👩🏾🎓- Cardiac & Shock Test Flashcards
Arrhythmias can be affected by
Disease states CAD and ACS Electrolyte imbalance Hypoxia Drugs/medications Trauma
Motivation
This is your LAST lecture test of your associates level nursing career. You have come to far to punk out now ! Study this material like your life depends on it, cuz well IT DOES ! With GOD by your side you can and will do this !
-amen
Normal sinus rhythm
Rate: 60-100 bpm
Origin: SA node
Rhythm: P-P interval regular, R-R interval regular
P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike
PR Interval: 0.12-0.20 sec and constant from beat to beat
QRS Complex: 0.10 sec or less unless an intraventricular conduction delay
Sinus arrhythmia
Rate: Usually 60-100 bpm, but may be slower or faster
Origin: SA Node
Rhythm: Irregular, phasic with respiration; heart rate increases gradually during inspiration and decrease with expiration
P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike
PR Interval: 0.12-0.20 sec and constant from beat to beat
Sinus tachycardia
Origin, rate, pwave, Cause, symptoms, treatment
Origin: SA node
Rate: greater than 100bpm (in adults)
P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike. At very fast rates, differentiating a P wave from a T wave may be difficult.
Cause: activity, SNS stimulation, stress, pain, fever, anemia, hypoxia, hypotension, drugs, ACS, decreased CO, hypovolemia
Symptoms: likely asymptomatic, may experience palpitations, chest pain, fatigue, weakness, SOB, hypotension, anxiety
Treatment: determine and treat underlying cause
Sinus bradycardia
Origin, rate, pwave, Causes, symptoms, treatment
Origin: SA node
Rate: less than 60bpm/regular rhythm
P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike
Cause: well conditioned athletes, vagal stimulation (vomiting/straining), ACS, heart block, hypoxemia, drugs
Symptoms: possibly asymptomatic, may experience syncope, dizziness, confusion, weakness, hypotension, diaphoresis, SOB, CP
Treatment: determine and treat underlying cause! May include atropine or external pacing
Premature atrial contractions PAC’s
Origin, rate, pwave, cause, symptoms, treatment
Origin: anywhere in the atria ; often seen with NSR
Rate: variable/irregular rhythm
P Waves: Premature (occurring earlier than the next expected sinus P wave), positive (upright) in lead II, one before each QRS complex, often differ in shape from sinus P waves; may be flattened, notched, pointed, biphasic, or lost in the preceding T wave
Causes: irritation to the atria including stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol or drugs; electrolyte imbalance, damage to cardiac muscle
Symptoms: usually asymptomatic; May feel palpitations
Treatment: usually treatment of the PAC is not necessary, treatment for underlying disorder is considered
Supraventricular tachycardia SVT
Origin, rate, pwave, cause, symptoms, treatment
Origin: anywhere in the atria
Rate: 140+ bpm/regular rhythm
P Wave: One positive (upright) P wave precedes each QRS complex in lead II; P waves differ in shape from sinus P waves; an isoelectric baseline is usually present between P waves.
Causes: irritation to the atria including stress, fatigue, anxiety, caffeine, nicotine, etc
Symptoms: may feel palpitations and anxiety, if prolonged may deteriorate into angina, decreased CO, shock
Treatment: may not be necessary unless SVT is sustained. Vagal maneuver may stop rhythm. If necessary antidysrhythmics to slow conduction or cardioversion
Risks factors for afib & aflutter
Risk factors- htn, dm, hf, ACS, pe, age, male, valve disease, alcohol abuse, cardiac surgery
Two important things to note about afib & aflutter
HR must be controlled or CO will rapidly decrease
Patient at very high risk for cardioembolic event - must be on anticoagulant
Afib & aflutter
Origin, rate, causes, symptoms, treatment
Origin: anywhere or everywhere in the atria
Rate: variable, if elevated must be controlled
Causes: age + risk factors
Symptoms: asymptomatic when rate is controlled; if rate is uncontrolled symptoms of HF rapidly develop
Treatment: antidysrhythmics to control rate or convert to NSR; anticoagulants to prevent thrombus formation; cardioversion if no thrombus seen; ablation; pacemaker placement; MAZE procedure
Symptoms of HF
Fatigue Dizziness Activity intolerance Anxiety Palpitations Hypotension
Junctional dysthymias
Origin, rate, pwave, causes, symptoms, treatment
Origin: AV node or junctional area
Rate: 40-60bpm/regular rhythm
Pwave: absent; inverted of present; one P wave before each QRS complex if present
Causes: unknown, damaged electrical path
Treatment: usually none
Premature ventricular contractions PVC
Origin, rate, pwave, cause, symptoms, treatment
Origin: ventricle, one or various sites
Rate: variable/irregular rhythm
P Wave: Usually absent or, with retrograde conduction to the atria, may appear after the QRS (usually upright in the ST segment or T wave)
Causes: aging, irritation of ventricles, ACS, HF, hypoxemia, electrolyte imbalance, stress, nicotine, caffeine, alcohol, infection , drugs
Symptoms: may be asymptomatic, palpitations, diminished pulses with “run” of PVCs
Treatment: none if infrequent or no history of CV disease
monitor this may be a warning sign for further V-Tach
Idioventricular Rhythm
Origin, rate, pwave, cause, symptoms, treatment
(Agonal heartbeats)
Origin: ventricles
Rate: less than 40bpm
P Waves: usually absent or, with retrograde conduction to the atria, may appear after the QRS (usually upright in the ST segment or T wave)
Causes: hypovolemia, hypoxia, acidosis, potassium disturbances, overdose, hypothermia, tension pneumothorax, PE, ACS, tamponade
Symptoms: unstable and likely in shock, hypotensive, diaphoretic, unresponsive
Treatment: PREARE FOR CPR THIS IS A DYING ❤️
Ventricular tachycardia
Origin, rate, pwave, cause, symptoms, treatment
Origin: ventricle, one site
Rate: >40bpm
Pwave: absent
Causes: ACS, cardiomyopathy, potassium imbalance, hypoxia, HF, drug overdose, shock
Symptoms: maybe asymptomatic or experience palpitations initially, anxiety, chest pain, unresponsive
Treatment: THIS IS A LETHAL RHYTHM
Stable vs unstable
Treatment for ventricle tachycardia
Stable vs unstable
Stable: O2, vagal maneuver, antidysrhythmics
Unstable: COR, ACLS protocol including defibrillation & antidysrhythmics
Pulseless electrical activity PEA
origin, rate, pwave, cause, symptoms, treatment
Origin: anywhere
Rate: variable; seen on monitor only- looks like sinus rhythm but NO PULSE IS PALPABLE
Pwave: present and uniform, one pwave before each QRS complex
Cause; hypovolemia, hypoxia, acidosis, potassium disturbances, overdose, hypothermia, tension pneumothorax, PE, ACS, tamponade
Symptoms: unresponsive
Treatment: INITIATE CPR
Ventricular asystole
Origin, rate, pwave, cause, symptoms, treatment
Origin: none
Rate: 0/UTD
Pwave: absent
Causes: ACS, cardiomyopathy, potassium imbalance, HF, drug overdose, shock
Symptoms: unresponsive, pulseless, apneic, no BP
Treatment: THIS PATIENT IS IN FULL ARREST
(CPR, acls protocol, epinephrine, atropine, airway management, transcutaneous pacing, resolution of cause of known)
First degree AV block
Impulses from SA are slow to conduct to AV
Monitor for bradycardia or progressive block
Second degree heart block type I (wenckebach)
PR interval: longer longer longer drop that’s the way you wenkebach
Normal lab values
RAP or CVP: 2-8
PAS: 20-30
PAD: 8-15
PAOP: 8-12
CO: 4-8
Cardiac Index: 2.5-5
SVR: 800-1200
How often should shock patients receive vital signs
Q 15mins VS until stable and cardiac/tele monitoring
Commonalities in shock
Hypoperfusion
Hypercoagulability
Activation of inflammatory response (SIRS)
Body generally uses about what percent of circulating oxygen off of hemoglobin
25%
What does anaerobic metabolism cause
An increase in lactate lactic acidosis
Normal range: 0-1.5
What are some things that increase cellular oxygen demand
Decrease hemoglobin
Decrease O2 in body
Decreased volume
Pump problems
SIRS
symptoms
Systemic inflammatory response syndrome
Overwhelming infection
Symptoms- vasodilation, increased capillary permeability, microvascular clotting
SIRS criteria
2 or more of the following:
WBC > 12000 or < 4000 or 10% bands
Tachycardia
Temperature > 100.4 or < 96.8
Tachypnea
List the 4 classifications of shock
Initial
Compensatory (neural, endocrine, chemical)
Progressive stage
Refractory stage
Initial stage
The initial stage of shock is marked by hypoxia due to decreased deliver (DO2) to the cells.
Progressive stage
The progressive stage is marked by the failure of compensatory mechanisms to maintain adequate blood pressure and circulating fluid volumes…losing the battle, needs life support/medical assistance or they will die-still reversible
Refractory stage
The refractory stage is marked by prolonged inadequate blood supply to the cells, resulting in cell death and multisystem organ failure…prepare patient and family for death
Causes of cardiogenic shock
Number 1 cause: acute myocardial infarction
Cardiomyopathy
CHF
Arrhythmia
Papillary muscle rupture
Clinical symptoms of cardiogenic shock
Neuro, respiratory, CV, GI, GU, skin
Neuro: Anxious, restless, eventually decreased LOC
Respiratory: Crackles, rales, increased O2 demand, decreased pulse ox, tachypnea
CV: Chest pain, delayed capillary refill, weak pulses, S3, S4, JVD
GI: Nausea, vomiting, decreased bowel sounds
GU: Decreased urine output
Skin: Pale, cold, clammy, mottled
Cardiogenic shock diagnostics
A good patient history
Cardiac Cath
Echocardiogram
Chest X-ray
Elevated myocardial tissue markers
Creatine Phosphokinase Myocardial bands (CPK-MB), Troponin
Brain natriuretic peptide (BNP)
Brain natriuretic peptide
Hormone released by the ventricles in response to increased blood volume and blood pressure
What is the gold standard of cardiogenic shock treatment
Balloon pump
Increase O2 supply, decrease O2 demand
Cardiogenic shock management
“Strengthen the pump”
Increase O2 supply decrease O2 demand
•Coronary intervention PCI/OHS- fix the problem
•Balloon pump –gold standard can be done before or after tx
•Impella just got FDA approval
- Dobutamine, Primacor + inotropes decrease afterload however they increase oxygen demand can cause VT is some pts
- IF BP can tolerate after load reducers, vasodilators (ACEI)
- Careful with vasopressors, they increase SVR!
- Diuretics usually, if fluids its cautiously and small boluses i.e. 250 over an hour (diuretics decrease preload)
Cardiogenic shock
HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment
HR ⬆️
BP ⬇️
Skin: cold
SVR ⬆️
CVP ⬆️
PAWP ⬆️
LOC ⬇️
Treatment: O2 100% nonrebreather, prepare for intubation, fluids uses cautiously, drugs (dopamine, norepinephrine, dobutamine, diuretics) morphine sulphate, rest
Obstructive shock
Epidemiology, Pathophysiology
Epidemiology - extra cardiac disorders such as cardiac tamponade, tension pneumothorax, saddle pe
Pathophysiology- there is a physical barrier obstructing the great vessels or heart itself. Barrier to ventricular filling or emptying. Heart can’t pump effectively
Saddle pe
Diagnostic, s&s, treatment
Diagnostic- RV strain on echo, CT angio, VQ scan, +ddimer, abg low pao2 and low paco2
S&s- pleurtic chest pain (worse on inspiration) dry cough, possible cough up blood, anxiety, apprehension
Treatment- thrombolytics, embolectomy
Cardiac tamponade
Diagnostic , s&s, treatment
Excessive air, fluid or blood collecting in the pericardial sac
Diagnostic- echocardiogram, X-ray
S&s- tachypnea, tachycardia, dyspnea, Low urine output, confusion, cold, clammy extremities, pulsus paradoxus
Beck’s triad
Treatment- fluid and inotropes while waiting for definitive treatment, pericardialcentesis
Becks triad
Associated with cardiac tamponade 3 signs include:
Low arterial blood pressure, JVD, distant muffled heart sounds
(Muffled due to ⬆️ fluid)
Pulsus paradoxus
an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration.
Tension pneumothorax
Diagnostic, s&s, treatment
Accumulation of air or blood in the pleural space
Diagnostics- CXR
S&s- sudden onset cp, chest tightness, SOB, tachycardia, tachypnea, cough, desaturation, severe dyspnea, JVD, narrowing pulse pressure, absent or diminished breath sounds, tracheal deviation toward unaffected side
Treatment- needle decompression, chest tube
Obstructive shock
Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
HR ⬆️
BP ⬇️
Skin cold
SVR ⬆️
CVP ⬆️
PAWP ⬆️
Loc
Causes of hypovolemia
Hemorrhagic vs hypovolemic
Hemorrhagic- trauma, ruptured AAA/surgical, GI bleed, ectopic pregnancy
Hypovolemic- GI loss, burns, dehydration-poor intake, over use diuretics, third spacing, sirs (pancreatitis) DJA, hhnk, hhs
Hypovolemic shock diagnostics
Serum lactate
ABG (pH, base deficit)-fluid resuscitation
Metabolic studies (Chem 7, CMP)
CBC
H/H watch out for hemoconcentration
Coags (PT, PTT, INR)
May need CT angio, nuclear med, endo IR - stop bleeding
Lactate Acid
Draw, range
Lactic acid is used to test for sepsis
Draw- no turnicate because will ⬆️ anaerobic metabolism, put on ice
Range-
> 4 = death
Compensatory stage
Neural, endocrine, chemical
Body initiated compensatory mechanisms in an effort to maintain adequate volume, CO and blood flow to the tissues
Neural compensation- characterized by the detection of hypotension by barorecptors in the carotid sinus and aortic arch that results in the stimulation of the sympathetic nervous system and the release of catecholamines epinephrine and norepinephrine from the adrenal medulla
Endocrine compensation- or hormonal mechanisms that exert control over BP, include: angiotensin II, epinephrine and norepinephrine, aldosterone, and adh. Angiotensin II creates in response to ⬇️ BP is an end product of series of events
Chemical compensation- is produced through the reaction of chemoreceptors in the aorta and carotid arteries that are stimulated by low oxygen levels
Hypovolemic shock assessment
Neuro, respiratory, skin, cv, Gu
Neuro- ams, lethargy, unresponsive
Respiratory- rapid and deep respirations may become deep and labored as they deteriorate
Skin- cool, clammy
CV- pulse weak, threats, tachycardia then hypotension
GU- decreased urine output, urine is dark and concentrated
If invasive hemodynamic monitoring ⬇️ CVP, PCWP, CO and ⬆️ SVR
Hypovolemic shock if bleeding
Stop the bleeding
If bleeding nothing replaces blood (over treatment with NS/LR May make acidosis and coagulopathy worse)
Correct coagulopathy
Warm the patient
Monitor trends should be improving
Watch out for banked blood- potassium, 2,3 dpg, hypothermia, transfusion reactions
Hypovolemic shock medications- non bleeding patient
Volume resuscitation NS or LR
Colloids use in caution- SIRS
Add vsopressors only after fluid resuscitation initiated (don’t squeeze an empty tank)
Beware of dopamine , may ⬆️ HR
Hypovolemic shock
Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
Hr ⬆️
BP ⬇️
Skin- cold
SVR ⬆️
CVP ⬇️ due to dehydration
PAWP ⬇️
Loc ⬇️
UOP ⬇️
Treatment- O2 100% nonrebreather, 2 IV’s, fluid NS or LR
Hypovolemic shock
Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
Hr ⬆️
BP ⬇️
Skin- cold
SVR ⬆️
CVP ⬇️ due to dehydration
PAWP ⬇️
Loc ⬇️
UOP ⬇️
Distributive shock
Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone-fluid in the wrong space
Caused by loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, capillary leak
Blood volume distributed to interstitial tissues where it can’t circulate, deliver oxygen
Anaphylaxis, neurogenic, septic
Anaphylactic shock
Manifestations, management
Allergic reaction causing a release of histamine- resulting in widespread venous dilation, increased capillary permeability, and smooth muscle contraction
Vasodilation, ⬇️ venous return
Manifestations- early uticarial, redness. Airway compromise include sob, tachypnea, angioedema, wheezing, stridor, cyanosis and confusion due to hypoxia, hypotension
Management- treatment priorities include immediately removing the trigger, emergency airway management, antihistamines (benadryl), h2 blockers (Pepcid, zantac) corticosteroids, epinephrine SC (not IV) NS bolus if hypotension develops
Epinephrine administration in anaphylactic shock
.3 - .5 SQ/IM
No IV can redo shot in 5-10min if no improvement
Neurogenic shock
Epidemiology, pathophysiology, manifestations, treatment
Epidemiology- disruption of the sympathetic nervous system , spinal cord injury above T6
Pathophysiology- hypotension, bradycardia, hypothermia
Manifestations- skin is warm, dry and flushed due to systemic vasodilation. ⬇️ CO, CVP, PAOP, SVR
** different from other forms of shock **
Management- fluid administration, vasopressors, MAP 85-90 prevent secondary injury, watch for cord spread, temperature management, bowel and bladder protocols, may need airway/pacemaker assistance
Neurogenic
HR, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
HR ⬇️
BP ⬇️
Skin- warm, flushed
SVR ⬇️
CVP ⬇️
PAWP ⬇️
Loc ⬇️
UOP ⬇️
Treatment- IV fluids cautiously, drugs (atropine, norepinephrine, thrombolytics) transcutaneous pacing, ⬆️ hob
Anaphylactic
HR, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
HR ⬆️ with weak pulses
BP ⬇️
Skin- urticaria, angioedema, pale, cold
SVR ⬇️ due to systemic vasodilation
CVP ⬇️
PAWP ⬇️
Loc- sob, wheezing
UOP ⬇️
Treatment- remove trigger, O2 100% nonrebreather, IV fluids, drugs (epinephrine 0.3-0.5mg May repeat q 5-10mins, antihistamines, corticosteroids, bronchodilators)
P wave
Atrial depolarization
Atrial systole
QRS complex
Ventricle depolarization
Ventricle systole
T wave
Ventricle repolarization
Ventricular diastole
SIRS , sepsis , severe sepsis , septic shock
SIRS- temp > 38’c or <36’c, HR >90, RR >20 or PaCO2 < 32, wbc >1200 or <4000 or >10% bands
Sepsis- SIRS + infection
Severe sepsis- sepsis + end organ damage
Septic shock- severe sepsis + hypotension
What percentage of patients meet diagnostic criteria for SIRS on admission to hospital
68%
Severe sepsis
Criteria
Sepsis + organ dysfunction (one of the following criteria):
Lactate > 4 Oliguria < 0.5 ml/kg/hr Thrombocytopenia < 100,000 Coagulopathy: INR > 1.5 Creatinine > 2 Bilirubin > 2
Septic shock
Severe sepsis + hypotension despite adequate fluid resuscitation OR initial lactate of 4 or greater
Treatment 3 hours of presentation with septic shock
Measure lactate level
Obtain 2 blood cultures from 2 different sites (prior to administrating antibiotics)
Administer broad-spectrum antibiotics
Administer 30 ml/kg of crystalloid if patient hypotensive or lactate level at least 4 mg/dL
When would you and would not administer crystalloid at a rapid rate ?
Severe sepsis- optional
Hypotension, septic- required
Cardiogenic- no rapid
Treatment within 6hrs of presentation with septic shock
Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure >65 mmHg
Persistent hypotension after initial fluid administration OR initial lactate was >4 reassess volume status and tissue perfusion and document findings
Remeasure lactate within 6hrs if initial lactate elevated >2
How would you reassess fluid volume status
CVP
Hypoglycemia in a noninsulin receiving patient indicates what
Ominous sign of liver failure and gluconeogensis. Warrants emergency intervention and notification of the provider
What is something to remember about positioning and shock priorities
Don’t put patient in reverse trendeleburg or leave them flag for extended periods of time
What is something to remember about positioning and shock priorities
Don’t put patient in reverse trendeleburg or leave them flag for extended periods of time
Sepsis
HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment
HR ⬆️ bounding pulses
BP ⬇️
Skin- warm, flushed, fever (then changes to cold)
SVR ⬇️
CVP ⬇️
PAWP ⬇️
Loc ⬇️
UOP ⬇️
Treatment- meticulous handwashing, O2, prepare for intubation, mouth care, blood cultures, IV fluids, drugs (antibiotics, dopamine, norepinephrine)
Sepsis
HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment
HR ⬆️ bounding pulses
BP ⬇️
Skin- warm, flushed, fever (then changes to cold)
SVR ⬇️
CVP ⬇️
PAWP ⬇️
Loc ⬇️
UOP ⬇️
Treatment- meticulous handwashing, O2, prepare for intubation, mouth care, blood cultures, IV fluids, drugs (antibiotics, dopamine, norepinephrine)
Tranexamic acid
An antifibrinolytic Drug , has been shown to reduce blood loss in surgical patients
Tranexamic acid
An antifibrinolytic Drug , has been shown to reduce blood loss in surgical patients
Dopamine low dose, medium dose, high dose
Low dose 1-5 mcg/kg/min (⬆️ CO, contractility, renal flow)
Medium dose 5-15 (dose the same as low)
High dose 20-50 (vasoconstrict, severe ⬆️ BP, causes tachy arrythmias)
Dopamine low dose, medium dose, high dose
Low dose 1-5 mcg/kg/min (⬆️ CO, contractility, renal flow)
Medium dose 5-15 (dose the same as low)
High dose 20-50 (vasoconstrict, severe ⬆️ BP, causes tachy arrythmias)
Chronotropic drugs vs inotropic drugs
Inotropic drugs affect the force of cardiac contraction.
Chronotropic drugs affect the heart rate.
Chronotropic drugs vs inotropic drugs
Inotropic drugs affect the force of cardiac contraction.
Chronotropic drugs affect the heart rate.
In what shock state might lasix be appropriate
Cardiogenic
In what shock state might lasix be appropriate
Cardiogenic
If a patient had a low CVP what might be an appropriate intervention
Fluids (NS or LR)
Next vasopressor
Next impella
If a patient had a low CVP what might be an appropriate intervention
Fluids (NS or LR)
Next vasopressor
Next impella
Is heart failure ventricular or atrial failure
Ventricular failure
3 most common causes of HF and risk factors
Causes- hypertension , acute coronary syndrome , valve dysfunction
Risk factors- CAD, age, HTN, obesity, diabetes, smoking, high cholesterol, African American
Cardiac output, stroke volume, ejection fraction
Cardiac output- amount of blood the heart pumps per minute
Stroke volume- amount of blood the heart pumps per beat
Ejection fraction- percentage of blood ejected from left ventricle with each beat
Normal range of ejection fraction
50-70%
What 4 things affect CO
Preload- volume of blood in LV at the end of diastole
Afterload- (SVR) resistance heart must overcome to pump blood
Myocardial contractility
Heart rate
Left sided systolic (contraction) failure
Left ventricle has reduced function
- Can’t generate enough pressure
- Can’t eject end diastolic volume
- LV muscle overworks
- LV enlarges leading to hypertrophy
What is the hallmark sign of left sided systolic (contraction) failure
Decreased LV ejection fraction
EF < 40%
Left sided diastolic (filling) failure
Impaired ability of ventricles to fill during diastole
Usually the result of LV hypertrophy
Characterized by pulmonary congestion
Ejection fraction is normal
Systemic clinical manifestations of left HF
Systolic, diastolic dysfunction
Systolic- lightheadedness, marginal BP, change in pulses, diaphoresis, pale color, nocturia
Diastolic- exercise intolerance, S3 and S4 heart sounds
Pulmonary symptoms of left HF
Systolic, diastolic dysfunction
Systolic- tachypnea, DOE, bibasilar crackles, respiratory acidosis
Diastolic- orthopnea, DOE, bibasilar crackles, cough with frothy pink sputum, pulmonary edema, respiratory acidosis
Right heart failure may occur without LV dysfunction in presence of what ?
Pulmonary hypertension
Right ventricular MI
Pulmonary embolism
COPD
What is right heart failure characterized by
Increased volume and pressure in the venous system and peripheral edema
Right heart failure clinical manifestations
Venous congestion
Jugular vein distention
Peripheral edema
Hepatomegaly
Splenomegaly
Ascites
Oliguria, nocturia
Fatigue, weakness
Low BP
A client’s heart disease has resulted in a reduction of stroke volume. Which compensatory mechanism is expected
Increased heart rate
Acute vs chronic HF
Acute HF- heart is overwhelmed by abrupt alteration in cardiac function and unable to bring compensatory mechanisms into play
Chronic HF- compensatory mechanisms have time to partially or completely restore cardiac function
List 3 compensatory mechanisms of heart failure
Ventricular dilation and/or hypertrophy
Increased sympathetic response
RAAS responses lead to “remodeling”
Chronic HF clinical manifestations
Fatigue
Dyspnea (paroxysmal nocturnal dyspnea)
Tachycardia
Chest pain
Nocturia
Dusky appearance
Weight changes
Edema
Behavioral changes (restlessness, confusion, reduced attention span)
NYHA classifications of HF
Based on tolerance to physical activity
Class I: no limitations
Class II: slight limitation / mild symptoms with ordinary activities
Class III: marked limitation / marked limitation with physical activity but comfortable at rest
Class IV: inability to carry out any physical activity without discomfort / severe limitation and distress with physical activity or at rest
Nursing assessment of HF patient
Auscuaybof heart and lungs
Vitals
JVD
Edema
Weight gain
Ascites
Mental status
How is HF diagnosed
Chest X-ray ,Ekg , Bnp levels , ABG’s , Echocardiogram, EF and PA pressure, Cardiac catheterization , ANP, thallium scanning, hemodynamic monitoring
HF treatment goals
Improve CO
Reduce pulmonary and systemic congestion
Improve gas exchange and oxygenation
Prevent complications
Educate patient and family about disease
Maintain glycemic control
The nurses role in HF
How to prevent complications
Providing oxygen and rest
Controlling heart rate and BP
Daily weights
Monitoring I&O
Monitoring drug effects
Education about activity
Education about diet and fluid restrictions
Education about home care
Normal values part II (HF)
RAP or CVP: 2-6
PAP: 20-30/8-15
PCWP: 6-12
CO HR x SV: 4-8
SV HR x CO: 20-60
SVR ((MAP - RAP)*80)/CO): 900-1200
PVR ((PAP-PCW)*80/CO): 100-200
MAP (SBP + 2DBP)/3: needs to be > 60
PCWP offers a more accurate reading on which type of patient
Patient with pulmonary hypertension
Pulmonary catheter wedge pressure
PCWP treatment is too high or too low
Low- volume
High- diuretics, dilators
LVSW treatment if too high or too low
High- beta blockers
Low- positive inotropes
(Left ventricle stroke work)
SVR treatment if too high or too low
High- dilators
Low- vasopressors
Preload treatment if too high or too low
High- diuretics , dilators
Low- volume, arrhythmia control
Afterload if treatment is too high or too low
High- dilators, IABP
Low- vasopressors, IABP
Pharmacological management of HF
Primary goals of therapy:
- improve contractility = ⬆️ perfusion to maintain CO
- optimize heart rate
- reduce preload
- reduce afterload
- most HF patients will be on a combination of drugs to meet goals*
Types of drugs that optimize heart ❤️ rate
Positive inotropes
Antidysrhythmics
Beta blockers
Types of drugs that ⬇️ afterload
Acute care
Ace inhibitors , ARB’s
Acute care- nitrates, b type natriuretic peptides
Types of drugs that improve contractility
Acute care
Positive inotropes , beta blockers
Acute care- dopamine, dobutamine, b type natriuretic peptide
Drugs that ⬇️ preload
Acute care
Diuretics, ace inhibitors, arbs
Acute care- nitrates, morphine
Example of inotropic and human b-type natriuretic peptide drugs to treat HF
Inotropes- digoxin, dobutamine, dopamine
B type natriuretic peptide- natrecor, primacor
Cardiac glycosides and inotropic agents are used to treat HF and arterial dysrhythmias how
Work through
Positive inotropic action- increase force of contraction
Negative chronotropic action- decrease heart rate
Negative dromotropic action- decrease speed of conduction
Digoxin
Route, Half life, therapeutic range, contraindications, toxicity, antidote
Route- maybe given PO or IV
Half life- very long 30 to 40hrs
Therapeutic range- 0.5-2.0
Contraindications- DO NOT GIVE with ventricular dysrhythmias, 2nd or 3rd Degree HB
Monitor closely for hypokalemia
Toxicity- bardaycardia, blurry vision, yellow halos, diplopia, GI distress, drowsiness, confusion, heart block, dysrhythmias
Antidote- digibind
Beta blockers
Use, action, monitor for
Used to treat chronic HF, hypertension, dysrhythmias and ACS
Works through- interference with the RAAS to lower BP through vasodilation, lowers HR through sympathetic response
Monitor closely for coughing
Metoprolol
Route, contraindications, Monitor for, patient education
Cardioselective B1
Maybe given PO or IV
DO NOT give in presence of heart block or bradycardia
Monitor closely for- bradycardia, hypotension, orthostatic hypotension, heart block, cough, rebound hypertension
Patient education- BP & HR monitoring, avoid orthostatic hypotension, risk of hypoglycemia, caution with OTC preparations, sexual side effects, don’t skip doses, lifestyle changes
Ace inhibitor: lisinopril / arb: losartan
Action, contraindications, Monitor for, patient education
Action- both interfere with RAAS to lower BP through vasodilation
DO NOT take with potassium sparing diuretics
Monitor closely for- hypotension, orthostatic hypotension, rebound hypertension, reflex tachycardia, renal Function, ANGIOEDEMA
Patient education- BP monitoring, avoid orthostatic hypotension, caution with OTC preparations, sexual side effects, pregnancy risk, don’t skip doses, lifestyle changes, dry cough is likely
How do diuretics work
Reduce preload & afterload by lowering BP and/or removing excess fluid
Work by inhibiting the reabsorption of sodium
Furosemide
Excretes, contraindications, Monitor for, patient education
Water, Na, K, Ca & Mg are lost
Very potent, only use if less potent diuretics don’t work
Highly protein bound
DO NOT give with another loop diuretic
Monitor closely for- hypokalemia, electrolyte imbalance, hypotension, digitalis toxicity, hyperglycemia, renal Function, dehydration, I&O, falls
Patient education- take exactly as prescribed, potassium supplement, fluid restrictions, daily weight, monitor BP , monitor glucose levels
Hydrochlorothiazide
Excretes, contraindications, Monitor for, patient education
Water, Na, K, Mg, chloride are excreted, Ca is retained
More effective at lowering BP than fluid elimination
Not used in patients with renal dysfunction
Monitor closely for- hypotension, hypercalcemia, hypokalemia, electrolyte imbalance, digitalis toxicity, lithium toxicity, hyperglycemia, renal function, I&O
Patient education- take in morning, fluid restriction, monitor BP , monitor glucose levels
Spironolactone
Excretes, contraindications, Monitor for, patient education
Water and Na are excreted, K is retained
Least effective at removing excess fluid, often prescribed in combination with other diuretics
SHOULD NOT be given with acei’s or arb’s
Monitor for- hyperkalemia, electrolyte imbalance, renal function, hypotension, I&O
Patient education- take in morning, fluid intake, BP monitoring, daily weight
How does an IABP work
Inflates during diastole= ⬆️ contractility in aorta (t wave)
Deflates during systole= creates pressure to pull blood from left ventricle
Mitral valve stenosis
Valve doesn’t open completely
Results in ⬇️ blood flow from LA to LV, leads to pulmonary congestion and right side HF
Fatigue, DOE, orthopnea, NVD, hepatomegaly, edema afib
Rumbling apical DIASTOLIC murmur
Low pitch, loud sound heard best with bell of stethoscope
Mitral valve stenosis
Valve doesn’t open completely
Results in ⬇️ blood flow from LA to LV, leads to pulmonary congestion and right side HF
Fatigue, DOE, orthopnea, NVD, hepatomegaly, edema afib
Rumbling apical DIASTOLIC murmur
Low pitch, loud sound heard best with bell of stethoscope
Mitral valve regurgitation
Valve doesn’t close completely
(flappy doors, won’t stay closed)
Results in blood ejected from LV into LA during systole (returns during diastole), leads to increased volume in LV and left side HF
High pitched SYSTOLIC murmur at apex heard best with diaphragm of stethoscope
fatigue, DOE, orthopnea, afib, NVD, edema
Mitral valve regurgitation
Valve doesn’t close completely
(flappy doors, won’t stay closed)
Results in blood ejected from LV into LA during systole (returns during diastole), leads to increased volume in LV and left side HF
High pitched SYSTOLIC murmur at apex heard best with diaphragm of stethoscope
fatigue, DOE, orthopnea, afib, NVD, edema
Mitral valve is opened/closed during what
Open during diastole
Closed during systole
Mitral valve is opened/closed during what
Open during diastole
Closed during systole
Aortic valve is opened/closed during what
Closed during diastole
Open during systole
Aortic valve is opened/closed during what
Closed during diastole
Open during systole
Mitral valve prolapse
Valve prolapses into LA during systole (when it should be closed)
Mitral valve prolapse
Valve prolapses into LA during systole (when it should be closed)
Infective endocarditis
Risk factors, symptoms, complications
Infection of inner lining of heart or valves, most commonly strep/staph
Risk factors- structural cardiac defects, systemic infection, valve replacement, IV drug use, poor oral health
Symptoms & complications- HF, vegetation on valve, valve dysfunction, new or changing murmur, arterial embolization, splenic rupture, petechia, janeways lesions
Janeway’s lesions
Irregular, erythematous, flat, painless macular on the palms of hands and soles of feet.
Associated with infective endocarditis
Rheumatic carditis
Symptoms & complications
Inflammatory response following group A beta-hemolytic strep upper respiratory infections
Symptoms & complications- Aschoff bodies that develop scar tissue, cardiomegaly, new or changing murmur, pericardial rub, valve dysfunction, HF, tachycardia, EKG changes
PREVENTION IS KEY !
(once damage is done it is often irreversible)
Pericarditis
Risk factors & causes, symptoms & complications
Inflammation of or fluid accumulation in the pericardial sac
Risk factors & common causes- malignancy, infection, MI, cardiac surgery, connective tissue disorder, renal failure
Symptoms & complications- CP, pericardial rub, LHF in acute phase, RHF in chronic phase, fatigue, elevated WBC’s, EKG changes/afib, pericardial effusion, CARDIAC TAMPONADE!
Dilated cardiomyopathy
Cause, treatment
Chronic disease involving damage to cardiac muscle
Often causes by alcohol abuse, chemotherapy, infection, inflammation, inadequate nutrition
Ventricles are enlarged but wall thickness is normal, results in ⬇️ cardiac output, ⬆️ size of chambers, systolic dysfunction, fatigue, weakness, S3 and S4, signs of LHF
Treatment- inotropes, antidysrhythmics, heart transplant
Hypertrophic cardiomyopathy
S&s, treatment
Chambers are reduced, muscle is thickened
S&s- diastolic dysfunction, mitral regurgitation, syncope as cardiac output can’t increase with increased demand, dyspnea, angina, S4, sudden death common, HF S&s
Treatment- b blockers, Ca channel blockers, ablation, NO INOTROPES NO DILATORS
Restrictive cardiomyopathy
s&s, treatment
Ventricular wall rigidity
s&s- diastolic dysfunction, low cardiac output, orthopnea, venous enforcement
Treatment- remove fluid, low Na diet, improve pump
(transplant may be only treatment for late stage disease)
Heart transplant
Criteria, complications
Criteria- life < 1yr, < 65, normal PVR, no infection, psychosocial, no abuse
Bicaval vs orthotopic (2 p waves)
Debervation (only isuprel) - atropine won’t work
Complications- infection, tamponade, rejection
