Cardiovascular

OBJECTIVE 1 — Cardiovascular Disorders

Your objective says you need to know etiology, risk factors, pathophysiology, and clinical manifestations for the listed disorders. Your lecture also repeatedly connects these with medical management, complications, and nursing care.

1. HEART VALVE DISORDERS

Basic idea

A valve disorder interferes with the normal one-way movement of blood.

Stenosis = valve opening is narrowed → blood has difficulty moving forward.

Regurgitation/insufficiency = valve does not close properly → blood flows backward.

Over time, either problem reduces cardiac efficiency/stroke volume and increases the workload of the heart. This can eventually produce ventricular hypertrophy and heart failure. Left-sided valve disease can increase pulmonary pressures and decrease cardiac output.

AORTIC VALVE DISORDERS

The aortic valve normally allows blood to move:

Left ventricle → aorta

Aortic stenosis

The opening becomes narrowed, creating resistance to blood leaving the LV.

Risk factors/causes from your study guide include:

• Degenerative calcification

• Inflammatory changes

• Atherosclerosis

• Commissural fusion/adhesions

As resistance increases, the LV must work harder → LV hypertrophy can develop → stroke volume/cardiac output eventually decrease.

Advanced manifestations include:

Exertional dyspnea, fatigue, pulmonary edema, dizziness, syncope and angina.

The guide specifically emphasizes low pulse pressure <30 mmHg in advanced disease.

Aortic regurgitation

The valve does not close completely → blood moves backward from the aorta into the LV.

Risk factors/causes:

• Infective endocarditis

• Rheumatic endocarditis

• Congenital defects

• Syphilis

• Dissecting aortic aneurysm

• Trauma

• Valve deterioration

Clinical manifestations listed include:

Forceful heartbeat, carotid/temporal pulsations, exertional dyspnea, orthopnea, fatigue, diastolic murmur, widened pulse pressure and water-hammer pulse.

Diagnostics

Know:

CXR: chamber enlargement/LVH.

12-lead ECG: chamber hypertrophy and rhythm abnormalities.

Echocardiogram/TEE: evaluates valve structure/function, EF and degree of regurgitation.

Angiography/cardiac catheterization: evaluates coronary arteries and helps confirm valvular disease.

Treatment

Your guide lists:

• Mechanical valve replacement

• Tissue valve replacement

• Antidysrhythmics

• Valvuloplasty

• Commissurotomy

• Balloon valvuloplasty

• TAVR for high-risk clients

• Afterload reduction

• ACE inhibitors

• Certain calcium-channel blockers

• Management of HTN, diabetes and hypercholesterolemia

Mechanical valve: lifelong anticoagulation; study guide gives therapeutic INR 2–3.5.

Tissue valve: used in selected populations such as pregnant, geriatric or pediatric patients; your mitral section states tissue valves may need replacement in 7–10 years.

Your guide also emphasizes infection prevention/prophylactic antibiotics before dental procedures.

Patient teaching

Know:

• Daily weights

• Recognize HF symptoms

• Follow prescribed exercise

• Sodium restriction

• Limit caffeine/alcohol

• Energy conservation

• Wound care

• Read OTC medication labels

• Infection prevention/dental care

Interprofessional resources include cardiology, respiratory therapy, nutrition and rehabilitation.

MITRAL VALVE DISORDERS

Three types are listed:

Mitral stenosis = valve too narrow.

Mitral regurgitation = valve leaks/backward flow.

Mitral valve prolapse (MVP) = floppy valve; the guide associates this with congenital disease in children.

Poor mitral valve function → reduced cardiac output → increased cardiac workload → heart enlargement/LVH → pulmonary fluid accumulation → dyspnea/PND.

Risk factors

• Rheumatic fever/strep infections

• Lupus/connective-tissue disease

• HTN

• Atherosclerosis

• Congenital heart disease

Clinical manifestations

• SOB, especially with activity

• Fatigue

• Weakness

• Palpitations

• Atrial fibrillation

• Orthopnea

• PND

• Heart murmur

• Edema

• JVD

• Hepatomegaly

Diagnostics

Echo = best test

Also:

• ECG → rhythm/hypertrophy

• CXR → enlargement

• TEE → detailed valve visualization

• Cardiac cath/angiography

Treatment

• Valve repair/replacement

• ACE inhibitors

• ARBs

• Beta blockers

• Diuretics

• Digoxin

• Cardioversion for AFib

• Anticoagulation

Nursing care

Monitor for emboli and bleeding, daily weights, potassium with diuretics, heart rhythm/sounds, oxygen needs, fluid/sodium intake and activity tolerance.

Encourage rest/energy conservation.

Major complications emphasized are heart failure and atrial fibrillation.

2. PERICARDITIS

Definition

Inflammation of the pericardium.

Your lecture lists several classifications/types:

• Acute

• Chronic

• Recurring

• Adhesive/constrictive

• Serous

• Purulent

• Calcific

• Fibrinous

• Sanguineous

• Malignant

• Exudative/non-effusive

Recurring inflammation can cause:

Repeated inflammation → pericardial thickening → decreased elasticity → constrictive pericarditis → decreased cardiac output.

Restricted diastolic filling → increased systemic venous pressure → peripheral edema and potentially hepatic failure.

Dressler syndrome

Can occur 10 days–2 months after an acute MI.

Your lecture describes it as an immune response to cardiac injury and notes that it may occur after:

• AMI

• Heart surgery

• Chest injury

Manifestations:

Chest pain + fever + SOB.

Pathophysiology

Inflammation can cause fluid accumulation:

Pericarditis → pericardial effusion → increased pericardial pressure → cardiac compression → decreased ventricular filling → decreased CO → possible cardiac tamponade.

Constrictive pericarditis similarly prevents adequate diastolic filling.

Clinical manifestations

The patient may initially be asymptomatic.

Important findings:

Chest pain

• Constant

• Worse with deep inspiration

• Worse lying down

Pericardial friction rub

• Creaky/scratchy

• Best heard at left lower sternal border

• Synchronous with heartbeat

• Best heard at end of exhalation

Other findings:

• Mild fever

• ↑ WBC

• Anemia

• ↑ ESR

• ↑ CRP

• Nonproductive cough

• Hiccups

• Dyspnea

• Respiratory splinting

• Compensatory tachycardia

• HF symptoms

Your lecture also mentions a ~10-mmHg inspiratory systolic BP difference in relation to paradoxical BP/pulse.

Diagnostics

• History/physical

• Echocardiogram

• TEE

• CT

• MRI

ECG: ST elevation in all leads is emphasized in the lecture, along with PR changes and possible atrial dysrhythmias.

Treatment

• Treat underlying cause

• Analgesics

• Colchicine

• Bed rest if CO is impaired

• Pericardiocentesis if significant fluid accumulation/tamponade

Fluid removed during pericardiocentesis can be cultured/evaluated for bacterial, viral or neoplastic disease.

3. PERICARDIAL EFFUSION & CARDIAC TAMPONADE

Pericardial effusion

Accumulation of fluid in the pericardial sac.

As fluid/pressure increases:

↑ pericardial pressure → atrial compression → ↓ venous return → ventricles cannot fill/distend → ↓ stroke volume/CO → tamponade → obstructive shock.

Normal CO listed in your lecture:

4–8 L/min at rest.

A slowly accumulating effusion can become quite large before symptoms occur because the pericardium has time to stretch.

A rapidly developing effusion is much more dangerous because there is no time for adaptation.

CARDIAC TAMPONADE = know Beck's triad

1. Hypotension → decreased CO

2. Distended neck veins/JVD → increased pericardial pressure

3. Muffled heart sounds

This is a very testable combination.

Treatment: pericardiocentesis

Removal of fluid relieves cardiac compression.

Successful treatment produces:

↓ CVP + ↑ BP

Afterward monitor:

• Heart rhythm

• BP

• Venous pressure

• Heart sounds

• Recurrence

• Follow-up echo

Recurrent effusion may require another aspiration or open surgical drainage.

Nursing actions

• Notify provider

• IV fluids for hypotension

• CXR/echo

• Prepare for pericardiocentesis

• Obtain consent

• Prepare equipment

• Monitor hemodynamics

• Continuous cardiac monitoring

• Monitor for recurrence

Pericardiocentesis complications

• Coronary artery puncture

• Myocardial trauma

• Dysrhythmias

• Pleural laceration

• Gastric puncture

A pericardiotomy/pericardial window creates an opening allowing drainage and may be used for recurrent effusions, particularly those associated with neoplastic disease.

4. CARDIOGENIC SHOCK

Definition/pathophysiology

Cardiogenic shock occurs when:

Heart cannot pump effectively → ↓ cardiac output → inadequate tissue perfusion → shock syndrome.

Lecture-associated causes include:

• Acute MI

• End-stage HF

• Cardiac tamponade

• PE

Your shock lecture describes cardiogenic shock as failure of the cardiac pump.

Clinical manifestations

• Angina/chest pain

• Dysrhythmias

• Fatigue

• Feeling of doom

• ↑ HR

• ↓ BP

• ↑ RR

• ↓ O₂ saturation

• Hypothermia

General shock stages

Initial: no obvious parameter changes; changes occur at cellular level.

Compensatory/nonprogressive: body attempts to restore CO/perfusion through vasoconstriction and sympathetic activation.

Progressive: compensatory mechanisms fail.

Refractory: irreversible shock/organ failure.

General shock nursing care in your lecture

• High-flow O₂

• Flat position with legs elevated to increase venous return

• Hemodynamic monitoring

• Isotonic crystalloids/colloids

• Other treatment based on shock type

Your lecture also lists anticoagulation, pantoprazole and vasodilators in its general shock-management section.

Mechanical circulatory support

IABP — intra-aortic balloon pump

Temporary catheter-based device.

Purpose:

Increase coronary artery blood flow + decrease cardiac workload.

It reduces the work of contraction but does not perform the actual work of the heart.

Used for short-term support, typically days.

VAD

Ventricular assist device can circulate approximately as much blood/minute as the heart.

Can be short- or long-term.

One device supports one ventricle; two can provide biventricular support.

The lecture describes an LV VAD as:

LV apex → inlet cannula → pump → outlet into aorta.

ECMO

A VAD-type circulatory system can be combined with an oxygenator when both cardiac pumping and pulmonary oxygenation are inadequate.

5. ANEURYSMS

Definition

An aneurysm is a localized dilation/sac at a weak point in an arterial wall.

Types

Saccular: projects from one side.

Fusiform: entire arterial segment dilates.

Mycotic: small aneurysm associated with localized infection.

All aneurysms involve damage to the media layer of the vessel.

Damage may arise from:

• Congenital weakness

• Trauma

• Disease

After formation, an aneurysm tends to enlarge.

Major risk factors:

• Genetic predisposition

• Tobacco

• HTN

• Atherosclerosis

More than half of patients with aneurysms in the lecture have hypertension.

Thoracic aortic aneurysm

Lecture notes:

• ~70% attributed to atherosclerosis

• More common in men 50–70

• Thoracic aorta is the most common site for a dissecting aneurysm

• Major concern = hemorrhage/death

Clinical manifestations

Can be asymptomatic.

Pain is the most prominent symptom.

Pain may be constant and boring and sometimes occur when supine.

Compression of nearby structures can produce:

• Dyspnea

• Brassy/paroxysmal cough

• Hoarseness

• Stridor

• Weak/lost voice

• Dilated superficial chest/neck/arm veins

• Chest-wall edema

• Cyanosis

• Unequal pupils

• Dysphagia

Aphonia can occur from laryngeal nerve pressure; dysphagia from esophageal compression.

Diagnostics

• CXR

• CTA

• MRA

• TEE

Management

Preoperatively the lecture gives:

SBP ~90–120 mmHg

to maintain:

MAP ~65–75 mmHg.

For endovascular thoracic repair, lumbar spinal drainage may reduce spinal cord ischemia/paraplegia risk. Lecture target:

CSF pressure ≤10 mmHg and MAP >90 for first 36–48 hours post-op.

Medical management includes:

• Control BP/risk factors

• Beta blockers

• ARBs

• Sodium nitroprusside

Surgery aims to repair the aneurysm and restore vascular continuity with a graft.

Abdominal aortic aneurysm — AAA

Most common cause:

Atherosclerosis

More common according to your lecture in:

• Men

• Age >65

• Caucasian men compared with Black men

Most are infrarenal, below the renal arteries.

Untreated aneurysms may eventually rupture and cause death.

Clinical manifestations

Only about 40% are symptomatic in your lecture.

Possible:

• Feeling heartbeat in abdomen while lying down

• Abdominal pulsation

• Abdominal mass

• Low-back pain

If thrombus forms → embolization/occlusion can occur → cyanotic/mottled toes.

IMPENDING RUPTURE — very important

Think:

Severe abdominal/back pain + falling BP + falling hematocrit.

Pain may be middle/lower abdomen, especially left of midline.

Intraperitoneal rupture can rapidly be fatal.

Retroperitoneal rupture can cause hematomas involving:

• Scrotum

• Perineum

• Flank

• Penis

Rupture into vena cava can cause a loud bruit and potentially right-sided HF.

Diagnosis

Duplex ultrasound or CTA

Small aneurysms may be followed by ultrasound at 6-month intervals in the lecture.

Post-endovascular repair nursing care

• Supine × 6 hours

• HOB may be elevated to 45° after 2 hours

• Check circulation

• Temperature q4h

• Prevent hemorrhage

• Fluids to support blood flow and contrast excretion

• Assist ambulation after 6 hours

• Monitor pulmonary, cardiovascular, renal and neurologic systems

Complications:

• Arterial occlusion

• Hemorrhage

• Infection

• Ischemic bowel

• Kidney injury

• Impotence

Postimplantation syndrome

Usually starts within 24 hours of stent graft placement.

Features:

Fever + leukocytosis ± transient thrombocytopenia.

6. CARDIOMYOPATHY

Main pathophysiology

All cardiomyopathies eventually impair cardiac output.

Sequence:

↓ stroke volume → sympathetic nervous system activation + RAAS activation → ↑ systemic vascular resistance + sodium/fluid retention → ↑ cardiac workload → HF.

Your lecture emphasizes sodium/fluid retention.

Clinical manifestations

• DOE

• Fatigue

• PND

• Cough, especially with exertion

• Orthopnea

• Fluid retention

• Weight gain — lecture says 5 lb/week

• Peripheral edema

• Nausea from poor GI perfusion

• Chest pain

• Palpitations

• Dizziness

• Syncope with exertion

With HCM, sudden cardiac arrest may be the first manifestation, including in young athletes.

Major outcomes:

Severe HF + lethal dysrhythmias + death.

Heart failure manifestations associated with cardiomyopathy

Right-sided

Think systemic backup:

• JVD

• Dependent leg edema

• Ascites

• Nausea/anorexia

• Fatigue/weakness

• Weight gain

• Hepatomegaly

Left-sided

Think lungs:

• Nocturnal dyspnea

• Cough

• Orthopnea

• SOB

• Fatigue

• Frothy sputum

• PND

• Altered LOC

• Oliguria

• Nocturia

• S3 gallop

Assessment/diagnostics

Possible findings:

S3: early diastole; lecture describes "sloshing" associated with dilated ventricle.

S4: late diastole; "stiff" ventricle/increased resistance to filling.

Also:

• Tachycardia

• Murmurs

• Crackles

• JVD

• Pitting edema

• Hepatomegaly

Echo

One of the most useful tests because it shows ventricular structure/function.

Cardiac MRI

Especially useful for HCM.

ECG

May show:

• AFib

• Ventricular dysrhythmias

• LVH

• Left-axis deviation

• Wide QRS

• ST changes

• Inverted T waves

CXR

Cardiomegaly ± pulmonary congestion.

BNP

Lecture states BNP >400 pg/mL in CHF and explains BNP is released from overdistended cardiac chambers.

Cardiac cath may rule out CAD; endomyocardial biopsy can evaluate myocardial cells.

Treatment

• Medications

• Low-sodium diet

• Exercise/rest regimen

• Control dysrhythmias

• ICD

• CRT pacemaker

• VAD

• Systemic anticoagulation

• Fluid limit listed as 2 L/day

• Avoid dehydration

• Beta blockers

• Activity limitations

Other options:

• Pacemaker

• Septal ablation

• Myectomy

• Mitral valve surgery

• Heart transplant

For the HCM material, your lecture specifically says nitrates and morphine are not used because coronary dilation is contraindicated.

Major procedural complication = dysrhythmia.

7. MULTIPLE ORGAN DYSFUNCTION SYNDROME — MODS

The core problem to remember:

MODS = HYPOPERFUSION

Inadequate tissue perfusion causes progressive dysfunction of multiple organ systems.

Lecture specifically lists:

• Lungs

• Kidneys

• Heart

• GI system

Nursing priorities:

• Assess organ function

• Improve tissue perfusion

• Ventilatory support

• Inotropic medications

• Replace/support failed functions

• Clotting factors as needed

• Dialysis as needed

Lecture target:

MAP 70–100 mmHg

and states that below 60 mmHg organs do not receive adequate blood flow.

Progression/findings

Respiratory: ARDS → mechanical ventilation.

Cardiovascular: ↓ BP and ↓ CO → IV fluids + vasoactive medications.

Labs: ↑ glucose, ↑ lactic acid, ↑ BUN.

Liver: ↑ bilirubin and LFTs.

Kidneys: ↑ creatinine → anuria.

Hematologic: increased bleeding.

Metabolic: severe muscle loss/autocatabolism.

Neurologic/end-stage: unresponsive/coma.

Eventually the cardiovascular system fails to respond.

OBJECTIVE 2 — LABS & DIAGNOSTIC PROCEDURES

Your lecture groups cardiovascular labs into:

• Cardiac biomarkers

• Blood chemistry

• Hematology

• Coagulation studies

• Lipid profile

• BNP

• CRP

• Homocysteine

Cardiac biomarkers

Your teacher's practice-question answer specifically identifies:

CK-MB + troponin + myoglobin = cardiac markers associated with myocyte injury.

BNP

Associated with ventricular/cardiac chamber stretching and HF.

Lecture emphasizes >400 pg/mL in CHF.

Echocardiogram

Noninvasive ultrasound.

Evaluates:

• EF

• Size

• Shape

• Motion of cardiac structures

• Direction of blood flow

• Velocity of blood flow

TEE

Transducer passes:

Mouth → esophagus

Produces clearer cardiac images and can detect left atrial thrombi.

Before:

• NPO 4–6 hours

• Informed consent

After:

• Check gag reflex

• Lecture lists HOB 45°

Cardiac catheterization

Invasive procedure used to diagnose structural/functional heart and great-vessel disease.

Risks include:

• Bleeding

• Hematoma

• Contrast reaction

• Contrast-induced nephropathy

Baseline labs include:

• CBC/Hgb/Hct/platelets

• Coagulation studies

Your lecture flags metformin with iodinated contrast.

Before cath

• NPO 8–12 hr

• Arrange transportation home

• Explain procedure

• IV medication for comfort

• Explain possible palpitations

• Patient may be instructed to cough/deep breathe

• Contrast may cause flushing/feeling of needing to urinate

After

Assess:

Access site + bleeding + hematoma + peripheral pulses

Know the 6 Ps:

Pallor
Pulselessness
Pain
Paralysis
Paresthesia
Poikilothermia

Lecture positioning:

Flat ~6 hr, HOB ≤30°, affected hip/leg extended for the described approach.

Monitor for orthostatic hypotension.

Complications:

• Arterial dissection

• Cardiac tamponade

• Hematoma

• Embolism

• Restenosis

• Retroperitoneal bleeding

• AKI

OBJECTIVE 5 — DYSRHYTHMIAS

Before the individual rhythms, know the conduction basics.

SA node: primary pacemaker, 60–100/min

AV node: secondary pacemaker, 40–60/min

Ventricular pacemaker sites: 30–40/min

Depolarization = electrical stimulation

Systole = mechanical contraction

Repolarization = electrical relaxation

Diastole = mechanical relaxation

ECG basics

Rate using 6-second strip:

Number of R-R intervals × 10

R-R = ventricular rhythm

P-P = atrial rhythm

P wave = atrial depolarization.

Normal P duration ≤ 0.11 sec.

QRS = ventricular depolarization.

Normal QRS < 0.12 sec.

ATRIAL FIBRILLATION

Recognition

Think:

No discernible P waves + irregularly irregular rhythm

AFib is described as the most common sustained dysrhythmia.

Risk factors include:

• Hyperthyroidism

• Cardiac ischemia

• Pericarditis/myocarditis

• Myocardial hypertrophy/fibrosis/dilation

• Increasing age

• HTN

• Diabetes

• Obesity

• Valvular disease

• HF

• OSA

• Alcohol

• Atrial remodeling

• Cardiac surgery

Pathophysiology

Electrical and structural atrial remodeling → rapid disorganized atrial activity → uncoordinated atrial twitching.

You lose the effective atrial kick.

Atrial kick contributes about 25–30% of cardiac output according to the lecture.

Rapid ventricular response shortens filling time → ↓ stroke volume.

Manifestations

• May be asymptomatic

• Palpitations

• SOB

• Hypotension

• DOE

• Fatigue

• Pulse deficit

• Angina/ischemia

Use a manual BP is specifically emphasized.

Blood stasis can produce thrombi, especially in the left atrial appendage.

Major complications

STROKE

plus:

• HF

• Myocardial ischemia

• Other embolic events

Diagnostics

• Thyroid tests

• Renal function

• Hepatic function

• TEE

• CXR

• Exercise stress test

• Holter/event monitor

• EP study

Treatment

Main goals include prevention of emboli and control of rate/rhythm.

Lecture includes:

• Heparin → warfarin

• INR 2–3

• Beta blockers

• Calcium-channel blockers

• Antiarrhythmics

• Cardioversion

• LAA occlusion

• Catheter ablation

• Convergent procedure

Hemodynamically unstable AFib with altered mental status, chest discomfort or hypotension → electrical cardioversion when medication is unsuccessful.

Catheter-ablation risks include:

• AV block

• Tamponade

• Phrenic nerve injury

• Stroke

• Hematoma

• Retroperitoneal bleeding

• Pulmonary vein stenosis

• Atrioesophageal fistula

ATRIAL FLUTTER

Recognition

Saw-tooth F waves

Pathophysiology:

Atrial conduction defect → rapid but regular atrial impulses.

Atrial rate: 250–400

Ventricular rate: usually 75–150

Because the AV node cannot conduct every atrial impulse, ratios may be:

2:1, 3:1 or 4:1.

Symptoms:

• Chest pain

• SOB

• Hypotension

Treatment:

• Vagal maneuvers

• Adenosine

• Antithrombotic therapy

• Rate control

• Rhythm control

• Electrical cardioversion

Adenosine in the lecture is given rapid IV, immediately followed by 20-mL saline flush, with arm elevation to promote rapid circulation.

PVC — PREMATURE VENTRICULAR COMPLEX

This one is on your objective, but the uploaded dysrhythmia lecture does not give a separate PVC teaching section. It only states that ventricular dysrhythmias include PVCs and that:

VT = 3 or more PVCs in a row at >100 bpm.

So I would not assume additional PVC details are coming specifically from these uploaded slides unless your teacher covered them verbally or in another resource.

VENTRICULAR TACHYCARDIA

Definition

≥3 PVCs in a row at a rate >100 bpm.

Risk factors/causes:

• Large MI

• Low EF

• Cardiac ischemia/infarction

• HF/increased cardiac workload

• Digitalis toxicity

• Hypoxia

• Acidosis

• Electrolyte imbalance, especially hypokalemia

• Caffeine

• Nicotine

• Alcohol

ECG

Rate: 100–200 bpm

Rhythm usually regular.

QRS ≥0.12 sec, wide/bizarre.

P waves difficult to see.

Treatment depends on pulse/hemodynamic status

This distinction is extremely important:

VT WITH pulse

Antiarrhythmics may be used.

Lecture identifies IV amiodarone for patients with impaired cardiac function/acute MI.

Symptomatic/unstable VT with pulse

Synchronized cardioversion

PULSELESS VT

DEFIBRILLATION + CPR

Treat like VF.

Long-term:

• EF <35% → consider ICD

• Catheter ablation

• Amiodarone in selected patients

VENTRICULAR FIBRILLATION

Recognition

Chaotic electrical activity + no organized QRS + NO PULSE.

The ventricles quiver rather than pump.

Common cause:

CAD/acute MI

Other causes:

• Untreated VT

• Cardiomyopathy

• Valvular disease

• Proarrhythmic medications

• Acid-base abnormalities

• Electrolyte abnormalities

• Electrical shock

• Brugada syndrome

Clinical findings:

No heartbeat + no pulse + no respirations.

Death is imminent without treatment.

Treatment

IMMEDIATE DEFIBRILLATION + CPR

Then ACLS medications such as:

• Epinephrine

• Amiodarone

Minimize interruptions in compressions.

Look for reversible Hs and Ts as listed in your lecture.

ASYSTOLE — CARDIAC STANDSTILL

Recognition

Flatline/no ventricular electrical activity.

Absent QRS complexes should be confirmed in two different leads.

There may briefly be P waves.

Patient has:

• No heartbeat

• No pulse

• No respirations

VERY IMPORTANT:

ASYSTOLE IS NOT SHOCKABLE.

Your lecture explicitly states it does not respond to defibrillation.

That is a classic exam distinction:

VF/pulseless VT → shock

Asystole → DON'T shock

GENERAL DYSRHYTHMIA NURSING CARE

Assess:

• BP

• Pulse/rhythm

• Respiratory rate/depth

• Breath sounds

• Hemodynamic effect

• Lightheadedness

• Dizziness

• Syncope

• Fatigue

• Chest discomfort

• Palpitations

• Medications

• Labs

• Oxygenation

• Electrolytes

• Acid-base status

• Caffeine

• Medication adherence

Home teaching:

• Maintain therapeutic antiarrhythmic levels

• Take pulse before medication as directed

• CPR training

• Recognize embolic symptoms

CARDIOVERSION VS DEFIBRILLATION

Cardioversion

SYNCHRONIZED

Timed to the QRS/R wave to prevent shock delivery during the vulnerable T-wave period.

Used for certain tachydysrhythmias when the patient still has organized cardiac activity.

Lecture preparation:

• If rhythm >48 hr, anticoagulation beforehand may be needed

• Digoxin usually withheld 48 hr in the lecture

• NPO ≥4 hr

• Anterior-posterior pads

• IV moderate sedation

• Analgesia/anesthesia

Defibrillation

UNSYNCHRONIZED

Used for:

VF + pulseless VT

Safety:

• Good pad/paddle contact

• Make sure nobody touches patient/bed during discharge

After successful cardioversion look for:

• Sinus rhythm

• Adequate peripheral pulses

• Adequate BP

• Stable airway

• Recovery from sedation

OBJECTIVE 7 — PACEMAKERS

A pacemaker provides electrical stimuli to the myocardium.

Used for:

• Slow impulse formation

• Symptomatic AV conduction disturbance

• Ventricular conduction disturbance

• Certain tachydysrhythmias unresponsive to medication

Can be:

Temporary or permanent.

Temporary pacemakers are hospital-based.

Permanent pacemaker battery life in the lecture:

~6–12 years.

ERI = elective replacement indicator, signaling battery depletion.

For symptomatic bradycardia with a pulse that does not respond to atropine:

Emergency transcutaneous pacing may be initiated.

Pacemaker complications

Know these:

• Infection

• Pneumothorax

• Bleeding

• Hematoma

• Hemothorax

• Ventricular ectopy

• VT

• Lead displacement

• Myocardial perforation

• Phrenic/diaphragmatic stimulation

• Pericardial effusion

• Cardiac tamponade

• Twiddler syndrome

• Pacemaker syndrome

HICCUPS after pacemaker placement

Report them.

They may indicate diaphragmatic/phrenic nerve stimulation, possibly associated with lead displacement.

ICD

Implantable cardioverter-defibrillator detects and terminates dangerous tachycardia/VF.

Lecture indications include CAD patients ≥40 days post-MI with significant LV dysfunction and EF ≤35%, and selected patients with nonischemic dilated cardiomyopathy.

Pacemaker/ICD nursing care & teaching

• Monitor ECG/rhythm

• Know device settings

• Assess cardiac output/hemodynamic stability

• Wear ID bracelet

• Restrict activity

• Do not lift affected arm above shoulder ×2 weeks

• Avoid tight clothing

• Report hiccups

• Teach family that an ICD shock is not harmful to someone nearby

• Avoid strong magnetic fields

• Inform security personnel about device

• Small household appliances are generally okay per lecture

• Keep phone on opposite side

Assess incision for:

• Bleeding

• Hematoma

• Infection

• Swelling

• Tenderness

• Drainage

• Warmth

Take temperature daily.

CXR before discharge verifies lead position and checks for pneumothorax.

Device function requires lifelong surveillance.

OBJECTIVE 9 — CARDIOVASCULAR MEDICATIONS

Your objective specifically lists:

Dobutamine
Milrinone
Quinidine
Procainamide
Lidocaine
Flecainide
Propranolol
Amiodarone
Verapamil
Atropine
Epinephrine
Magnesium
Vasopressin

The medication PowerPoint establishes the antiarrhythmic classes, but several individual-drug slides appear to contain information that did not parse into text. An exact search of the uploaded medication file only returned epinephrine in the atropine discussion; it did not return readable lecture text for quinidine, procainamide, lidocaine, flecainide, propranolol, amiodarone, verapamil, magnesium or vasopressin.

So here is everything the readable lecture material actually provides.

CLASS I — SODIUM CHANNEL BLOCKERS

Your lecture's key class statement:

Slow conduction

Your blueprint divides these into:

IA: quinidine, procainamide
IB: lidocaine
IC: flecainide

The uploaded PPT does not provide additional readable text for the individual drugs.

CLASS II — BETA-ADRENERGIC BLOCKERS

Blueprint drug: propranolol

The lecture explains the beta-blocker class using metoprolol.

Effects:

• Block beta-adrenergic sympathetic stimulation

• ↓ HR

• Slow conduction

• ↓ BP

• ↓ myocardial contractility

• ↓ myocardial O₂ consumption

• Balance myocardial O₂ supply/demand

Think:

Negative chronotropic = ↓ HR

Negative inotropic = ↓ contraction strength

Negative dromotropic = ↓ conduction

Possible contraindications/adverse effects:

• Hypotension

• Bradycardia

• Advanced AV block

• Acute HF

• Fatigue

• Dizziness

• Depressed mood

• Decreased libido

Nonselective beta blockers can cause bronchoconstriction and are contraindicated in significant pulmonary disease such as asthma.

Do not stop abruptly → can worsen angina and potentially precipitate MI.

Beta blockers can mask hypoglycemia in diabetics.

CLASS III — POTASSIUM CHANNEL BLOCKERS

Blueprint drug: amiodarone

Class effect:

Prolong action potential and refractory period.

The dysrhythmia lecture uses amiodarone in:

• VT

• VF

• Selected long-term ventricular dysrhythmia management

It is listed with epinephrine as a medication that may facilitate ROSC after VF defibrillation.

CLASS IV — CALCIUM CHANNEL BLOCKERS

Blueprint drug: verapamil

The medication lecture explains this class using amlodipine/diltiazem.

Effects:

• ↓ SA-node automaticity

• ↓ AV-node conduction

• ↓ HR

• ↓ myocardial contractility

• ↓ cardiac workload

• Coronary arteriole dilation

• ↑ myocardial O₂ supply

• ↓ systemic arterial pressure

• ↓ myocardial O₂ demand

Adverse effects:

• Hypotension

• AV block

• Bradycardia

• Constipation

MILRINONE

Phosphodiesterase inhibitor

Causes:

↑ intracellular Ca²⁺ in myocardial cells → ↑ contractility

Also causes vasodilation:

↓ preload + ↓ afterload → ↓ cardiac workload

Used IV for severe HF, including patients awaiting transplant.

Major adverse effects:

• Hypotension

• Ventricular dysrhythmias

Nursing:

Monitor BP + ECG closely.

Hypovolemia increases risk of a sudden BP drop.

Lecture specifically states:

Do not give with nitrates.

DOBUTAMINE

Sympathomimetic/catecholamine.

Stimulates beta-1 receptors.

Used for:

Significant LV dysfunction + hypoperfusion

Effects:

↑ myocardial contractility + ↑ renal perfusion → ↑ urine output

Can also:

• Increase HR

• Cause ectopic beats

• Cause tachydysrhythmias

ATROPINE

Used for symptomatic/unstable bradycardia in your lecture.

Signs of instability include:

• Acute altered mental status

• Chest discomfort

• Hypotension

Your lecture slide states:

0.5 mg rapid IV bolus

repeat:

q3–5 min

maximum:

3 mg

If unresponsive → transcutaneous pacing; dopamine/epinephrine may be used.

Important for studying: I would memorize the dose exactly as your teacher's slide presents it for this exam, since that is the source you're being tested from.

EPINEPHRINE

The medication lecture only mentions it as a catecholamine option when symptomatic bradycardia is unresponsive to atropine. The dysrhythmia lecture also lists epinephrine during VF resuscitation.

MAGNESIUM

Listed on your blueprint and also listed among medications associated with defibrillator/ACLS management, but the uploaded slides do not contain additional readable medication-specific teaching for it.

VASOPRESSIN

Listed on the objective, but the uploaded lecture's readable text does not provide a drug-specific explanation.

OBJECTIVES 6 & 8 — IMPORTANT GAP IN THE UPLOADED RESOURCES

Your actual blueprint specifically says you need:

Hemodynamics

• Central venous pressure monitoring

• Intra-arterial BP monitoring

• Pulmonary artery pressure monitoring

and:

Central venous access devices

• Implanted ports

• Percutaneous/non-tunneled central venous access devices

• PICCs

• Tunneled central catheters

I searched the lecture files specifically for these topics. The uploaded resources do not contain actual teaching sections for them. The only CVP reference is that CVP should decrease after successful pericardiocentesis for tamponade.

So these are definitely on your blueprint, but the lecture files you uploaded don't give me enough source material to build those sections without bringing in outside information.

THE BIG EXAM CONNECTIONS I WOULD MAKE FROM YOUR BLUEPRINT

These are relationships repeatedly emphasized by your teacher's materials:

Pericarditis → effusion → tamponade → ↓ filling → ↓ CO → obstructive shock

Cardiomyopathy → ↓ SV → SNS/RAAS → vasoconstriction + fluid retention → ↑ workload → HF

Cardiogenic shock → pump failure → ↓ CO → hypoperfusion

MODS → prolonged hypoperfusion → multiple organs fail

AAA + sudden severe abdominal/back pain + falling BP/Hct → suspect rupture

AFib → loss of atrial kick + blood stasis → ↓ CO + LAA thrombus → stroke risk

A-flutter → saw-tooth F waves

VT → ≥3 PVCs, wide QRS

Pulseless VT/VF → DEFIBRILLATE

Asystole → DON'T defibrillate

Unstable tachydysrhythmia with pulse → synchronized cardioversion

Symptomatic bradycardia → atropine → pacing if unsuccessful

Pacemaker + hiccups → possible diaphragmatic/phrenic stimulation/lead problem

Mechanical valve → lifelong anticoagulation

Cardiac tamponade → Beck's triad = hypotension + JVD + muffled heart sounds

Pericarditis ECG → diffuse/all-lead ST elevation

Milrinone → ↑ contractility + vasodilation → watch BP and ventricular dysrhythmias

Dobutamine → beta-1 → ↑ contractility/renal perfusion, but may cause tachydysrhythmias