Cardiac 2 PDF

Cardiac 2 Lead placement Interpreting ECG rhythm strips 1.) Heart rate: count the number of QRS complexes and times by 10 to get BPM. - atrial rate = number of P waves. - ventricular rate = total QRS x 10. 2.) Rhythm: sequential beating of the heart as a result of...

Cardiac 2 Lead placement Interpreting ECG rhythm strips 1.) Heart rate: count the number of QRS complexes and times by 10 to get BPM. - atrial rate = number of P waves. - ventricular rate = total QRS x 10. 2.) Rhythm: sequential beating of the heart as a result of the generation of electrical impulses. - regular pattern: interval between QRS (R) waves is regular. May vary by less than 0.06 seconds or 1.5 boxes. - irregular pattern: interval between the QRS (R) waves is not regular. Vary by longer than 0.06 seconds, or 1.5 boxes. - Basically, the measurement between the QRS (R) waves should all be the same. If they are not, the rhythm is considered irregular. 3.) P wave: produced when left and right atria depolarize. It is the first deviation from the isoelectric line. It should be rounded and upright. - P wave is the SA node pacing or firing at regular intervals. - normal duration is 0.06-0.12 seconds. - possible variation may result from a problem in conduction with the atria. 5 questions to ask... Are P waves present? Are P waves occurring regularly? Is there one P wave present for every QRS complex present?  Are the P waves smooth, rounded, and upright in appearance, or are they inverted? Do all P waves look similar? 4.) PR interval: measured from beginning of P wave to beginning of QRS. Measures the time interval from the onset of atrial contraction to onset of ventricular contraction. - normal interval is 0.12-0.20 seconds, or 3-5 small squares. - possible variation may result from a problem in conduction in the AV node, bundle of his, or bundle branches but can also be in the atria. 3 questions to ask... Are the PR intervals greater than 0.20 seconds? Are the PR intervals less than 0.12 seconds? Are the PR intervals consistent across the EKG strip? 5.) QRS complex Q wave: first negative (downward) deflection after P wave, short and narrow, not present in several leads. R wave: first positive (upward) deflection in QRS. S wave: first negative (downward) deflection after the R wave. - Normal duration < 0.03 seconds. - Possible variation may result from an MI which can cause wide Q waves. QRS interval: measured from beginning to end of QRS complex. Represents time taken for depolarization (contraction) of both ventricles (systole). - Normal duration < 0.12 seconds. - Possible variation may result from problem in conduction in bundle branches or in the ventricles. QT interval: measured from beginning of QRS to end of T wave, represents time taken for entire electrical depolarization and repolarization of the ventricles. - Normal duration 0.34-0.43 seconds. - Possible variation from problems affecting repolarization such as drugs, electrolyte imbalances, and changes in HR. 3 questions to ask... Are the QRS complexes greater than 0.12 seconds (in width)? Are the QRS complexes less than 0.06 seconds (in width)?  Are the QRS complexes similar in appearance? T wave: represents the time for ventricular repolarization. Usually, the first upward or positive deflection following the QRS complex. - Normal duration 0.16 seconds. - Possible variation may be from changes caused by fluid and electrolyte imbalances, ischemia, or infarction. U wave: usually not visible on EKG strips, if visible follows the T wave. Appears much smaller than the T wave, rounded, upright, or positive deflection following the QRS complex. - May indicate hypokalemia. Artifact: EKG waves from sources outside of the heart. Interference seen on the monitor or EKG strip. Causes may include patient movement or muscle tremor, loose or defective electrodes, or faulty EKG apparatus. Normal sinus rhythm: normal/regular rhythm of the heart set by the natural pacemaker of the heart called the sinoatrial node. Sinus bradycardia: regular but unusually slow heartbeat (less than 60 bpm). Often seen as a normal variation in athletes, during sleep, or in response to a vagal maneuver. - Rate: < 60 - Rhythm: regular  - P wave present before each QRS, upright and uniform - Length of PR interval: 0.12-0.20 - QRS complex: 0.06-0.10 Causes: hypoglycemia, hypothermia, hypothyroidism, medications, MI, sick sinus syndrome S/S: syncope (passing out), dizziness, SOB, cool, clammy skin Tx: If due to drugs, these may have to be stopped, held, or reduced. For the patient with symptoms, treatment consists of giving IV atropine (anticholinergic). If this is ineffective, transcutaneous pacing or a dopamine, atropine, or epinephrine infusion are options. The patient may need a permanent pacemaker. Sinus tachycardia: fast heartbeat related to rapid firing of the SA node. This may be normal for the patient. Will appear uniform and upright. High heart rate = high respiratory rate. Palpitations are possible. Try the vagal maneuver before meds. - Rate: > 100 - Rhythm: regular - P wave present before each QRS, upright and uniform - PR interval: 0.12-0.20 - QRS complex: 0.06-0.12 Causes: damage to heart tissues from heart disease, hypertension, hyperthyroidism, fever, stress, excess alcohol, caffeine, nicotine or drugs, side effect of medications, response to pain, imbalance of electrolytes (potassium) S/S: dizziness, SOB, lightheaded, palpitations, chest pain, syncope Tx: vagal maneuvers first, then IV beta blockers such as metoprolol, adenosine, or calcium channel blockers such as diltiazem. Unstable patients may need synch. cardioversion.  When the SA node fails to generate an impulse; atrial tissues or internodal pathways may initiate an impulse. The four most common atrial arrhythmias include: atrial flutter, atrial fibrillation, supraventricular tachycardia, and premature atrial complexes. Atrial fibrillation: uncoordinated electrical signal circles through the muscles of the atria, causing them to quiver (sometimes more than 400 times per minute), without contracting. The ventricles do not receive regular impulses and contract out of rhythm, the heartbeat becomes uncontrolled and irregular. Decrease in CO because of ineffective atrial contractions (loss of atrial kick) and/or a rapid ventricular response. Thrombi may form in the atria because of blood stasis. An embolized clot could move to the brain and cause a stroke. Patient will be on blood thinners. Causes: heart failure, COPD, pericarditis, heart disease, stress, high use of alcohol or caffeine. S/S: palpitations, irregular pulse that may feel too rapid or too slow, dizziness, fainting, fatigue, confusion, trouble breathing especially when lying down, tightness in chest. Tx: rate control, goal is to slow ventricular rate to 80-100 BPM. - Digoxin - Beta blockers - Calcium channel blockers (verapamil IV for quick rate control) - Antithrombotic therapy - Chemical or electrical cardioversion Check the patient’s BP if on amiodarone drip. Heparin stopped when PT returns to normal. Patients may have longer periods of Afib, causing palpitations. Tachypnea can cause fluid and electrolyte imbalances and acidosis. - Rate: 300-600 - Rhythm: irregular - No P wave QRS complex: < 0.12 seconds Atrial Flutter: coordinated rapid beating of the atria. Identified by recurring, regular, sawtooth-shaped flutter waves. - Atria beat faster than the ventricles. - 4:1 ratio, 4 f waves to each QRS. - Atrial rate could be as high as 350-600. Causes: heart failure, pulmonary embolism, MI, digoxin toxicity, CAD, valve probs, drugs, hyperthyroidism, cor pulmonale, hypertension S/S: palpitations, SOB, anxiety, weakness, angina, syncope Tx: cardioversion, anti arrhymics such as procainamide, diltiazem, verapamil, digitalis, or beta blocker to slow ventricular rate. Heparin to reduce incidence of thrombus formation. - Rate: 200-350, ventricular or = to 0.12 seconds) and bizarre in appearance. Risk of death if not fixed Rhythms that are lethal if untreated - Idioventricular rhythm (20-40 BPM) - Accelerated idioventricular rhythm (> 40 BPM) - Agonal rhythm (20 or less BPM) - Ventricular tachycardia (> 150 BPM) - Ventricular fibrillation - Torsade's de Pointes - Pulseless electrical activity (PEA) - Asystole (cardiac standstill) Premature ventricular contractions: contraction coming from an ectopic focus in the ventricles. Premature (early) occurrence of a QRS complex. Will appear wide and distorted in shape compared with compared with a QRS complex coming down the normal conduction pathway. - Same shape are unifocal PVC - Arise from different foci are multifocal PVC - Every other beat is a PVC, ventricular trigeminy - 2 consecutive PVCs is a couplet  - Associated with stimulants such as caffiene, alcohol, nicotine, epinephrine, and isoproterenol - Associated with electrolyte imbalances, heart disease, hypoxia, fever, exercise, and emotional stress - Usually not harmful in a patient with a normal heart - Assess for pulse deficit - More than 3 PVC in a row = vtach Tx: assess patient’s hemodynamic status to determine if treatment with drug therapy is needed. Drug therapy may include Beta blockers, lidocaine, or amiodarone. Accelerated idioventricular rhythm: last-ditch effort of the ventricles to try and prevent cardiac standstill. - SA node and AV node have both failed, no P wave - Rate is usually between 40-100 beats per minute - Cardiac output is compromised - Amiodarone should not be used Causes: drugs, MI, metabolic imbalances, hyperkalemia, cardiomyopathy S/S: pale, cool skin, weakness, dizziness, hypotension, alterations in mental status Treatment: usually tolerated well and doesn’t need treatrment. If pt becomes symptomatic (hypotensive, chest pain), atropine is an option. Temporary pacing may be needed. Rate: 40-100 Rhythm: regular No P wave QRS wide and distorted Ventricular tachycardia: a run of 3 or more PVCs. Occurs when an ectopic focus fires repeatedly and the ventricle takes control as the pacemaker. Different forms exist and depend on the QRS configuration. Life threatening dysrhythmia because of decreased CO and the possible development of VF, which is lethal. - Monomorphic VT (A) has QRS complexes that are the same in shape, size, and direction - Polymorphic VT occurs when the QRS complexes gradually change back and forth from one shape, size, and direction to another over a series of beats.  - Torsades de pointes (french for twisting of the points) is a polymorphic VT associated with a prolonged QT interval (B). Usually terminates spontaneously but frequently reoccur and may degenerate into Vfib. The hallmark finding is upward and downward deflection of the QRS complexes around the baseline. Causes: underlying heart disease, MI, meds that prolong QT interval, electrolyte imbalance, digitalis toxicity, CHF S/S: angina, syncope, light headed/dizzy, palpitations, shortness of breath, absent or rapid pulse, loss of consciousness, hypotension Tx: if no pulse begin CPR, if there is a pulse and pt is unstable, cardiovert and begin drug therapy. Amiodarone, lidocaine, antiarrhythmics, ablation, long term ICD. Rate: 150-250 Rhythm: regular or irregular No P wave QRS wide and distorted Ventricular Fibrillation: severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude. Represents the firing of multiple ectopic foci in the ventricle. The ventricle is quivering with no effective contraction, so no cardiac output occurs. Vfib is a lethal dysrhythmia. Patient will be conscious, defibrilation will be needed. Causes: AMI, untreated VT, electrolyte imbalance, hypothermia, myocardial ischemia, drug toxicity, trauma. S/S: loss of consciousness, absent pulse Tx: CPR with immediade defibrilation. Rate: not measurable Rhythm: irregular No P wave, QRS not measurable Asystole: the absence of ventricular electrical activity. P waves seen occasionally. No ventricular contraction because depolarization does not occur. This is a lethal dysrhythmia that needs to be treated immediately. - Patients may be unresponsive, pulseless, and apneic - Always assess the rhythm in more than one lead - Usually a result of advanced heart disease, severe cardiac conduction system problem, or end stage HF. - Generally, the patient with asystole has end-stage heart disease or has a prolonged arrest and cannot be resuscitated. - If the patient is dead and has no electrical activity, then no shock is needed. There are other issues going on outside of the heart. Treat with epinephrine instead. Brain damage and other tissues seen if pt lives. Pulseless electrical activity: situation in which organized electrical activity is seen on the ECG, but there is no mechanical heart activity, and the patient has no pulse. It is the most common dysrhythmia seen after defibrillation. - Prognosis is poor unless the underlying cause is quickly identified and treated. Causes: hypovolemia, hypoxia, metabolic acidosis, hyperkalemia, hypokalemia, hypoglycemia, hypothermia, toxins, cardiac tamponade, thrombosis, tension pneumothorax, and trauma. Tx: CPR, followed by drug therapy such as epinephrine, and intubation. Correcting the underlying cause is critical. inflammatory and structural heart disorders Infective Endocarditis: disease of the endocardium, innermost layer of the heart, and the heart valves. Associated with a poor prognosis and a decreased life expectancy. - Increase in the number of cases largely linked to an increase in IV drug use - Subacute affects those with preexisting valve disease - Acute form affects those with healthy valves - Most commonly caused by staphylococcus aureus and streptococcus viridians Risk factors: previous history of valve or heart issues such as rheumatic heart disease, congenital heart disease, or marfan’s syndrome. - Open wounds, abscesses, procedures, infected needles, prosthetic valves, prior history Occurs in three stages (bacteremia, adhesion, vegetation) - Vegetation is masses of bacteria, fibrin, and platelets that form on the heart valves or the endocardium in patients with endocarditis. Parts of the mass can break off and leak into the bloodstream (embolization). - Left sided vegetation can move to brain, kidneys, spleen, and extremities. - Right sided vegetation can move to the lungs (PE) Any kind of damage to the heart will result in HF, dysrhythmias, kidney probs, night sweats, and shortness of breath. Clinical manifestations: - Chills - Roth spots (on the eye) - Malaise - Fatigue - Anorexia - Splinter hemorrhages (under fingernails) - Petechiae - Osler’s nodes (tender purple/pink nodules usually on fingers and/or toes)  - Janeway’s lesions (painless, small flat hemorrhages on the palms or soles) - Fever Assess for heart disease, previous hx of IE, staph or strep infection, IV drug use, weight changes, cough, night sweats, joint/muscle tenderness, petechiae, splinter hemorrhages, Osler's nodes, Janeway's lesions and alcohol abuse. Diagnostic studies: - 2 to 3 blood cultures in one hour all from different sites - ESR, C-reactive protein, CBC - Echo will show vegetation Dx: will include 2 major criteria and 1 minor, 1 major and three minor, or 5 minor. - Major criteria: positive blood culture, new valvular vegetation - Minor criteria: predisposing heart condition (rheumatic fever) or IV drug use This is why we need to stress how important it is to take and finish the antibiotics prescribed to you after dental procedures, respiratory tract incisions, tonsillectomy/adenoidectomy, and surgical procedures that involve the skin or musculoskeletal tissue Tx: after accurate identification of the organism is completed to determine which type of antibiotic will work best, IV antibiotics for 4-8 weeks will be given inpatient. Most likely vancomycin or penicillin. - Two sets of blood cultures should be done every 24-48 hours until the infection is cleared - Follow up with echo and inflammatory markers (blood work) at 1,3,6, and 12 months after antibiotics are finished. - Valve replacement if needed Patient teaching: stress need to stay away from people with infections, avoid stress and fatigue, plan rest periods, regular dental visits, importance of completing antibiotic regimen, and drug rehab. Teach to monitor body temp (can alternate tylenol and ibuprofen for fever), s/s of complications, nature of disease and how to prevent reinfection, stress follow up care, good nutrition, and prompt treatment of common infections. - Assess home setting and coping strategies - Assess IV lines (DO NOT LET PT LEAVE WITH IV) - Compression stockings  - Deep breathe and cough every 2 hours xcd Pericarditis is a condition caused by inflammation of the pericardial sac (pericardium), often with fluid (10-15mL) accumulation. - Most often, the cause is unknown or idiopathic. - Acute pericarditis develops rapidly, causing the pericardial sac to become inflamed and leak fluid. (Pericardial effusion) The characteristic finding is inflammation. - Subacute pericarditis occurs weeks to months after an event. - Chronic pericarditis lasts longer than 6 months. Myocardial infarction causes 5-8% of acute pericarditis cases. Post MI syndrome (Dressler syndrome) can occur 4-6 weeks after a transmural MI. This syndrome is more common after a large anterior artifact. - Viral pericarditis can be seen after a respiratory or GI illness. Clinical manifestations - Progressive, severe, sharp chest pain that is worse with deep respiration and when laying flat. Sitting up and leaning forward will relieve the pain. - The pain may also radiate to the neck , arms, or left shoulder, similar to angina.  The hallmark finding in pericarditis is the pericardial friction rub. This is a scratching, grating, high-pitched sound believed to result from friction between the pericardial and epicardial surfaces. Best heard at the lower left sternal border with the patient leaning forward. Complications - Major complications include pericardial effusion and cardiac tamponade. Pericardial effusion is a build-up of fluid in the pericardium. - Pulmonary tissue compression can cause cough, dyspnea, and tachypnea. - Phrenic nerve compression can cause hiccups. - Laryngeal nerve compression can result in hoarseness. - Heart sounds will be distant and muffled. - Cardiac tamponade develops as the pericardial effusion volume increases and compresses the heart. The speed of fluid accumulation affects the severity of clinical signs. The patient may report chest pain and confusion. - It can occur acutely from rupture of heart or trauma, or sub acutely from renal failure or cancer. - Pulsus paradoxus can also be present. This is a large decrease in systolic BP during inspiration. Diagnostic studies - ECG reveals a widened ST segment - An echo can determine the presence of a pericardial effusion or cardiac tamponade. - Doppler imaging and color mode can diagnose constrictive pericarditis. - CT scan and MRI can visualizr the pericardium and pericardial space. - Common laboratory findings indicate leukocytosis and increased CRP with ESR. - Troponin levels may be increased. Treatment - Antibiotics will treat bacterial pericarditis and NSAIDs control pain and inflammation. - Steroids may be used for patients with pericarditis from lupus, patients who were previously on them, or patients who do not respond to NSAIDs. - Pericardiocentesis is usually done for pericardial effusion with acute cardiac tamponade, purulent pericarditis, or suspected cancer. - Give steroids with milk, avoid alcohol, PPIs may be given to reduce stomach acid. Myocarditis - Focal or diffuse inflammation of the myocardium - Causes include viruses, bacteria, fungi, radiation therapy, and pharm/chemical factors. - As the infection progresses, an autoimmune reaction occurs, causing further destruction of myocytes. - Myocarditis will result in heart dysfunction. - Dilated cardiomyopathy can occur. Clinical manifestations - May begin without any symptoms - Progressive HF - Dysrhythmias - Sudden cardiac death - Fever, fatigue, malaise, myalgias  - Pharyngitis - Dyspnea - Lymphadenopathy - Nausea/vomiting - Early cardiac signs appear 7-10 days after viral infection because pericarditis often accompanies myocarditis. The signs of this include chest pain with a pericardial friction rub and effusion. - Late cardiac signs refer to the development of HF with an S3 sound, crackles, JVD, syncope, peripheral edema, and angina. - ECG changes are often nonspecific but reflect associated pericardial involvement, such as ST segment changes. - Endomyocardial biopsy may be done to confirm myocarditis. Treatment Consists of managing symptoms - ACE inhibitors and Beta blockers used if the heart is enlarged or to treat HF. - Diuretics reduce fluid volume and preload. - If the patient is not hypotensive, IV drugs such as nitroprusside may be used to reduce afterload and improve cardiac output by decreasing resistance. - Digoxin improves heart contractility and reduces HR. Used cautiously in patients with myocarditis because of increased sensitivity to the adverse effects such as dysrhythmias and the potential toxicity. - Anticoagulants reduce the risk of clot formation from blood stasis in patients with low ejection fraction. - Myocarditis predisposes to digoxin toxicity, use cautiously. Rheumatic fever & Rheumatic heart disease An acute inflammatory disease that can involve all of the heart layers. Chronic scarring and deformity of the heart valves resulting from Rheumatic fever - Occurs as a complication 2-3 weeks after a group A streptococcal pharyngitis. - An abnormal immune response to strep - Affects the heart, skin, joints, and CNS. Rheumatic heart disease, caused by Rheumatic fever, mainly affects children and young adults. About 50% of all RF episodes are rheumatic pancarditis, involving all layers of the heart (endocardium, myocardium, and pericardium). - Rheumatic infective endocarditis (IE) is mainly found in the valves in vegetation forms. The lesions initially create a thickening of the valve leaflets. - Valve leaflets may become calcified, resulting in stenosis. - Some of the valve leaflets may not close properly, resulting in regurgitation. - Mitral and aortic valves are most often affected. - Major criteria such as arthritis or polyarthritis are required for diagnosis, minor criteria of fever, monoarthralgia, or evidence of labratory findings of A streptococci. Complications Chronic rheumatic carditis results from changes in valve structure months to years after an episode of RF. Rheumatic IE can result in fibrous tissue growth in valve leaflets and chordae tendineae with scarring and contractures. The mitral valve is most often involved. The aortic and tricuspid valves may be affected. Diagnostic studies o No single diagnostic test exists for RF. An echocardiogram may show valvular insufficiency and pericardial fluid or thickening. o A chest x-ray may show an enlarged heart. o The most consistent ECG change is a prolonged PR interval from delayed AV conduction. Care/ Treatment Antibiotic therapy does not change the course of the acute disease or the development of carditis. o Eliminates residual group A streptococci in the tonsils and pharynx and prevents the spread of organisms through close contact. Salicylates, NSAIDs, and corticosteroids are the 3 inflammatory agents most widely used to control fever and joint manifestations. Interprofessional Care Rheumatic Fever Diagnostic Assessment History and physical assessment Laboratory studies (Table 40.7) Chest x-ray Echocardiogram ECG Management Bed rest or limited activity Drug therapy Antibiotics NSAIDs Salicylates Corticosteroids Nursing management Inspect the skin for subcutaneous nodules and erythema marginatum. Palpate for subcutaneous nodules over all bony surfaces and along extensor tendons of the hands and feet. T he nodules range in size from 1 to 4 cm and are hard, painless, and freely movable. Erythema marginatum can occur on the trunk and inner aspects of the upper arm and thigh. Assess for these bright pink maculae in good light because the rash is hard to see, especially in patients with dark skin. Early detection and immediate treatment of group A streptococcal pharyngitis can prevent RF. Treatment with an initial dose of intramuscular Benzathine Penicillin G is the most widely used antibiotic to treat. If the patient is allergic to penicillin, a narrow-spectrum cephalosporin (e.g., cephalexin), clindamycin (Cleocin), or azithromycin (Zithromax) Therapy requires strict adherence to the full course of treatment. Acute Care Give antibiotics as prescribed to treat the streptococcal infection. Teach the patient that completing the full course of antibiotics is vital to successful treatment Promote optimal rest. Give salicylates, NSAIDs, and corticosteroids as prescribed for joint pain. Implement measures to manage fever (see Table 12.5). Check Your Practice Ambulatory Care The aim of secondary prevention is to stop a recurrence of RF. Prior history of RF makes the patient more susceptible to a second attack after a streptococcal infection. The best prevention is treatment with prophylactic antibiotics. Patients with RF without carditis need prophylaxis until age 20 and for a minimum of 5 years. Patients with rheumatic carditis and residual heart disease (e.g., persistent valve disease) need lifelong prophylaxis.  Tell the patient to seek medical care for symptoms, such as excessive fatigue, dizziness, palpitations, unexplained weight gain, or exertional dyspnea. EKG is a graphic record of the heart’s electrical activity, or it’s conduction of impulses. The P wave represents depolarization of the atria, a problem with the P wave indicates swelling of the atria. The QRS complex represents depolarization of the ventricles, and atrial repolarization. If QRS wave is prolonged, this indicates that ventricular conduction delay is occurring. The T wave reflects repolarization of the ventricles. Inverted T wave often seen after myocardial damage. - P wave: 0.06-0.12 (variation indicates problem in atria) - PR interval 0.12-0.20 (variation indicates problem in AV node, bundle of his, or atria) - QRS variation: MI may develop if wide and deep Q wave. - QRS interval (beginning to end of QRS complex), represents time taken for depolarization (contraction) of both ventricles (systole) (0.20 seconds), everything else normal. - Can be normal for some patients or caused by MI or calcium channel blockers, beta blockers, or digoxin. - The patient may or may not have symptoms, continue to monitor either way to be sure it doesn't progress to a worse block or abnormal rhythm. 2nd degree, type 1: electrical signal going from the atria to the ventricles is slowing down until it doesn’t stimulate the ventricles to contract. QRS complex will be missing here and there, from gradually widened PR interval. When QRS is present, it will be normal. - Can be caused by MI, calcium channel blockers, beta blockers, digoxin. - Treatment: assess for symptoms, if none preset continue to monitor. Meds that slow the AV system may be stopped. Be sure patient is not having MI. - If symptoms are present, activate rapid response, may need atropine or temporary pacing. 2nd degree, type 2: Ventricular rate will be slower, due to missed QRS complexes. - Can be caused by MI, CAD, or meds such as calcium channel blockers, beta blockers, digoxin that show the AV conduction system. Ventricular rate is lower than previous type, more likely to have symptoms since lower cardiac output. - Treatment: temporary pacing, permanent pacemaker. 3rd degree: electrical signal from the atria doesn’t make it to the ventricles. - Regular P waves, making the atrial rhythm regular and its rate normal. QRS complexes will be regular, making the ventricular rhythm regular. - Fewer QRS complexes than P waves. - Causes: congenital, heart disease, MI, digoxin toxicity, structural damage, heart valve problem. - Symptoms will likely be present: low cardiac output, low blood pressure, weak pulse, mental status changes, pale clammy skin. - Treatment: activate rapid response, possibly give atropine to help the heart pump effectively.