👩🏾🎓- 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
