W8-Cardiology Flashcards
Function of the circulatory system
The main function of the circulatory system is to deliver oxygen,
nutrients, and
hormones to
various cells and tissues throughout the body and
to remove metabolic wastes such as carbon dioxide and nitrogenous wastes
Oxygen extraction and general oxygenation via coronary arteries
Etiology: The coronary arteries arise from the aorta and supply oxygen-rich blood to the myocardium.
Pathophysiology: They extract oxygen from blood that is ejected by heart contractions and deliver it to heart muscle tissues critical for sustaining cardiac function.
Manifestations: Proper function manifests as normal cardiac function, while blockage or disease results in myocardial ischemia.
Diagnostics: Evaluated using angiography or coronary CT angiograms.
Clinical course: Compromise can lead to myocardial infarction.
Other: Preventative measures include managing risk factors such as HTN & HLD
RCA: (RV), R marginal branch (RV to apex) & post desc branch
LCA: LAD (L/R vent and septum) and Circ (LA and lateral wall of LV)
Blood flow through the heart
Periph ➡️ I/SVC➡️ RA ➡️ Tricuspid Valve ➡️ RV
➡️ Pulmonic Valve ➡️ Pulmonary Artery (deoxygenated) ➡️ Lungs
Lungs 🫁 ➡️ Pulmonary Vein (+O2) ➡️ LA
➡️ Mitral Valve ➡️ LV ➡️aortic valve➡️
aorta 🫀➡️ Periphery
Blood Flow by Diastole and Systole
■ During DIASTOLE, blood flows into the atria, the atrioventricular valves are pushed open, and blood begins to fill the ventricles. Atrial systole squeezes the blood remaining in the atria into the ventricles.
■ During ventricular SYSTOLE, the ventricles contract, pushing the blood out through the semilunar valves into the pulmonary artery (right ventricle) and the aorta (left ventricle).
Influencers of blood flow through the vasculature- what 3 factors could determine this?
Vessel diameter: Vasoconstriction reduces diameter, slowing flow, while vasodilation increases it. (pressure)
Blood (viscosity): Higher viscosity increases resistance, impeding flow. (or opposition to Bflo, diameter/length of BV contributes, vessel radius)-High Hct
(resistence)
Cardiac output: The amount of blood the heart pumps influences overall flow through the vasculature.
Velocity: distance blood travels in a unit of time
High hematocrit reduces the flow through the blood vessels
Done by: baroreceptors, chemoreceptors, arterial pressure effects, epi/norepi-vasoconstrict, ADH Antidiuretic-Increase blood volume by reabsorption of water from the distal tubule and collecting duct of nephron,
RAAS: Aldosterone: stimulates reabsorption of sodium, chloride and water to increase blood volume and stimulate thirst
Angiot-II: vasoconstrict
Nat-peptides: Cause loss of sodium, chloride, and water through their effects of kidney function and decreased blood flow.
Tell me about Baroreceptors
Nerve cells in aortic arch or carotid sinus
can decr preload or dias filling, thereby decr CO
Pressure/stretch
Bain Bridge Reflex w/vagus nerve
ex: if CPB get less stretched, effects reverse: dec HR, dec ANP, Incr ADH= decr H20/NA excretion, restoring blood volume
Decr CO since the BP is roughly greater than COx total periph resistance
Venous stasis ulcers
Etiology: Typically occur due to chronic venous insufficiency.
Pathophysiology: Blood pools in veins causing pressure that leads to ulcers on the skin.
Manifestations: Painful ulcers, typically on the lower limbs.
Diagnostics: Clinical examination and Doppler U/S (venous insuff), ABI’s (r/o arterial ds)
Clinical course: Can lead to infections and more severe complications.
Other: Compression stockings and proper wound care can prevent progression.
TX: elevation, compression stockings/bandages; skin grafting, endovenous ablation, sclerotherapy, phlebectomy, or vein bypass.
Risks for DVT, and Ischemic Heart Disease
Etiology: Commonly arises from blood clotting abnormalities (DVT) and atherosclerosis (Ischemic Heart Disease), increased O2 demands, pregnancy, cancer, genetics, oral Birth control, obesity, smoking
Pathophysiology: DVT involves clots in deep veins, whereas ischemic injury to cardiac muscle is due to reduced coronary blood flow.
Manifestations: DVT presents as limb swelling and pain; Ischemic Heart ds as chest pain or heart attack.
**Virchow’s Triad: **
-venous stasis
-Venous endothelial damage
-hypercoaguable states
Diagnostics: U/s for DVT; cardiac stress tests and angiography for Ischemic Heart Disease.
Clinical course: Both can be fatal if untreated. dysrhymias, HF, CRF
Other: Preventative strategies include lifestyle modification and medication adherence
*NSaids are linked to CAD related ischemic events
RHF manifestations versus LHF manifestations (think physical exam)
RHF: usually d/t LHF; RV too weak to pump B. to lungs,
leads to back up of fluid in the system=fluid retention/edema
s/s: fluid retention; swelling (legs/feet), heart palpitations and wt gain.
Can be c/b: COPD, pulm emb, and pulm HTN.
LHF: when LV fails to pump B. to periph
MC than RHF
2 types:
systolic (HFrEF)-loss of contractility
Dia (HFpEF) LV stiff, no relax=not approp filling
S/s: DOE/SOA, cough esp w/ phys
C/b: CAD, MI, long-term HTN
Interpretation of cardiac lab markers (CKMB/troponin etc) and role of the ECG
Both rise within 2-4 hours,
troponin stays elevated for 7-10 days after event
Troponin-cardiac specific
CKMB- non cardiac specific-can also indicate skeletal muscle damage (rhabdomyolysis)
ECG: detect electrical changes in the heart,
MI- Areas of Infarct and ECG changes to expect-extra
ACS s/s and what to treat first
Patho of ACS on 1079 figure 32.4
Etiology: Occurs due to sudden, reduced blood flow to the heart.
Pathophysiology: Plaque rupture and subsequent clot formation restrict coronary blood flow.
Manifestations: Chest pain (stable and unstable) , nausea, heartburn-like symptoms, or breathlessness.
*Classic: Sudden/Severe CP, SOA, Pallor, diaphoresis.
W/ DM-neurpathy may not have symptoms “Silent”
Diagnostics: ECG and cardiac biomarkers.
STMI and NSTEMI
Clinical course: Without treatment, can lead to heart damage or death.
Other: Immediate treatment includes aspirin and anticoagulants to minimize heart damage.
Stable and Unstable Angina-Extra
Unstable Angina: angina occurring at rest, unrelieved with
nitroglycerin, angina that increase in severity or frequency, dyspnea, diaphoresis and
anxiety.
Stable: attacks have a trigger (such as stress or exercise) and stop within a few minutes of resting
Prinzmetal agina: vasoplastic/vasospasmic, Levin’s sign (fist over chest), transmural ischemia
Causes of HF
● CAD – where the arteries that supply blood to the heart become clogged up with fatty substances (atherosclerosis), which may cause angina or a heart attack
● HTN – this can put extra strain on the heart, which over time can lead to heart failure
● conditions affecting the heart muscle (cardiomyopathy)
● heart rhythm problems (arrhythmias), such as Afib
● damage or other problems with the heart valves
● congenital heart disease – birth defects that affect the normal workings of the heart
Obesity, anemia, etoh, hyperthyroid, pulm HTN
Pathophysiology: Impaired cardiac function leads to insufficient blood flow to meet the
bodys needs.
Manifestations: Fatigue, dyspnea, and fluid retention.
Diagnostics: Echocardiography, ECG, cardiac MRI.
Clinical course: Can progress to severe, life-limiting conditions.
Other: Management includes lifestyle changes, medications, and possibly surgical
interventions.
Hypertensive organ damage
- Etiology: Chronic systolic HTN causing damage to body organs.
- Pathophysiology: Persistent pressure load leads to arterial damage and subsequent organ impairment.
- Manifestations: May be asymptomatic initially; later, organ dysfunction becomes apparent.
- Diagnostics: Blood pressure monitoring, organ function tests (e.g., kidney, heart, brain, eyes).
- Clinical course: Can lead to chronic kidney disease, heart failure, or vision loss.
- Other: Control of hypertension through lifestyle and medication is crucial.
Weight reduction and increased physical activity effects
- Etiology: Lifestyle modifications aimed at improving health.
- Pathophysiology: Reduces the body’s fat stores, improves metabolism, and increases functional capacity.
- Manifestations: Weight loss, improved physical fitness, enhanced metabolic profiles.
- Diagnostics: BMI, lipid profiles, glucose tolerance tests.
- Clinical course: Reduces risk of chronic conditions like type 2 diabetes, heart disease.
- Other: Sustainable changes entail a balanced diet and regular physical activity.
USA presentation
(Assumed topic is general health care or heart health in the USA)
Etiology: State of healthcare influencing disease prevalence and management.
Pathophysiology: Lifestyle, healthcare access, and preventive care play roles in the
national health profile.
Manifestations: Variability in disease prevalence and health outcomes across different
populations.
Diagnostics: Nationwide health statistics and disease incidence reports.
Clinical course: Impacts public health policies and healthcare provisions.
Other: Ongoing need for improved healthcare access and preventive measures.
Metabolic syndrome - what is it?
- Etiology: Defined by a cluster of conditions including high blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol levels.
- Pathophysiology: Increases risk for heart disease, diabetes, and stroke. by atherosclerosis and endothelial damage over time
- Manifestations: Often asymptomatic until complications arise.
- Diagnostics: Physical exam, blood tests for glucose and lipid levels.
- Clinical course: Can lead to more severe metabolic disorders.
- Other: Management involves addressing each of the components through lifestyle and medications.
