Week 1; Acute Care Cardiac Flashcards
BLOOD FLOW REVIEW (1)
The __ atrium receives deoxygenated blood from the body through the __ and __ __ __ and also receives blood from the heart muscle through the __ __.
right, superior, inferior, vena cava, coronary sinus
BLOOD FLOW REVIEW (2)
Most blood flows passively from the right atrium through the __ __ and to the __ __ during ventricular __
tricuspid valve, right atrium, diastole
BLOOD FLOW REVIEW (3)
The right atrium propels remaining venous return through the right ventricle during __ __
Atrial systole
BLOOD FLOW REVIEW (4)
The right ventricle is a __ __. It generates enough pressure to close the __ __, open the __ __, and propel blood into the __ __ and __.
Muscular pump, tricuspid valve, pulmonic valve, pulmonary artery, lungs
BLOOD FLOW REVIEW (5)
After oxygenated in the lungs, blood flows from the four pulmonary veins into the __ __. Then, through the __ __ into the __ __ during ventricular __.
Left atrium, mitral valve, left ventricle, diastole.
BLOOD FLOW REVIEW (5)
The left ventricle generates enough pressure to close the __ __ and open the __ __. Blood is then pumped into the __ and into __ __
mitral valve, aortic valve, aorta, systemic circulation.
Blood Flow Order
- superior vena cava
- right atrium
- tricuspid valve
- right ventricle
- pulmonic valve
- pulmonary artery to lungs
- lungs to pulmonic veins
- left atrium
- mitral valve
- left ventricle
- aortic valve
- aorta
Mean Arterial Pressure (MAP)
An average blood pressure in an individual during a single cardiac cycle. MAP is altered by cardiac output and systemic vascular resistance
MAP parameter
Must be at least 60 mm Hg to maintain adequate blood flow through coronary arteries and perfuse major organs (brain)
Systolic BP
The amount of pressure or force generated by the left ventricle to distribute blood into the aorta. It is a measure of how effectively the heart pumps and is an indicator of vascular tone
Diastolic BP
The amount of pressure against the arterial walls during the relaxation phase of the heart
Blood pressure regulation; autonomic nervous system:
Baroreceptors –
Chemoreceptors-
inhibition results in drop in BP
Hypercapnia, sensitive to hypoxemia; when stimulated, send impulses along the Vagus nerve to activate a vasoconstrictive response to increase BP
Blood pressure regulation; renal system
Kidneys
Help regulate cardiovascular activity. When renal blood flow decreases, pressure decreases and kidneys retain sodium and water. BP tends to rise because of fluid retention and activation to the renin-angiotensin-aldosterone mechanism
Blood pressure control; endocrine system
vasopressin from the pituitary gland that releases ADH
Blood pressure control; external factors
emotional factors also affect BP
Cardiovascular System Assessment
Patient history – examples: demographics, history of medical issues, smoking, drug use
Nutritional history
Family history and genetic risk
Current health problems
Pain, discomfort
Dyspnea, Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea
Fatigue
Palpitations
Edema
Syncope
Extremity pain
Cardiovascular system assessment; physical
General appearance – BMI/HT/WT
Skin
Cyanosis, rubor
Extremities
Clubbing, edema
Blood pressure
Hypotension and hypertension
Postural (orthostatic) hypotension
Precordium (area over heart) assessment
Inspection
Palpation
Percussion
Auscultation;
Normal heart sounds
Gallops and murmurs
Pericardial friction rub
Assessing chest discomfort
Quality and Severity
Location and Radiation
Duration and relieving factors helps distinguish but many times these mimic one another:
angina, MI, pericarditis, pleuropulmonary, esophageal-gastric, anxiety
Serum marker of myocardial damage: Troponin
Troponin T and troponin I – myocardial muscle protein released when injury, rise indicates necrosis or acute MI.
Serum marker of myocardial damage: creatine kinase (CK) –
exists in skeletal, heart muscle, brain and lungs Cardiac is specifically CK-MB, present within first 48 hours
Serum marker of myocardial damage: myoglobin –
general damage to skeletal or cardiac muscle (increased in numerous conditions including MI, Cardiac surgery, rhabdomyolysis, shock, chronic kidney disease, cocaine use)
Serum marker of myocardial damage: homocysteine –
risk factor for cardiovascular disease
Additional serum markers of myocardial damage:
High-sensitive C-reactive protein and serum lipids
Blood coagulation studies
PT/INR – prothrombin time and international normalized ratio
PTT – partial thromboplastin time
ABG –
arterial blood gas – tissue oxygenation, acid base status
Fluid and electrolyte balance – chem panel
Low serum K+- increased electrical instability, ventricle dysrhythmias, hypocalcemia can cause ventricular dysrhythmias, prolonged QT wave
Erythrocyte count (RBC) –
decreased in infective endocarditis, increased in heart diseases to compensate for decreased oxygen
H&H –
hemoglobin and hematocrit, decreased can lead to angina or aggravate heart failure
Leukocyte count(WBC) –
elevated in infection, and after MI
Diagnostic assessments
PA and lateral CXR
Angiography/Arteriography – by interventional radiology
Cardiac catheterization
ECG
Electrophysiologic study (EPS)
Stress test
Echocardiography
Pharmacologic stress echocardiogram (dobutamine or dipyridamole). These increase heart’s contractility and one coronary artery dilator.
Transesophageal Echocardiography – cardiac structure, transducer placed behind heart in the esophagus or stomach
Myocardial nuclear perfusion imaging (MNPI) - radioactive tracers for nuclear imaging
CT
MRI
Cardiac catheterization can measure
intracardiac pressures, take samples, detect valve problems, regurgitation.
Dysrythmias
Abnormal rhythms of the heart’s electrical system that can affect its ability to effectively pump oxygenated blood throughout the body. Some are life threatening. Result of disturbances in cardiac electrical impulse formation, conduction, or both.
Automaticity –
pacing function
Excitability –
ability to respond to impulses
Conductivity –
ability to send electrical stimulus from cell membrane to cell membrane
Contractility –
ability of atrial and ventricular muscle cells to shorten their fiber length in response to stimulation (mechanical activity of the heart)
Normal sinus rhythm
Rate: 60 to 100 beats/min
Rhythm: Regular
P waves: Present, consistent configuration, one P wave before each QRS complex
PR interval: 0.12 to 0.20 second and constant
QRS duration: 0.04 to 0.10 second and constant
Sinus arrhythmia
Variant of NSR; results from changes in intrathoracic pressure during breathing
Common dysrhythmias include
Premature complexes
Bradydysrhythmias
Tachydysrhythmias
Sinus dysrhythmias include
Sinus tachycardia
Sinus bradycardia
ID this rhythm
Sinus tachycardia
ID this rhythm
Bradycardia
ID this rhythm
Premature atrial contractions
ID this rhythm
Atrial flutter
ID this rhythm
Atrial fibrillation
ID this rhythm
Premature ventricular contractions
ID this rhythm
Ventricular tachycardia
ID this rhythm
Ventricular fibrillation
Pacemakers
Temporary pacing—invasive and noninvasive, permanent pacemakers
Premature atrial complexes
Ectopic focus of atrial tissue fires an impulse before next sinus impulse is due
Supraventriular tachycardia
Rapid stimulation of atrial tissue occurs at rate of 100 to 280 beat/min with mean of 170 beats/min (adults)
Paroxysmal supraventricular tachycardia rhythm is intermittent, terminated suddenly with or without intervention
Atrial fibrillation
Chaotic rhythm with no clear p wave and irregular ventricular response
Decreases ventricular filling and reduces cardiac output
**Alteration in cardiac function allows for blood to pool, placing the patient at risk
**CLOTTING CONCERNS such as embolic stroke, dvt, or pulmonary embolism (PE)
Etiology and genetic risk – heart disease, increases with age, htn, diabetes, European and African American ancestry
Most common dysrhythmia
What is the most common dysrhymia?
Atrial fibrillation
Biggest concerns with AFIB
CLOTTING CONCERNS such as embolic stroke, dvt, or pulmonary embolism (PE)
For PE and VTE
Assessment:
Analysis:
Planning and implementation:
Noticing, signs of poor perfusion, anxiety, 12 lead ECG
Interpreting, potential for embolus formation, potential for heart failure
Responding. preventing embolus formation, preventing heart failure
Non-surgical interventions for PE/VTE
Electrical cardioversion
Left atrial appendage closure
Radiofrequency catheter ablation
Bi-ventricular pacing
For PE/VTE
Surgical interventions
Maze procedure – open chest procedure often performed with a coronary artery bypass graft (CABG). This procedure is being replaced by catheter procures using minimally invasive form.
Common antidysrythmic drugs; class 1 sodium Channel Blockers act by
Decrease automaticity, slow conduction, prolong repolarization
monitor BP and HR, hypotension and bradycardia can occur, Monitor for CNS Side effects, dizziness
Common antidysrythmic drugs; Class II Beta Blockers act by
Decrease heart rate and conduction velocity
Monitor HR and BP; bradycardia and decreased BP are expected, assess for wheezing or SOB. Can cause bronchospasm, assess for insomnia, fatigue, dizziness
Ventricular dysrhythmias include
Premature ventricular complexes
Ventricular tachycardia
Ventricular fibrillation
Ventricular asystole
Ventricular dysrhythmias
More life-threatening than atrial dysrhythmias
Premature ventricular complexes
Result of increased irritability of ventricular cells—early ventricular complexes followed by a pause
Ventricular tachycardia (VTACH)
repetitive firing of irritable ventricular ectopic focus, usually at 140 to 180 beats/min
Ventricular fibrillation (V-fib)
result of electrical chaos in ventricles
Ventricular asystole
Also called ventricular standstill—complete absence of any ventricular rhythm
Management of cardiac arrest
CPR; maintain patent airway, ventilate with mouth-to-mask device/bag, start chest compressions
Advanced cardiac life support
Defibrillation
Asynchronous countershock that depolarizes critical mass of myocardium simultaneously to stop re-entry circuit and allow sinus node to regain control of heart; disrupts the chaotic rhythm
Early defibrillation is critical in resolving pulseless __ or __. It must not be delayed for any reason aft the equipment and skilled personnel are present. The earlier it is performed, the greater the chance of __
VT, VF, survival
Shockable rhythms
Ventricular fibrillation and ventricular tachycardia
AED
AED’s create an opportunity for laypersons to respond to cardiac arrest. They analyze the rhythm and shocks are delivered for ventricular fibrillation or pulseless ventricular tachycardia only
A 28-year-old woman with a history of hypertension and tachycardia comes to the hospital clinic stating that she doesn’t feel well. You connect her to a cardiac monitor and observe that she is in supraventricular tachycardia (SVT) with a rate varying between 160 and 180. She reports shortness of breath, palpitations, and weakness. She appears very nervous and anxious, and her BP is 88/56 mm Hg.
What is your priority intervention?
Oxygen should be administered at 2 L per nasal cannula.
Ten minutes later, the patient is still in SVT and reports substernal chest pain and dizziness.
Which action will you expect the physcian to take to treat the dysrhythmia?
a. Order a 12-lead ECG.
b. Perform carotid massage.
c. Administer amiodarone (Cordarone) IV push.
d. Instruct the patient to take several deep breaths.
ANS: B
The physician may perform vagal stimulation such as carotid massage, which may be successful in terminating the dysrhythmia; however, it may only be temporarily successful.
The patient’s SVT returns after 30 minutes. What medication do you anticipate will be ordered for the patient?
a. Magnesium sulfate 1 g IVP
b. Lidocaine (Xylocaine) 75 mg IVP
c. Adenosine (Adenocard) 6 mg IVP
d. Mexiletine (Mexitil) 300 mg PO q8h
Ans is C. Adenosine
The appropriate medication to administer is adenosine (Adenocard), which is the drug used for SVT. The nurse should give the medication as ordered to include 6 mg IV over 1 to 3 seconds followed by 20 mL saline flush.
Adenosine priority
The nurse should monitor the patient’s heart rate and rhythm carefully after administration of the medication. Be sure to have the crash cart available because a short period of asystole is common after administration. Bradycardia and hypotension may also occur.
The SVT resolves immediately after IV adenosine (Adenocard) is administered. Because the patient has experienced repeated episodes of symptomatic SVT, a cardiologist has been consulted and treatment options discussed.
What is the preferred treatment for recurrent SVT?
a. Atrial overdrive pacing
b. Synchronized electrical shock
c. Radiofrequency catheter ablation
d. Daily administration of diltiazem (Cardizem)
Answer: C
If SVT is continuous, the patient should be studied in the electrophysiology laboratory.
The preferred treatment is radiofrequency catheter ablation.
Radiofrequency ablation
a procedure that can cure many types of fast heart rates. Using special wires or catheters that are threaded into the heart, radiofrequency energy (low-voltage, high-frequency electricity) is targeted toward the area(s) causing the abnormal heart rhythm, permanently damaging small areas of tissue with heat. The damaged tissue is no longer capable of generating or conducting electrical impulses. If the procedure is successful, this prevents the dysrhythmia from being generated, thereby curing the patient.
Heart failure review
Inability of the heart to work effectively as a pump. Major types include left and right-sided and high-output
__ __ __ and other functional problems may lead to HF
acute coronary disease
Left-sided HF review
Also known as CHF, caused by HTN, CAD, valvular disease. Most HF starts off left sided and progress to right.
Systolic HF
Reduced ejection fraction; heart cannot contract forcefully enough during systole to eject adequate amounts of blood into circulation. EF drops below 40%. Tissue perfusion diminishes and blood accumulates in pulmonary vessels.
Normal ejection fraction
50-70%
Diastolic HF (left sided)
HF with preserved left ventricular function occurs when the left ventricle cannot relax adequately. Stiffening prevents the ventricle from filling with sufficient blood to ensure adequate cardiac output
Right-sided HF can be caused by
Right ventricle MI, pulmonary HTN, obstructive sleep apnea, right ventricle cannot empty completely, increased volume and pressure in venous system and peripheral edema
High output failure
CO remains normal or above average caused by increased metabolic needs of hyperkinetic conditions such as septicemia, anemia, hyperthyroidism.
Compensatory mechanisms d/t insufficient C/O
SNS stimulation, RAS system activation, chemical responses, myocardial hypertrophy
HF etiology
Systemic HTN most common as well as structural changes
Left sided failure s/s
• WEAKNESS
• FATIGUE
• DIZZINESS
• ACUTE CONFUSION (LOW FLOW)
• PULMONARY CONGESTION
• FROTHY, PINK-TINGED SPUTUM
• BREATHLESSNESS
• OLIGURIA
L=lung!!!!!!!
Right sided HF s/s
(R – ROCKS BODY WITH FLUID)
• JUGULAR VEIN DISTENTION
• INCREASED ABDOMINAL GIRTH
• DEPENDENT EDEMA, PERIPHERAL EDEMA
• HEPATOMEGALY
• HEPATOJUGULAR REFLUX
• ASCITES
• WEIGHT MOST RELIABLE INDICATOR OF FLUID
GAIN/LOSS
Hemodynamic monitoring
Direct assessment of cardiac fxn and volume status in acutely ill patients. A balloon tipped, flow-directed cath is inserted percutaneously or into a large vein. It is inflated and then blood flow carries the cath through the tricuspid valve, right ventricle, and pulmonary valve into the pulmonary artery. The balloon wedges into a branch of the pulmonary artery and the wedge pressure (PAWP) is obtained.
HOPE mnemonic used for interventions for HF patients
H = HEAD OF BED TO HIGH FOWLER’S 45 DEGREES
O = OXYGEN
P = PUSH LASIX, MORPHINE (DECREASES WORKLOAD ON
HEART) FUROSEMIDE OR BUMETANIDE
E = ENDING SODIUM AND FLUIDS, SALT RESTRICTION,
FLUID RESTRICTION, I&O. NUTRITION TEACHING
Nursing consideration when caring for HF patients
QUESTION ANY MD ORDER THAT ORDERS FLUIDS FOR HF
PATIENT. TED HOSE TO INCREASE CIRCULATION AND DECREASE
VENOUS POOLING AND INCREASE VENOUS RETURN.
Decreasing fatigue
energy management, cardiac rehab, functional level, activity plan
Preventing or managing pulmonary edema
Assess for early signs like crackles in the base of the lungs, dyspnea at rest, disorientation, confusion. High fowler’s position, O2 therapy, nitroglycerin, rapid-acting diuretics, IV morphine sulfate, cont. assessment
Indications for worsening HF
Rapid weight gain: 3 lbs a week or 1-2 lbs overnight, decrease in exercise tolerance lasting 2-3 days, cold sx, excessive nocturia, dyspnea/angina at rest, increased edema in feet, ankles, and hands
Infective endocarditis
Microbial infection involving the endocardium (lines inside of heart and forms the valves)
Risk factors for endocarditis
IV drug abusers, valve replacement recipients, systemic infxn, structural cardiac defects
S/s of infective endocarditis
Pain, murmur, HF, arterial embolization, neurologic changes, petechiae, splinter hemorrhages (black, longitudinal lines on nails)
Diagnostic assessment for infective endocarditis
Positive blood cultures, new regurgitant murmurs, evidence of endocardial involvement by echocardiography
Infective endocarditis treatment
Antimicrobials, activity with adequate rest, removal of infected valve, repair or removal of congenital shunts, repair of injured valves, draining of abscesses in heart or elsewhere
Myocarditis
Inflammation of the heart muscle; result of infectious process or autoimmune disorder, hypersensitivity rxn, or exposure to chemicals or toxins
Myocarditis s/s
Can be asymptomatic, chest pain, respiratory distress, fatigue, cyanosis, dysthymias, necrosis
Myocarditis dx
Based on hx, exam and myocardial biopsy
Myocarditis treatment
Correct identifiable causes, ACE inhibitors, diuretics, beta blockers, sodium restriction, steroids, immunoglobulins, anticoagulants, and bed rest.
Pericardium
Covers the heart and provides mechanical protection for the heart, as well as large vessels by reducing friction between the heart and surrounding structures
Substernal precordial pain
Radiates to left side of neck, shoulder, or back. It is grating and oppressive. It is aggravated by breathing, coughing, swallowing, and supine position. Sitting up and leaning forward relieve this pain.
S/s of pericarditis
Substernal precordial pain, pericardial friction rub, and cardiac tamponade
What can cause cardiac tamponade?
Pericarditis, chest injury, or MVA
Acute cardiac tamponade treatment
Increased fluid volume, hemodynamic monitoring, and pericardiocentesis, monitor for pericardial effusion
Pericardial effusion
Occurs when the space between the parietal and visceral layers of pericardium fills with fluid. Worsening effusion puts pt at risk for cardiac tamponade.
What is cardiac tamponade?
Compression of the heart d/t rapid fluid accumulation of the pericardium, leading to a sudden drop in CO
s/s of cardiac tamponade
Early: hypoxemia, restlessness, confusion, tachycardia (first sign of decreased CO)
Also JVD, paradoxical pulse, decreased hr, dyspnea, fatigue, muffled heart sounds, hypotension, circulatory collapse
Paradoxical pulse
a phenomenon in which the peripheral pulse is markedly diminished, or even abolished, during ordinary or quiet inspiration; it promptly reappears during expiration.
First sign of decreased cardiac output
tachycardia
Pericardial effusion nursing care
Assess pain, auscultate friction rub, position comfortably, anti-inflammatory drugs (avoid aspirin and anticoagulants together)
Pericardial effusion treatment
Fluid replacement, pericardiocentesis, hemodynamic monitoring
Rheumatic carditis
Sensitivity response from upper respiratory tract infection with group A beta-hemolytic streptococci, leading to inflammation in all layers of the heart, formation of Aschoff bodies, and impaired contractile fxn of myocardium, thickening of pericardium, and valvular damage.
Aschoff bodies
Nodules found in the hearts of individuals with rheumatic fever. They result from inflammation in the heart muscle and are characteristic of rheumatic heart disease.
Rheumatic carditis s/s
Tachycardia, cardiomegaly, new murmur, pericardial friction rub, precordial pain, prolonged PR, indications of HF, evidence of strep throat.
A 51-YEAR-OLD MAN CAME TO THE HOSPITAL 2 DAYS AGO FOR
RECURRENT EXACERBATION OF HEART FAILURE. HE WEIGHS 237
LBS AND IS 5ʹ8ʺ TALL. HE HAS IV ACCESS IN HIS LEFT FOREARM
AND IS ON OXYGEN AT 2 L PER NASAL CANNULA. WHEN YOU
ASSESS THE PATIENT, HE IS SITTING ON THE SIDE OF THE BED
AND APPEARS TO BE SHORT OF BREATH. HE TELLS YOU THAT HE
HAS JUST RETURNED FROM THE BATHROOM. HE IS SWEATING
AND HIS NASAL CANNULA IS LAYING ON THE BEDSIDE TABLE.
WHICH ACTION SHOULD YOU TAKE FIRST?
A. TAKE HIS VITAL SIGNS.
B. REPLACE THE NASAL CANNULA.
C. SIT HIM UP IN A BEDSIDE CHAIR.
D. CALL THE RAPID RESPONSE TEAM.
IFTEEN MINUTES AFTER THE OXYGEN IS REPLACED VIA
NASAL CANNULA AND HE HAS RESTED, THE PATIENT
DENIES BEING SHORT OF BREATH. YOU OBTAIN AN OXYGEN
SATURATION, WHICH IS 96%.
BASED ON THIS RESULT, WHAT SHOULD YOU DO NEXT?
A. CALL THE PROVIDER AS SOON AS POSSIBLE.
B. ENCOURAGE THE PATIENT TO TAKE SOME DEEP
BREATHS.
C. INCREASE THE OXYGEN LEVEL TO 5 L PER NASAL
CANNULA.
D. CONTINUE THE ASSESSMENT, AS 96% IS
CONSIDERED ACCEPTABLE.
AFTER ASSESSING THE PATIENT, YOU DOCUMENT THE FOLLOWINGJUGULAR VENOUS DISTENTION
2+ EDEMA IN FEET AND ANKLES
SWOLLEN HANDS AND FINGERS
DISTENDED ABDOMEN
BIBASILAR CRACKLES ON AUSCULTATION
PRODUCTIVE COUGH WITH PINK-TINGED SPUTUM
WHAT IS YOUR MOST LIKELY INTERPRETATION OF THESE FINDINGS?
A. BIVENTRICULAR FAILURE (BOTH LEFT AND RIGHT SIDED HEART FAILURE)
B. CARDIOMEGALY
C. LEFT-SIDED HEART FAILURE
D. RIGHT-SIDED HEART FAILURE
ANS: A
THE PATIENT HAS KEY FEATURES OF BOTH RIGHT-SIDED
AND LEFT-SIDED HEART FAILURE.
DURING THE EVENING SHIFT, THE PATIENT HAS A BEDSIDE
ECHOCARDIOGRAM, WHICH REVEALS AN EJECTION FRACTION OF
30%.
BASED ON THIS FINDING, WHICH MEDICATIONS MIGHT THE
PROVIDER ORDER? (SELECT ALL THAT APPLY.)
A. MULTIVITAMIN 1 PO EACH DAY
B. LISINOPRIL (ZESTRIL) 5 MG PO DAILY
C. DIGOXIN (LANOXIN) 0.25 MG PO DAILY
D. IBUPROFEN (ADVIL) 200 PO MG TWICE DAILY
E. FUROSEMIDE (LASIX) 20
ANS: B, C, E
COMMONLY PRESCRIBED DRUG CLASSES FOR PATIENTS
WITH HEART FAILURE INCLUDE ACE INHIBITORS
(LISINOPRIL), DIURETICS (FUROSEMIDE), NITRATES
(DIGOXIN), HUMAN B-TYPE NATRIURETIC PEPTIDES,
INOTROPICS, AND BETA-ADRENERGIC BLOCKERS.
LISINOPRIL TO LOWER BP, DIGOXIN TO INCREASE
CONTRACTILITY AND, AND LASIX AS DIURETIC.
