disease
Sudden onset or slow development of symptoms over many years.
Question client about history of rheumatic fever, infective endocarditis, and IV drug use/abuse.
Common diagnostics include chest x-ray, echocardiogram (TT, TEE), and exercise tolerance test.
Common Nursing Diagnoses related to Valvular Heart Disease
- Decreased Cardiac Output related to altered stroke volume
- Impaired Gas Exchange related to ventilation perfusion imbalance
- Activity Intolerance related to inability of the heart to meet metabolic demands during activity
- Acute Pain related to physiologic injury agent (hypoxia)
Nonsurgical Management for Valvular Heart Disease
Nitrates dilate to allow less resitance and doesn’t make heart work as hard
Surgical Management for Valvular Heart Disease
- Reparative procedures
- Balloon valvuloplasty
- Direct, or open, commissurotomy
- Mitral valve annuloplasty: go in scrape off
- Replacement procedures
(Lifelong anticoagulants r/t mechanical artificial valve.)
Xenograft from other species (pig) do not last as long as artificial (mechanical).
Infective endocarditits
Microbial infection involving the endocardium – most common
Streptococcus viridans or Staphlocococcus aureus
Occurs primarily with IV drug abuse, valvular replacements, systemic infections, or structural cardiac defects
Ports of entry: mouth, skin rash, lesion, abscess, infections, surgery, or invasive procedures including IV line placement
High mortality rate
Manifestations of Endocarditis
- Murmur
- Heart failure – most common complication
- Arterial embolization
- Splenic infarction
- Neurologic changes : TIA, CVA, confusion, dysphagia
- Petechiae (pinpoint red spots)
- Splinter hemorrhages – distal third of nail bed
Interventions for endocarditis
- Antimicrobials – 4-6 weeks, most penicillins or cephalosporins
- Home Care or outpatient therapy for IVs
- Rest, balanced with activity
- Supportive therapy for heart failure
- Anticoagulants if pt has prosthetic valve
- Surgical management to remove or repair infected valve
Pericarditis
Inflammation or alteration of the pericardium
the membranous sac that encloses the heart
Dressler’s syndrome (1-12 wks after MI)
Fever, pericarditis, pleural & pericardial effusions
Postpericardiotomy syndrome
After cardiac surgery
Chronic constrictive pericarditis
Assessment of pericarditis
Substernal precordial pain radiating to left side of the neck, shoulder, or back.
Grating, oppressive pain, aggravated by breathing, coughing, swallowing, position.
Pain worsened by the supine position; relieved when the client sits up and leans forward.
Pericardial friction rub
Elevated WBC and fever
Intervention for pericarditis
Hospitalization for diagnostic evaluation, observation for complications, and symptom relief
Pharmacologic therapy: Nonsteroidal anti-inflammatory drugs, Corticosteroid therapy
Comfortable position, usually sitting
Pericardial drainage
What is cardiac tamponade?
Cardiac tamponade:an extreme emergency
When the space between the parietal and visceral layers of the preicardium fills with fluid
restricts ventricular filling and cardiac output falls.
Symptoms: JVD, paradoxical pulse, ↓CO, muffled heart sounds, circulatory collapse
Pericardiocentesis :draw off fluid, “tap”
Pericardial window : for recurrence of tampanode or pericarditis
Pericardiectomy – removal of the pericardium
Ischemia
Ischemia: oxygen supply insufficient to meet requirements of the myocardium
Infarction
Infarction: necrosis or cell death that occurs when severe ischemia is prolonged and irreversible damage to tissue results
Coronary artery disease
Includes stable angina pectoris and acute coronary syndromes
Angina
Temporary imbalance between the coronary arteries’ ability to supply oxygen and the cardiac muscles’ demand for oxygen.
Chronic Stable Angina (CSA)
Chronic Stable Angina (CSA)
-The ischemia is of limited duration and does not cause permanent myocardial tissue damage.
- Predictable, remains the same over several months.
- Doesn’t go past a 3 on a 0-10, predicatable, same treatment works usually nitro
Metabolic syndrome
Hypertension Low HDL High Triglycerides Elevated blood glucose Large waist size Increased pro-thrombotic state Increased pro-inflammatory state (C-reactive protein
Chest pain diagnostics
- Electrocardiogram (12 lead EKG)
- Stress Test
- Myocardial perfusion imaging
- -Magnetic resonance imaging (-MRI)
- Cardiac Catheterization (Angiogram)
- Cardiac Markers
- Troponin T
- Troponin I
- Myoglobin
- CPK MB
- C-reactive Protein
Chemical stress test
Chemical stress test: dubetamide, persentine
Gold standard for diagnosing chest pain
GOLD STANDARD: ANGIOGRAM ( look and see)
True or false
Dysrhythmias the leading cause of death in clients with MI who die prior to hospitalization
True
Which mind-body therapy intervention would it be most appropriate to implement for a patient reporting pain and anxiety in the hospital setting?
Music therapy
What percentage of Americans age 50 or older are estimated to use some form of complementary and/or alternative medicine?
44%
What health history do you want to know when doing a cardiovascular assessment ?
- Congenital Heart Disease
- Rheumatic Fever
- Heart Murmur
- Hypertension
- High cholesterol
- Diabetes Mellitus
- Confusion: not adequate oxygen perfusion -possibly because of a blockage in the carotid arteries
- Fatigue: Anemia
- Dental Status
Cardiovascualr medications
- Beta Blockers
- ACE Inhibitors
- Angiotensin Receptor Blockers
- Calcium Channel Blockers
- Antidysrhythmic Agents
- Diuretics
Beta blockers
Metoprolol, decreases heart rate, know HR, cardiac rhythm & BP before and after giving med. IV Esmolol can be used in emergency situations (on test)
ACE Inhibitors
Angitoensin converting enzyme, Lisinopril, cough is a side effect of ACE inhibitors, used to treat hypertension
Calcium Channel Blockers
Block calcium during action potentials, slows down impulses and rhythms, Verapamil
Antidysrhythmic Agents:
Digoxin, Amiodarone,
Diuretics
Lasix (furosemide), Bumex,
Look carefully at renal labs such as creatine, BUN and potassium when giving ACE inhibitors and ARBS
True
Ausculating the heart
Auscultation Heart Sounds S1 S2 S3 S4 Murmur: graded 1-6, 1 is the softest, 6 is the loudest, when they occur systolic/diastolic Pericardial Rub Prosthetic Valve : sounds like fingernails rubbing together
S3 and S4 can come and go
What is the hallmark of CHF?
S3 is the hallmark of CHF, when the extra fluid is gone the S3 is gone too
How to distinguish pericardial rub vs pleural rub
if you ask patient to hold breath and it continues its probably pericardial, rubs can come and go, can go after taking chest tubes out
How many sites do you listen to for the heart?
Listen to 4 or 5 sites, one on right and 4 on left going top to bottom of chest
Age related cardiovascular issues
- Calcification in valves
- Pacemaker cells decrease in number
- Conduction time increases
- Left ventricle increases
- Aorta and large vessels thicken and become stiffer
- Baroreceptors less sensitive : Barioreceptors are a lot less sensitive so give them a minte to adjust because their blood doesn’t go by barocrecptors as strong and they wiill feel faint
Classic heart attack symptoms
Nausea, vomiting, pallor, sweating, anxiety
Cardiac diagnostics
- Blood studies (Labs)
- Chest x-ray
- ECG
- Exercise/Stress Testing
- Echocardiogram/TEE
- Nuclear studies
- Magnetic Resonance Imaging
- Cardiac Catheterization
Serum markers of myocardial damage
- Troponin (10 min)
- Creatine kinase
- Myoglobin - muscle
- Serum lipids
- Homocysteine
- C-reactive protein
- Blood coagulation
What causes S1?
S1 is created by the closure of the mitral and tricuspid valves
What causes S2?
S2 is caused by the closing of the aortic and pulmonic valves…S2 is shorter than s1
What is paradoxical splitting?
Abnormal splitting of the S2 is referred to as paradoxical splitting and has a wider split heard on expiration. Paradoxical splitting is heard in patients with severe myocardial depression such as MI, left bundle branch block, aortic stenosis, aortic regurgitation, and righ ventricular pacing
