Cardiovascular System Study Guide

Cardiac Anatomy & Physiology

Core Goals of the Cardiovascular System

• Primary goal: Deliver oxygen to tissues and remove metabolic waste
• Oxygen Delivery (DO2) depends on cardiac output and arterial oxygen content
• Oxygen consumption (VO2) must be balanced with delivery
• When demand exceeds supply: ischemia develops, potentially leading to infarction

Heart Structure

• Four chambers: Right atrium, Right ventricle, Left atrium, Left ventricle
• Four valves: Tricuspid (right AV), Pulmonary (right semilunar), Mitral/Bicuspid (left AV), Aortic (left semilunar)
• Right side: Low-pressure system, pumps deoxygenated blood to lungs
• Left side: High-pressure system, pumps oxygenated blood to body
• Heart wall layers: Epicardium (outer), Myocardium (muscle), Endocardium (inner lining)

Coronary Circulation

• Left main coronary artery branches into LAD and Circumflex
• LAD supplies anterior wall and septum
• Circumflex supplies lateral and posterior walls
• Right coronary artery (RCA) supplies inferior wall and SA/AV nodes in most people
• Coronary perfusion occurs primarily during diastole
• Coronary Perfusion Pressure = Diastolic BP - PAOP (or LVEDP)

Electrical Conduction System

• SA Node: Primary pacemaker (60-100 bpm)
• AV Node: Delays impulse for ventricular filling (40-60 bpm)
• Bundle of His → Bundle Branches → Purkinje fibers (20-40 bpm)
• Cardiac cell properties: Automaticity, Excitability, Conductivity, Contractility

Hemodynamic Monitoring

Key Hemodynamic Parameters

• Blood Pressure = Cardiac Output × Systemic Vascular Resistance
• Cardiac Output (CO) = Heart Rate × Stroke Volume (normal: 4-8 L/min)
• Cardiac Index (CI) = CO ÷ Body Surface Area (normal: 2.5-4.0 L/min/m²)
• Stroke Volume determined by: Preload, Contractility, Afterload

Preload

• Definition: Ventricular wall stretch at end-diastole (volume)
• Right heart preload measured by CVP/RAP (normal: 2-6 mmHg)
• Left heart preload measured by PAOP/PCWP (normal: 8-12 mmHg)
• Frank-Starling Law: Increased stretch = increased contractile force (to a point)
• Causes of increased preload: Fluid overload, heart failure, renal failure
• Causes of decreased preload: Hypovolemia, vasodilation, diuresis

Afterload

• Definition: Resistance the ventricle must overcome to eject blood
• Right ventricular afterload: Pulmonary Vascular Resistance (PVR) - normal: 100-250 dynes
• Left ventricular afterload: Systemic Vascular Resistance (SVR) - normal: 800-1200 dynes
• Increased afterload: Vasoconstriction, hypertension, aortic stenosis
• Decreased afterload: Vasodilation, sepsis, anaphylaxis

Pulmonary Artery Catheter Values

• RAP (Right Atrial Pressure): 2-6 mmHg - reflects right heart preload
• PA Systolic: 20-30 mmHg
• PA Diastolic: 8-15 mmHg
• PA Mean: 10-20 mmHg
• PAOP/Wedge: 8-12 mmHg - reflects left heart preload
• Mixed venous O2 saturation (SvO2): 60-80% - oxygen supply/demand balance

Acute Coronary Syndrome

ACS Overview

• Umbrella term for sudden reduction in coronary blood flow
• Spectrum: Unstable Angina → NSTEMI → STEMI
• Pathophysiology: Atherosclerotic plaque rupture → thrombus formation
• Key principle: "Time is muscle" - early reperfusion saves myocardium

Types of Angina

• Stable Angina: Predictable chest pain with exertion, relieved by rest/nitroglycerin
• Unstable Angina: New onset, worsening pattern, or occurs at rest - NO troponin elevation
• Variant/Prinzmetal Angina: Coronary vasospasm, ST elevation that resolves, often at rest

STEMI vs NSTEMI

• STEMI: Complete coronary occlusion, ST elevation on ECG, positive troponins
• NSTEMI: Partial occlusion, ST depression or T-wave inversion, positive troponins
• Troponin I normal: <0.04 ng/mL - elevated indicates myocardial injury
• ECG leads correlate to coronary territories (II, III, aVF = inferior/RCA)

ACS Treatment

• MONA: Morphine (if needed), Oxygen (if hypoxic), Nitro, Aspirin (325mg)
• Dual Antiplatelet Therapy: Aspirin + P2Y12 inhibitor (Plavix, Brilinta)
• Anticoagulation: Heparin, Enoxaparin, or Bivalirudin
• STEMI: PCI (door-to-balloon <90 min) or Fibrinolytics (door-to-needle <30 min)
• NSTEMI: Risk stratification, early invasive strategy for high-risk patients
• Post-PCI monitoring: Groin site bleeding, hematoma, retroperitoneal bleed signs

Cardiogenic Shock

Definition & Causes

• Heart fails as a pump - inadequate tissue perfusion
• Most common cause: Large MI (>40% LV involvement)
• Other causes: Cardiomyopathy, valvular dysfunction, arrhythmias, mechanical complications
• Mechanical complications: Papillary muscle rupture, VSD, free wall rupture

Hemodynamic Profile

• Decreased CO/CI (<2.2 L/min/m²)
• Elevated PAOP (>18 mmHg)
• Elevated SVR (compensatory vasoconstriction)
• Hypotension: SBP <90 mmHg or MAP <65 mmHg
• Low SvO2 (<60%) indicating increased oxygen extraction

Clinical Presentation

• Cold, clammy skin (poor perfusion)
• Altered mental status
• Oliguria (<0.5 mL/kg/hr)
• Elevated lactate (tissue hypoperfusion)
• Pulmonary congestion (crackles, dyspnea)

Management

• Optimize oxygenation - may need mechanical ventilation
• Inotropes: Dobutamine (increases contractility, vasodilation)
• Vasopressors: Norepinephrine if severely hypotensive
• Avoid excessive fluids - already volume overloaded
• Mechanical support: IABP, Impella, LVAD, ECMO
• Treat underlying cause: Revascularization for MI

Shock Categories & Classification

Overview of Shock

• Definition: Inadequate tissue perfusion leading to cellular hypoxia
• Four main categories: Distributive, Cardiogenic, Hypovolemic, Obstructive
• Common endpoint: End-organ dysfunction from oxygen supply-demand mismatch
• Early recognition and treatment essential to prevent irreversible damage

Distributive Shock

• Characterized by widespread vasodilation and loss of vascular tone
• SEPTIC: Most common - caused by infection (Gram+, Gram-, fungal, viral)
• NEUROGENIC: Spinal cord injury disrupts sympathetic tone (bradycardia + hypotension)
• ANAPHYLACTIC: Severe allergic reaction causing massive histamine release
• Other causes: Liver failure, SIRS, toxic shock syndrome, transfusion reactions
• Hemodynamics: Low SVR, high CO (warm shock initially), elevated or normal PAOP

Cardiogenic Shock

• Primary pump failure - heart cannot maintain adequate cardiac output
• Cardiomyopathic causes: MI, RV infarct, heart failure exacerbation, myocarditis
• Drug-induced: Beta-blocker overdose, calcium channel blocker toxicity
• Stunned myocardium: Post-arrest, post-cardiopulmonary bypass
• Hemodynamics: Low CO/CI, elevated PAOP, elevated SVR
• Clinical: Cold extremities, pulmonary edema, oliguria

Hypovolemic Shock

• Inadequate circulating volume leading to decreased preload
• HEMORRHAGIC: Trauma, GI bleeding, surgical blood loss, retroperitoneal bleed
• NON-HEMORRHAGIC: Severe dehydration, vomiting/diarrhea, burns, third-spacing
• Hemodynamics: Low CO, low PAOP/CVP, elevated SVR (compensatory)
• Treatment: Volume resuscitation - crystalloids, blood products for hemorrhagic
• Massive transfusion protocol: 1:1:1 ratio PRBC:FFP:Platelets

Obstructive Shock

• Mechanical obstruction to blood flow impairs cardiac output
• PULMONARY VASCULAR: Massive PE, severe pulmonary hypertension, air embolism
• MECHANICAL: Tension pneumothorax, cardiac tamponade, constrictive pericarditis
• Key feature: JVD with hypotension (blood cannot enter or leave heart)
• Treatment: Relieve obstruction (needle decompression, pericardiocentesis, thrombolytics)
• Hemodynamics: Low CO, elevated CVP, variable SVR

Shock Differentiation by Hemodynamics

• Distributive: ↓SVR, ↑CO (early), normal/low PAOP
• Cardiogenic: ↑SVR, ↓CO, ↑PAOP
• Hypovolemic: ↑SVR, ↓CO, ↓PAOP
• Obstructive: Variable SVR, ↓CO, ↑CVP
• SvO2 <60% in all types indicates inadequate oxygen delivery
• Lactate elevation indicates tissue hypoperfusion regardless of type

Heart Failure

Types of Heart Failure

• Systolic HF (HFrEF): Reduced ejection fraction (<40%), impaired contractility
• Diastolic HF (HFpEF): Preserved EF (>50%), impaired relaxation/filling
• Left Heart Failure: Pulmonary congestion (dyspnea, crackles, orthopnea)
• Right Heart Failure: Systemic congestion (JVD, peripheral edema, hepatomegaly)

BNP - Brain Natriuretic Peptide

• Released by ventricles in response to stretch/volume overload
• BNP >100 pg/mL suggests heart failure
• NT-proBNP >300 pg/mL suggests heart failure
• Used to differentiate cardiac from pulmonary causes of dyspnea

RAAS System in Heart Failure

• Decreased renal perfusion triggers renin release
• Renin converts angiotensinogen to Angiotensin I
• ACE converts Ang I to Ang II (potent vasoconstrictor)
• Ang II stimulates aldosterone release (sodium/water retention)
• This creates a vicious cycle worsening heart failure

Heart Failure Treatment

• ACE Inhibitors/ARBs: Block RAAS, reduce afterload and remodeling
• Beta Blockers: Reduce heart rate, improve survival (start low, go slow)
• Diuretics: Reduce preload and congestion
• Aldosterone antagonists: Spironolactone - reduces mortality
• Digoxin: Increases contractility, controls rate in AFib
• Hydralazine/Nitrate: Alternative for ACE-intolerant patients

Cardiomyopathies

Dilated Cardiomyopathy

• Enlarged, weakened ventricles with poor systolic function
• Causes: Viral, alcoholic, peripartum, idiopathic
• Treatment: Standard HF therapy (ACE-I, BB, diuretics)
• Tako-Tsubo (Stress) Cardiomyopathy: Apical ballooning from catecholamine surge

Hypertrophic Cardiomyopathy (HCM/HOCM)

• Thickened ventricular walls, especially septum
• Diastolic dysfunction - stiff, non-compliant ventricle
• Can cause LVOT obstruction during systole
• Risk of sudden cardiac death, especially in young athletes
• AVOID: Inotropes, volume depletion, vasodilators (worsen obstruction)
• Treatment: Beta blockers, calcium channel blockers, ICD if high risk

Restrictive Cardiomyopathy

• Rigid, non-compliant ventricles from infiltrative disease
• Causes: Amyloidosis, sarcoidosis, hemochromatosis
• Impaired filling (diastolic dysfunction)
• Poor prognosis, treatment is supportive

Valvular Disorders & Heart Sounds

Heart Sounds

• S1: Closure of AV valves (mitral/tricuspid) - "Lub"
• S2: Closure of semilunar valves (aortic/pulmonic) - "Dub"
• S3: Early diastole, ventricular filling - suggests HF or volume overload
• S4: Late diastole, atrial kick against stiff ventricle - suggests hypertrophy

Stenosis vs Regurgitation

• Stenosis: Valve narrowing, restricted blood flow forward
• Regurgitation: Valve incompetence, backward blood flow
• Aortic Stenosis: Systolic crescendo-decrescendo murmur, syncope, angina, HF
• Aortic Regurgitation: Diastolic decrescendo murmur, widened pulse pressure
• Mitral Stenosis: Diastolic rumble, atrial fibrillation common
• Mitral Regurgitation: Systolic blowing murmur radiating to axilla

Endocarditis & Pericarditis

• Endocarditis: Infection of heart valves (vegetation formation)
• Risk factors: IV drug use, prosthetic valves, poor dentition
• Treatment: Prolonged IV antibiotics, possible valve surgery
• Pericarditis: Inflammation of pericardium
• Classic findings: Chest pain relieved by sitting forward, friction rub
• ECG: Diffuse ST elevation, PR depression
• Treatment: NSAIDs, colchicine, watch for tamponade

Vascular Emergencies

Aortic Aneurysm

• Permanent dilation of aorta (>50% normal diameter)
• Risk factors: Hypertension, atherosclerosis, connective tissue disorders
• Often asymptomatic until rupture or dissection
• Ruptured AAA: Severe back/abdominal pain, hypotension, pulsatile mass
• Treatment: Emergent surgical repair, BP control

Aortic Dissection

• Tear in intimal layer allows blood between vessel wall layers
• Type A: Involves ascending aorta - surgical emergency
• Type B: Descending aorta only - medical management possible
• Classic presentation: Tearing chest pain radiating to back
• BP differential between arms, widened mediastinum on CXR
• Management: BP control (SBP <120, HR <60), beta blockers first, then vasodilators

Peripheral Arterial Disease

• Arterial insufficiency: Acute (6 Ps) - Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia
• Chronic arterial insufficiency: Claudication (cramping with walking)
• Venous insufficiency: Edema, skin changes, chronic, DVT risk
• Treatment: Revascularization for arterial, anticoagulation for venous

Hypertensive Crisis

• Hypertensive Urgency: Severely elevated BP without end-organ damage
• Hypertensive Emergency: Elevated BP WITH end-organ damage
• Target organs: Brain (stroke, encephalopathy), Heart (MI, HF), Kidneys, Eyes
• Treatment: IV antihypertensives (Nicardipine, Labetalol, Nitroprusside)
• Goal: Reduce MAP by 20-25% in first hour, avoid precipitous drop
• Nitroprusside: Watch for cyanide/thiocyanate toxicity

Malignant Hypertension

• DBP typically >140 mmHg with end-organ damage
• Classic findings: Papilledema, retinal hemorrhages
• Other manifestations: Encephalopathy, acute kidney injury, heart failure
• Requires ICU admission and continuous BP monitoring
• Treatment: Gradual BP reduction - rapid drops can cause stroke/ischemia

ACS & MI Detailed Management

Acute Coronary Syndrome Spectrum

• ACS = Sudden blockage of coronary blood flow from atherosclerosis/clots
• CRITICAL CONCEPT: "Time is Tissue" - early reperfusion = best outcomes
• Spectrum from least to most severe: Unstable Angina → NSTEMI → STEMI
• Troponin determines presence of myocardial necrosis
• EKG changes indicate extent and location of injury

📊 Angina Types Comparison

• ═══════════════════════════════════════════════════════════════════════════════════════════════
• TYPE │ PATTERN │ TROPONIN │ TREATMENT
• ═══════════════════════════════════════════════════════════════════════════════════════════════
• Stable Angina │ Predictable with exertion │ NEGATIVE │ Rest, Nitroglycerin,
• │ Relieved by rest │ │ Risk factor modification
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Unstable Angina │ New onset, increasing │ NEGATIVE │ Anticoagulation, ASA,
• │ severity, occurs at REST │ │ Risk stratification
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Variant │ Vasospasm, often early │ NEGATIVE │ Calcium Channel Blockers,
• (Prinzmetal) │ morning, at rest │ │ Nitrates. Avoid beta blockers
• │ Triggers: stress, cold, │ │ (can worsen spasm)
• │ tobacco, cocaine │ │
• ═══════════════════════════════════════════════════════════════════════════════════════════════

📊 NSTEMI vs STEMI Comparison

• ═══════════════════════════════════════════════════════════════════════════════════════════════
• FEATURE │ NSTEMI │ STEMI
• ═══════════════════════════════════════════════════════════════════════════════════════════════
• Vessel │ PARTIAL occlusion │ COMPLETE occlusion
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• EKG │ ST DEPRESSION or │ ST ELEVATION >1mm limb leads
• │ T-wave inversion │ or >2mm precordial leads
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Troponin │ ELEVATED (>0.4 mcg/L) │ ELEVATED
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Management │ Heparin drip, monitoring, │ EMERGENT reperfusion:
• │ ischemia-guided strategy │ PCI goal <90 min OR
• │ │ Fibrinolytics <30 min
• ═══════════════════════════════════════════════════════════════════════════════════════════════

STEMI Reperfusion Goals

• ═══ DOOR-TO-TREATMENT TIMES ═══
• PCI (Cath Lab): Door-to-balloon <90 minutes
• Fibrinolytics: Door-to-needle <30 minutes
• Transfer for PCI: Door-in-door-out <30 minutes if no on-site cath lab
• SYMPTOMS: Dyspnea, diaphoresis, chest pain NOT relieved by nitroglycerin
• PATHOLOGIC Q WAVE: Width >40ms OR depth >25% of R wave = indicates INFARCTION/NECROSIS

Nitroglycerin Precautions

• Vasodilator that reduces preload and myocardial oxygen consumption
• ⚠️ CAUTION with INFERIOR MI (Leads II, III, aVF):
• • Often involves RIGHT VENTRICLE (RCA territory)
• • RV is preload-dependent
• • Nitroglycerin reduces preload → can cause severe hypotension
• • Always check RIGHT-SIDED LEADS (V4R) before giving nitrates
• ⚠️ CONTRAINDICATED with PDE-5 inhibitors (Sildenafil/Viagra)
• • Can cause dangerous hypotension
• ⚠️ OXYGEN: Only supplement if SpO2 <94% or respiratory distress
• • Excessive O2 can cause peripheral vasoconstriction

Post-PCI Nursing Care

• CHECK PEDAL PULSES: Ensures no arterial occlusion from procedure
• MONITOR RENAL FUNCTION: Contrast dye can cause nephropathy
• • Watch for rising creatinine, decreased urine output
• • Ensure adequate hydration
• INSERTION SITE MONITORING:
• • Hematoma formation
• • Active bleeding
• • RETROPERITONEAL BLEEDING: Flank pain + hypotension = emergency
• MEDICATIONS: Continue dual antiplatelet therapy (Aspirin + P2Y12 inhibitor)

Papillary Muscle Rupture

• LOCATION: Most commonly after INFERIOR or LATERAL MI
• • Posteromedial papillary muscle has SINGLE blood supply (RCA)
• • Anterolateral has dual supply (less commonly ruptures)
• TIMING: Typically 2-7 days POST-MI
• CLINICAL SIGNS:
• • Acute LOUD SYSTOLIC MURMUR (mitral regurgitation)
• • Sudden pulmonary edema
• • Cardiogenic shock
• HEMODYNAMIC FINDING: Large "V" wave on PAOP tracing
• TREATMENT: Emergent surgical repair, may need IABP for stabilization

Peripheral Vascular Disorders

Carotid Artery Stenosis

• CAUSE: Atherosclerosis at carotid bifurcation reduces cerebral blood flow
• IMPACT: Accounts for 15-25% of all strokes
• ASSESSMENT:
• • Carotid BRUIT or THRILL on auscultation
• • Symptoms: Visual changes, syncope, TIA symptoms
• INTERVENTION: Endarterectomy or stenting if occlusion >70%

Post-Carotid Endarterectomy Nursing

• AIRWAY MONITORING: Watch for stridor, edema (surgical site near airway)
• CRANIAL NERVE ASSESSMENT:
• • CN IX (Glossopharyngeal): Swallowing difficulty
• • CN X (Vagus): Hoarseness, vocal changes
• • CN XII (Hypoglossal): Tongue deviation
• BLOOD PRESSURE CONTROL: Maintain <160 mmHg to prevent bleeding
• NEUROLOGICAL CHECKS: Frequent assessment for stroke signs

📊 Arterial vs Venous Insufficiency

• ═══════════════════════════════════════════════════════════════════════════════════════════════
• FEATURE │ ARTERIAL │ VENOUS
• ═══════════════════════════════════════════════════════════════════════════════════════════════
• Pain Character │ Claudication (cramping │ Crampy, aching pain
• │ with walking), rest pain │
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Temperature │ COOL (poikilothermia) │ WARM
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Skin Changes │ Pale, shiny, hairless │ Brown pigmentation at
• │ │ ankles, stasis dermatitis
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Edema │ Minimal or absent │ SIGNIFICANT edema
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Pulses │ DIMINISHED or ABSENT │ Present
• ═══════════════════════════════════════════════════════════════════════════════════════════════

Acute Arterial Occlusion - The 6 Ps

• ═══ CRITICAL LIMB ISCHEMIA SIGNS ═══
• 1. PAIN - Severe, sudden onset
• 2. PALLOR - Pale, waxy appearance
• 3. PULSELESSNESS - No distal pulses
• 4. PARESTHESIA - Numbness, tingling
• 5. PARALYSIS - Cannot move extremity (late sign)
• 6. POIKILOTHERMIA - Cold (unable to regulate temperature)
• TREATMENT:
• • Bypass grafting for larger vessels
• • Fibrinolysis for smaller vessels
• • Fasciotomy if compartment syndrome develops
• THIS IS A SURGICAL EMERGENCY - "Time is muscle"

Venous Insufficiency & DVT

• SYMPTOMS: Crampy pain, warm extremities, edema, brown ankle pigmentation
• DVT RISK FACTORS: Virchow triad - Stasis, Endothelial injury, Hypercoagulability
• PREVENTION: Ambulation, anticoagulation, SCDs
• ⚠️ WARNING: Do NOT use compression sleeves on existing DVT (risk of embolization)
• TREATMENT: Anticoagulation, elevation, eventually compression after acute phase

Structural Heart Disease & Emergencies

Cardiac Tamponade Detailed

• Fluid accumulation in pericardial space compresses heart
• ═══ BECK'S TRIAD ═══
• 1. JVD (Jugular Venous Distension)
• 2. Hypotension
• 3. Muffled/distant heart sounds
• PULSUS PARADOXUS: SBP drop >10 mmHg during inspiration
• • Inspiration increases venous return to right heart
• • Compressed heart cannot accommodate → LV filling decreases
• • Stroke volume and BP drop during inspiration
• TREATMENT: Pericardiocentesis (emergent fluid removal)

Endocarditis

• Bacterial infection causing vegetation on heart valves
• USUALLY AFFECTS LEFT-SIDED VALVES (mitral, aortic)
• RISK FACTORS: IV drug use, prosthetic valves, dental procedures
• CLASSIC SIGNS:
• • Petechiae (skin, conjunctivae)
• • Splinter hemorrhages (nail beds)
• • Osler nodes (painful, fingers/toes)
• • Janeway lesions (painless, palms/soles)
• DIAGNOSIS: Duke criteria, blood cultures, echocardiogram
• TREATMENT: Prolonged IV antibiotics (4-6 weeks), may need valve surgery

Pericarditis

• Inflammation of the pericardial sac
• CLASSIC SYMPTOMS:
• • Sharp chest pain RELIEVED by sitting up and leaning forward
• • Worsened by lying flat, deep breathing
• • Pericardial friction rub on auscultation
• EKG FINDINGS: DIFFUSE ST elevation (not confined to coronary territory)
• CAUSES: Viral (most common), post-MI (Dressler syndrome), uremia, autoimmune
• TREATMENT: NSAIDs, Colchicine
• ⚠️ WATCH FOR: Progression to tamponade (worsening symptoms, Beck's triad)

📊 Aortic Dissection vs Rupture

• ═══════════════════════════════════════════════════════════════════════════════════════════════
• FEATURE │ DISSECTION │ RUPTURE
• ═══════════════════════════════════════════════════════════════════════════════════════════════
• Pathology │ Tear between arterial │ Complete perforation
• │ layers (false lumen) │ of vessel wall
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Presentation │ Sudden severe chest pain, │ Sudden severe pain,
• │ "tearing" quality, │ PROFOUND HYPOTENSION,
• │ radiating to back │ Shock, syncope
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Blood Pressure │ May be hypertensive │ HYPOTENSIVE (bleeding out)
• ─────────────────────────────────────────────────────────────────────────────────────────────────
• Priority │ BP CONTROL critical │ RAPID TRANSFUSION,
• Treatment │ (Nipride, Beta-blockers) │ Emergent surgery
• ═══════════════════════════════════════════════════════════════════════════════════════════════
• ⚠️ NIPRIDE TOXICITY: Watch for thiocyanate toxicity with prolonged use

Cardiac Cycle Dynamics

Understanding the Cardiac Cycle

• One complete heartbeat from beginning of one contraction to the next
• Composed of systole (contraction/ejection) and diastole (relaxation/filling)
• Duration varies inversely with heart rate
• At 60 bpm: cycle lasts 1 second (systole 30%, diastole 70%)
• At 120 bpm: cycle lasts 0.5 seconds (systole 60%, diastole 40%)

Systole and Diastole Proportions

• At rest (60 bpm): Diastole dominates at 70% - optimal filling time
• At 90 bpm: Diastole reduced to 55% of cycle
• At 120 bpm: Diastole only 40% - filling time significantly reduced
• Higher HR = proportionally more time in systole, less in diastole
• Tachycardia compromises ventricular filling time

Clinical Significance for Critical Care

• Shortened diastole decreases coronary perfusion (occurs during diastole)
• Rapid heart rates can compromise preload and stroke volume
• Patients with diastolic dysfunction are sensitive to rate increases
• Heart rate control crucial in ischemia and heart failure
• Beta blockers extend diastole, improving filling and coronary flow

Phases of Ventricular Systole

• Isovolumetric contraction: Ventricles contract, all valves closed
• Rapid ejection: Aortic/pulmonic valves open, blood ejected rapidly
• Reduced ejection: Flow slows as pressure equalizes
• About 2/3 of stroke volume ejected in first 1/3 of systole

Phases of Ventricular Diastole

• Isovolumetric relaxation: Ventricles relax, all valves closed
• Rapid filling: AV valves open, blood rushes into ventricles
• Diastasis: Slow passive filling from atria
• Atrial contraction (atrial kick): Contributes 15-25% of ventricular filling
• Loss of atrial kick (AFib) reduces cardiac output by 15-25%

Cardiac Waveforms & Hemodynamic Monitoring

ECG and Arterial Waveform Correlation

• ECG represents electrical activity; arterial waveform represents mechanical output
• QRS complex triggers ventricular contraction → systolic upstroke
• T wave corresponds with ventricular repolarization → diastolic phase
• Time delay between electrical and mechanical events is normal
• Arrhythmias visible on ECG will affect arterial waveform

Arterial Waveform Components

• Systolic upstroke: Rapid rise as ventricle ejects blood
• Systolic peak: Maximum arterial pressure
• Dicrotic notch: Represents aortic valve closure
• Diastolic runoff: Gradual decline as blood flows to periphery
• Diastolic pressure: Lowest point before next systole

Central Venous Pressure (CVP) Waveform

• A wave: Atrial contraction (absent in AFib)
• C wave: Tricuspid valve bulging during isovolumetric contraction
• X descent: Atrial relaxation and downward movement of tricuspid valve
• V wave: Atrial filling against closed tricuspid valve
• Y descent: Tricuspid valve opens, blood flows into ventricle

Pulmonary Artery Waveform

• Similar to arterial waveform but at lower pressures
• Normal PA systolic: 20-30 mmHg
• Normal PA diastolic: 8-15 mmHg
• Elevated PA pressures suggest pulmonary hypertension or left heart failure
• PAWP obtained by inflating balloon and measuring "wedge" pressure

Waveform Troubleshooting

• Dampened waveform: Air in line, clot, kinked catheter, hypotension
• Overdamped: Loss of dicrotic notch, falsely low systolic
• Underdamped: Exaggerated oscillations, falsely high systolic
• Catheter whip: Excessive movement creating artifact
• Square wave test: Used to assess dynamic response of system