Cardiovascular System: Shock

Week 1: Shock

• Definition of Shock: Life-threatening circulatory failure resulting in cellular and tissue hypoxia, characterized by insufficient blood flow and an imbalance of oxygenated and non-oxygenated blood in the body.
• Impact on Cardiac Output:
  • Decreased stroke volume due to fluid loss
  • Increased heart rate as the heart tries to compensate
  • Overall decrease in cardiac output
  • Impaired tissue perfusion leading to organ dysfunction and failure
• Clinical Manifestations of Shock:
  • Hypotension
  • Altered mental state
  • Tachycardia
  • Elevated respiratory rate
  • Decreased urine output
  • Hypoxia
  • Delayed capillary refill
  • Elevated lactate levels
  • Mottled, clammy skin
  • Metabolic acidosis

Types of Shock and Treatment

• Distributive Shock:
  • Causes: sepsis, anaphylaxis, neurogenic
  • Characterized by vasodilation, decreased systemic vascular resistance, and redirected blood flow away from vital organs
  • Treatment: Sepsis 6, treat underlying cause, and provide pain relief
• Cardiogenic Shock:
  • Causes: heart damage or dysfunction (MI, arrhythmias, myocarditis, cardiomyopathy)
  • Treatment: reperfusion therapy, cardioversion
• Hypovolemic Shock:
  • Causes: decreased circulating blood volume (bleeding, trauma, dehydration)
  • Treatment: haemorrhage control, surgical intervention, IV fluids, blood products, and TXA
• Obstructive Shock:
  • Causes: physical obstruction to blood flow (PE, pneumothorax, cardiac tamponade, aortic stenosis)
  • Treatment: thrombolytic, decompression, removal of pericardial fluid

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Week 2: Respiratory Anatomy, Physiology, and Assessment

Systemic vs Pulmonary Circulation

• Pulmonary Circulation:
  • Function: facilitates gas exchange in the lungs
  • Pathway: pulmonary arteries, capillaries, and pulmonary veins
  • Operates under lower pressure to prevent lung damage and facilitate gas exchange
• Systemic Circulation:
  • Function: delivers oxygenated blood to body tissues and returns deoxygenated blood to the heart
  • Pathway: arteries, arterioles, capillaries, venules, and veins
  • Operates under higher pressure due to the pumping action of the left ventricle and peripheral resistance

Oxygen Delivery

• Variables of O2 Delivery:
  • Cardiac output (CO)
  • Haemoglobin (Hb) concentration
  • SaO2 (percentage of haemoglobin bound to oxygen)
  • PaO2 (partial pressure of oxygen in arterial blood)
• Steps of Oxygen Delivery:
  1. O2 available to breathe
  2. Airway - into the alveoli
  3. Transmembrane diffusion (A-a gradient)
  4. Vascular - red cells available for binding
  5. Cardiac output - blood moving to take O2 to tissues
  6. Hb releasing O2 adequately - tissue uptake
  7. Use of O2 by tissue

Lactate Levels

• Elevated lactate levels: indicate anaerobic metabolism due to inadequate oxygen supply, tissue hypoxia, hypoperfusion, or impaired lactate clearance

Oxyhaemoglobin Dissociation Curve

• Shift to the left:
  • Lungs: oxygen has a higher affinity for haemoglobin in alkalotic conditions
  • Lower temperature
  • Higher oxygen levels
  • More affinity - holds onto oxygen
  • Less 2,3 DPG
• Shift to the right:
  • Muscles/placenta: oxygen has a lower affinity for haemoglobin in acidic conditions
  • Higher temperature
  • Higher CO2 levels
  • Less affinity - needs to unload oxygen
  • More 2,3 DPG

Hypoxia vs Hypoxemia

• Hypoxemia: low oxygen levels in arterial blood (measured by PaO2)
• Hypoxia: condition where tissues are deprived of adequate oxygen supply

V/Q Mismatch

• Definition: imbalance between ventilation and perfusion in the lungs, leading to impaired gas exchange and hypoxemia
• Consequences:
  • Shunting effect: blood passes through poorly ventilated alveoli without efficient gas exchange
  • Dead space: areas with adequate ventilation but reduced perfusion, contributing to wasted ventilation

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Week 3: Acute Respiratory Failure and Common Respiratory Disorders

Definition of Respiratory Failure

• Respiratory failure: respiratory system fails to perform gas exchange (oxygenation or elimination of carbon dioxide)
• Type 1 Respiratory Failure: failure to oxygenate (PaO2 < 60 mmHg)
• Type 2 Respiratory Failure: failure to ventilate (PaCO2 > 45 mmHg)

Management of Respiratory Failure

• Treatment: address underlying cause, improve gas exchange, and support respiratory function
• Supplemental oxygen: improves oxygenation and reduces work of breathing
• Mechanical ventilation: supports respiratory function in severe cases

Causes of Respiratory Failure

• Airway disease
• Lung disease
• Pulmonary circulation
• Pulmonary oedema

Clinical Features of Respiratory Failure

• Dependent on the degree of:
  • Hypoxaemia
  • Hypercarbia
  • Acidosis

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Week 4: Invasive and Non-Invasive Ventilation

Principles of Oxygen Therapy

• Oxygen therapy: administration of oxygen as a medical intervention to maintain adequate tissue oxygenation
• Primary goals:
  • Correct hypoxemia: increase oxygen levels in the blood
  • Reduce work of breathing: decrease effort required to breathe
  • Reduce myocardial workload: lower oxygen demand on the heart

Delivery Systems

• Low-flow systems:
  • Nasal specs
  • Simple face mask
  • Non-rebreather
• High-flow systems:
  • Nasal high flow
  • NIV
  • IPPV

Physiological Dangers of Oxygen Therapy

• CO2 retention: high oxygen levels can reduce the hypoxic drive to breathe, leading to respiratory acidosis
• V/Q mismatch: high oxygen levels can worsen ventilation-perfusion mismatch, leading to increased dead space

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Week 5: Cardiovascular Anatomy and Physiology

Properties of Cardiac Cells

• Automaticity: cardiac cells can generate electrical impulses spontaneously
• Excitability: cardiac cells respond to electrical stimuli by depolarizing and generating action potentials
• Conductivity: cardiac cells can propagate electrical impulses rapidly through intercalated discs and gap junctions
• Contractility: cardiac cells contract in response to depolarization, leading to the pumping action of the heart
• Rhythmicity: synchronized action of cardiac cells ensures rhythmic beating of the heart
• Ion channel regulation: specialized ion channels regulate the flow of ions across the cell membrane, crucial for action potential generation and contraction

Cardiac Cycle

• Atrial contraction (atrial systole):
  • Initiated by depolarization of the atria
  • Causes contraction, increasing atrial pressure and forcing blood into the ventricles
• Ventricular filling (early diastole):
  • Ventricles relax, lowering pressure and allowing blood from the atria to fill them### Cardiac Function and Blood Pressure Regulation
• Atrioventricular valves open due to higher atrial pressure than ventricular pressure, while semilunar valves remain closed
• Ventricular contraction (systole) triggers atrioventricular valve closure, increasing ventricular pressure and opening semilunar valves to eject blood into the pulmonary artery and aorta
• Ventricular relaxation (diastole) leads to semilunar valve closure, atrioventricular valve reopening, and refilling of ventricles

Blood Pressure Regulation

• Blood pressure (BP) is the force exerted by circulating blood against arterial walls
• Autonomic nervous system (ANS) regulates BP through sympathetic nervous system (SNS) and parasympathetic nervous system (PNS)
  • SNS releases norepinephrine, causing vasoconstriction and increased heart rate
  • PNS releases acetylcholine, causing vasodilation and decreased heart rate
• Renin-angiotensin-aldosterone system (RAAS) regulates BP through:
  • Renin release, triggered by low BP or SNS stimulation, converting angiotensinogen to angiotensin I
  • Angiotensin-converting enzyme (ACE) converting angiotensin I to angiotensin II, a potent vasoconstrictor
  • Aldosterone release, promoting sodium and water reabsorption by the kidneys, increasing blood volume and pressure
• Kidneys regulate BP through renal regulation of sodium and water retention/excretion, influenced by RAAS and atrial natriuretic peptide (ANP)

Cardiac Output and Cardiovascular Disease

• Cardiac output (CO) is the volume of blood pumped by the heart per minute, calculated as CO = Heart Rate (HR) × Stroke Volume (SV)
• Factors affecting cardiac output include:
  • Heart rate (HR)
  • Stroke volume (SV)
• Cardiovascular disease can impact cardiac output, including:
  • Heart failure: reduced cardiac output due to impaired heart function
  • Hypertension: increased systemic vascular resistance leading to increased workload on the heart and potentially reduced cardiac output
  • Coronary artery disease (CAD): reduced blood flow to the heart muscle, impairing its ability to pump effectively and reducing cardiac output
  • Arrhythmias: abnormal heart rhythms affecting heart rate and cardiac output

Myocardial Oxygen Supply and Demand

• Coronary blood flow determines myocardial oxygen supply, influenced by:
  • Coronary artery diameter and resistance
  • Systemic blood pressure
  • Diastolic perfusion pressure
  • Autoregulation
• Oxygen content of coronary blood depends on:
  • Systemic arterial oxygen content
  • Coronary venous oxygen extraction
• Endothelial function maintains vascular tone and regulates coronary blood flow
• Collateral circulation provides alternate pathways for blood flow to the myocardium in the presence of coronary artery occlusion
• Factors affecting myocardial oxygen demand include:
  • Heart rate
  • Contractility
  • Preload (volume of blood in the ventricles at the end of diastole)
  • Afterload (resistance against which the heart must pump)

Coronary Arteries and Conduction Pathway

• Left coronary artery (LCA) branches into:
  • Left anterior descending (LAD) artery, perfusing the anterior wall and septum
  • Left circumflex (LCx) artery, perfusing the lateral wall
• Right coronary artery (RCA) branches into:
  • Posterior descending (PDA) artery, perfusing the back wall
  • Right marginal artery, perfusing the right side
• The conduction pathway includes:
  • SA node, initiating the impulse
  • AV node, delaying the impulse briefly
  • Bundle of His and its branches (right and left bundle branches, Purkinje fibers), ensuring coordinated contraction of the heart chambers

Rhythm Analysis and Bundle Branch Block

• Interpret a rhythm strip systematically, considering:
  • Calibration and patient details
  • Rhythm regularity or irregularity
  • Rate (atrial and ventricular)
  • P-wave presence and morphology
  • PR interval
  • QRS complex duration and morphology
• Identify bundle branch blocks, including:
  • Right bundle branch block (RBBB): wide QRS complex with rSR' morphology in lead V1
  • Left bundle branch block (LBBB): wide QRS complex with W morphology in lead V1
• Bundle branch blocks can indicate underlying cardiac pathology and may require management with devices like pacemakers

Junctional and Ventricular Arrhythmias

• Junctional rhythm originates from the AV node, resulting in:
  • Abnormal heart rhythm
  • No relationship between P waves and QRS complexes
  • QRS complex duration and morphology
• Junctional escape rhythm has a rate of 40-60 bpm
• Mechanisms of junctional and ventricular arrhythmias include:
  • Abnormal automaticity
  • Reentry
  • Triggered activity

12-Lead ECG and Axis Deviation

• Identify cardiac axis and axis deviation on a 12-lead ECG:
  • Normal cardiac axis: positive reflections in leads I and II
  • Right axis deviation: negative reflection in lead I, positive in lead III
  • Left axis deviation: positive reflection in lead I, negative in leads II and III
• Relate ECG leads to coronary territories:
  • Anterior leads (V1-V4): LAD territory (anterior wall)
  • Lateral leads (I, aVL, V5-V6): LCx territory (lateral wall)
  • Inferior leads (II, III, aVF): RCA or LCx territory (inferior wall)
  • Right ventricular leads (V1-V2): RCA territory (right ventricle)

Bundle Branch Block and Clinical Significance

• Bundle branch block refers to a delay or blockage in conduction down one of the bundle branches
• Right bundle branch block (RBBB) and left bundle branch block (LBBB) have distinct ECG features
• Bundle branch blocks can indicate underlying cardiac pathology and may require management with devices like pacemakers

Acute Coronary Syndrome and Sepsis

• Acute coronary syndrome (ACS) refers to a spectrum of conditions associated with sudden, reduced blood flow to the heart
• Categories of ACS include:
  • Unstable angina (UA)
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)
• ACS is diagnosed based on symptoms, ECG findings, and biomarkers
• Sepsis is a clinical syndrome characterized by life-threatening organ dysfunction
• Causes of sepsis include infections, pathogens, and underlying conditions
• Management of sepsis involves fluids, vasopressors, antibiotics, and supportive care

Hemodynamic Monitoring and Vasoactive Medications

• Inotropes, chronotropes, and vasopressors are used in critically ill patients
• Inotropes increase cardiac contractility, chronotropes affect heart rate, and vasopressors cause vasoconstriction
• Examples of inotropes include dobutamine, dopamine, and milrinone
• Vasopressors include norepinephrine, epinephrine, vasopressin, and phenylephrine
• Hemodynamic monitoring involves balancing cardiac output with peripheral resistance and blood pressure

Massive Transfusion and Hypertensive Crisis

• Critical bleeding is associated with hemodynamic instability, coagulopathy, and organ dysfunction
• Massive transfusion can lead to complications such as coagulopathy, metabolic disturbances, volume overload, and transfusion reactions
• Nursing care during massive transfusion involves monitoring, fluid and electrolyte management, coagulopathy management, and temperature management
• Hypertension is a major public health burden, and hypertensive crisis requires prompt management to prevent end-organ damage